Endurance Sports Medicine: A Clinical Guide [2nd ed. 2023] 3031265998, 9783031265990

Table of contents :
Contents
Contributors
Part I: Medical Conditions
1: Taking a Holistic Approach to Treating Endurance Athletes
Introduction
Behavioral Health
Nutrition
Compression Garments
Hydrotherapy
Acupuncture
Dry Needling
Iontophoresis
Ultrasound
Kinesiology Tape
Blood Flow Restriction
Conclusion
References
2: Cardiovascular Evaluation and Treatment in the Endurance Athlete
Introduction
Pre-Participation Cardiovascular Screening
History and Physical Examination
Masters Athletes
Young Athletes
Dose
Exercise-Induced Cardiac Remodeling
Overview of Exercise Physiology and the Cardiovascular System
Remodeling of the Cardiac Chambers
Aortic Adaptation
Electrical Remodeling
Demographic Impact on EICR
Approach to Cardiovascular Symptoms
Chest Pain
Syncope
Palpitations
Approach to Athletes with Established Cardiovascular Disease
Atherosclerotic Cardiovascular Disease (ASCVD)
Atrial Fibrillation
Hypertension
COVID-19
Conclusion
References
3: Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction
Chapter
Vocal Cord Dysfunction
References
4: Low Ferritin and Anemic Conditions in Endurance Athletes
Introduction
Clinical Presentation
The Function of Iron
Causes of Iron Deficiency
Diet and Nutrition
Iron Absorption
Diagnostic Testing: Hematologic Markers
Stages of Iron Deficiency
Sports Anemia (Dilutional Anemia)
Sources of Iron Loss in Athletes
Intravascular Hemolysis
Gastrointestinal
Renal
Metabolic Disturbances
Genetics and Medications
Extravascular Hemolysis
Sweat
Exercise
Menses and Hypothalamic Dysfunction
Dietary Needs and Treatment
Iron Supplementation and Periodization
Conclusion
References
5: Evaluation and Treatment of Exertional Heat Illness, Rhabdomyolysis, and Hyponatremia
Exertional Heat Illness
Introduction
Epidemiology and Risk Factors
Pathophysiology
Diagnosis
Treatment
Return to Play
Prevention
Exercise-Associated Hyponatremia
Introduction
Epidemiology and Risk Factors
Pathophysiology
Diagnosis
Treatment
Return to Play
Prevention
Exertional Rhabdomyolysis
Introduction
Epidemiology and Risk Factors
Pathophysiology
Diagnosis
Treatment
Outpatient Treatment
Inpatient Treatment
Return to Play and Prevention
References
6: Evaluation and Treatment of Cold- and Altitude-Related Injuries and Illnesses
Part 1: Cold-Related Injuries and Illnesses
Hypothermia
Hypothermia Diagnosis
Hypothermia Treatment
Hypothermia Prevention
Frostbite
Frostbite Treatment
Chilblains
Nonfreezing Cold Injury
Raynaud’s
Cold Agglutinin Syndrome
Cold-Induced Urticaria
Cold Effect on Chronic Medical Conditions
Part 2: Altitude Medicine
High-Altitude Physiology
High-Altitude Pathophysiology
High-Altitude Illness Risk Factors
High-Altitude Illness: Acute Mountain Sickness
Diagnosis
Prevention
Gradual Ascent
Medication Prophylaxis
Treatment
High-Altitude Illness: High-Altitude Cerebral Edema
Diagnosis
Prevention
Treatment
High-Altitude Illness: High-Altitude Pulmonary Edema
Diagnosis
Prevention
Treatment
High-Altitude Pathology: High-Altitude De-Acclimation Syndrome
Diagnosis
Prevention and Treatment
References
7: Pregnancy and Other Considerations for the Female Endurance Athlete
Introduction
The Menstrual Cycle and the Endurance Athlete
Female Athlete Triad/RED-S and Long-Term Health/Contraception Issues
Pathogenesis
Investigations
Management
Pregnancy and the Endurance Athlete
Physiological Adaptations to Pregnancy
Cardiorespiratory Adaptations
Metabolic Adaptations
Thermoregulation
Effects of Endurance Exercise on Maternal and Fetal Health
Guidelines for Exercise during Pregnancy (See Fig. 7.1 [67])
Considerations for Pregnant Endurance Athletes
Postpartum and the Endurance Athlete
Physiological Adaptations
Considerations for the Postpartum Endurance Athlete
Menopause and Exercise in the Masters Athlete
Bone Health
Cardiorespiratory Health
Menopausal Symptoms
Summary
References
8: Considerations for Treating the Pediatric Endurance Athlete
Introduction
Recommendations for Youth Participation in Running as a Sport
Potential Health Concerns Related to Endurance Training
Apophyseal Injuries
Tendon Injuries
Bone Stress Injury (BSI)
Low Energy Availability in the Youth Runner
Overtraining Syndrome
Risk Factors for Running-Related Injuries
Intrinsic Factors
Growth-Related
Age
Female Gender
Body Mass Index (BMI)
Bone Health
Alignment and Strength
Prior Injury
Extrinsic Factors
Training Characteristics: Volume, Intensity, Terrain, and Footwear
Biomechanical Factors: Cadence and Footstrike Mechanics
Sports Specialization
Injury Screening Tools and Preventative Strategies
Conclusions
References
9: Effects of Exercise and Aging in the Masters-Level Athlete
Performance Changes
Cardiopulmonary Changes
Musculoskeletal Changes
Metabolic, Psychosocial, and Nutritional Impact
Conclusions
References
Part II: Musculoskeletal Conditions
10: Biologic Advancements in the Treatment of Stress Fractures
Introduction
Pathophysiology and Risk Stratification
Taking a Holistic Approach
Biologic Healing Enhancement
Conclusion
References
11: Orthobiologic Treatment Options for Injuries in Endurance Athletes
Introduction
What Are Orthobiologics?
Platelet-Rich Plasma
Advanced Autologous Cellular Therapy
Bone Marrow Concentrate (BMC)
Adipose
Birth-Product Injectables
Culture-Expanded Mesenchymal Stem Cells
Orthobiologic Use in Lower Limb Pathologies
Hamstring Pathology
A Practical Clinical Perspective
Technical Pearls for Optimizing Patient Experience and Clinical Outcomes
Sterility
Peri- and Post-Procedural Pain Control
Joint Injections
Tendon Injections
Conclusion
References
12: Special Considerations for the Periodic Health Evaluation of Endurance Athletes
Introduction to the PHE
Start with Why PHE Design Strategy
Choosing the Elements of the PHE
Health History and Physical Examination
Cardiovascular Screening
Hematologic Screening
Musculoskeletal Screening and Functional Evaluations
The Role of Body Composition and Bone Density Measurement in the Endurance Athlete
Putting it all Together
References
13: Chronic Leg Pain in Running Athletes
Introduction
Evaluation
Medial Tibial Stress Syndrome
Chronic Exertional Compartment Syndrome
Popliteal Artery Entrapment Syndrome
Stress Fractures
Nerve Entrapments
Conclusion
References
14: Hip Injuries and Conditions in the Endurance Athlete
Introduction
Anatomy
Layer I
Layer II
Layer III
Layer IV
History
Physical Examination
Inspection
Palpation
Motion, Strength, and Special Testing
Imaging Evaluation
Differential Diagnosis Evaluation
Treatment
Conclusions
References
15: Common Injuries and Conditions in Rowers
Introduction
Rowing Stroke
Back
Lower Extremity
Hip Impingement
Knee
Ribs and Upper Extremity
Rib Stress Fracture
Upper Extremity Deep Vein Thrombosis and Thoracic Outlet Syndrome
Shoulder Instability and Dislocation
Forearm Compartment Syndrome
Intersection Syndrome
Skin
References
16: Common Injuries and Conditions in Crossfit Participation
Introduction
Weightlifting
Endurance
Gymnastics
Other
Conclusion
References
17: Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation
Introduction
Blood Flow Restriction
Mechanism
Clinical Application
Safety and Side Effects
Conclusion
Dry Needling
Mechanism
Clinical Application
Safety and Side Effects
Conclusion
Cryotherapy
Safety and Side Effects
Conclusion
Manual Therapy Techniques
Foam Rolling
Mechanism
Clinical Application
Side Effects and Safety
Conclusion
Percussive Massage
Mechanism
Clinical Application
Safety and Side Effects
Conclusion
Instrument-Assisted Soft Tissue Mobilization
Mechanism
Clinical Application
Side Effects and Safety
Conclusion
Muscle Energy Techniques
Mechanism
Clinical Application
Safety and Side Effects
Conclusion
Active Release Technique
Mechanism
Clinical Application
Safety and Side Effects
Conclusion
Cupping
Mechanism
Clinical Application
Safety and Side Effects
Conclusion
References
Part III: Performance Optimization and Event Coverage
18: Clinical Aspects of Running Gait Analysis
Introduction
Getting Started
Patient Setup and Video Capture
Analysis of the Recorded Video
Sagittal Plane
Initial Contact
Foot Inclination Angle
Horizontal Distance from Foot to COM
Leg Inclination Angle
Knee Flexion Angle
Mid-Stance
Peak Knee Flexion Angle
Peak Ankle Dorsiflexion Angle
Additional Sagittal Measures
COM Vertical Excursion
Hip Extension and Pelvic Tilt
Forward Trunk Lean
Frontal Plane
Mid-Stance
Trunk Side Bend
Lateral Pelvic Drop
Knee Center Position
Base of Gait
Rearfoot and Forefoot Position
Other Variables
Summary
Appendix 1. Disclosure
References
19: Clinical Applications of Bike Fitting
Introduction
Anatomy of a Bike
Pedal Cycle
Common Clinical Presentations
Neck Pain
Back Pain
Hip Pain
Hand Numbness
Perineal Symptoms
Knee Pain
Foot Pain and Numbness
Setup for a Basic Bike Fit
Helpful Tools and Equipment
Saddle Positioning
Foot and Cleat Alignment
Hand Positioning and Handlebars
Summary
References
20: Clinical Application of Swim Stroke Analysis
Introduction
The Four Competitive Strokes
Freestyle Biomechanics
Freestyle Upper Extremity Movement
Freestyle Lower Extremity Movement
Freestyle Stroke Mechanics
Backstroke Biomechanics
Backstroke Upper Extremity Movement
Backstroke Lower Extremity Movement
Backstroke Mechanics: General Notes
Butterfly Biomechanics
Butterfly Upper Extremity Movement
Butterfly Lower Extremity Movement
Butterfly Stroke Mechanics: General Notes
Breaststroke Biomechanics
Breaststroke Upper Extremity Movement
Breaststroke Lower Extremity Movement
Breaststroke Stroke Mechanics: General Notes
Common Stroke Technique Errors
Freestyle Errors
Injury Prevalence and Incidence
Performance Considerations
The Pediatric Swimmer
The Masters Swimmer
Common Injuries and Rehabilitation
Shoulder Injuries
Shoulder Rehabilitation
Knee Injuries
Knee Rehabilitation.
Spine Injuries
Spine Rehabilitation
Cervicothoracic
Lumbar
Hip Injuries
Hip Rehabilitation
Ankle Injuries
Ankle Rehabilitation
Breathing
Breath Control/Pulmonary Function
Mobility
Elastic Therapeutic Taping
Return to Sport Considerations
Swimming Injury and Rehabilitation Conclusion
Return to Swimming Protocol
Training Considerations
Equipment
Coach/Teacher/Trainer Safety Awareness
Efficacy of Dryland Strength Training
Efficacy of Swim Training Regimen
Training Effort and Communication with Coaches
Injury Prevention
Video Swim Stroke Analysis
Feedback
Injury Screening
A Proposed Dynamic Warm-Up
Appendix 1: Part 1—Dynamic Shoulder, Spine, Hip, Knee, and Ankle Warm-Up (all 2 × 15 reps) ([191]; Edelman 2015)
Appendix 2: Part 2—Strength/Plyometric/Balance/Reaction Time Progression [191]
Appendix 3: Part 3—Aquatic Swimming-Specific Drills ([191]; Edelman 2015)
References
21: High-Intensity Interval Training and Resistance Training for Endurance Athletes
Physiological and Neuromuscular Determinants of Endurance Performance
Training Principles and Periodization for Endurance Performance Enhancement
Effects of HIT on Endurance Performance
Considerations of HIT Programming
Effects of Strength Training on Endurance Performance
Considerations for Strength Training Programming
References
22: Mental Skills Training for Endurance Sports
Introduction
Motivation
Goal Setting
Energy Management
Self-Talk
Concentration
Imagery
Performance Routines
Mindfulness
Balanced Exercise
Medication Considerations
Conclusion
References
23: Performance-Based Nutrition for Endurance Training
Introduction
Carbohydrate
Pre-Competition: “Loading”
During Competition: “Fueling”
Post-Competition: “Repleting”
Protein
Pre- and during Exercise Protein
Post-Exercise Protein
Fat
Hydration
Micronutrients, Electrolytes, and Dietary Supplements/Ergogenic Aids
Sodium
Caffeine
Nitrates
Iron
Environmental Considerations
Conclusion
References
24: Coordination of Medical Coverage for Endurance Sporting Events
Overview
Coordination
Weather
Staffing
Equipment and Medications
Communications and Medical Records
Illness
Unique Event Considerations
Event Types
Remote Settings
Infection Control: COVID-19 Pandemic Considerations
Summary
References
25: Return to Sport Decision-Making for Endurance Athletes
Return to Play Versus Return to Sport Versus Return to Performance
Return to Participation
Return to Sport
Return to Performance
Team Approach and Empowering the Athlete
Psychological Aspects
Step 1: Assessment of Health Risk (Tissue Health)
Step 2. Assessment of Activity Risk (Tissue Stresses)
Step 3: Assessment of Risk Tolerance (Acceptable Risk)
References
Index

Citation preview

Endurance Sports Medicine A Clinical Guide Timothy L. Miller Editor Second Edition

123

Endurance Sports Medicine

Timothy L. Miller Editor

Endurance Sports Medicine A Clinical Guide Second Edition

Editor Timothy L. Miller Department of Orthopedic Surgery The Ohio State University Wexner Medical Center New Albany, Columbus, OH, USA

ISBN 978-3-031-26599-0    ISBN 978-3-031-26600-3 (eBook) https://doi.org/10.1007/978-3-031-26600-3 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2016, 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Contents

Part I Medical Conditions 1 Taking  a Holistic Approach to Treating Endurance Athletes��������������������������������������������������������������������������   3 Gloria Beim, Kyle R. Brena, Bridget Holroyd Jones, Adam Lindsay, William Sterett, and Jared D. Heinze 2 Cardiovascular  Evaluation and Treatment in the Endurance Athlete ��������������������������������������������������������������������������  19 Andrew Hornick and Curt J. Daniels 3 E  xercise-Induced Bronchoconstriction and Vocal Cord Dysfunction ����������������������������������������������������������  37 Alexys Monoson and Jonathan Parsons 4 Low  Ferritin and Anemic Conditions in Endurance Athletes��������������������������������������������������������������������������  49 Holly J. Benjamin and Marci Goolsby 5 Evaluation  and Treatment of Exertional Heat Illness, Rhabdomyolysis, and Hyponatremia ��������������������������������������������  63 Jordan Romick, Rukayat Balogun, and Nathaniel Nye 6 Evaluation  and Treatment of Cold- and Altitude-Related Injuries and Illnesses������������������������������������������  77 Katie E. Krebs, Jake Fletcher, and Michael R. Tiso 7 Pregnancy  and Other Considerations for the Female Endurance Athlete��������������������������������������������������������������  95 Michelle F. Mottola, Jane Thornton, and Margie H. Davenport 8 Considerations  for Treating the Pediatric Endurance Athlete �������������������������������������������������������������������������� 113 Stephanie DeLuca and Adam S. Tenforde 9 Effects  of Exercise and Aging in the Masters-Level Athlete���������������������������������������������������������������������� 127 Jenny Berezanskaya and Thomas M. Best

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vi

Part II Musculoskeletal Conditions 10 Biologic  Advancements in the Treatment of Stress Fractures�������������������������������������������������������������������������������� 137 Elise Grzeskiewicz and Timothy L. Miller 11 Orthobiologic  Treatment Options for Injuries in Endurance Athletes�������������������������������������������������������������������������� 151 Elena Randazzo and Michael R. Baria 12 Special  Considerations for the Periodic Health Evaluation of Endurance Athletes�������������������������������������������������� 167 Dustin Nabhan, Carlos Jimenez, Julia Johnson, and Kevin Pierce 13 Chronic  Leg Pain in Running Athletes������������������������������������������ 175 Leonard Tiger Onsen, Jeniffer Lima, and Mark Hutchinson 14 Hip  Injuries and Conditions in the Endurance Athlete���������������� 187 Joshua D. Harris 15 Common  Injuries and Conditions in Rowers�������������������������������� 213 Kristine A. Karlson and Genevra L. Stone 16 Common  Injuries and Conditions in Crossfit Participation ������������������������������������������������������������������������������������ 221 Brian D. Giordano and Mina Botros 17 Blood  Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation������������������������������������������������������ 237 Kathryn Thomas Part III Performance Optimization and Event Coverage 18 Clinical  Aspects of Running Gait Analysis������������������������������������ 269 Amanda Pipkin and Bryan Heiderscheit 19 Clinical  Applications of Bike Fitting���������������������������������������������� 285 Andrea Cyr and Joseph Ascher 20 Clinical  Application of Swim Stroke Analysis ������������������������������ 301 Katherine Wayman, Joshua A. Pintar, and Sarah Depp 21 High-Intensity  Interval Training and Resistance Training for Endurance Athletes���������������������������������������������������� 355 Joshua F. Feuerbacher and Moritz Schumann 22 Mental  Skills Training for Endurance Sports ������������������������������ 373 Jennifer E. Carter and Joshua L. Norman

Contents

Contents

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23 Performance-Based  Nutrition for Endurance Training �������������� 387 Steven Liu, Shawn Hueglin, Jacque Scaramella, and Kenneth Vitale 24 Coordination  of Medical Coverage for Endurance Sporting Events�������������������������������������������������������������������������������� 411 Amadeus Mason and Sara Raiser 25 Return  to Sport Decision-Making for Endurance Athletes���������� 427 Bryant Walrod Index���������������������������������������������������������������������������������������������������������� 433

Contributors

Joseph Ascher  PhysioPartners, Chicago, IL, USA Rukayat  Balogun Emergency Department, Osan Air Base, Pyeongtaek, Gyeonggi Province, Republic of Korea Michael R. Baria  Department of Physical Medicine and Rehabilitation, The Ohio State University, Columbus, OH, USA Gloria Beim, MD  Department of Orthopaedic Surgery and Sports Medicine, Vail-Summit Orthopaedics and Neurosurgery–Alpine, Elk Avenue, Crested Butte, CO, USA Holly  J.  Benjamin Department of Orthopaedic Surgery, Rehabilitation Medicine & Pediatrics, University of Chicago, Chicago, IL, USA Jenny  Berezanskaya Department of Family Medicine, Sports Medicine, Cleveland Clinic Martin Health, Port Saint Lucie, FL, USA Thomas M. Best  Department of Orthopedics, University of Miami, Miami, FL, USA Mina Botros  Department of Orthopeadic Surgery, University of Rochester Medical Center, Rochester, NY, USA Kyle  R.  Brena, BS  Department of Research and Education, Vail-Summit Orthopaedics and Neurosurgery–Research and Education Foundation, Vail, CO, USA Jennifer  E.  Carter Psychiatry and Behavioral Health, Jameson Crane Sports Medicine Institute, Ohio State University Wexner Medical Center, Columbus, OH, USA Andrea Cyr  Department of Orthopedics and Sports Medicine, University of Illinois Hospital and Health Sciences System, Chicago, IL, USA Curt  J.  Daniels  Division of Cardiology, The Ohio State Wexner Medical Center, Ross Heart Hospital, Columbus, OH, USA Margie  H.  Davenport Program for Pregnancy and Postpartum Health, Physical Activity and Diabetes Laboratory, Faculty of Kinesiology, Sport and Recreation, Women and Children’s Health Research Institute, Alberta Diabetes Institute, University of Alberta, Edmonton, AB, Canada

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x

Stephanie  DeLuca Department of Physical Medicine & Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Charlestown, MA, USA Sarah Depp  Wexner Medical Center, Ohio State University Medical Center, Columbus, OH, USA Joshua  F.  Feuerbacher Department of Molecular and Cellular Sports Medicine, Institute of Cardiovascular Research and Sports Medicine, German Sport University, Cologne, Germany Jake Fletcher  Department of Family Medicine, Cleveland Clinic, Lakewood, OH, USA Brian  D.  Giordano Department of Orthopeadic Surgery, University of Rochester Medical Center, Rochester, NY, USA Marci Goolsby  Primary Care Sports Medicine, Hospital for Special Surgery, New York, NY, USA Elise  Grzeskiewicz Department of Orthopaedic Surgery and Sports Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA Joshua D. Harris  Department of Orthopedics and Sports Medicine, Houston Methodist Hospital, Houston, TX, USA Bryan  Heiderscheit Departments of Orthopedics and Rehabilitation and Biomedical Engineering, UW Health Runners’ Clinic, Badger Athletic Performance Program, University of Wisconsin-Madison, Madison, WI, USA Jared  D.  Heinze, MPH Department of Research and Education, VailSummit Orthopaedics and Neurosurgery–Research and Education Foundation, Vail, CO, USA Andrew Hornick  Division of Cardiology, The Ohio State Wexner Medical Center, Ross Heart Hospital, Columbus, OH, USA Shawn Hueglin  Sports Performance, United States Olympic and Paralympic Committee, Chula, CA, USA Mark  Hutchinson Department of Orthopaedic Surgery, University of Illinois, Chicago, IL, USA Carlos Jimenez  Health and Performance, Canyon Ranch, Tucson, AZ, USA Julia Johnson  United States Olympic and Paralympic Committee, Colorado Springs, CO, USA Bridget Holroyd Jones, PT, DPT, OCS  Department of Physical Therapy, Avalanche Physical Therapy, Frisco, CO, USA Kristine A. Karlson  Community and Family Medicine, Orthopaedics and Pediatrics, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA

Contributors

Contributors

xi

Katie E. Krebs  Premier Health, Centerville, OH, USA Jeniffer Lima  Department of Family Medicine, Amita Health Saints Mary and Elizabeth Medical Center, Chicago, IL, USA Adam  Lindsay, MD Department of Orthopaedic Surgery and Sports Medicine, Vail-Summit Orthopaedics and Neurosurgery–Alpine, Crested Butte, CO, USA Steven Liu  Department of Internal Medicine, Providence Portland Medical Center, Portland, OR, USA Amadeus  Mason Departments of Orthopaedics and Family Medicine, Emory School of Medicine, Atlanta, GA, USA Timothy L. Miller  Department of Orthopaedic Surgery and Sports Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA The Jameson Crane Sports Medicine Institute, Columbus, OH, USA Alexys  Monoson Division of Pulmonary, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA Michelle  F.  Mottola R. Samuel McLaughlin Foundation-Exercise and Pregnancy Laboratory, School of Kinesiology, Faculty of-Health Sciences, Department of Anatomy & Cell Biology, Schulich School of Medicine and Dentistry, Children’s Health Research Institute, The University of Western Ontario, London, ON, Canada Dustin Nabhan  Health and Performance, Canyon Ranch, Tucson, AZ, USA Joshua  L.  Norman Psychiatry and Behavioral Health, Jameson Crane Sports Medicine Institute, Ohio State University Wexner Medical Center, Columbus, OH, USA Nathaniel  Nye Department of Sports Medicine, Ft. Belvoir Community Hospital, Fort Belvoir, VA, USA Leonard  Tiger  Onsen  Department of Orthopaedic Surgery, University of Illinois, Chicago, IL, USA Jonathan  Parsons Division of Pulmonary, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA Kevin Pierce  United States Olympic and Paralympic Committee, Colorado Springs, CO, USA Joshua  A.  Pintar Department of System Health Solutions, Indiana University Health, Indianapolis, IN, USA Amanda  Pipkin Department of Physical Therapy, Nova Southeastern University, Clearwater, FL, USA

xii

Sara  Raiser Departments of Orthopaedics and Rehabilitation Medicine, Emory School of Medicine, Atlanta, GA, USA Elena Randazzo  Department of Physical Medicine and Rehabilitation, The Ohio State University, Columbus, OH, USA Jordan Romick  Department of Family Medicine, St. Elizabeth’s Hospital, O’Fallon, IL, USA Jacque Scaramella  Sports Dietitian, San Diego, CA, USA Moritz Schumann  Department of Molecular and Cellular Sports Medicine, Institute of Cardiovascular Research and Sports Medicine, German Sport University, Cologne, Germany William Sterett, MD  Department of Research and Education, Vail-Summit Orthopaedics and Neurosurgery–Research and Education Foundation, Vail, CO, USA Department of Orthopaedic Surgery and Sports Medicine, Vail-Summit Orthopaedics and Neurosurgery, Vail, CO, USA Genevra  L.  Stone Harvard Affiliated Emergency Medicine Residency at Beth-Israel Deaconess Medical Center, Boston, MA, USA Adam  S.  Tenforde Department of Physical Medicine & Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Charlestown, MA, USA Kathryn Thomas  Co-Kinetic, Centor Publishing, London, UK Jane  Thornton  Return to Health and Performance Lab, Fowler Kennedy Sport Medicine Clinic, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada Michael  R.  Tiso Department of Sports Medicine, Ohio State University Medical Center, Columbus, OH, USA Kenneth Vitale  Department of Orthopedic Surgery, University of California San Diego, La Jolla, CA, USA Bryant Walrod  Department of Family and Community Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA Katherine Wayman  Wexner Medical Center, Ohio State University Medical Center, Columbus, OH, USA

Contributors

Part I Medical Conditions

1

Taking a Holistic Approach to Treating Endurance Athletes Gloria Beim , Kyle R. Brena , Bridget Holroyd Jones, Adam Lindsay , William Sterett, and Jared D. Heinze

Abbreviations

Introduction

BW Body weight CWI Cold-water immersion DN Dry needling Kg Kilogram MPS Myofascial pain syndrome MTrP Myofascial trigger point PHQ Personal Health Questionnaire

Endurance athletes participating in sports such as cycling, running, and swimming strive to maintain peak performance by alternating between periods of intensive training and periods of rest and recovery. Maintaining balance between periods of rest and recovery can be difficult due to the nature of prolonged physical exercise both during training and competition. Because of this, endurance athletes are most at risk for experiencing “overuse” injuries, which are usually a result of an imbalance between overly intensive training and inadequate recovery [1]. Sports medicine providers and orthopedic surgeons who provide care for endurance athletes are technicians and experts in treating injury and diseases related to the musculoskeletal system, with the ability to restore physical function and relieve pain. But for high-level endurance athletes, surgery is often viewed as a “last resort” given it likely means time away from sport, less training, and more emphasis on recovery. Also, despite the overwhelming success of most orthopedic procedures, functional improvements after surgery still vary widely. In fact, suboptimal functional outcomes have been associated with poor emotional health in a variety of orthopedic specialties, including sports-related surgery. It is well documented that emotional health of a patient influences the outcome of many common orthopedic surgeries [2]. This is especially important to consider when providing care for endur-

G. Beim · A. Lindsay Department of Orthopaedic Surgery and Sports Medicine, Vail-Summit Orthopaedics and Neurosurgery–Alpine, Elk Avenue, Crested Butte, CO, USA e-mail: [email protected]; [email protected] K. R. Brena · J. D. Heinze (*) Department of Research and Education, Vail-Summit Orthopaedics and Neurosurgery–Research and Education Foundation, Vail, CO, USA e-mail: [email protected]; [email protected] B. H. Jones Department of Physical Therapy, Avalanche Physical Therapy, Frisco, CO, USA e-mail: [email protected] W. Sterett Department of Research and Education, Vail-Summit Orthopaedics and Neurosurgery–Research and Education Foundation, Vail, CO, USA Department of Orthopaedic Surgery and Sports Medicine, Vail-Summit Orthopaedics and Neurosurgery, Vail, CO, USA e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_1

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ance athletes because emerging evidence suggests that endurance athletes, along with being at increased risk of physical injury, also experience a higher risk of psychological issues and mental health disorders [3]. Given the complexity surrounding the physical and psychological needs of endurance athletes to reach peak performance, it is important to take a holistic approach to providing care. Holistic care is that which takes a multidimensional perspective and aims to target all ­components of an individual athlete’s specific needs. Holistic care is comprehensive, integrative care and can be best understood through a biopsychosocial health model. The biopsychosocial health model was developed by George Engel to complement the traditional biological model of disease that views a disease solely because of biological malfunction. The biopsychosocial model offers a multidimensional perspective by recognizing the impact of psychological and social factors on the development and outcomes of illness and disease [4]. Taking the complex nature of endurance athlete’s needs into consideration allows for comprehensive care planning and considerations to be made so that peak performance can be attained while minimizing the risk of injury and need for invasive surgeries. What follows are different components of a holistic program of care that should be included for consideration that encompass the diverse and multidimensional needs of endurance athletes.

Behavioral Health Elite and recreational endurance athletes are susceptible to a unique variety of stressors which may increase their vulnerability to behavioral health issues and disorders. The psychological impact of injury, overtraining, burnout, and need to manage competitive pressures to perform are important factors which may increase susceptibility to stress. It is widely accepted that overtraining is often required of endurance athletes to achieve peak performance despite growing evidence that extreme overtraining can result in declined performance. Along with the risk of decrement in performance, more research is

showing that overtraining may also lead to declines in mood and increased risk of behavioral affective disorders [5, 6]. Although a dose-­ response relationship between exercise volume and physiologic benefit has been documented in previous studies [7], less is known regarding the relationship between exercise volume and effects on psychological well-being. Some existing studies point to a potential inverse relationship between mental health and training volume. One such study of 400 swimmers at the University of Wisconsin-Madison assessed the mood of athletes at monthly intervals during the entire duration of their training season over a 10-year period [8]. Throughout all 10 years of the study, mood disturbances were reported to be at their highest level during the time of highest volume training blocks. Currently, there is still a lack of research on prevalence and types of mental health disorders in endurance athletes. This gap in knowledge hinders the ability to generate evidence-based guidelines and standards for clinicians in sports medicine and orthopedics to utilize when treating the complex needs, including psychological needs, of the endurance athlete population. Behavioral screening tools, such as the Personal Health Questionnaire (PHQ) series, exist and should be utilized during clinic visits to identify any psychological issues. Other tools available to endurance athletes which may be beneficial include psychological and mental toughness coaching, resilience training, goal setting, verbal encouragement, and head-to-head competition. These recommended tools can be used to meet a specific athlete’s needs and should be evaluated for use on a case-by-case basis.

Nutrition Nutrition is a key component in the integrated approach for the treatment of endurance athletes. Its effects can promote both physical and mental well-being after an injury, surgery, or hard training session. With a suboptimal diet, endurance athletes can encounter delayed recovery, a decrease in performance, or an increased risk for injury [9–12]. The goal of rehabilitation nutrition

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is to maintain a recommended body weight and body fat percentage according to an athlete’s specific sport to reduce the effects of muscle disuse atrophy [10]. When an athlete is in the inactivity or immobilization phase of recovery, muscle disuse atrophy can cause a 0.5% decrease in muscle mass per day with an overall 50% decline in muscle ­protein synthesis. Muscle atrophy etiology is a multifactorial process that can be attributed to acute inflammatory cytokines, hormonal changes, bone calcium loss, decreased metabolic rate and insulin sensitivity, and increases in fat deposition [10]. An important factor when attempting to counteract the effects of muscle atrophy is sustaining the amount of available hepatic or muscular glycogen, which can be used for rebuilding damaged tissue after an injury or training session [9–12]. A recent systematic review on rehabilitation nutrition for injured athletes concluded that sufficient intake to maintain glycogen stores requires a caloric intake of approximately 25–30  calories per kilogram (kg) of body weight (BW) with simultaneous intake of carbohydrates and protein [10]. The co-ingestion of protein with carbohydrates increases serum insulin secretion, which leads to better glycogen resynthesis in the presence of carbohydrates. Other research supports these recommendations and has added evidence to the specifics of timing, amount, and other nutrients that may aid to recovery. In summary, it is recommended that recovering or rehabilitating endurance athletes ingest five to six meals throughout the day, including immediately after exercise, with an average of 0.75  g of carbohydrates/kg of BW/meal with 0.25 g of protein/kg of BW/meal [9, 11, 12]. Previous studies have also demonstrated that long-term intake (>8 weeks) of 4 g/day of omega-3 fatty acids may enhance sensitivity to amino acids, as well as provide anti-inflammatory properties, all of which could aid in optimizing recovery [10]. Nutrition does not only provide elements of recovery but also contains preventative properties as well. Stress fractures are a common overuse injury in active populations, occurring in approximately 20% of all athletes [13]. Repeated submaximal loads can cause stress fractures, as

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endurance athletes may experience from frequently running long distances or from jumping repeatedly. Without proper nutrition (and appropriate time) for recovery, the repeated submaximal loading can eventually cause an accumulation of stress fractures which can be debilitating for an athlete. Studies that have extensively examined active populations have identified correlations between low calcium and/or vitamin D levels and the prevalence of stress fractures [14– 19]. Calcium is the main mineral present in the bones which provides strength, as well as helps maintain appropriate blood calcium levels. Vitamin D helps regulate calcium absorption and bone remodeling [20]. Therefore, low levels of either calcium, vitamin D, or both may contribute to the risk of stress fractures and muscular strain in athletes [21]. It is currently recommended that athletes consume 2000  mg of calcium and 800 international units of vitamin D daily to reduce the risk associated with deficiency [13], though 2000–5000 international units per day may be required if an athlete is Vitamin D insufficient or deficient. Foods or supplements that contain probiotics, nitrates, and antioxidants may also have benefits for recovery or injury prevention; however, the body of evidence is currently incomplete and inconclusive [11]. The recommendations provided above on nutrition should be considered for all athletes that are aiming to optimize recovery after a training session or an injury. By consuming the appropriate micro- and macronutrients, athletes can maximize recovery between training sessions and can potentially reduce the time to return to their respective sport after an injury. The nutritional recommendations in this section are consistent across literature; however, it is important to acknowledge that everyone’s metabolism varies, and therefore the athlete should consult their physician or nutritionist before following specific protocols. In conclusion, a well-balanced diet plays a fundamental role in the multimodal, holistic approach to the recovery of an endurance athlete and should not be overlooked when aiming to optimize performance or the recovery and rehabilitation process.

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Compression Garments Compression garments are articles of clothing such as knee sleeves, socks, and tights that are frequently worn during endurance training and recovery. The theory behind use of compression garments is that during activity, these garments help to prevent excessive swelling in the muscles, as well as improve circulation and removal of waste products such as lactic acid and muscle metabolites. As a result, manufacturers claim compression wear can improve exercise performance and speed up muscle recovery. The research behind these garments indicates that there is little to no benefit to using compression clothing during exercise to improve performance [22–27]. However, there is research that supports the use of compression wear for recovery, especially for reducing delayed-onset muscle soreness (DOMS) and improving next-day muscle performance [22, 24, 25, 27]. One systematic review and meta-analysis that aimed to review efficacy of compression garments on measures of DOMS, muscular strength, muscular power, and creatinine kinase concluded that compression garments are effective at enhancing recovery from muscle damage [25]. Another review also concluded that compression garments could be beneficial to enhance next-day endurance performance [26]. In a third systematic review, authors attempted to compare low- vs. high-pressure garments, as well as wear times. The authors found that there was a high level of variation in pressures as well as wear time for garments and were unable to identify a correlation between either measurement. However, the review concluded that in many studies, muscle performance improved, and DOMS was reduced with garment wear during recovery following exercise with a variety of wear times and garment pressures [27]. Overall, more research is needed to determine optimal parameters for compression garments, but many reviews and studies conclude that compression wear is likely to be beneficial for endurance athlete recovery [22, 24–27]. While there is no apparent harm in wearing compression garments during exercise, there is likely limited objective benefit to wearing these

to enhance immediate metabolic performance. The benefit of wearing compression garments is mostly identified as the ability to enhance recovery and reduce post-performance inflammation, so while garments can be worn during activity, most of the benefit of compression wear is use after exercise. Typically, compression garments are purchased by the athlete for personal use, so these are not often used during formal rehab such as in physical therapy. When treating endurance athletes, we recommend wearing compression garments for the affected treatment area after activity to reduce post-activity soreness and inflammation. However, if wearing compression garments provides increased subjective performance during activity, it should not necessarily be discouraged. Compression may provide a sense of increased support, comfort, and the ability to minimize swelling in an injured area during exercise.

Hydrotherapy The shift in youth and adolescent sports from a school-based, seasonal format to a club or travel team, year-around format has led to an early specialization in one sport, which increases the likelihood of overuse injuries [28, 29]. As a result, parents and athletes are searching for accessible and inexpensive recovery modalities. A particular interest has developed in hydrotherapy, specifically cold-water immersion (CWI) and contrast baths. These treatments may be an effective recovery tool which do not require expensive equipment or a specialist which would be needed for treatments such as dry needling or acupuncture. Cold-water immersion is one of the most widely implemented and researched recovery modalities for athletes. The exposure to cold water is hypothesized to provide benefits in muscle recovery and subsequent performance from the reduced temperature of the muscles, skin, and core [30, 31]. A systematic review on available literature revealed that CWI can significantly reduce the symptoms of delayed-onset muscle

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soreness up to 96  h after exercise as well as decrease ratings of perceived exertion 24 h after exercise when compared to passive recovery [32]. The exact physiological mechanisms for reduction in delayed-onset muscle soreness and rating of perceived exertion are not well understood; however, it could be explained by the vasoconstrictive properties of CWI [32, 33]. Vasoconstriction reduces the muscle cell’s metabolism, which may reduce the number of metabolites that cause muscle soreness [32]. Vasoconstriction also alters hydrostatic pressure in blood, which may promote muscle metabolite removal, further reducing the number of harmful metabolites in the recovering area [34]. Lowering body temperature reduces the perception of pain by slowing down nerve conductions, which may improve psychological recovery following an intense training session or event [35]. There are numerous protocols for duration and temperature for CWI; however, literature has cited that the optimal time for submersion is between 11 and 15 min at 11–15 °C [36]. Contrast baths are different from CWI in that they utilize repeated immersions of hot then cold water for a specified time, duration, and temperature [37]. The alternating temperature changes from hot to cold cause periodic vasodilation and vasoconstriction that induce a vascular pumping effect. Vascular pumping increases blood flow and oxygenation and thus enhances tissue waste product transportation and removal that can improve recovery [37]. Like studies on CWI, those examining benefits of contrast baths have conflicting evidence on their effectiveness for recovery [38–42]. There is evidence, however, that contrast baths decrease perception of fatigue, but not perceptions of soreness [42]. There is also evidence that contrast baths help athletes maintain performance on subsequent exercise bouts when compared to CWI and passive recovery modalities. The contrast bath strategy utilized in the study included alternating between cold water at 10–12 °C and warm water at 38–40 °C for 60 s in each cycle, through 7 cycles [41]. Contrast baths and CWI are an inexpensive and accessible recovery modality that may be of benefit for endurance athletes. However, the lack

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of knowledge about the underlying mechanisms of recovery with respect to hydrotherapy limits the ability to conclude whether an athlete will recover more rapidly in comparison with use of other modalities. We recommend that athletes utilize CWI or contrast baths within these guidelines if they believe hydrotherapy provides perception of decreased fatigue and/or muscle soreness. The psychological benefits of perceived recovery may also provide a better frame of mind for the athlete, thus potentially enhancing the athlete’s subsequent physical performances [42].

Acupuncture Acupuncture is a therapeutic intervention in which a clinician inserts small, filiform needles into the skin to stimulate specific points on the body [43–45]. This practice is most frequently associated with a system of medical theory and practice called “traditional Chinese medicine,” wherein health is seen as the result of harmony among bodily functions and between body and nature [44, 45]. The main idea behind acupuncture is that stimulation of specific body regions, or “acupoints,” can have effects on one’s physiology at distant sites [46]. Traditional acupuncture treatment is not based on Western empirical research; however, recent studies have yielded promising results that support the use of acupuncture for reducing the body’s inflammatory response and managing certain pain conditions. For the endurance athlete, this may be a useful tool for recovery and more rapid return to sport following injury. Current research indicates that it is possible to reduce systemic inflammation with acupuncture treatment [43, 46, 47]. In two studies using acupuncture needles stimulated with electric current, termed “electroacupunture,” it was shown that researchers could reduce systemic inflammation in mice [43, 46–48]. Two other independent studies that aimed to determine the effect of acupuncture on bone healing produced promising results, indicating that acupuncture can improve outcomes in fractures of the tibia, fibula, and humerus [49, 50]. These studies determined that

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the addition of acupuncture to usual care protocols can increase positive outcome rates and result in improved function at the injured sites, specifically with improvements in range of motion and reduction in swelling [49, 50]. Studies have also been conducted on human subjects to determine immediate effects of strength and endurance performance. While some of these studies failed to confirm improved ability to produce force with acupuncture [51], several studies indicate that acupuncture may reduce discomfort and delayed-onset muscle soreness and improve muscle activation [44, 51–53]. Evidence to support acupuncture is developing, and more research is needed to narrow down treatment parameters such as needle placement, treatment duration, and treatment intensity to optimize outcomes for the endurance athlete [43, 46, 47]. Currently, parameters for how and when to use acupuncture are widely variable. There is evidence to indicate that acupuncture used immediately prior to performance can reduce pain and rating of perceived exertion during activity, thus improving overall performance times [49–53]. Other studies have aimed at using acupuncture as a recovery tool where treatment is provided following strenuous activity or injury. The theory behind treatment post-activity is to reduce pain and inflammation, which can lead to faster recovery times and earlier improvements in function. If inflammation and pain are controlled early following strenuous activity or injury, we would predict that an athlete should be able to return to training sooner and at a higher intensity that may otherwise be limited.

Dry Needling Dry needling (DN), also referred to as trigger point dry needling or functional dry needling, is a minimally invasive technique in which a fine, solid filiform needle is inserted through the skin into muscle tissue, often targeting a “knot” or “trigger point” in the muscle. A myofascial trigger point (MTrP) is characterized as a “hypersensitive spot, usually within a taut band of skeletal muscle or in the muscle’s fascia, they can have

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strong focal points of tenderness, a few millimeters in diameter, and can be found at multiple sites in the tissue” [54–57]. Myofascial trigger point can further be classified as active or latent. Active MTrPs are painful and cause a pattern of referred pain at rest and/or while in motion. Latent MTrPs are also areas of hypersensitivity but only refer pain when palpated or pressed on [54, 55, 57–59]. Dry needling is used to influence muscular, neural, and connective tissues such as muscle, tendons, and scar tissue [56]. Dry needling can be used for both active and latent TPs. Typically, DN is performed by a licensed physical therapist, chiropractor, medical doctor, or acupuncturist. Dry needling is frequently confused with acupuncture, but these are separate treatment approaches that differ both in technique and theory behind the practice [56]. Traditional acupuncture is based on Eastern medicine theories related to meridians and balance of yin and yang, and Western medical acupuncture is meant to target ah shi points, which are acupuncture points that are painful with palpation [56, 59]. Dry needling is meant to target MTrPs with the intent of influencing muscle function and reducing pain [54, 57, 59]. Most DN therapy is used to target myofascial pain syndrome (MPS) associated with hyperalgesic zones in MtrPs. Current research generally supports the effectiveness of DN to reduce pain in patients with MPS of the upper quarter. One previous systematic review identified 246 articles on the subject, of which 12 randomized clinical trials were chosen for meta-analysis. The findings of three studies which compared DN to sham or placebo produced evidence that DN can immediately decrease pain in patients with upper-­ quarter MPS.  Two other studies in this meta-­ analysis suggested that DN, when compared to sham or placebo, decreased pain after 4 weeks in patients with upper-quarter MPS.  In addition to reducing pain, there is evidence that DN can increase muscle blood flow and oxygenation by causing vasodilation in small vessels. However, it is unclear whether the increase in blood flow is restricted to the needling site, or if DN increases blood flow to remote areas as well, or how long these effects last [56, 58]. Finally, there is limited

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evidence that DN has a direct effect on MTrPs by disrupting the “taut band” that forms, resulting in relaxation of the muscle and possible improvements in flexibility and range of motion [56, 58, 60]. Based on the current body of available ­evidence, recommending DN for management of acute pain should be considered for endurance athletes. Treatment could be combined with other modalities immediately following rigorous activity for management of acute pain as well. Dry needling is frequently performed by accredited and trained physical therapists and occasionally performed by chiropractors, acupuncturists, and medical doctors to treat individuals before, during, and after endurance activities. Clinicians can perform a variety of treatment techniques using filiform needles with or without electric stimulation to target the affected muscles. Some techniques include needle “pistoning,” in which the needle is rapidly moved up and down in the muscle, needling with electric stimulation where the needle is placed in the muscle and the electrical stimulation unit is attached to the needles, and even placing the needle and leaving it for a set period of time (Fig. 1.1). The techniques used will vary based on the clinician’s experience level and training. The needles used are sterile a

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Fig. 1.1  Dry needling. Illustration demonstrating a physical therapist’s (a) dry needling technique for a supraspinatus myofascial trigger point with (b) electrical stimulation. During electric stimulation, the current and frequency were held constant, while the intensity was slowly increased on the (c) electrical stimulation machine

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and disposable and come in various lengths and gauges, typically between 0.16–0.3 mm thick and 1.5–6 cm long in size. The length and gauge of needle are determined by the depth of the trigger point in the tissue, as well as the technique used for treatment. As athletes prepare to train for endurance activities, they may consult a medical professional to identify impairments such as decreased range of motion, decreased flexibility, weakness, and poor motor patterns that could contribute to injury. These evaluations are often performed by a physical therapist, and the physical therapist may decide that DN is an appropriate intervention to treat these impairments as the athletes begin their training plan. In some instances, professional athletes may have access to physical therapy during endurance events. For example, if an athlete sustains a minor calf or hamstring strain while competing and a clinician is available to perform DN immediately after injury at the competition site, this could allow the athlete to continue in the competition. Following rigorous training regiments or endurance events, athletes may experience muscle tightness, pain, or even weakness. Clinicians can use needling techniques to release tension in the muscles or place c

(E-Stim II) until a slight twitch occurred in the target muscle, which was seen around an intensity of 2 Watts/cm2 out of 10. The physical therapist allowed for continuous stimulation until a noticeable change was observed in the twitch response

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needles into weak muscles and stimulate them with electricity to improve overall muscle fiber recruitment. Often this treatment is followed by corrective exercises to improve movement patterns that may have contributed to the pain or tightness in the first place. Dry needling should be considered as a treatment option for endurance athletes at any stage of training and competition, from preparation to recovery.

Iontophoresis Steroids administered orally or through injection are often used to treat chronic inflammation in athletes. Although these administration modalities provide short-term relief, they do not come without risk. Injections can disturb the underlying tissue and potentially increase the chance of tendon rupture and cartilage damage [61]. Steroids taken orally allow systemic administration, increasing the chance fluid retention, upset stomach, and high blood pressure [62]. To minimize the risk of steroid administration, iontophoresis was developed as a noninvasive and localized modality for chronic, inflammatory injuries. Iontophoresis is a transdermal drug delivery technique utilized to reduce inflammation in various musculoskeletal conditions without the use of needle. The principle behind iontophoresis is that the application of a same-charge current can repel a charged drug into the desired area. There are two commonly used methods of iontophoresis. The traditional way in which a current is generated is with lead wires connected to an active and dispersion pad. This method is conducted during the physical therapy session and lasts between 15 and 20 min. The other method is conducted through a battery-charged patch that is loaded with the appropriate medication and administers a current for up to 24 h after application (Fig. 1.2) [63]. Iontophoresis is mainly used for chronic, overuse injuries that endurance athletes may experience over the course of their career. Lateral epicondylitis (tennis elbow), plantar fasciitis, patellar/Achilles tendonitis, and any other superficial soft tissue pathology tend to be the most

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common injuries that may benefit from iontophoresis. Several randomized studies have evaluated the effectiveness of iontophoresis in the treatment of lateral epicondylitis and have observed that when paired with a strengthening program, iontophoresis results in quicker improvement of strength and decreased pain level [64–66]. One study in particular evaluated the 24-h iontophoresis patch loaded with dexamethasone versus corticosteroid injection in patients undergoing formal physical therapy for lateral epicondylitis. The authors concluded that iontophoresis produced greater short-term strength benefits over injections, possibly due to the lack of deep tissue damage caused by a needle [64]. Iontophoresis may be a useful drug administration technique for athletes battling chronic injuries to superficial soft tissues. For medical professionals and athletes interested in utilizing iontophoresis, there are a few things to consider:

Fig. 1.2 Iontophoresis. Illustration demonstrating the placement of a battery-charged, 80 mA-min iontophoresis patch used for Achilles tendonitis. Prior to application, the negatively charged terminal was loaded with 1.3  mL of dexamethasone and applied with the negatively charged terminal over the injured area

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• The type of medication used. – – In order to be effective, the medication must be water-soluble and have a small molecular size and an ionic charge [63, 64]. • Which application (traditional or patch) is best for the athlete’s situation? –– The traditional method, which is conducted during the physical therapy session, can potentially reduce the time to perform supervised stretches or exercises with the therapist, whereas the patch can be used after the session and administered for a longer period. • Depth of injury. –– A study conducted with dexamethasone phosphate determined that a therapeutic concentration could reach depths of only 4 mm below the skin, with a higher concentration at the more superficial depths [67]. • Dose period and current strength. –– The recommended dose, expressed in milliampere-­ minutes (mA-min), is 40 mA-­min, which can vary depending on the subject’s comfort level and type of administration [63].

a

b

Fig. 1.3  Ultrasound. Illustration demonstrating a physical therapist utilizing ultrasound treatment for (a) plantar fasciitis and (b) supraspinatus tendinopathy. The treatment area must be approximately twice the size of the probe, as indicated by the red circle. The (c) ultrasound

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It is important to note that the athlete should consult with his or her physician prior to using iontophoresis because this technique is introducing a drug.

Ultrasound An imbalance between training and recovery can lead to overuse injuries that may impact athletic performance. An endurance athlete’s training protocol requires a perfect balance between training sessions and rest/recovery periods. It is very important for athletes, coaches, and physical therapists to use various modalities to ensure proper recovery. Like iontophoresis, ultrasound is a noninvasive, atraumatic recovery modality used by physical therapists to treat painful musculoskeletal conditions, but without the use of a drug. Ultrasound machines emit high-frequency sound waves (above the threshold of human hearing), through a probe which is applied to the skin (Fig.  1.3). The passing of the ultrasound waves through the skin can produce a variety of effects, such as increased tissue temperature, increased

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machine’s parameters were set to an intensity of 1.2 Watts/ cm2 and frequency of 1 MHz; however, these parameters may vary depending on the athlete’s tolerance to the treatment and type of injury

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tissue metabolism, increased localized blood flow, increased extensibility of collagen fibers, reduced viscosity of fluid elements of the tissue, ultrasonic cavitation, and gas body activation [68, 69], all of which can enhance the recovery process. Therapeutic ultrasound has been used to treat many types of injuries. Ligament sprains, muscle strains, tendonitis, joint inflammation, plantar fasciitis, facet irritation, bursitis, and scar tissue adhesion are among the typical injuries that can be treated with ultrasound therapy [68, 69]. Literature is inconclusive regarding the effectiveness of ultrasound therapy [70–75]; however, this may be due to differences in the severity of the treated injuries, the specific techniques used by the physical therapist, and/or the evaluations of results (subjective versus objective scores, animal models, etc.). In animal models, where confounding factors are limited, it has been shown that ultrasound therapy can increase cell proliferation during muscle generation, accelerate patellar-bone tendon junction healing, and facilitate tendon healing with increased tensile strength and collagen alignment [76–81]. Ultrasound may be a useful tool for physical therapists to optimize an athlete’s recovery when administered concurrently with a strengthening and/or stretching program. The adjustability of the ultrasound machine allows it to treat a variety of injuries/conditions; however, an improper technique may diminish its benefits. Below are a few considerations for medical professionals utilizing ultrasound in their treatment protocol [69]. • Size of the injured area –– The therapeutic effects of ultrasound derive from its ability to heat localized tissues through continuous mechanical disturbances from sound waves. Only small areas, roughly twice the size of the ultrasound probe, are recommended. Hot packs or baths should be used for any injury that is larger. • Correct intensity, frequency, and duration –– The ultrasound’s maximum benefit typically occurs when the injured area’s temperature is increased by 4  °C.  When

applied with an intensity of 1.5 Watts/cm2, heating will take 10–15 min at 1 MHz frequency or 3–5 min at 3 MHz frequency. It is important to note that ultrasound may create a feeling of warmth/burning, which will be tolerated differently by each athlete. Adjusting the intensity of the ultrasound machine can reduce discomfort; however, if the intensity is adjusted, then the duration of treatment should also be adjusted. • Injured tissue –– The depths of tissues treated are inversely proportional to the frequency used. A 3  MHz frequency is recommended for superficial tissue injuries less than 3  cm deep, whereas a frequency of 1 MHz is recommended for tissue injuries at 2.5–5 cm deep. –– The type of tissue may also influence the therapist’s decision regarding technique (e.g., tendons typically heat up faster than muscles). • Appropriate speed of probe movement –– The recommended speed of the probe is approximately 4 cm/s. This allows for even distribution of the sound waves and helps the therapists stay within a small application area. • Therapeutic window after application –– The average time it takes for heated tissues to drop to baseline temperature is approximately 15 min. Therapists should conduct stretching and/or strengthening exercises immediately after application.

Kinesiology Tape Athletes are always searching for the next best and innovative product or technology to help improve their performance and expedite recovery. In recent years, most of the focus has been on external garments, dietary supplements, hot/cold baths, electro-stimulus, drug therapy, etc.; however, kinesiology tape gained international attention after its notable use in the 2008 Summer Olympics.

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Kinesiology tape was developed in the 1970s by a Japanese chiropractor, Dr. Kenzo Kase. The application of the tape was designed to provide support without limiting range of motion (Fig.  1.4) [82]. Today, the innovative blend of nylon, cotton, and medical grade adhesive is believed by some to increase range of motion and strength, stabilize joints, facilitate recovery, and improve blood flow through mechanical stimulation of structures underneath the skin [83]. A magnetic resonance imaging study observed that when kinesiology tape was applied over the tibialis anterior, changes were noted in both the underlying and distant tissues [84]; however, other studies have not been able to consistently demonstrate that kinesiology tape can prevent injury or improve recovery. Additionally, a systematic literature review on kinesiology tape’s effect on athletic performance evaluated 11 studies and observed that out of the 193 comparisons, a

Fig. 1.4  Kinesiology tape. Illustration of kinesiology tape placement for (a) shoulder stabilization and (b) patellar tendonitis. This particular (a) shoulder stabilization technique required three strips of kinesiology tape, originating from the deltoid tuberosity and extending (a1) posteriorly, (a2) medially, and (a3) anteriorly to stabilize the

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only two reached statistical significance [83]. Another systematic review and meta-analysis of ten studies showed that there is a low quality of evidence to support kinesiology tape in the prevention and treatment of injuries in athletes [85]. While there is limited evidence on the efficacy of kinesiology tape, the placebo affect may be substantial enough to facilitate a positive psychological response. In a single-blinded, placebo-­ controlled crossover trial evaluating quadriceps force output with kinesiology tape, the authors observed that even when there were no statistical differences in force output, approximately 45% of subjects in the experimental group reported feeling stronger, compared to only 30% of subjects in the placebo group [86]. This indicates that the benefits advertised for kinesiology tape may be strictly due to psychological factors. Kinesiology tape may be a useful tool for select athletes who find it beneficial. It is b

humeral head within the glenohumeral joint. (b) The patellar tendonitis technique entailed placing two strips of kinesiology tape along the (b1) lateral and (b2) medial side of the patella with an additional strip of kinesiology tape placed (b3) horizontally across the patella tendon in order to provide support for the tendon when under stress

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i­mportant to note that the application technique may vary depending on the body part and desired treatment outcome [87]. We recommend athletes consult a medical professional before applying.

Blood Flow Restriction A significant percentage of athletes will experience an injury over the course of their career. Not all these injuries require surgery; however, some form of physical therapy is frequently prescribed to help the athlete recover. This process is often slow and can be further delayed by the inability to perform high-load resistance exercises (defined as ≥70% of an individual’s 1 repetition maximum), which have been shown to promote muscle hypertrophy and strength gains [88, 89]. Various modalities have been investigated to determine whether the physiologic response to a high-load resistance exercise could be mimicked, but without the physical stress. Dr. Yoshiaki Sato developed a training philosophy that we now

a

b

Fig. 1.5  Blood flow restriction. Illustration demonstrating pneumatic cuff placement for (a) targeting the upper extremity blood flow restriction prior to and (b) during bicep curl exercise movement and (c) targeting the lower extremities prior to and (d) during lunge exercise movement. Pneumatic cuff must be placed on the most proxi-

refer to as blood flow restriction training, which seems to produce a physiologic response similar to that of a high-load resistance exercise [90]. Blood flow restriction training involves applying a pneumatic tourniquet system to the most proximal region of the upper and/or lower limbs while doing a low-load resistance exercise (Fig. 1.5). The pressure from the pneumatic tourniquet or cuff reduces arterial blood flow and inhibits all venous blood flow. It is believed that when resistant exercises are done under this altered state of blood flow, hypoxia is induced in the muscles. Under hypoxic conditions, there is a greater recruitment of motor units, like that of a high-load resistance exercise, and an increase in cellular metabolites that are known meditators of muscle hypertrophy [88, 90, 91]. Current research indicates that low-load blood flow restriction training stimulates muscle hypertrophy through the synergistic effects of muscle activation and hypoxic conditions [88, 91–93]. In an 8-week rehabilitation study conducted in the United Kingdom, 24 patients undergoing anterior

c

d

mal portion of the extremity with an occlusion pressure that restricts arterial flow by approximately 40–80%. Athletes should use a working load of 20–40% of their 1 rep max and aim for four sets of high repetitions (i.e., 30, 15, 15, 15) as tolerated with 30–60 s between sets

1  Taking a Holistic Approach to Treating Endurance Athletes

cruciate ligament reconstruction were randomized into either a high-load resistance training group (70% of the individual’s 1 repetition maximum) or a blood flow restriction resistance training group with loads at 30% of the individual’s 1 rep max. The investigators found that blood flow restriction resistance training improved skeletal muscle hypertrophy and strength to a similar extent as the high-load resistance training group, but with a greater reduction in joint pain and effusion [94]. These findings are corroborated by other independent studies, systematic reviews, and meta-analyses [88, 89, 92, 93, 95–98]. Low-load blood flow restriction training does not appear to be superior to high-load resistance training in muscle hypertrophy or strength; however, it could be a useful tool for athletes aiming to regain lost muscle due to an injury or maintain in-season conditioning without risking further injury with a high-resistance load. Literature has cited that the working load should be 20–40% of the individual’s 1 repetition maximum. Ideally, athletes should do four sets of high repetitions (i.e., 30, 15, 15, 15) as tolerated with 30–60  s between sets [90, 91, 94]. Caution should be taken when using pneumatic cuffs as they present some risk when not used properly. The amount of pressure applied to the upper and/or lower limb will be athlete dependent. Limb size, resting blood pressure, cuff size/shape, and athlete tolerance to pressure should all be considered during application. The ideal amount of pressure applied should restrict arterial blood flow by 40–80% of its resting pressure, which can be monitored by newer technologically advanced cuffs [90].

Conclusion Providing comprehensive and holistic care to endurance athletes is often complex and can be challenging when considering the appropriate action. The authors of this chapter have described various preventative and recovery treatments that encompass the diverse and multidimensional needs of endurance athletes. Physicians, physical therapists, and athletic trainers should implement a holistic and individualized approach for treat-

15

ing endurance athletes that considers the athlete’s specific injury, mental status, and desired outcome.

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2

Cardiovascular Evaluation and Treatment in the Endurance Athlete Andrew Hornick and Curt J. Daniels

Introduction The decade leading up to 2020 saw significantly increased participation in endurance races in the United States. During that time frame, tens of millions of athletes participated in endurance events including road races, multisport competitions, and endurance cross-training events. Though centralized databases do not exist, the majority of reports indicates that the trends in participation continued to increase over this time frame, with some segments of endurance racing seeing up to a 50% increase in participation over the decade [1, 2]. Exercise confers numerous health benefits. Results of recent longitudinal cohort analyses have indicated that the most physically active adults gain up to 7–8  years in life expectancy compared with sedentary peers [3, 4]. Despite this, exercise does not render active persons immune from diseases of the cardiovascular system. Many reports indicate that athletes above the age of 35, so-called masters athletes, have similar cardiovascular risk factors as age-matched peers [5, 6]. Therefore, assessing a patient for cardio-

A. Hornick · C. J. Daniels (*) Division of Cardiology, The Ohio State Wexner Medical Center, Ross Heart Hospital, Columbus, OH, USA e-mail: [email protected]; [email protected]

vascular health prior to and while engaging in endurance athletics, as well as the resultant effects on the cardiovascular system secondary to endurance athletics, is of increasing importance for clinicians. Sports cardiology is an emerging subspecialty within the field of cardiology, spurred by tremendous increases in the amount of scientific literature examining the impact of exercise on the cardiovascular system [7, 8]. Perhaps most notably, increasing access to various means of cardiovascular imaging, like transthoracic echocardiography, cardiac computed tomography (CT), and cardiac magnetic resonance imaging (MRI), has allowed for novel insights into differentiating pathologic from physiologic changes in the athlete’s heart [7]. The term exercise-induced cardiac remodeling (EICR) has recently become an accepted terminology to describe physiologic adaptations secondary to exercise and to differentiate them from pathologic findings. Becoming familiar with the common forms of adaptive cardiovascular physiology is foundational to providing care and advice for endurance athletes. The aim of this chapter is to provide clinicians with a focused review of training-related cardiovascular adaptations and an approach to endurance athletes with cardiovascular symptoms and preexisting disease.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_2

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A. Hornick and C. J. Daniels

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Pre-Participation Cardiovascular Screening The composition and performance of the pre-­ participation cardiovascular screen (PPCS) for athletes is an important topic for clinicians seeing athletes in their practice. Numerous health societies have produced guidelines aimed at a systematic approach to screening athletes for occult cardiovascular disease with the aim of reducing the risk of sudden cardiac death during exercise [9–12]. Studies have indicated that while physical activity reduces all-cause and cardiovascular mortality, the risk of sudden cardiac death increases transiently during vigorous exercise [13–16]. It is notable and worth discussing with athletes that while the risk of sudden cardiac arrest or death does increase transiently during exercise, the absolute risk remains very low. Precise data regarding prevalence of sudden cardiac death related to exercise is limited by a lack of a centralized database in athletes. Extrapolated data from databases of runners and marathoners indicate a range of 1 in 15,000 per year to 1 in 50,000 per year. Commonly accepted prevalence in college athletes is 1 in 50,000 per year. Risk is often stated to be higher among athletes engaging in vigorous activity who were previously sedentary [16, 17]. Multiple professional sporting organizations mandate advanced screening, including the International Olympic Committee (IOC), Federation Internationale de Football Association (FIFA), and the majority of North American professional leagues [10, 11, 16, 18, 19]. However, it is worth noting that there is limited data substantiating the value of pre-participation cardiovascular screening, and published recommendations are considered expert opinion. Universal screening for all persons is a matter of some debate, with no clear consensus on indications for screening. Regardless, preparticipation cardiovascular evaluation is a common reason for referral to clinicians seeing athletes in practice, and some considerations are presented below.

History and Physical Examination Guidelines from the American Heart Association (AHA) and the American College of Cardiology (ACC) have traditionally advocated for a focused medical history and physical examination prior to participation as the core component of PPCS for athletes [20]. The American Heart Association has published a standardized 14-point focused history and physical to promote consistency in screening [10]. This history and physical focuses on traditional cardiovascular risk factors and targets identifying cardiovascular disease that may cause a significant morbidity with exertion. Most society guidelines and recommendations divide their recommendations by age, with 35 years of age being a common cutoff. Athletes over the age of 35 are commonly referred to as “masters athletes,” whereas athletes under the age of 35 are referred to as “young athletes.” The rationale for this age cutoff is based upon the prevalence of pathology causing exercise-­ induced sudden cardiac death in these two age groups.

Masters Athletes Multiple studies have indicated that the most common cause of sudden cardiac death during exercise for masters athletes is coronary artery disease (CAD) [21, 22]. Specific assessment for patients with either occult or clinical CAD, as well as other forms of diagnosed cardiovascular pathology, will be covered in depth in a later section; the vast majority of these patients should undergo specialty assessment by a cardiologist regarding their fitness for exercise participation [23]. Recent expert recommendations [17] have called into question whether referring all masters athletes for pre-participation cardiovascular screening creates barriers to sedentary persons engaging in physical activity [24]. These barriers may limit sedentary persons from garnering the substantial mortality and cardiovascular benefits of routine exercise. A recent scientific statement

2  Cardiovascular Evaluation and Treatment in the Endurance Athlete

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from the American Heart Association published in 2020 proposed individualizing exercise recommendations in individuals without known cardiovascular disease and focusing on their prior level of activity and presence of cardiovascular symptoms. Specifically, physically active individuals without cardiovascular disease or symptoms may continue their usual moderate or vigorous exercise and progress as tolerated, without seeking further care or testing, unless signs or symptoms of cardiovascular disease develop. Physically inactive individuals without known cardiovascular disease or symptoms may begin light to moderate intensity exercise without specific cardiovascular testing and, provided they remain asymptomatic, progress gradually in intensity. Those with any concerning symptoms should seek evaluation with medical professionals and undergo focused history, physical examination, and appropriate testing [17].

tiate physiologic from pathologic changes on an ECG of an athlete [24]. Despite the possible benefits of pre-­ participation ECG, evidence also consistently indicates a high degree of variability in interpretation between readers [26, 27]. There are also concerns regarding false-positive results leading to inappropriate further testing or inappropriate limitation in athletic participation. Due to these concerns, the AHA expert panels have convened three separate times (1996, 2007, and 2014) to consider adding ECG to pre-participation cardiovascular assessment for young athletes, and each time has recommended against mandatory ECG screening [10]. Therefore, guidelines in the United States continue to discourage routine ECG testing and advocate for focused history and physical.

Young Athletes

Part of the pre-participation cardiovascular screening history is determining the amount of exercise, or dose, that the athlete intends to participate in on a regular basis. Exercise dose is frequently thought of as a combination of three discrete variables: frequency, duration, and intensity [28]. The type of exercise is also an important variable and will be discussed in detail in the following section. While frequency and duration of exercise are intuitive variables, intensity of exercise is a more complex concept. Endurance exercise is often defined as either kilocalories expended over time or in metabolic equivalents, with one MET being defined as the resting metabolic rate [28]. Other relative terms may be used, such as percentage of maximal heart rate or VO2max [11]. Current ACC/AHA recommendations for the dose of physical activity in adults are 150 min of moderate intensity exercise, or 75 min of vigorous intensity exercise, accumulated over 1 week [29]. As described briefly above, these recommendations are based on a growing body of evidence that indicates this dose of exercise provides both cardiovascular and all-cause mortality benefit [14, 15].

For athletes below the age of 35, exercise-related cardiac death is generally caused by a variety of congenital and genetics-based diseases affecting the structure of the heart, like hypertrophic cardiomyopathy (HCM), congenital coronary artery anomalies, and arrhythmogenic right ventricular cardiomyopathy (ARVC) [17, 21]. The addition of an ECG to history and physical examination screening for young athletes has been an ongoing topic of debate in the sports medicine and sports cardiology communities. Evidence consistently indicates that pre-participation ECG can increase the detection of cardiac disorders that are linked to sudden cardiac arrest or death in young athletes [10, 25, 26]. Because of this, expert recommendations cautiously allow for use of pre-participation ECG in some specific situations and at centers with the ability for expert interpretation. As will be covered in depth in subsequent sections, becoming familiar with the expected electrical remodeling of the athlete’s heart and normal variants seen on the ECG is an important part of cardiovascular care for the athlete. Guidelines have been published to help differen-

Dose

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Endurance athletes, especially those engaging in competition, will frequently far exceed the recommended amount of exercise. Exercise health benefit does not track with increasing amount of exercise in a linear fashion; rather, studies indicate that accrued benefit reaches a plateau at an amount of weekly exercise approximately 3–4× the recommended amount. Some studies have indicated that athletes participating in the highest amount of exercise may lose some of that benefit, though these findings are limited by self-reported exercise data and small sample size; further studies are required to validate this finding [15]. Dose of exercise is highly relevant to cardiovascular care of endurance athletes. As described above, athletes initiating vigorous activity that are not accustomed to this are reported to have a higher incidence of cardiovascular events or death [17]. Additionally, knowing the dose of planned exercise informs the likely exercise-­ induced cardiac remodeling.

Exercise-Induced Cardiac Remodeling Exercise dosage is highly relevant given the possible benefits to the athlete but also the anticipated cardiovascular adaptations. The term exercise-induced cardiac remodeling (EICR) has become a common term for the cardiovascular adaptations to repeated exercise stimuli. Studies utilizing advanced cardiovascular imaging have assessed the minimum dose of exercise required to produce EICR. In a small study of previously sedentary individuals who underwent a progressive training regimen leading up to a marathon run, anatomic changes occurred in as little as 3 months at 3–4 h per week [30]. The degree of EICR is dependent on the dose and type of exercise [8]. Multiple studies have confirmed that the unique load that different types of exercise place on the heart causes different phenotypes of EICR [31, 32]. Understanding the various pressure and volume loads applied to the heart requires a basic understanding of the role of the cardiovascular system within normal exercise physiology.

A. Hornick and C. J. Daniels

 verview of Exercise Physiology O and the Cardiovascular System It is well established that sustained participation in physical activity results in cardiovascular adaptations [28]. Cardiovascular adaptations to exercise are mediated by the physiologic demands placed on the heart by exercise activities. On a cellular level, exercise increases skeletal muscle energy expenditure above the resting metabolic rate of ~3.5 mL O2/min/kg, which is defined as 1 metabolic equivalent (MET) [28]. Most contemporary literature reviewing cardiovascular adaptations to exercise draws specific focus to the type of exercise, generally breaking exercise into two broad categories of skeletal muscle activity: static and dynamic [7, 33, 34]. Static activities refer to strength-type activities requiring forceful skeletal muscle contractions; these activities are also occasionally referred to as isotonic. Weightlifting is a specific example of static activity. Dynamic activities refer to endurance-type activities requiring regular contraction of large muscle groups; these activities are also occasionally referred to as isometric [11]. Specific examples of dynamic activities include long-distance running and cycling [34]. It would be overly simple to describe exercise as purely static or purely dynamic. The majority of exercise involves some combination of static and dynamic movements, and efforts have been made to adjudicate the static and dynamic components of different types of exercise (Fig. 2.1). The classification of exercise into these categories is useful to the clinician seeing highly active patients, as the adaptation and stresses on the cardiovascular system vary based on the subset of exercise. During sustained dynamic activity, as in endurance sports, the volume of oxygen uptake via the lungs for metabolic use is increased. This volume of oxygen is referred to as the VO2, and it is directly related to the cardiac output via the Fick equation: Cardiac output  =  VO2 /arteriovenous oxygen difference (a-VO2 difference).

II. Moderate (10-20%) I. Low (30%)

2  Cardiovascular Evaluation and Treatment in the Endurance Athlete Bobsledding/Luge Field events (throwing) Gymnastics*+ Martial arts Rock climbing Sailing Water skiing*+ Weight lifting*+ Windsurfing*+

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Body building*+ Downhill skiing Skateboarding*+ Snowboarding*+ Wrestling*

Boxing Canoeing Kayaking Cycling*+ Decathlon Rowing Speed skating Triathlon*+

Archery Auto racing*+ Diving*+ Equestrian*+ Motorcycling*+

American football* Field events (jumping) Figure skating Rodeoing*+ Rugby Running (sprint) Surfing Synchronized swimming+ “Ultra” racing

Basketball* Ice hockey* Cross-country skiing (skating technique) Lacrosse* Running (middle distance) Swimming Team handball Tennis

Bowling Cricket Curling Golf Riflery Yoga

Baseball/softball Fencing Table tennis Volleyball

Badminton Cross-country skiing (classic technique) Field hockey* Orienteering Race walking Racquetball/Squash Running (long distance) Soccer*

A. Low (75%)

Increasing Dynamic Component

Fig. 2.1  Classification of sporting activity by static or dynamic component. Reprinted from Levine BD, Baggish AL, Kovacs RJ, Link MS, Maron MS, Mitchell JH. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities:

task force 1: classification of sports: dynamic, static, and impact: a scientific statement from the american heart association and american college of cardiology. J Am Coll Cardiol. 2015; 66 (21): 2350–2355. With permission from Elsevier

Increased cardiac output is required to distribute the increased volume of oxygen taken in to meet metabolic demand at the cellular level, and cardiac output may increase 5–six-fold during maximal exercise efforts [35–37]. Cardiac output in the equation above can be further simplified and is classically defined as the product of the left ventricular stroke volume (difference in volume at end diastole and end systole) and heart rate. Peak heart rate is a function of age, sex, and genetics rather than exercise habits; thus, the ability to generate a large stroke volume with exercise is a classic adaptation of an endurance athlete. Increased stroke volume is mediated by increases in the end diastolic volume. Thus, dynamic exercise exerts a volume load on the heart [38, 39].

Static activity results in increased afterload on the heart, and the heart has to maintain cardiac output against this increased afterload [7, 33]. During static activity there is generally little change in the heart rate or stroke volume, with increased contractility of the heart overcoming the increased afterload. Most descriptions of static exercises consider it to be a pressure load on the heart [33].

Remodeling of the Cardiac Chambers Using the above descriptions of static and dynamic exercise helps to inform the likely EICR of different types of athletes. Classically, the volume load of dynamic exercise leads to dilation of

A. Hornick and C. J. Daniels

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Increasing static Component

participating in wrestling and shot put. The athletes participating in the endurance disciplines with primarily dynamic components were shown to have eccentric LV hypertrophy, whereas those in the static disciplines had concentric LV hypertrophy. Papers reporting on adaptations of the left ventricle utilize a common nomenclature for two different types of LV hypertrophy in echocardiography: eccentric hypertrophy vs. concentric hypertrophy [40]. Eccentric hypertrophy is both LV wall thickening and chamber enlargement, whereas concentric hypertrophy is isolated LV wall thickening. Contemporary studies have confirmed the early findings of Morganroth [43]. In athletes, increased chamber size of the left ventricle is common, and recently published recommendations for cardiovascular imaging in athletes now consider this to be a normal variant in athletes engaging in endurance sports [40, 44, 45]. Interestingly, in studies of competitive athletes

Concentric LVH

Eccentric LVH & RV Dilation

Eccentric LV Remodeling & RV Dilation Normal Morphology

Low

Fig. 2.2 Expected exercise-induced cardiac remodeling based on increasing static or dynamic exercise component. Reprinted from Baggish AL, Battle RW, Beckerman JG, et al. Sports cardiology: core curriculum for providing cardiovascular care to competitive athletes and highly active people. J Am Coll Cardiol. 2017; 70 [15]: 1902–1918. With permission from Elsevier

High

all four chambers of the heart, whereas the pressure load of static exercise leads to at least mild thickening of the ventricles, predominantly the left ventricle (LV) [40]. The most common EICR findings are summarized in Fig. 2.2. As referenced previously, most exercise is a combination of static and dynamic movements. It follows that EICR exists often as a combination of both chamber dilation and wall thickening. Studies using echocardiography to evaluate the dimensions of the left ventricle in athletes have shown that average thickness of the LV wall is 15–20% greater than nonathlete controls, and LV cavity size is 10% larger [41]. The discrepant remodeling caused by static vs. dynamic exercise has been reported for upwards of 40  years, with a classic study from Morganroth and colleagues published in 1975 being among the first to document these differences [42]. That study used echocardiography to assess endurance athletes participating in swimming and running and compare them to athletes

Low

Increasing Dynamic Component

High

2  Cardiovascular Evaluation and Treatment in the Endurance Athlete

competing in a variety of exercise disciplines, up to 25% of athletes exceed gender-specific limits for LV chamber size, and in some studies that number is as high as 40% of male athletes exceeding recommended upper limits of normal [46–48]. Ejection fraction (EF) of the LV is generally normal in endurance athletes even with a significant increase in chamber dimension, though values at the lower limit of normal may be seen. A classic study comparing Tour de France athletes to age- and size-matched male physicians via echocardiography indicated the cyclists had normal-­range EF, but that their EF was statistically significantly lower than the physician group. Invasive hemodynamics were used to calculate cardiac output, and the cyclist group, despite a lower ejection fraction, had a higher cardiac output [49]. Physiologic dilation of the left ventricle among endurance athletes participating in large volumes of dynamic exercise is often accompanied by dilation of the right ventricle (RV) [50, 51], as well as dilation of the left and right atrium [52–54]. Expert recommendations from professional societies have referred to this as a harmonic and consistent increase in the dimension of the cardiac chambers and that this is a reassuring finding in endurance athletes [11]. Consistent with this, isolated dilation of a single ventricle in endurance athletes potentially indicates a pathologic process. Compared with LV dilation, which frequently exceeds the upper limit of normal ranges in endurance athletes, LV hypertrophy from static type exercise is generally mild and remains within accepted limits [40, 55]. Mild thickening meeting the definition for concentric hypertrophy has been demonstrated to occur in primarily static activities, like American football players competing in the lineman position. However, the early development of concentric hypertrophy in college-aged American football linemen corresponded to increased blood pressure and reduced markers of systolic function, raising the possibility that this form of remodeling had pathologic implications rather than physiologic [56].

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LV wall thickness in athletes rarely exceeds 12  mm, though hypertrophy in the 13–14  mm range has been described as a “gray zone” and may be seen in sports with high isotonic load or athletes of African and Caribbean descent, described in more detail below [40]. Attention should be drawn to athletes with LV wall thickness > 15 mm, as this is in the range of hypertrophic cardiomyopathy, a pathology that is frequently implicated in exercise-induced sudden cardiac death.

Aortic Adaptation Studies measuring the dimensions of the aorta in athletes have demonstrated a relationship between aortic dimension and exercise training. A recent paper reviewing athletes engaging in rowing and running demonstrated that 24% of the study cohort had at least one aortic dimension at least 2 standard deviations above the normal values for their age and gender [57]. Meta-analyses have also demonstrated larger aortic diameters in athletes compared with sedentary controls [58]. Further studies have assessed the aortic dimensions of former National Football League (NFL) players and found that being a former athlete was associated with a larger ascending aorta independent of body size, age, race, and a variety of clinical risk factors, including hypertension, diabetes, smoking status, or lipid profile [59]. The authors in the above studies have noted that the clinical implication of these findings is unclear, as in nonathletes, increased aortic size is considered a risk factor for aortic syndromes including aortic dissection, aneurysm, or rupture [60]. It is important to note that understanding regarding remodeling of the aorta and aortic dimensions is incomplete, and literature published on this topic urges further study. While studies have defined athletic populations with increased aortic dimensions compared with sedentary controls, the aortic dimensions of athletes should still fall within normal ranges for age, gender, and height, all of which are known to have bearing on the aortic size. Large studies of ath-

A. Hornick and C. J. Daniels

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letes reporting aortic dimensions have demonstrated low prevalence of athletes with dimensions exceeding normal values [61]. Recommendations consistently state that athletes with aortic dimensions that exceed normal values warrant careful workup as would be done for nonathletes [11, 40].

Electrical Remodeling As discussed previously, pre-participation ECG screening is a matter of some controversy within the field of sports medicine and sports ­cardiology. Despite this controversy, electrical remodeling of the athletes heart is well described, and recognition of patterns of electrical remodeling on the ECG of an athlete is an important and relevant skill to the clinician evaluating athletes. As such, the past decade has seen multiple international recommendations published in an attempt to improve recognition of both normal and abnor-

Normal ECG Findings • Increased QRS voltage for LVH or RVH • Incomplete RBBB • Early repolarization/ST segment elevation • ST elevation followed by T wave inversion V1-V4 in black athletes • T wave inversion V1-V3 age 1 mm and TWI confined to leads V1–V4 have excluded cardiomyopathy with 100% negative predictive value, regardless of ethnicity [73, 75]. The previous paragraphs highlight the importance of considering each athlete as an individual and that assessing the EICR of an athlete cannot follow a “one size fits all” approach. Further study will be required to fully define the role of demographics like gender and ethnicity in the degree of physiologic adaptation to endurance exercise.

Approach to Cardiovascular Symptoms Providers evaluating endurance athletes in the clinic should be prepared to assess common cardiovascular symptoms, including chest pain and palpitations. The following sections will aim to provide an initial framework for addressing these issues prior to referral to a cardiovascular specialist.

Chest Pain Chest pain is one of the most common chief complaints encountered in medical practice, and in the United States, it is the second most common reason for presentation to the emergency department [76]. As is standard practice, any athlete presenting for clinical evaluation with symptoms suggestive of severe or unstable pathology should be immediately referred for triage in an emergency setting. In the ambulatory setting, the differential diagnosis for athletes is similar to that for non-active persons and includes noncardiac pathology. Among common noncardiac patholo-

A. Hornick and C. J. Daniels

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gies causing chest pain are gastroesophageal reflux, anxiety, and respiratory infections. Especially among young athletes, underlying cardiovascular disease is not a common cause of chest symptoms [77]. Possible cardiac etiologies for chest pain in young athletes include hypertrophic cardiomyopathy, anomalous coronary arteries, and congenital valvular disease [7]. The presentation of patients with these pathologies may not mimic that of classic exertional angina; thus, a thorough history of present illness, family history, and a high degree of suspicion are required for diagnosis. Among athletes over the age of 35, atherosclerotic coronary vascular disease (ASCVD) prevalence increases significantly [23]. Classic exercise-induced chest symptoms may be expected in athletes with significant CVD. A variable syndrome of “warm-up” angina has been described, wherein chest discomfort related to coronary artery disease begins at the onset of exercise, and subsides with rest, and does not return on resumption of activity [78]. Testing in athletes with chest discomfort and classic risk factors for ASCVD like tobacco use, diabetes, and hypertension should follow expert guidelines, including the possible use of stress testing for appropriate patients [79]. Athletes should additionally be asked regarding performance-­ enhancing substances. Expert recommendations indicate that when possible, if obstructive cardiovascular disease has been ruled out, exercise testing should be tailored to the athlete in order to best simulate their preferred method and intensity of exercise [7].

Syncope Syncopal events are defined by transient loss of consciousness and postural tone as a result of cerebral hypoperfusion. This is a common clinical problem, and it is estimated that up to 40% of the general population will experience a syncopal event in their lifetime [80]. Syncopal events during exercise are an emergency, and athletes with this presentation should be immediately referred for emergency evaluation, as this may be a har-

binger of pathology predisposing to serious morbidity or sudden cardiac death. The majority of causes of syncope is benign and unrelated to a cardiovascular condition [81]. These include neurally mediated etiologies like vasovagal syncope, which is frequently preceded by either change in position or prodromal symptoms of warmth, lightheadedness, and a gradual onset of symptoms, which may allow time for the affected person to ease themselves to the ground [7]. Postexercise syncope is also neurally mediated by increased contractility and paradoxical bradycardia, termed the Bezold-Jarisch reflex, a reflex triggered by decreased blood return to the heart immediately following exercise with relaxation of the lower extremity muscles [82]. Cardiovascular etiologies of syncope include both tachy- and bradyarrhythmias, structural heart disease like hypertrophic cardiomyopathy that may cause obstruction of the left ventricular outflow tract, or anomalous coronary arteries [83]. Arrhythmic-mediated syncope, in contrast to neurologic or vasovagal syncope, is often accompanied by sudden collapse secondary to abruptly decreased cardiac output. The mainstay of syncope evaluation is a thorough history of present illness [84], including family history, to assess for familial risk factors or syndromes. ECG and echocardiography may be added if the history is unrevealing. If these tests are negative, the addition of prolonged ambulatory telemetry monitoring may be considered if the clinical suspicion for arrhythmia remains high.

Palpitations Palpitations are a subjective symptom characterized by an unpleasant awareness of the beating of the heart. Some of the descriptions may include a forceful, irregular, or fluttering heartbeat [85]. As described previously, athletes commonly have sinus bradycardia, sinus arrhythmias, and occasionally Mobitz type 1. These findings may result in a sensation of atypical heart beats. Athletes as a group also may be more keenly aware of their physical symptoms [86].

2  Cardiovascular Evaluation and Treatment in the Endurance Athlete

Palpitations are most frequently the result of arrhythmia, though these may be benign arrhythmias, like sinus tachycardia. The duration of the symptom may provide clues to the etiology, with only occasional skipped beats followed by a pause being more likely premature atrial or ventricular contractions and prolonged symptoms potentially a manifestation of sustained arrhythmia like paroxysmal atrial fibrillation or other supraventricular tachycardias [87]. The age of the athlete may also be a clue, with older athletes more likely to have atrial fibrillation as a cause of their palpitations. If the athlete is experiencing palpitations during exercise, exercise testing may be performed. Expert consensus documents recommend exercise testing with an attempt to reproduce the exercise modality during which the athlete experiences the symptom [7]. Resting ECG can also be performed and is of utility especially if the athlete is having ongoing or highly frequent symptoms. Ambulatory telemetry monitoring can also be performed, with the duration tailored to frequency of the symptom.

Approach to Athletes with Established Cardiovascular Disease Engagement in endurance athletics by masters aged athletes continues to increase. Despite the improved cardiovascular outcomes demonstrated among persons who participate in regular physical activity [14], these athletes still are at risk for cardiovascular pathology [88]. The following sections will review common cardiovascular comorbidities prevalent particularly in masters aged athletes, in order to introduce familiarity with the considerations for care of these athletes. The majority of the following conditions will require subspecialty engagement by a cardiologist with at least some knowledge of the practice of sports cardiology

29

Atherosclerotic Cardiovascular Disease (ASCVD) The leading cause of sudden cardiac death and myocardial infarction in athletes over the age of 35 is coronary artery disease [21, 89]. A recent survey-based study of masters aged athletes sought to define the atherosclerotic cardiovascular risk profile of this segment of athletes. In this study there was a high prevalence of traditional risk factors, with at least 64% of the athletes surveyed having at least one traditional ASCVD risk factor [88]. ASCVD may be clinically concealed or asymptomatic. Recently, due to the increasing prevalence of computed-tomography screening for coronary artery calcium (CAC), more athletes with clinically concealed ASCVD are being detected. A higher burden of CAC is associated with a higher risk of future cardiovascular events in the general population [90]. There has been some controversy regarding the role of exercise in accelerating the formation of coronary artery calcification. Several studies have indicated that athletes have a higher CAC burden compared to nonathletic peers, though the clinical significance of this is unknown, and it has been proposed that the higher CAC burden can often be explained by traditional risk factors [91, 92]. These findings came with several caveats, including the fact that studies find that patients with elevated CAC who exercise more often have better outcomes compared with those with similarly high CAC who exercise less [93]. Athletes with clinical ASCVD, defined as those who have had a cardiac event or have findings of ischemia on stress testing, are at much greater risk for adverse cardiovascular events than those with clinically concealed ASCVD.  Published recommendations from the ACC/AHA support maximal exercise testing and evaluation of left ventricular function for patients with established ASCVD [23]. The majority of these athletes is indicated for and should undergo

A. Hornick and C. J. Daniels

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a formal exercise-based cardiac rehabilitation program [15]. Systematic reviews have consistently shown mortality benefit and decreased readmission for patients completing cardiac rehabilitation after cardiac events [94]. All endurance athletes with coronary artery disease should be treated with aggressive risk factor modification in accordance with published guidelines, including the use of lipid lower therapy. It should be noted that initiation of statin therapy generally leads to increased CAC, though achieving lipid-lowering targets decreases cardiac events [95]. Evaluation and management of these patients should involve the input of a cardiologist.

strategy with restoration and maintenance of sinus rhythm may be preferred, including consideration for catheter-based ablation [83]. Anticoagulation to decrease thromboembolic risk is also a cornerstone of atrial fibrillation management for patients who have risk factors for embolic phenomenon as defined by the CHA2DS2-VASC score [99]. Though many athletes may have low risk factor profiles and not be indicated for anticoagulation, those who do meet criteria for anticoagulation need to be cautioned against high-impact activities to decrease the risk of pathologic bleeding [83].

Atrial Fibrillation

As with other forms of cardiovascular disease, athletes may be underdiagnosed or undertreated for hypertension, the most common cardiovascular disease in the general population [100]. Exercise, along with diet adjustment, is one of the first-line lifestyle changes for treatment of hypertension, though many endurance athletes may meet or exceed the levels of physical activity correlated with lowering blood pressure [28]. Athletes should be assessed for underlying causes of hypertension. Some areas of focus in the history taking for endurance athletes include usage patterns of nonsteroidal antiinflammatory medications and screening for anabolic steroid usage [100]. As with all hypertensive patients, emphasis should be placed on correct acquisition of blood pressure, including three separate readings in each arm, separated by 1  min. Appropriate cuff size should be selected, with the bladder of the cuff encircling 80% of the arm circumference. Expert recommendations from the ACC/ AHA suggest that stage 1 hypertension, or resting systolic blood pressure in the range of 130– 139  mmHg and diastolic blood pressure 80–89  mmHg [101], should not preclude athletes from participation in exercise [100]. Athletes otherwise may be managed according to guidelines published for the general population [101].

Among the general population, atrial fibrillation is the most prevalent arrhythmia in the United States [95], and data suggest that endurance athletes have a higher risk of developing atrial fibrillation [96]. A study published in 2016 evaluated a Scandinavian population across several decades of life and found that moderate levels of physical activity, defined as up to 4 h per week, seemed to attenuate lifetime risk of atrial fibrillation, whereas highly or vigorously active persons had a similar risk to sedentary persons [96]. Other analyses have indicated that endurance athletes are at a higher risk for atrial fibrillation [97]. Though the pathophysiology of atrial fibrillation in endurance athletes is not well understood [98], expert recommendations published by the ACC/ AHA suggest standard workup for atrial fibrillation, including assessment for coronary artery disease, hypertension, and sleep disordered breathing [83]. Management of atrial fibrillation may pose several challenges for the endurance athlete. Primary among these would be the limitations of a rate-control strategy that utilizes atrioventricular nodal agents like beta blockers or calcium channel blockers that decrease heart rate and may place a limit on exertional capacity in the endurance athlete. For this reason, a rhythm control

Hypertension

2  Cardiovascular Evaluation and Treatment in the Endurance Athlete

COVID-19 Coronavirus disease 2019 (COVID-19) has been associated with a variety of cardiovascular pathologies [102]. Perhaps the most well publicized and investigated in athletes is myocarditis, and screening for myocarditis and the development of return-to-play protocols after its diagnosis remain an area of intense focus. Though an ongoing topic of debate, proposed criteria for diagnosis of COVID-19-associated myocarditis suggest the following triad: cardiac symptoms, elevated troponin, and any of an abnormal ECG, cardiac MRI, echocardiogram, or biopsy finding [103]. The clinical relevance of this diagnosis is that myocarditis historically (though not ­specifically with COVID-19) is a recognized risk factor for sudden cardiac death in athletes [104]. The incidence of COVID-19 myocarditis is unclear, but widespread screening with cardiac MRI indicated a higher prevalence of subclinical myocardial involvement than would be detected with symptom-driven screening alone [105]. Return-to-play protocols following COVID-­19 infection without myocarditis have been published and generally recommend resumption of activity when symptoms have ceased. The most recent among these recommends that for asymptomatic athletes with COVID-19 infection, 3 days of abstinence from training is preferred to ensure symptoms do not develop [103]. Studies have additionally indicated that there is no clinically significant myocardial involvement in athletes with mild COVID-19, lending credibility to only a brief pause in training following documented infection [8]. In athletes with cardiopulmonary symptoms, screening with ECG, troponin, and echocardiogram is the current expert recommendation and, if there are abnormal findings, then cardiac MRI.  If myocarditis is excluded on MRI, exercise testing may be pursued if cardiopulmonary symptoms persist [103]. For athletes who have confirmed myocarditis, the most recent expert consensus statement recommends exercise abstinence for 3–6 months [103]. The early studies of professional athletes in the United States completing return-to-play pro-

31

tocols after COVID-19 infections have yielded good outcomes, without any episodes of cardiac arrest or severe disease [106]. More data are required to further define this clinical entity, the optimal management, and return-to-play protocols for athletes. In the interval, cautious return to play following appropriate testing is the cornerstone of expert recommendations.

Conclusion In summary, athletes represent a unique population presenting for cardiovascular care. The recent rapid increase in the amount of scientific literature describing cardiovascular adaptations to exercise and defining normal findings in various cohorts of endurance athletes has allowed for the development of expertise in the new field of sports cardiology. As participation in large-scale endurance events resumes with lifting of social distancing restrictions related to the COVID-19 pandemic, clinicians will be well positioned to serve the cardiovascular care needs of endurance athletes.

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39. Baggish AL, Wood MJ. Athlete’s heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011;123(23):2723–35. 40. Baggish AL, Battle RW, Beaver TA, et  al. Recommendations on the use of multimodality cardiovascular imaging in young adult competitive athletes: a report from the American society of echocardiography in collaboration with the society of cardiovascular computed tomography and the society for cardiovascular magnetic resonance. J Am Soc Echocardiogr. 2020;33(5):523–49. 41. Maron BJ. Structural features of the athlete heart as defined by echocardiography. J Am Coll Cardiol. 1986;7(1):190–203. 42. Morganroth J, Maron BJ, Henry WL, Epstein SE.  Comparative left ventricular dimensions in trained athletes. Ann Intern Med. 1975;82(4):521–4. 43. Wasfy MM, Weiner RB, Wang F, et  al. Endurance exercise-induced cardiac remodeling: not all sports are created equal. J Am Soc Echocardiogr. 2015;28(12):1434–40. 44. Prakken NH, Velthuis BK, Teske AJ, Mosterd A, Mali WP, Cramer MJ.  Cardiac MRI reference values for athletes and nonathletes corrected for body surface area, training hours/week and sex. Eur J Cardiovasc Prev Rehabil. 2010;17(2):198–203. 45. Weiner RB, Wang F, Isaacs SK, et  al. Blood pressure and left ventricular hypertrophy during American-style football participation. Circulation. 2013;128(5):524–31. 46. Churchill TW, Petek BJ, Wasfy MM, et al. Cardiac structure and function in elite female and male soccer players. JAMA Cardiol. 2021;6(3):316–25. 47. Pelliccia A, Culasso F, Di Paolo FM, Maron BJ.  Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med. 1999;130(1):23–31. 48. Weiner RB, Wang F, Hutter AM, et al. The feasibility, diagnostic yield, and learning curve of portable echocardiography for out-of-hospital cardiovascular disease screening. J Am Soc Echocardiogr. 2012;25(5):568–75. 49. Abergel E, Chatellier G, Hagege AA, et  al. Serial left ventricular adaptations in world-class professional cyclists: implications for disease screening and follow-up. J Am Coll Cardiol. 2004;44:144–9. 50. Oxborough D, Sharma S, Shave R, Whyte G, Birch K, Artis N, et  al. The right ventricle of the endurance athlete: the relationship between morphology and deformation. J Am Soc Echocardiogr. 2012;25(3):263–71. 51. Scharhag J, Schneider G, Urhausen A, Rochette V, Kramann B, Kindermann W.  Athlete’s heart: right and left ventricular mass and function in male endurance athletes and untrained individuals determined by magnetic resonance imaging. J Am Coll Cardiol. 2002;40(10):1856–63. 52. D’Andrea A, Riegler L, Golia E, Cocchia R, Scarafile R, Salerno G, et  al. Range of right heart measurements in top-level athletes: the training impact. Int J Cardiol. 2013;164(1):48–57.

34 53. Grünig E, Henn P, D’Andrea A, et  al. Reference values for and determinants of right atrial area in healthy adults by 2-dimensional echocardiography. Circ Cardiovasc Imaging. 2013;6(1):117–24. 54. Iskandar A, Mujtaba MT, Thompson PD. Left atrium size in elite athletes. JACC Cardiovasc Imaging. 2015;8(7):753–62. 55. Pelliccia A, Spataro A, Caselli G, Maron BJ.  Absence of left ventricular wall thickening in athletes engaged in intense power training. Am J Cardiol. 1993;72:1048–54. 56. Lin J, Wang F, Weiner RB, DeLuca JR, Wasfy MM, Berkstresser B, et al. Blood pressure and LV remodeling among American-style football players. JACC Cardiovasc Imaging. 2016;9(12):1367–76. 57. Churchill TW, Groezinger E, Kim JH, et  al. Association of ascending aortic dilatation and long-­ term endurance exercise among older masters-level athletes. JAMA Cardiol. 2020;5:522–31. 58. Iskandar PDT. A meta-analysis of aortic root size in elite athletes. Circulation. 2013;127:791–8. 59. Gentry JL, Carruthers D, Joshi PH, Maroules CD, Ayers CR, de Lemos JA, et  al. Ascending aortic dimensions in former national football league athletes. Circ Cardiovasc Imaging. 2017;10(11):e006852. 60. Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg. 2002;73(1):17–27. 61. D'Andrea A, Cocchia R, Riegler L, Scarafile R, Salerno G, Gravino R, Vriz O, Citro R, Limongelli G, Di Salvo G, Cuomo S, Caso P, Russo MG, Calabro R, Bossone E.  Aortic root dimensions in elite athletes. Am J Cardiol. 2010;105:1629–34. 62. Corrado D, Pelliccia A, Heidbuchel H, Sharma S, Link M, Basso C, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31(2):243–59. 63. Drezner JA. Standardised criteria for ECG interpretation in athletes: a practical tool. Br J Sports Med. 2012;46(Suppl 1):i6–8. 64. Riding NR, Sheikh N, Adamuz C, Watt V, Farooq A, Whyte GP, et al. Comparison of three current sets of electrocardiographic interpretation criteria for use in screening athletes. Heart. 2015;101(5):384–90. 65. Wasfy MM, DeLuca J, Wang F, Berkstresser B, Ackerman KE, Eisman A, et al. ECG findings in competitive rowers: normative data and the prevalence of abnormalities using contemporary screening recommendations. Br J Sports Med. 2015;49(3):200–6. 66. Stein R, Medeiros CM, Rosito GA, Zimerman LI, Ribeiro JP. Intrinsic sinus and atrioventricular node electrophysiologic adaptations in endurance athletes. J Am Coll Cardiol. 2002;39(6):1033–8. 67. Calore P, Melacini AP, et  al. Prevalence and clinical meaning of isolated increase of QRS voltages in hypertrophic cardiomyopathy versus athlete’s

A. Hornick and C. J. Daniels heart: relevance to athletic screening. Int J Cardiol. 2013;168:4494–7. 68. Aagaard P, Baranowski B, Aziz P, Phelan D. Early repolarization in athletes: a review. Circ Arrhythm Electrophysiol. 2016;9(3):e003577. 69. Quattrini FM, Pelliccia A, Assorgi R, et al. Benign clinical significance of J-wave pattern (early repolarization) in highly trained athletes. Heart Rhythm. 2014;11:1974–82. 70. Pelliccia A, Maron BJ, Culasso F, Spataro A, Caselli G.  Athlete's heart in women. Echocardiographic characterization of highly trained elite female athletes. JAMA. 1996;276:211–5. 71. Whyte GP, George K, Sharma S, Firoozi S, Stephens N, Senior R, et al. The upper limit of physiological cardiac hypertrophy in elite male and female athletes: the British experience. Eur J Appl Physiol. 2004;92(4–5):592–7. 72. Sheikh N, Sharma S.  Impact of ethnicity on cardiac adaptation to exercise. Nat Rev Cardiol. 2014;11(4):198–217. 73. Papadakis M, Carre F, Kervio G, Rawlins J, Panoulas VF, Chandra N, Basavarajaiah S, Carby L, Fonseca T, Sharma S. The prevalence, distribution, and clinical outcomes of electrocardiographic repolarization patterns in male athletes of African/Afro-Caribbean origin. Eur Heart J. 2011;32:2304–13. 74. Sheikh N, Papadakis M, Ghani S, et al. Comparison of electrocardiographic criteria for the detection of cardiac abnormalities in elite black and white athletes. Circulation. 2014;129:1637–49. 75. Calore A, Zorzi N, Sheikh A, Nese M, Facci AM, et al. Electrocardiographic anterior T-wave inversion in athletes of different ethnicities: differential diagnosis between athlete's heart and cardiomyopathy. Eur Heart J. 2016;37:2515–27. 76. CDC ambulatory healthcare data. https://www.cdc. gov/nchs/ahcd/web_tables.htm. 77. Perron AD. Chest pain in athletes. Clin Sports Med. 2003;22(1):37–50. 78. Lockie TPE, Rolandi MC, Guilcher A, Perera D, De Silva K, Williams R, et  al. Synergistic adaptations to exercise in the systemic and coronary circulations that underlie the warm-up angina phenomenon. Circulation. 2012;126(22):2565–74. 79. Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, et al. 2021 AHA/ACC/ASE/ CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain: a report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines. Circulation. 2021;144(22):e368–454. 80. Task Force for the Diagnosis and Management of Syncope, European Society of Cardiology (ESC), European Heart Rhythm Association (EHRA), Heart Failure Association (HFA), Heart Rhythm Society (HRS), Moya A, Sutton R, Ammirati F, Blanc J-J, Brignole M, Dahm JB, et al. Guidelines for the diag-

2  Cardiovascular Evaluation and Treatment in the Endurance Athlete nosis and management of syncope (version 2009). Eur Heart J. 2009;30:2631–71. 81. Madan S, Chung E. The Syncopal Athlete. American College of Cardiology; 2016. 82. Campagna JA, Carter C.  Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology. 2003;98:1250–60. 83. Zipes DP, Link MS, Ackerman MJ, Kovacs RJ, Myerburg RJ, Estes NAM 3rd. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: task force 9: arrhythmias and conduction defects: a scientific statement from the American Heart Association and American college of cardiology. J Am Coll Cardiol. 2015;66:2412–23. 84. O'Connor FG, Levine B. Syncope in athletes of cardiac origin: 2B.  From personal history and physical examination sections. Curr Sports Med Rep. 2015;14:254–6. 85. Zimetbaum P, Josephson ME.  Evaluation of patients with palpitations. N Engl J Med. 1998;338(19):1369–73. 86. Lawless CE, Briner W.  Palpitations in athletes. Sports Med. 2008;38(8):687–702. 87. Giada F, Raviele A.  Clinical approach to patients with palpitations. Card Electrophysiol Clin. 2018;10(2):387–96. 88. Shapero K, Deluca J, Contursi M, Wasfy M, Weiner RB, Lewis GD, et al. Cardiovascular risk and disease among masters endurance athletes: insights from the Boston master (masters athletes survey to evaluate risk) initiative. Sports Med Open. 2016;2:29. 89. Parker MW, Thompson PD.  Assessment and management of atherosclerosis in the athletic patient. Prog Cardiovasc Dis. 2012;54(5):416–22. 90. Hou ZH, Lu B, Gao Y, Jiang SL, Wang Y, Li W, Budoff MJ. Prognostic value of coronary CT angiography and calcium score for major adverse cardiac events in outpatients. JACC Cardiovasc Imaging. 2012;5:990–9. https://doi.org/10.1016/j. jcmg.2012.06.006. 91. Merghani V, Maestrini SR, et al. Prevalence of subclinical coronary artery disease in masters endurance athletes with a low atherosclerotic risk profile. Circulation. 2017;136:126–37. 92. Aengevaeren VL, Mosterd A, Braber TL, et  al. Relationship between lifelong exercise volume and coronary atherosclerosis in athletes. Circulation. 2017;136:138–48. 93. DeFina LF, Radford NB, Barlow CE, et  al. Association of all-cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiol. 2019;4:174–81. 94. Anderson L, Thompson DR, Oldridge N, Zwisler AD, Rees K, Martin N, et al. Exercise-based cardiac rehabilitation for coronary heart disease. Cochrane Database Syst Rev. 2016;(1):CD001800.

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95. Zhao XQ, Dong L, Hatsukami T, Phan BA, Chu B, Moore A, et al. MR imaging of carotid plaque composition during lipid-lowering therapy a prospective assessment of effect and time course. JACC Cardiovasc Imaging. 2011;4(9):977–86. 96. Morseth B, Graff-Iversen S, Jacobsen BK, et  al. Physical activity, resting heart rate, and atrial fibrillation: the Tromsø study. Eur Heart J. 2016;37:2307–13. 97. Grimsmo J, Grundvold I, Maehlum S, Arnesen H. High prevalence of atrial fibrillation in long-term endurance cross-country skiers: echocardiographic findings and possible predictors: a 28-30 years follow-up study. Eur J Cardiovasc Prev Rehabil. 2010;17:100–5. 98. Sorokin AV, Araujo CGS, Zweibel S, Thompson PD. Atrial fibrillation in endurance-trained athletes. Br J Sports Med. 2011;45(3):185–8. 99. Friberg L, Rosenqvist M, Lip GYH.  Net clinical benefit of warfarin in patients with atrial fibrillation: a report from the Swedish atrial fibrillation cohort study. Circulation. 2012;125(19):2298–307. 100. Black HR, Sica D, Ferdinand K, White WB, American Heart Association Electrocardiography and Arrhythmias Committee of Council on Clinical Cardiology, Council on Cardiovascular Disease in Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and American College of Cardiology. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: task force 6: hypertension: a scientific statement from the American Heart Association and the American College of Cardiology. Circulation. 2015;132(22):e298–302. 101. Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C, et  al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APHA/ASH/ ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. Hypertension. 2018;71(6):e13–115. 102. Sandoval Y, Januzzi JL, Jaffe AS. Cardiac troponin for assessment of myocardial injury in COVID-19: JACC review topic of the week. J Am Coll Cardiol. 2020;76:1244–58. 103. Gluckman TJ, Bhave NM, Allen LA, Chung EH, Spatz ES, et al. 2022 ACC expert consensus decision pathway on cardiovascular sequelae of covid-19  in adults: myocarditis and other myocardial involvement, post-acute sequelae of sars-cov-2 infection, and return to play: a report of the American College of Cardiology solution set oversight committee. J Am Coll Cardiol. 2022;79(17):1717–56. 104. Eichhorn C, Biere L, Schnell F, et  al. Myocarditis in athletes is a challenge: diagnosis, risk stratifica-

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3

Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction Alexys Monoson and Jonathan Parsons

Chapter

may improve athlete performance and quality of life. Exercise-induced bronchoconstriction (EIB) EIB is common in athletes, with a prevalence describes acute, transient airway narrowing that of 35–39% among elite and varsity athletes [4, 5] occurs in association with exercise. There are and 13.2% among recreationally active adults implications for athletes both on and off the play- [6]. This is likely even more common among proing field. It is estimated that 5–20% of the general fessional athletes and those participating in winpopulation and 90% of people with asthma ter sports. Wilber and associates [7] found that experience EIB [1]. In 2011, the EIB Landmark 18–26% of Olympic winter sports athletes, Survey was the first comprehensive study on including 50% of cross-country skiers, had exercise-related respiratory symptoms in the EIB.  In contrast, the US Olympic Committee United States. Not only was there a general lack reported an 11.2% prevalence of EIB in all athof awareness and treatment adherence for EIB, letes who competed in the 1984 Summer but exercise-related respiratory symptoms were Olympics [8]. Other studies have reported the also found to negatively impact people’s activity prevalence of EIB among Olympic athletes to be levels. Almost half (45.6%) of the adult patients between 30% and 70% [2, 9]. EIB is also often surveyed with asthma reported that they avoid seen among adolescent athletes. Of 549 Swedish physical activity altogether due to respiratory students enrolled at a sports high school, 23.1% symptoms [1]. EIB is not only physically limiting, were found to have EIB [10]. This trend is similar but it also adversely impacts quality of life. among children, with an estimated prevalence of Adolescent athletes who self-reported dyspnea 12% [11] among the general pediatric population with exercise had a significantly lower health-­ and 23% among school children [12]. Ethnicity related quality of life, including scores for well-­ may have an impact on the prevalence of EIB, but being and emotional functioning [2, 3]. Increasing this data is less conclusive as there has been only awareness of the diagnosis and treatment of EIB one study examining this. Within inner-city Scottish and English schools, the prevalence of EIB among children of Asian descent was 12.3%, those of Afro-Caribbean descent was 9.1%, and A. Monoson · J. Parsons (*) those of Caucasian descent was 4.5% [13]. Department of Internal Medicine, Division of Studies conducted in Kenya and India have sugPulmonary, Critical Care, and Sleep, The Ohio State University Wexner Medical Center, gested that there may be a higher prevalence of Columbus, OH, USA disease among those living in urban areas [2, 14]. e-mail: [email protected]; Jonathan. A recent meta-analysis suggests that EIB may [email protected] © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_3

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also have a sexual disparity among athletes. Among studies reviewed, there was no increased prevalence of EIB itself; however, atopy was more common among male than female athletes [15]. Although there are numerous reports on the prevalence of EIB in asthmatic athletes, few ­studies have investigated the prevalence of EIB in those without a known history of asthma or EIB. Mannix and associates [16] found that 19% of subjects without a previous asthma diagnosis had EIB.  Rupp and colleagues [17] evaluated 230 middle and high school student athletes and, after excluding those with known asthma and EIB, found that 29% had EIB.  A study among college athletes found that only 14% of those who tested positive for EIB had a previous diagnosis of asthma or EIB [5], raising concern that EIB is likely underdiagnosed among this population. The prevalence of EIB may be further underestimated because patients with asthma and EIB have been shown to be poor perceivers of bronchospasm [18, 19]. In a previous study of varsity athletes, only 36% of participants who were found to have EIB reported symptoms [5]. Among elite athletes, there was no difference in reported symptoms between those with and without EIB [20]. Even if they do recognize they have a medical problem, athletes may not want to admit this to health personnel for fear of social stigma and loss of game time. Healthcare providers and coaches may also not consider EIB as a possible explanation for respiratory symptoms occurring during exercise. Athletes are generally healthy, and the possibility of a significant medical problem is often not taken into account. The athlete is frequently considered to be “out of shape”; vague symptoms of chest discomfort, breathlessness, and fatigue are often ignored. Athletes who compete in high-ventilation or endurance sports may be more likely to experience symptoms of EIB than those who participate in low-ventilation sports [21]. For example, athletes who participate in cross-country skiing, swimming, and long-distance running have a high prevalence of EIB [21]. In fact, the prevalence of EIB among cross-country skiers is

A. Monoson and J. Parsons

typically four times higher than among other skiers [22, 23]. Environmental triggers may predispose athletes to EIB.  Chlorine compounds in swimming pools have been linked to reactive airway dysfunction [24, 25]. Swimmers (both synchronized and racing) have an increased prevalence of EIB [23, 26]. Cyclists, particularly those who ride on roads, are often exposed to carbon monoxide, a common component of vehicle exhaust [23, 27]. Athletes who compete on ice rinks such are often subjected to high levels of pollutants that have been linked to airway dysfunction including carbon monoxide, nitrogen dioxide, sulfur dioxide, and fine particulate matter from ice resurfacing machines [23, 28, 29]. Sports such as ice hockey, track and field, skating, cross-country skiing, mountain biking, cycling, swimming, and rowing have the highest prevalence of EIB without known underlying asthma [30]. Interestingly, these sports tend to have both a high ventilatory requirement and frequent exposure to air toxins. Badminton and weightlifting, which have a low ventilation and toxin exposure, have an EIB prevalence similar to that of the general population [23, 27]. The clinical manifestations of EIB are variable and can range from mild impairment of performance to severe bronchospasm and respiratory failure. Common symptoms include coughing, wheezing, chest tightness, and dyspnea. More subtle evidence of EIB includes fatigue, symptoms that occur in specific environments (e.g., ice rinks or swimming pools), postexercise cough, poor performance for conditioning level, and avoidance of activity (Table 3.1). Symptoms of EIB occur after at least a few minutes of exercise and typically peak 5–10 min after physical activity is complete [31]. In order to generate bronchospasm in most athletes, a patient must achieve a workload representing at least 80% of the maximal predicted oxygen consumption for 5–8  min [32] or ventilation corresponding to 17.5–21 times the forced expiratory volume (FEV1) [33, 34]. Symptoms persist for 30  min or longer without bronchodilators. Though some athletes are able

3  Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction Table 3.1 Common symptoms of exercise-induced bronchoconstriction Dyspnea on exertion Chest tightness Wheezing Fatigue Poor performance for conditioning level Activity avoidance Post-exercise cough Fatigue Symptoms that occur in specific environments (e.g. ice rinks or swimming pools)

to return to baseline airflow within 60  min without treatment [31], it is currently impossible to predict which athletes will recover without therapy. Athletes who experience symptoms for extended periods often perform at suboptimal levels for significant portions of their competitive or recreational activities. The presence of EIB can be challenging to recognize because symptoms are often nonspecific. A complete history and physical ­ examination should be performed on every athlete with exertional dyspnea because self-reported symptoms alone are neither sensitive nor specific for a diagnosis of EIB. Hallstrand and colleagues [35] found that screening history identified subjects with symptoms or a previous diagnosis suggestive of EIB in 40% of participants, but only 13% of these persons actually had EIB after objective testing. Similarly, Rundell and associates [20] demonstrated that only 61% of EIB-positive athletes reported symptoms of EIB, whereas 45% of athletes with normal objective testing reported symptoms. Other medical problems that can mimic EIB and need to be considered in the initial evaluation of exertional dyspnea include exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, diaphragmatic paralysis, obesity, gastroesophageal reflux disease, allergic rhinitis, pulmonary hypertension, myopathy, parenchymal lung disease, and cardiac disease [36] (Table 3.2). In a young and athletic population, many of these diagnoses are rare. Keeping this in mind, they should be considered in atypical presentations or with patients not responding to standard therapy.

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Table 3.2  Diseases that may mimic exercise-induced bronchoconstriction Exercise-induced laryngeal dysfunction (including vocal cord dysfunction) Exercise-induced anaphylaxis Gastroesophageal reflux disease Allergic rhinitis Obesity Pulmonary hypertension Cardiac disease Parenchymal lung disease Diaphragmatic paralysis Myopathy Deconditioning

A comprehensive history and examination are recommended to evaluate for other disorders, and specific testing such as echocardiography may be required. A detailed history of specific symptoms as they relate to the patient’s activity and environment, occupational history, and a detailed family history is also recommended. A family history is particularly important in patients suspected to have underlying asthma, as a positive family history is correlated with increased risk of developing asthma themselves [37]. Objective testing should begin with spirometry before and after inhaled bronchodilator therapy to identify athletes with asthma. Many people who experience EIB have normal baseline lung function (i.e., FEV1 ≥ 70%) [36], which may lead to a significant number of false-negative results if adequate exercise and environmental stress are not provided. Indirect bronchoprovocation testing is indicated for patients being evaluated for EIB with normal spirometry [36]. A positive bronchoprovocation test is consistent with the diagnosis of EIB. Patients with spirometry showing reversible airway obstruction (generally an increase in FEV1 of ≥12% after beta2 agonist administration) may carry a diagnosis of asthma which would put them at a high risk of EIB.  It should be noted that not all patients who have reversible airway obstruction on spirometry have asthma, and results must be interpreted in the right clinical setting. Persistent symptoms and a lack of reversibility to a beta2 agonist suggest an alternative diagnosis [36].

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A positive bronchoprovocation test indicates the need for treatment of EIB. Specific tests have varying positive values, but a change (generally ≥10% decrease in FEV1) between pretest and posttest values is suggestive of EIB [38]. Not all bronchoprovocation techniques are equally valuable or accurate in assessing EIB in athletes. The 2016 practice update in the Journal of Allergy and Clinical Immunology recommends using an indirect graded challenge (such as exercise or surrogate testing with eucapnic voluntary hyperventilation) rather than a direct graded challenge (such as methacholine) due to the increased sensitivity of an indirect challenge [36]. Though this guideline does not specify which type of indirect challenge is preferable in athletes, the International Olympic Committee recommends eucapnic voluntary hyperventilation (EVH) testing for documentation of EIB in Olympians [39]. EVH involves hyperventilation of a gas mixture of 5% carbon dioxide and 21% oxygen at a target ventilation of 85% of the patient’s maximal voluntary ventilation in 1 min (MVV). The MVV is usually calculated as 35 times the baseline FEV1. The patient hyperventilates for 6 min, and assessment of FEV1 occurs at specified intervals up to 20 min after the test. Not only does EVH have a high specificity for EIB, but it is also more sensitive than field or lab-based testing [40]. Field exercise challenge testing involves assessing the athlete’s FEV1 before and after they participate in their normal sport. Because of the inherent challenges in this testing, it offers little opportunity for standardization. The goal of therapy is to minimize symptoms and improve athletic performance. It is important for a patient to have regular visits with their clinician, as treatment needs may fluctuate throughout the year and the athlete’s training schedule [36]. Non-pharmacologic treatments offer an easy and effective way to reduce symptoms. Athletes should perform warm-up exercises, avoid exposure to air pollutants and allergens if able, and wear a scarf or face mask to warm and humidify inhaled air [2, 34, 36]. Many athletes find that a period of pre-competition warm-up induces a “refractory period,” during which they do not

A. Monoson and J. Parsons

experience symptoms of EIB. It has been shown that this refractory period occurs in some athletes with asthma and can last for up to 2 h after the warm-up [41, 42]. This has not been consistently proven across different populations [43]. In patients with underlying asthma, EIB symptoms may be a sign of inadequate asthma control. In these patients, treatment should focus on optimizing their asthma medication regimen [2]. If asthma is otherwise well controlled, treatment should focus on EIB alone. The most effective pharmacologic therapy is use of a shortacting beta2 agonist (SABA) approximately 15  min prior to exercise [36]. SABAs work by inducing airway smooth muscle relaxation and bronchodilation to prevent FEV1 from falling during exercise. Peak bronchodilation is achieved approximately 15–60 min after use and lasts for 3  h. Interestingly when SABAs are combined with warm-up exercise, they provide additive protection against EIB that is greater than SABA or warm-up therapy alone [2, 34, 44]. Regular use of SABAs leads to medication tolerance and should only be used as monotherapy when intermittent treatment is required (generally less often than daily) [2, 34]. Long-acting bronchodilators (LABAs) work similarly to short-acting bronchodilators and last up to 12  h [45]. As with SABAs, medication tolerance is a concern with LABAs. A metaanalysis suggested that the bronchoprotective effect of salmeterol at 9  h posttreatment is reduced after 4  weeks [2, 46]. Long-acting bronchodilators are not recommended as monotherapy in EIB given the increased risk of adverse outcomes and are generally prescribed in combination with an inhaled corticosteroid [47]. For patients with underlying asthma, inhaled corticosteroids (ICS) represent a fundamental aspect of treatment. The most recent Global Initiative for Asthma (GINA) guidelines recommend an as-needed ICS-LABA inhaler as first-­line treatment. If a patient requires further control beyond this, a standing ICS is the next recommended step [47]. ICS inhalers have been shown to decrease the frequency and severity of EIB [36]. Some degree of bronchoprotection against EIB with a high

3  Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction

dose ICS has been seen as early as 4 h after the first dose though it may take weeks to months to reach peak effect [36, 48]. Leukotriene modifiers have also been shown to be effective in treating EIB. Unlike SABA and LABA medications, daily use of a leukotriene inhibitor does not lead to tolerance or rebound worsening lung functioning after treatment cessation [36]. Leff and colleagues [49] evaluated the ability of montelukast, a leukotriene receptor antagonist, to protect asthmatic patients against EIB.  Montelukast therapy offered a greater ­protection against EIB than placebo therapy and was also associated with a significant improvement in the maximal decrease in FEV1 after exercise. There is a high level of variability in leukotriene inhibitors among patients with EIB [50], and thus they may not work for all patients. Mast cell stabilizers have been studied extensively for EIB, but they are not often used due to their lack of ability in the United States as inhalers and their short duration of action (generally 1–2  h). In a meta-analysis of the prevention of EIB in asthmatic patients, nedocromil sodium was found to improve FEV1 by an average of 16% and to shorten the duration of EIB symptoms to less than 10 min [51]. They may be effective alone or in addition to other drugs for EIB [36]. Other pharmacologic therapies have been studied for the treatment of EIB, though results have been mixed. Drug classes studied thus far include anticholinergic agents, methylxanthines, antihistamines, caffeine, calcium channel blockers, inhaled furosemide, and inhaled heparin among others [36]. These drugs are not currently recommended for treatment of EIB, although research is ongoing. Dietary modifications (low-­ sodium diet, supplementation with vitamin C, lycopene, or fish oil) have similarly been studied with mixed results [34].

Vocal Cord Dysfunction Vocal cord dysfunction (VCD) is a disorder characterized by inappropriate adduction of the vocal cords during inspiration that causes wheezing, stridor, and dyspnea [52]. The first modern case

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report of VCD was in 1974, when Patterson and colleagues described what they believed to be a purely psychogenic case of respiratory distress that they labeled “Munchausen’s stridor” [53]. Since this time there have been a number of research studies demonstrating that VCD is in fact a complex, multifactorial disorder with a variety of triggers. It can be challenging to diagnose, as it often mimics and coexists with EIB and asthma and is often triggered by exercise. This is particularly important for athletes, as VCD has implications both on and off of the playing field. VCD leads to decreased exercise tolerance [54] and is an independent risk factor for a poorer quality of life [55]. The prevalence of VCD is difficult to determine due to the lack of a uniform definition and standardized diagnostic criteria [56]. Among the general population, the prevalence of VCD has been estimated to be somewhere between 2.8% and 59% [57–59]. In a study by Jain and colleagues, 22% of patients at a Texas hospital who presented to the emergency room with acute dyspnea had a diagnosis of VCD [60]. The prevalence among athletes appears to be similar to that of the general population. At the US Olympic Training Center in Lake Placid, VCD was present in approximately 5.1% of athletes [61]. There is evidence that the disorder is more prevalent among women. After performing a systematic literature review of 1530 patients with VCD, Brugman [62] found that 3 out of 4 patients were female. Another systematic review by Morris et  al. [63] had similar results. Among 1161 patients with VCD, there was a female-tomale ratio of 2:1. Both reviews showed that VCD may occur at any age, with presentation from infancy to old age. There have been many studies examining the symptoms of VCD, which are summarized in Table 3.3. Across three large systematic reviews, the most common symptoms were dyspnea, wheezing, cough, and stridor [62, 64, 65]. Other presenting symptoms include exercise-induced voice changes, throat tightness, stridor, chest pain, throat pain, and choking. The severity of symptoms is variable, ranging from limited episodes with minimal impact on the patient to

42 Table 3.3  Symptoms of vocal cord dysfunction Wheezing Stridor Dyspnea Chest tightness Neck or throat tightness Cough Exercise-induced voice changes Failure to respond to standard therapies for bronchospasm Choking

severe presentations prompting treatment at an emergency department. Newman et  al. [64] found that the average patient with VCD had visited the emergency department 9.7 times in the past year and had been admitted for evaluation 5.9 times. Though VCD by itself is not lifethreatening, failure to recognize the diagnosis has led to intubation in 28% of patients with VCD [64] and has even led to patients undergoing tracheostomy [63]. Although EIB and VCD can be difficult to distinguish due to their overlapping symptoms, there are aspects of the patient’s history that may suggest one diagnosis over another. The timing of symptoms is often a feature that differs between the two disorders. EIB typically presents 5–10  min after initiating exercise and may last for up to an hour after exercise [31]. VCD is often abrupt in both onset and cessation, frequently with symptoms lasting less than 2 min [56, 63]. Not only can the timing of symptoms after initiation of exercise be suggestive of a diagnosis, but the timing of symptoms within the respiratory cycle may suggest one diagnosis or another. High-pitched inspiratory sounds loudest when auscultated at the neck are consistent with stridor, which is more suggestive of VCD. On the other hand, wheezing with expiration over the lung fields may be more suggestive of EIB [56, 63]. Though this may be helpful if examining a patient with symptoms, it is often difficult for patients to distinguish between these symptoms. Patients with VCD are often misdiagnosed with asthma or EIB and may present for treatment after they have failed to respond to multiple rounds of oral steroids and bronchodilator therapies. Morris and

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colleagues [63] found that among 380 patients with VCD, 32.7% had been previously misdiagnosed with asthma. Oral corticosteroids are a cornerstone of therapy for acute asthma exacerbations, but they are unhelpful in treatment of VCD.  Despite this, Newman et  al. [64] discovered that among a large cohort of patients with VCD, the average patient was taking the equivalent of 29.2 mg of prednisolone per day. A further diagnostic challenge is that there are many patients who have coexistent VCD, asthma, and EIB. Among a case series of 95 patients with VCD, 56% also had a diagnosis of asthma by bronchoprovocation or peak flow variability [64]. Out of 20 patients diagnosed with VCD in the ambulatory setting, 7 also held a diagnosis of asthma [66]. Similarly, when VCD was evaluated in the emergency department, 60% of patients with laryngoscopic evidence of VCD also had portable spirometry consistent with asthma [60]. There are a number of known triggers for VCD that can be categorized as either organic or inorganic. The pathogenesis behind these various triggers is poorly understood and likely differs by the type of trigger. Many of the organic causes are known to cause chronic laryngeal irritation. These triggers include gastroesophageal reflux (GERD), allergic rhinitis, and chronic exposure to smoke and chemical fumes [63, 67]. Among patients with VCD, it is estimated that 17–56% have GERD symptoms [58, 68]. Furthermore, after effective treatment of GERD, many patients experienced resolution of their VCD symptoms [69]. Exposure to a multitude of chemicals including air pollutants and perfume has also been shown to induce VCD [70]. Balkissoon and colleagues hypothesized that these irritants may accentuate glottic closure as a protective measure to prevent toxins from entering the lungs [71]. Ayres and Gabbot suggested that chronic irritant exposure may lead to an autonomic imbalance [72]. Morrison et al. furthered this hypothesis by postulating that frequent irritant exposure alters the cell genome and induces a chronic hyperexcitable state in the portion of the brainstem that controls laryngeal function [73]. Inorganic VCD triggers include a number of psychiatric conditions such as depression, factitious disorder,

3  Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction

obsessive-compulsive disorder, anxiety, and conversion disorder [63]. It has been suggested that for patients with psychologically mediated VCD, there is a dysregulation of the central respiratory mechanism that is triggered by anxiety or panic [74]. Treatment of underlying psychiatric disorders has been shown to alleviate VCD symptoms among select patients [75]. Evaluation of VCD begins with symptom recognition. Given the strong personal drive among many athletes, they may fail to recognize that they have an underlying medical condition. Instead they may blame symptoms on deconditioning and only present to medical care after prompting by coaches or teammates. Once they establish with a clinician, the initial step is to perform a thorough history and physical exam. If VCD is suspected, the patient should undergo pulmonary function testing. Spirometry, lung volumes, and diffusion capacity may be suggestive of other pulmonary disorders that may be contributing to a patient’s dyspnea, although the presence of these disorders does not rule out a concomitant diagnosis of VCD. The flow-volume loop is of particular importance in the evaluation of VCD and is illustrated in Fig. 3.1. The inspiratory limb from the patient with VCD is flattened when compared to that from a healthy patient. This has been referred to as the “sail sign,” or “up arrow,” and is suggestive of variable extra-­ thoracic obstruction. While this is not diagnostic, VCD is the most common disorder that causes this pattern. If pulmonary function testing is normal, bronchoprovocation testing should be pursued as outlined earlier in this chapter. If this is nondiagnostic for EIB or if clinical suspicion for VCD remains, direct visualization via video laryngoscopy (VLS) should be performed. This serves to diagnose VCD, rule out other structural causes of variable extra-thoracic obstruction, and identify exacerbating conditions such as vocal cord polyps, chronic sinusitis, and GERD. The diagnostic characteristics of VCD on VLS include the following: adduction of the vocal cords during inspiration (or both expiration and inspiration), >50% closure of the cords, and a diamondshaped “chink” (narrow opening in the posterior

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one third of the vocal cords) [76, 77]. Otolaryngologists often perform the VLS examination in the office with the patient at rest, though Heinle et al. [78] suggest that the test be performed with exercise if this is thought to be the cause of the patient’s VCD. The treatment of VCD should begin with addressing comorbid conditions. Some authors have suggested empiric treatment of GERD given the high incidence in this population and the data suggesting VCD symptoms improve with aggressive GERD management [69, 79]. Treatment for asthma, EIB, rhinitis, underlying psychiatric conditions, and other comorbidities should be optimized with referral to a specialist if needed. Laryngeal control therapy (LCT) is the cornerstone of treatment for VCD. LCT is a type of cognitive behavioral therapy administered by speech and language therapists that focuses on recognizing the symptoms of VCD and implementing behaviors to prevent and control symptoms. These techniques retrain the patient to breathe using the muscles of the chest and abdomen instead of with their larynx. Not only is it important for the athlete to master these techniques, but it is often helpful for their coach or trainer to be familiar with LCT [76]. There are a number of exercises for VCD control. Sandage and Zelazny [80] suggest three common techniques: tightening and relaxing exercises, low breathing, and breathing recovery. Tightening and relaxing involves a therapist asking a patient to perform sequential muscle contractions throughout their body, focusing on identifying areas of tension. Low breathing is a technique in which the patient decreases tension in their upper body by focusing on expanding their abdomen during inspiration. Breathing recovery (also known as sniffing) focuses on training a patient to inhale quickly through their nose, which causes abduction of the vocal cords. This is followed by a slow exhale through pursed lips. These techniques are often aided by use of biofeedback, which involves a patient observing themselves while performing relaxation exercises. This allows them to quickly adjust their movements and create a strong internal feedback loop with the correct technique.

A. Monoson and J. Parsons 12

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Fig. 3.1  This figure demonstrates a normal flow-volume loop (left) and a flow-volume loop for a patient with vocal cord dysfunction (right). Note the flattening of the inspiratory limb in the flow-volume loop from the patient with

vocal cord dysfunction. This is suggestive of variable extra-thoracic obstruction and is often referred to as the “sail sign” or “up arrow”

Biofeedback can be done in front of a mirror or via VLS. In VLS, the patient is able to see their own vocal cords projected onto a screen. This is a particularly effective technique that has shown a significant improvement in symptoms over a 3-month period [81]. After a patient has perfected their LCT exercises, they should continue to use them with physical activity and any VCD symptoms. Even when asymptomatic, athletes should continue to practice 3–5 times per day. It may also be helpful for a patient to keep a journal of their symptoms, activities, and stressors so they may better avoid triggers [70]. Although recurrences are common, they can be mitigated by rigorous adherence to LCT exercises [82]. The overall prognosis of VCD is quite good, with 69% of college athletes experiencing symptom improvement after therapy [83].

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46 Effect of repeated exercise challenge. Eur J Respir Dis. 1982;63(5):472–80. 42. McKenzie DC, McLuckie SL, Stirling DR. The protective effects of continuous and interval exercise in athletes with exercise-induced asthma. Med Sci Sports Exerc. 1994;26(8):951–6. 43. Rundell KW, Spiering BA, Judelson DA, Wilson MH.  Bronchoconstriction during cross-country skiing: is there really a refractory period? Med Sci Sports Exerc. 2003;35(1):18–26. 44. Mickleborough TD, Lindley MR, Turner LA.  Comparative effects of a high-intensity interval warm-up and Salbuterol on the Bronchoconstrictor response to exercise in asthmatic athletes. Int J Sports Med. 2007;28:456–62. 45. Bronsky EA, Yegen U, Yeh CM, Larsen LV, Della CG.  Formoterol provides long-lasting protection against exercise-induced bronchospasm. Ann Allergy Asthma Immunol. 2002;89(4):407–12. 46. Bonini M. Beta-2 agonists for exercise-induced bronchoconstriction in children. Paediatr Respir Rev. 2014;15:42–4. 47. Reddel HK, Fitz Gerald JM, Bateman ED, Bacharier LB, Becker A. GINA 2019: a fundamental change in asthma management. Eur Respir J. 2009;53:1901046. 48. Koh MS, Tee A, Lasserson TJ, Irving LB.  Inhaled corticosteroids compared to placebo for prevention of exercise induced bronchoconstriction. Cochrane Database Syst Rev. 2007;2007(3):CD002739. 49. Leff JA, Busse WW, Pearlman D, Bronsky EA, Kemp J, Hendeles L, et  al. Monteleukast a leukotriene-­ receptor antagonist, for the treatment of mild asthma and exercise-induced bronchoconstriction. N Engl J Med. 1998;339(3):147–52. 50. Vidal C, Esperanza FO, Pineiro J, Nunez R, Gonzalez-­ Quintela A.  Comparison of Monteleukast versus budesonide in the treatment of exercise-induced bronchoconstriction. Ann Allergy Asthma Immunol. 2001;86(6):655–8. 51. Kelly KD, Spooner CH, Rowe BH.  Nedocromil sodium verses cromoglycate for the pre-treatment of exercise induced bronchoconstriction in asthma. Cochrane Database Syst Rev. 2000;2:CD002169. 52. Maschka DA, Bauman NM, McCray PB Jr, Hoffman HT, Karnell MP, Smith RJ.  A classification scheme for paradoxical vocal cord motion. Laryngoscope. 1997;107(11 Pt 1):1429–35. 53. Patterson R, Schatz M, Horton M.  Mucnchausen’s stridor: non-organic laryngeal obstruction. Clin Allergy. 1974;4:307–10. 54. Roksund OD, Halvorsen T, et  al. Exercise inducible laryngeal obstruction: diagnosis and management. Pediatr Respir Rev. 2017;21:86–94. 55. Tay RT, Radhakrishna N, Horce-Lacy F, Smith C, Hoy R, Dabscheck E, Hew M. Comorbidities in difficult to asthma are independent risk factors for frequent exac-

A. Monoson and J. Parsons erbations, poor control and diminished quality of life. Respirology. 2016;21:1384–90. 56. Kenn K, Balkissoon R. Vocal cord dysfunction: what do we know? Eur Respir J. 2011;37:194–200. 57. Doshi DR, Weinberger MM.  Long-term outcome of vocal cord dysfunction. Ann Allergy Asthma Immunol. 2006;96(6):794–9. 58. Morris MJ, Christopher KL.  Diagnostic criteria for the classification of vocal cord dysfunction. Chest. 2010;138(5):1213–23. 59. Kenn K, Willer G, Bizer C, et al. Prevalence of vocal cord dysfunction in patients with dyspnea: first prospective clinical study. Am J Respir Crit Care Med. 1997;155:A956. 60. Jain S, Bandi V, Zimmerman J.  Incidence of vocal cord dysfunction in patients presenting to emergency room with acute asthma exacerbation. Chest. 1997;11:243. 61. Rundell KW, Spiering BA. Inspiratory stridor in elite athletes. Chest. 2003;123(2):468–74. 62. Brugman S.  The many faces of vocal cord dysfunction. what 36 years of literature tells us. Am J Repir Crit Care Med. 2003;167:A588. 63. Morris MJ, Allan PF, Perkins PJ.  Vocal cord dysfunction etiologies and treatment. Clin Pulm Med. 2006;13(2):73–86. 64. Newman KB, Mason UG III, Schmaling KB. Clinical features of vocal cord dysfunction. Am J Respir Crit Care Med. 1995;152:1382–6. 65. Perello MM, Gurevich J, Fitzpatrick T, et al. Clinical characteristics of vocal cord dysfunction in two military tertiary care facilities. Am J Respir Crit Care Med. 2003;167:A788. 66. O’Connell MA, Sklarew PR, Goodman DL. Spectrum of presentation of paradoxical vocal cord motion in ambulatory patients. Ann Allergy Asthma Immunol. 1995;74:341–4. 67. PerknerJJ FKP, Balkissoon R, et  al. Irritant-­ associated vocal cord dysfunction. J Enviorn Med. 1998;40:136–43. 68. Parsons JP, Benninger C, Hawley MP, Philips G, Forrest LA, Mastronarde JG.  Vocal cord dysfunction: beyond severe asthma. Respir Med. 2010;104(4):504–9. 69. Bucca C, Rolla G, Scappaticci E, Chiampo F, Bugiani M, et  al. (1995). Extrathoracic and intrathoracic airway responsiveness in sinusitis. J Allergy Clin Immunol. 1995;95:52–9. 70. Andrianopoulos MV, Gallivan GJ, Gallivan KH.  PVCM, PVCD, EPL, and irritable larynx syndrome: what are we talking about and how do we treat it? J Voice. 2000;14:607–18. 71. Balkissoon R.  Occupational upper airway disease. Clin Chest Med. 2002;23:717–25. 72. Ayres JG, Gabbott PL.  Vocal cord dysfunction and laryngeal Hyperresponsiveness: a function of altered autonomic balance? Thorax. 2002;57(4):284–5.

3  Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction 73. Morrison M, Rammage L, Emami AJ.  The irritable larynx syndrome. J Voice. 1999;13:447–55. 74. Balkissoon R, Jenn K. Asthma: vocal cord dysfunction (VCD) and other functional breathing disorders. Semin Respir Crit Care Med. 2012;33(6):596–605. 75. Thurston NL, Fiedorowicz JG. Improvement of paradoxical vocal cord dysfunction with integrated psychiatric care. Psychosomatics. 2009;50(3):282–4. 76. Wilson JJ, Wilson EM. Practical management: vocal cord dysfunction in athletes. Clin J Sport Med. 2006;16(4):357–60. 77. Forrest LA, Husein T, Husein O.  Paradoxical vocal cord motion: classification and treatment. Laryngoscope. 2012;122(4):844–53. 78. Heinle R, Linton A, Chidekel AS.  Exercise-induced vocal cord dysfunction presenting as asthma in pediatric patients; toxicity of inappropriate inhaled

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c­ orticosteroids and the role of exercise laryngoscopy. Pediatr Asthma Allergy Immunol. 2003;16:215–24. 79. Powell DM, Karanfilov BI, Beechler KB, et  al. Paradoxical vocal cord dysfunction in juveniles. Arch Otolayngol Head Neck Surg. 2000;126:29–34. 80. Sandage MJ, Zelazny SK.  Paradoxical vocal fold motion in children and adolescents. Lang Speech Hear Serv Sch. 2004;35:353–62. 81. LeBlanc RA, Aalto D, Jeffery CC.  Visual biofeedback for paradoxical vocal fold motion (PVFM). J Otolaryngol Head Neck Surg. 2021;50(1):13. 82. Matrka L. Paradoxical vocal fold movement disorder. Otolaryngol Clin N Am. 2014;47(1):135–46. 83. Marcinow AM, Thiompson J, Chiang T, Forrest LA, de Silva BW. Paradoxical vocal fold motion disorder in the elite athlete: experience at a large division I university. Laryngoscope. 2014;124(6):1425–30.

4

Low Ferritin and Anemic Conditions in Endurance Athletes Holly J. Benjamin and Marci Goolsby

Abbreviations

Introduction

EPO Erythropoietin Fe Iron GI Gastrointestinal Hb Hemoglobin Hct Hematocrit ID Iron deficiency IDA Iron deficiency anemia IDNA Iron deficiency nonanemia IL-6 Interleukin-6 IV Intravenous LEA Low energy availability MCV Mean corpuscular volume RBC Red blood cell RDW Red cell distribution width (RDW) RED-S Relative energy deficiency syndrome TIBC Total iron binding capacity Triad Female athlete triad and male athlete triad

Anemia is defined as low or inadequate hemoglobin. There are a variety of reasons, many of which are not related to sports, that an athlete could have anemia. The most common form of anemia is iron deficiency anemia (IDA), affecting approximately 5% of the general population. Iron deficiency is the most common nutritional deficiency both in the United States and the world, occurring in approximately 1–2% of all adults and 11% of females [1]. It is also the most common cause of anemia in athletes, affecting approximately 12.5% of athletes [1, 2]. Athletes, particularly endurance athletes, are at a significantly higher risk of experiencing ID as well as IDA with the average incidence ranging from approximately 30% in male athletes up to ≥50% in female athletes [2–7]. The vulnerability of athletes to iron deficiency is related to many factors including increased iron demands and increased losses. Concern over performance impairments related to iron deficiency, not just anemia, has spurred interest to better understand the relationship between exercise and iron regulation. Current research focuses on the effects of diet, training, hormones, and environmental stress on the iron status of athletes. These new insights into the pathogenesis of anemia and deficiency in sports have improved our understanding of the multifactorial and complex processes that affect iron metabolism.

H. J. Benjamin (*) Department of Orthopaedic Surgery, Rehabilitation Medicine & Pediatrics, University of Chicago, Chicago, IL, USA e-mail: [email protected] M. Goolsby Primary Care Sports Medicine, Hospital for Special Surgery, New York, NY, USA e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_4

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It is important to understand how to interpret lab results and to consider other medical conditions when evaluating an athlete with anemia. In fact, it would be erroneous to assume all anemia in endurance athletes is related to iron deficiency. Nevertheless, the focus of this chapter will be on iron deficiency and iron deficiency anemia. The evaluation of any symptomatic athlete with suspected anemia requires a good history and physical examination. Identification of more serious causes other than nutritional deficiency is critical to ensure diagnoses are not missed such as blood loss from heavy menstrual loss secondary to uterine fibroids, gastrointestinal (GI) blood loss from colon cancer, or an absorption issue from inflammatory bowel disease like Crohn’s disease [2]. Identification of the causes of ID, IDA, or any anemia is critical to ensure appropriate treatment regimens are instituted.

Clinical Presentation Making a clinical diagnosis of iron deficiency is challenging despite the frequency of occurrence. Numerous reports exist of athletes presenting with vague complaints of fatigue, weakness, decreased physical endurance, poor performance, feeling hot or cold, diminished immune response presenting as frequent illnesses, and changes in energy level, cognitive performance, and behavior. Iron deficiency is clearly not the only potential cause of these types of symptoms, as a variety of physical, lifestyle, training, and mental health issues can cause similar symptoms. Any athlete experiencing a decrease in training or performance coupled with even vague somatic symptoms should see a qualified healthcare provider for a thorough evaluation. Chronic iron deficiency anemia can progress in severity leading to more notable, specific signs and symptoms such as pallor (skin, tongue, conjunctiva), orthostatic hypotension, tachycardia, weak peripheral pulses, koilonychia (brittle spoonlike nails), angular stomatitis, glossitis, and atrophic skin [8]. By the time these symptoms are apparent, iron levels have likely been low or dropping for a prolonged period of time. In addi-

H. J. Benjamin and M. Goolsby

tion to prompt institution of treatment, avoidance of endurance or high-intensity training is required.

The Function of Iron Iron is a fundamental mineral involved in oxygen transport, energy metabolism, cognitive function, and immunity. It is an essential nutrient in the synthesis of heme and other metalloproteins such as iron-sulfur. Iron plays a key role in mitochondrial metabolism as well [9]. Most of the body’s iron is found circulating within red blood cells (RBCs). Ferritin protein is the body’s primary iron storage site, and the transferrin protein transports iron. Approximately 75% of the body’s iron is bound to hemoglobin in circulating erythrocytes (RBCs) as well as stored in myoglobin in muscles. Twenty five percent of the body’s iron is bound to ferritin. Iron is the active catalyst to bind oxygen to hemoglobin and myoglobin in the body that facilitates the transfer of oxygen from the lungs to the blood to the the exercising muscles [9]. Normal iron metabolism requires a meticulous balance between dietary uptake and loss. A certain amount of iron loss must occur daily, and therefore a daily source of iron is needed.

Causes of Iron Deficiency Diet and Nutrition Low iron stores may result from physiologic and pathophysiologic causes (Table 4.1). In athletes the most common causes of ID are both a lack of dietary intake and poor absorption. Iron losses, iron absorption, and quality/quantity of iron sources will affect individual needs. Ultimately, iron bioavailability is more important than the total amount of iron ingested [10, 11]. For many athletes, iron metabolism is impacted by a variety of iron losses occurring simultaneously resulting in a cumulative negative impact. Treatment, therefore, must focus on addressing these interactions to successfully improve the

4  Low Ferritin and Anemic Conditions in Endurance Athletes

overall iron status in athletes who struggle to maintain adequate iron stores. Future research is needed in the treatment of multifactorial iron deficiency in athletes [2]. Adequate dietary intake and effective absorption are the key components to an athlete having a healthy iron metabolism. While energy needs may change due to variations in the level of activity and overall body stresses, over time the average energy in must be equal or greater than the average energy out. Unfortunately, athletes, including elite and endurance athletes, may suffer from chronic low energy availability (LEA) that leads to various negative consequences, one of which is iron deficiency [8]. Iron absorption is decreased during endurance exercise so timing of iron intake is crucial to maximize absorption. Vegetarian and vegan diets are also risk factors for low iron storage in the body due to a lack of iron availability in the diet [12].

Table 4.1  Causes of iron deficiencya Reduced dietary intake – Restrictive diets, vegetarian, vegan, skipping meals, sky-high carbs, iron absorption inhibitors Reduced absorption – Diseases, GI dysfunction, endurance training, altitude training, exertional inflammation Blood loss – GI, urinary, menses, menstrual dysfunction, blood donation, inflammation, and excess breakdown (fragility) Iron sequestration –  Sweating, inflammation Increased iron demands –  Increased tissue remodeling GI gastrointestinal a  Modified from Damian (2021) [9]

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Iron Absorption It is well known that iron absorption is inefficient. Vegetarian athletes absorb an average of 2–20% of nonheme iron, often primarily from green leafy vegetables. Meat-eating athletes can absorb 5–35% of heme iron; however, even that is not a particularly efficient absorption process [13]. Heme sources of iron such as red meat are more easily absorbed than nonheme sources. The human body does not synthesize iron; therefore, it is completely dependent on dietary intake and recycling. A healthy gut microbiome also influences iron status. Iron metabolism is tightly regulated by the body. A minimum of 20 mg is required for daily function, yet only 1–2  mg is obtained through dietary intake and intestinal absorption. Most iron is reused or recirculated in the body. When iron is not bound, it is toxic to the body; therefore, dietary intake and supplementation must be monitored [13]. The timing of iron intake is important as many factors affect absorption including exercise, inflammation, and iron intake which increase the production of hepcidin by the liver. Circulating hepcidin feeds back to inhibit intestinal absorption of iron [13]. Co-ingestion of tannins (tea, coffee), calcium, polyphenols, and phytates can inhibit absorption. Iron-fortified foods that contain flours and derived food productions have a high phytic acid content which actually decreases iron absorption. Conversely, combining vitamin C intake with iron sources can enhance absorption and augment bioavailability. Carotenoids, fermented foods, and cooking your food promote iron absorption [14, 15] (Table 4.2: Dietary Factors).

Table 4.2  Dietary factors that inhibit and enhance absorption Inhibitors of nonheme iron absorption Calcium Dairy products (yogurt, milk, cheese) MVI Polyphenols Tea, coffee, wine, & chocolate Phytates Legumes, nuts, seeds, & whole-grain cereals Other Zinc, manganese minerals

Enhancers of nonheme iron absorption Vitamin C (ascorbic acid) Citrus fruits (oranges, kiwi), broccoli, tomato, capsicum Carotenoids Fermented foods (reduces phytates) Cooked food (reduces phytates)

Carrots, pumpkin, apricots, grapefruit Kimchi, miso, sauerkraut Cast iron pots; cooking process itself

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Diagnostic Testing: Hematologic Markers Debate exists as to the ideal hematologic variables and appropriate cutoff values used to assess an athlete’s iron status [2, 13]. The recommended minimum screening includes ferritin, hemoglobin, and transferrin saturation. Ferritin is the primary iron storage protein in the body and is essential to iron metabolism. Ferritin helps make iron available for critical cellular processes in our body, including converting food to energy. In clinical medicine, ferritin is a valuable blood marker for total body iron stores. It is known as an acute-phase reactant, so the measured value varies significantly depending on what acute stresses are affecting the body. Anything from lack of sleep, infection, liver or chronic diseases, inflammation, or intense exercise can have immediate effects on ferritin, causing it to rise. These “falsely normal or elevated” ferritin levels in an acute stress or inflammatory setting can be mistakenly reassuring, causing one to miss the signs of iron deficiency that an otherwise low ferritin would signal [16]. Sex, age, and type of sport also affect laboratory cutoff values for iron metabolism. Screening for anemia by measuring ferritin alone or obtaining a complete blood count (CBC) without ferritin is inadequate. It is best to measure ferritin in the morning before exercise and, ideally, after a day of rest [17]. Iron transport, distribution, and recycling are tightly regulated processes in the human body. Ironically, iron also has toxic effects on the body, and ferritin serves to buffer those negative effects. Ferritin, therefore, is an integral part of iron metabolism. Ferritin has a wide range of normal levels, typically 30–300 ng/mL in males and 10–200 ng/ dL in females [18]. Low ferritin is highly specific for iron deficiency anemia. One is considered iron deficient with a level below 10–30  ng/mL [19]. In clinical practice, particularly when caring for endurance and high-performance athletes, the use of a higher cutoff value of 40–50 ng/mL improves the likelihood of identifying the presence of iron deficiency [20, 21]. There is no consensus on the threshold value in athletes. In 1992,

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a systematic review concluded that ferritin of ≤15 ng/dL had a 52-fold greater likelihood ratio of correlating with the presence of iron deficiency, and 15–35  ng/dL was predictive of low iron stores [22]. Furthermore, female athletes with chronic fatigue who had ferritin levels less than 50 (but hemoglobin >12) had significant increases in ferritin level, hemoglobin, and, more importantly, resolution of fatigue, with iron supplementation [23]. Transferrin is a negative acute-phase protein in the blood that binds iron and transports it throughout the body. Transferrin saturation represents the current amount of iron bound to transferrin. Total iron binding capacity (TIBC) is an important blood marker and is a measure of the maximal ability of transferrin to bind iron [24]. As iron stores are depleted and iron is less available, TIBC rises. A simple example of supply and demand is illustrated here. As iron supply goes down, transferrin’s demand goes up, and its capacity to bind all available iron is maximized. Many clinicians assess serum iron and total iron binding capacity (TIBC) as well. Laboratory values typically affected in iron deficiency in chronological order include ferritin, serum iron, transferrin saturation, total iron binding capacity, red cell count, red cell distribution width (RDW), mean corpuscular volume (RDW), and hemoglobin [2, 3, 25] (Table 4.3). The most comprehensive clinical laboratory picture of a body’s iron stores involves obtaining a CBC, ferritin, transferrin, and complete iron studies.

Stages of Iron Deficiency There are three stages of iron deficiency called prelatent, latent, and true deficiency [26] (Table  4.4). The first two stages result in iron deficiency in the absence of anemia. Only the third stage reflects true anemia. In the prelatent phase, iron stores are depleted in the bone marrow, liver, and spleen, yet only a decrease in ferritin is seen on laboratory testing. In the latent phase, iron stores are exhausted, and iron deficiency nonanemia (IDNA) develops in which

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Table 4.3  Anemia laboratory values Fe Pseudoanemia deficiency Low Low

B12/folate deficiency Low

Anemia of chronic disease Low

Normal

Low

High

Normal

Normal

High

Normal

Sensitive marker for Fe Normal deficiency Transferrin 30 mmHg, or 5 min post exercise presSurgical and nonsurgical treatment options sure of 20  mmHg [24]. Debate exists over the exist for CECS. Mainstays of nonoperative manvalidity of these criteria as well as reproducibility agement for most musculoskeletal injuries are of compartment pressure testing in general for the rest, activity modification, massage, and stretchdiagnosis of CECS [25–27]. Continuous intra- ing. These methods provide some symptomatic compartmental pressure measurement have been improvement for CECS but are rarely able to described as an alternative and can provide a trend completely resolve the pathology and return the of pressures during or after exercise rather than athlete to unrestricted sport. Complete resolution pressures at one given time. Unfortunately, this via conservative means can occur with permamethod can be more difficult to use due to its con- nent activity restrictions or modifications but

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most athletes do not elect this pathway. Botox injections are an alternative treatment for CECS, which have been found to decrease compartment pressures and significantly reduce the incidence of symptoms. However, they do come with associated muscle weakness making this a less attractive option for athletes [30, 31]. Gait retraining is emerging as a promising nonsurgical treatment option for CECS. Retraining focuses on switching from hindfoot to forefoot striking pattern of gait. Other alterations include reducing stride length, increasing step cadence, and maintaining upright posture [32]. These modifications appear to impact CECS of the anterior compartment by decreasing ground reaction forces and reducing muscle activation specifically through less eccentric tibialis anterior activity [33]. The method has been found to decrease intra-compartmental pressures resulting in CECS symptom improvement and reducing the need for surgery [34–36]. In certain, military populations, a nonoperative first treatment approach has had a positive impact both on soldier retention as well as the reduction in the need for surgical intervention. Overall, a variety of nonsurgical treatment options exist for CECS and are often used in conjunction with one another prior to consider surgical treatment. Ultimately for athletes and runners with unrelenting exertional leg pain and/or who have incomplete symptom resolution from conservative measures, surgical fascial release is the definitive course of treatment. Fasciotomy techniques have evolved over time from the original one large incision to two small incision subcutaneous release, and now endoscopic-assisted techniques and fluoroscopic-guided techniques have been developed and reported. Regardless of the technique, it is important that at least 80–90% of the fascial length is released to be effective and reduce the risk of recurrence. As with any surgery, complications exist and for CECS fascial release these include: postoperative hematoma, superficial cellulitis or deep infection, nerve injury (especially of branches of the superficial peroneal nerve), incomplete fascial release, and postoperative scarring and adhesions leading to stiffness. Studies have shown surgery to have good results with resolution of symptoms and

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return to activities in 80–90% of patients [21, 37, 38]. Reduced success rates have been noted in females, military patients, and those with involvement of the deep posterior compartment.

 opliteal Artery Entrapment P Syndrome Popliteal artery entrapment syndrome (PAES) is a rare cause of chronic exertional leg pain in running athletes. This pathology involves anatomic variants leading to compression of the popliteal artery during activity resulting ischemia and pain. The term PAES was first used in 1965 with the condition being described earlier in 1959 and anatomic variant being first noted in the late 1800s [39–41]. Incidence of PAES ranges from 0.6% to 3.6%, with males being more commonly affected [42, 43]. It is important to be aware that bilateral extremity involvement has been found in up to two thirds of cases even if only unilateral symptoms are reported [44]. PAES can be subdivided into anatomic and functional causes. Majority of cases are due to anatomic variants. These include a more lateral attachment of the medial head of the gastrocnemius, an accessory band of the gastrocnemius entrapping the artery, popliteus running superficial to the artery, and the artery running medial to the medial head of the gastrocnemius [42]. Variants are demonstrated in Fig.  13.4. Functional causes center on muscle hypertrophy in the popliteal fossa leading to artery compression. PAES often presents mimicking CECS with exertional pain in the deep posterior compartment. Symptoms include activity-related pain, tightness, cramping, and or altered sensation in the affected leg. In PAES, these symptoms will always involve the calf, whereas CECS can involve any compartment, but more commonly impacts the anterior or lateral lower leg. Other findings that may favor PAES diagnosis are diminished pedal pulses with active planar flexion as well as cold feet and pallor associated with pain symptoms. Further evaluation of PAES begins with radiographs to rule out any potential osseous causes of

13  Chronic Leg Pain in Running Athletes Fig. 13.4  Demonstrating anatomic variants found in PAES. Type 1 with normal medial gastrocnemius origin but an aberrant popliteal artery course. Type 2 with normal popliteal artery course but a more lateral location of the medial gastrocnemius origin. Type 3 accessory muscle or tissue band from medial gastrocnemius that constricts the artery. Type 4 with constriction occurring from the popliteus muscle [45]

181 Type I

Type II Popliteal artery

Popliteal artery

Popliteal vein

Medial head of gastrocnemius muscle

Popliteal artery

Type III

Popliteal artery

Accessory slip of gastrocnemius muscle Medial head of gastrocnemius muscle

symptoms. Vascular specific testing includes performing an ankle brachial index (ABI) at rest and after symptoms develop. PAES will have a decreased ABI with exercise. No diagnostic criteria have been proposed for this exam, but previous reports have found decreases of 30–50% [46, 47]. Once decreased ABI values are noted further imaging can be performed. Duplex ultrasound of the popliteal artery can be performed and flow in the popliteal artery can be measured at various positions. One provocative maneuver described involves active plantar flexion with the knee at 15° of flexion [48]. A decrease in flow can be diagnostic of PAES; however, this test has a high false positive rate with similar results being produced in asymptomatic individuals on provocative testing [49, 50]. With a presumed diagnosis of PAES, advanced imaging of CT angiography or MR angiography can be performed at rest and with provocative maneuvers. These exams further confirm PAES with the added benefit of surgical planning by identifying the exact areas of compression that need to be addressed. When an anatomic cause is identified, surgery remains the primary treatment for PAES.  Procedures are commonly performed by vascular surgeons who utilize a posterior or medial approach depending on the location of

Type IV Popliteal vein Compressed popliteal artery Popliteus muscle

compression. Goals of the surgery are to release the site of compression on the artery and reroute the artery as needed. Excellent outcomes have been reported with maintained patency of greater than 90% at 5 and 10 years follow-up [51, 52]. Functional causes of PAES are more challenging to treat. Surgery can still be done to release areas of compression found on provocative testing, but no accepted standard procedure exists such as with anatomic variants. Botox injections are an emerging option for treating functional PAES, but further investigation is needed.

Stress Fractures While originally described in military recruits, runners are the most likely athletes to suffer from a stress fracture with the tibia being most affected [53, 54]. Stress fractures represent one segment of the continuum of bone stress injuries that are initiated by chronic repetitive overuse and loading on the bone. Overload leads to microinjury at the trabecular level bone that may not be visualized on imaging but represent the lowest level of bone stress injury. With increased or repetitive loading, the injury propagates and become more severe and diagnosable as a stress fracture on

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imaging. During this there is increased bone turnover and resorption compared to bone formation ultimately leading to a stress fracture. These injuries can be grouped into those related to fatigue or insufficiency. The fatigue grouping refers to overuse injuries in patients with normal bone density whereas insufficiency types are related to decreased bone mineral density [55]. Poor nutrition can contribute to reduced bone density and serve as a risk factor for stress fracture. Risk factors include females due to increased likelihood of decreased bone mineral density and decreased muscle mass [56]. Muscle is thought to play a role in stress fractures in both protective and causative manners. With each step muscles of the lower leg help to absorb impact forces and reduce the total force transmitted to the tibia. In the case of decreased or fatigued muscles, there are increased forces absorbed by the tibia and thus increased risk for stress fracture [55]. Furthermore, muscle may contribute to stress fracture by the forces they create at their bony insertion sites. Bone stress injuries present as impact-related leg pain, which improves with cessation of activity. Over time symptoms can progress to pain lasting longer after activity or occurring with day-to-day activities. It is important to ascertain the patient’s diet, nutritional status, and BMI to screen for relative energy deficiency in sports. Specifically, in female patients, menstrual history should be documented as well. On exam patients will have focal bony point tenderness on palpation at the region of the stress fracture. Subtle swelling may be present at the site of the pathology as well. A tuning fork can be put in contact with the tibia resulting in pain exacerbated by the vibration. It is important to assess overall alignment and muscle strength to identify any possible modifiable factors serving as contributors to this pathology. Imaging begins with standard radiographs. Oblique views and image magnification may be beneficial to assist in demonstrating subtle findings. Often, radiographs can be negative especially in the early aspects of the pathology. At later stages, periosteal reaction or even a fracture line can be present which is shown in Fig. 13.5.

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Fig. 13.5  AP and lateral radiographs of the tibia and fibula showing an anterior tibial diaphysis stress fracture [57]

Advanced imaging is far more accurate in evaluating the presence of bone stress injury and stress fractures. Bone scans are a sensitive modality, which show increased focal uptake on all three phases. The focal or linear area of uptake differentiates stress fractures from MTSS. MRI is the preferred imaging technique to evaluate for stress fractures demonstrating focal increased signal at the area of concern on T2 imaging. MRI also offers the benefit of showing the surrounding anatomy for evaluation of possible concomitant pathologies with no radiation exposure. MRI

13  Chronic Leg Pain in Running Athletes

scans have also been used to predict the time to return to play based on the presence or absence of findings on T1, T2, or fat suppressed T2 imaging. Most stress fractures can be treated nonoperatively and heal uneventfully. However, when the pathology progresses or fails to respond to nonoperative treatment, some cases do require surgical management. Stress fractures of the posterior-medial aspect of the tibia usually go on to heal. Stress fractures of the anterolateral aspect of the tibia have an elevated risk of nonunion and more commonly fail nonoperative attempts and require surgery. Nonoperative treatment focuses on rest, activity modification, immobilization with occasional periods of nonweight bearing. This is continued until symptoms begin to resolve. Subsequently, there is a gradual, progressive return to activity guided. If pain returns, the athlete should return to rest and/ or immobilization. The period of nonoperative treatment is a minimum of 6–12  weeks. Additional nonoperative measures that can be taken include optimizing overall nutrition and supplementing bone health with calcium and vitamin D. Modifiable contributing factors such as muscle weakness can be addressed with a focused therapy program. Anecdotal studies have supported the use of bone stimulation in some athletes to accelerate the healing process by a few weeks. Patients that fail a complete course of nonoperative management will be indicated for surgical treatment. Surgery focuses on stabilizing stress fracture to allow it to heal. In the tibia the preferred stabilization technique is an intramedullary nail.

Nerve Entrapments Though more common in the upper extremity, a variety of nerve entrapments of the lower extremity exist and can cause chronic leg pain in running athletes. Nerves involved in the lower extremity include the saphenous, sural, common peroneal, deep peroneal, superficial peroneal, and tibial nerves. Compression of these nerves can lead to pain, paresthesia, or altered sensation

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in their distributions. The saphenous nerve can become entrapped at the adductor canal between the sartorius and gracilis tendons. Compression will only lead to sensory effects at the medial leg, ankle, and arch without motor involvement given the function of the saphenous nerve [58]. Additional motor deficits can be found in other nerves of the lower extremity. Common peroneal can become compressed near the fibular neck resulting in altered sensation at the lateral leg and dorsum of the foot [59]. In addition to sensory symptoms, motor involvement can include weakness in ankle dorsiflexion, eversion, and great toe extension. Superficial peroneal nerve can be entrapped where it enters the lateral compartment leading to weakness in ankle eversion [60]. The deep peroneal nerve can be compressed at the anterior tarsal tunnel and have resulting weakness in great toe extension. The tibial nerve can be compressed at the tarsal tunnel resulting in pain or paresthesia at the medial and plantar foot. Nerve entrapment symptoms in the lower extremity can be present with activity or at rest. Symptoms may worsen with activity as muscles of the lower leg swell or become engorged with blood, which can worsen baseline nerve compression or pressure. A thorough neurovascular exam is performed to be able to identify the distribution of symptoms and possible motor deficits to relate them back to the associated nerve. A Tinel’s test can be performed over the nerve and may reproduce symptoms. Imaging evaluation can include ultrasound and MRI to be able track the course of the nerves to identify for any areas of compression. These modalities can also identify inciting anatomical causes of compression such as aberrant fibrous bands or ganglion cysts. Additionally, ultrasound can be used to aid in  localized diagnostic nerve blocks with local anesthesia to determine how much a given nerve is contributing to symptoms. Results of a diagnostic block can help provide some reference to the benefit of surgical release of the entrapped nerve. Electrodiagnostic studies such as electromyography can be used to evaluate for nerve entrapment by evaluating the conduction velocities. Nonoperative management again ­ involves rest, activity modification, and possible

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technique or shoe modifications. If symptoms persist surgical treatment with neurolysis and possible fascial release can be performed.

Conclusion Chronic leg pain is a prevalent complaint among running athletes. Symptoms often include activity-­related pain but may also involve paresthesia, altered sensation, or weakness. These symptoms often improve with activity cessation and a period of rest. Pathologic diagnoses leading to leg pain can come from the bone, neurovascular structures, or soft tissue. Though leg pain is common, accurate diagnoses can be challenging given vague symptoms and overlapping pathologies. Optimizing treatment based on arriving at an accurate diagnosis can be achieved by differentiating and considering contributing factors through history, exam, and imaging to aid in this process. Treatment often begins with nonoperative management, but certain diagnoses may require operative intervention for definitive resolution of symptoms. Overall, with a better understanding of these processes, all providers should be able to more accurately diagnose optimally manage leg pain in the athletes and patients they care for.

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185 36. Zimmermann WO, Hutchinson MR, Van den Berg R, Hoencamp R, Backx FJG, Bakker EWP. Conservative treatment of anterior chronic exertional compartment syndrome in the military, with a mid-term follow-up. BMJ Open Sport Exerc Med. 2019;5(1):e000532. 37. Nwakibu U, Schwarzman G, Zimmermann WO, Hutchinson MR.  Chronic exertional compartment syndrome of the leg management is changing: where are we and where are we going? Curr Sports Med Rep. 2020;19(10):438–44. 38. Schepsis AA, Martini D, Corbett M.  Surgical management of exertional compartment syndrome of the lower leg. Long-term followup. Am J Sports Med. 1993;21(6):811–7. discussion 7 39. Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am J Surg. 1965;109:620–4. 40. Hamming JJ. Intermittent claudication at an early age, due to an anomalous course of the popliteal artery. Angiology. 1959;10:369–71. 41. Stuart TP. Note on a variation in the course of the popliteal artery. J Anat Physiol. 1879;13(Pt 2):162. 42. Grimm NL, Danilkowicz R, Shortell C, Toth AP.  Popliteal Artery Entrapment Syndrome. JBJS Rev. 2020;8(1):e0035. 43. Mark LK, Kiselow MC, Wagner M, Goodman JJ.  Popliteal artery entrapment syndrome. JAMA. 1978;240(5):465–6. 44. Levien LJ.  Popliteal artery entrapment syndrome. Semin Vasc Surg. 2003;16(3):223–31. 45. Sellers W, Obmann M, Nikam S, Song B, Mariner D.  Popliteal artery entrapment syndrome presenting as acute limb ischemia in pregnancy. J Vasc Surg Cases Innov Tech. 2017;3(4):232–5. 46. McAree BJ, O'Donnell ME, Davison GW, Boyd C, Lee B, Soong CV. Bilateral popliteal artery occlusion in a competitive bike rider: case report and clinical review. Vasc Endovasc Surg. 2008;42(4):380–5. 47. Turnipseed WD. Popliteal entrapment in runners. Clin Sports Med. 2012;31(2):321–8. 48. di Marzo L, Cavallaro A, Sciacca V, Lepidi S, Marmorale A, Tamburelli A, et al. Diagnosis of popliteal artery entrapment syndrome: the role of duplex scanning. J Vasc Surg. 1991;13(3):434–8. 49. Erdoes LS, Devine JJ, Bernhard VM, Baker MR, Berman SS, Hunter GC.  Popliteal vascular compression in a normal population. J Vasc Surg. 1994;20(6):978–86. 50. Hoffmann U, Vetter J, Rainoni L, Leu AJ, Bollinger A.  Popliteal artery compression and force of active plantar flexion in young healthy volunteers. J Vasc Surg. 1997;26(2):281–7. 51. Lejay A, Delay C, Georg Y, Gaertner S, Ohana M, Thaveau F, et al. Five year outcomes of surgical treatment for popliteal artery entrapment syndrome. Eur J Vasc Endovasc Surg. 2016;51(4):557–64. 52. Tanaka H, Higashi M, Fukumoto Y, Ogino H.  Entrapment of the popliteal artery. J Vasc Surg. 2010;52(2):479. 53. Hulkko A, Orava S. Stress fractures in athletes. Int J Sports Med. 1987;8(3):221–6.

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Hip Injuries and Conditions in the Endurance Athlete

14

Joshua D. Harris

Introduction Endurance athletes require extended periods of repetitive hip motion, articular congruity, and balanced musculotendinous coordination in order to successfully perform their sport [1]. Over 80% of athletic hip and pelvis injuries are due to overuse [2]. The majority of endurance athletes with groin, hip, or pelvis pain have intra-articular diagnoses [3]. Recurrent episodes of high-­ intensity or extended duration sport without sufficient recovery may lead to overuse injury. These injuries may involve isolated single osseous or soft tissue structures or a combination of multiple separate musculoskeletal entities. Overuse hip injuries in endurance athletes may occur in the setting of normal or abnormal anatomy and mechanics (e.g., Femoroacetabular Impingement Syndrome [FAIS]) [4]. As the quantity and quality of athletic hip preservation literature evolves and improves, normal anatomy and abnormal pathology are better understood, classified, and managed. Anatomic evaluation of athletic hip complaints has led to utilization of the “layer concept,” categorizing diagnoses into different layers: I (osteochondral), II (inert), III (contractile), and IV (neuromechanical) [5]. This has permitted not only better assessment and treatment

J. D. Harris (*) Department of Orthopedics and Sports Medicine, Houston Methodist Hospital, Houston, TX, USA

of hip injuries, but also implementation of effective prevention programs [6].

Anatomy The hip is a deep, diarthrodial synovial ball-and-­ socket joint. Although the hip is not a perfect sphere, better characterized as conchoid shape, its deviation from sphericity is minimal and the highly congruous femoral head and acetabulum afford a highly stable, yet multiaxial, joint [7]. Recent recognition of variable degrees of severity of nonarthritic hip pathoanatomy relative to FAI, dysplasia, version disorders, and labral pathology have greatly improved the understanding of “normal hip anatomy.” The hip articulation, in conjunction with the pelvic ring, form the basis of the osteochondral layer, Layer I [5]. Layers II (inert) and III (contractile) comprise the stabilizing soft tissues enveloping the joint, working in synchronicity to prevent instability during normal physiologic motion. Layer II includes the static stabilizers (labrum, capsule, iliofemoral, pubofemoral, and ischiofemoral ligaments, zona orbicularis). Layer III includes the dynamic musculotendinous stabilizers crossing the hip joint, lumbosacral and pelvic floor complexes. Layer IV, the neuromechanical layer, includes the nervous and vascular structures that coordinate the kinetic chain in and around the hip.

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Altered bone mineral density has also been observed on both the proximal femoral head-­ The osteochondral layer provides the basis for neck junction and acetabulae of patients with arthrokinetic motion via joint congruity. Hip cam morphology [11, 12]. Cam morphology elemotion is primarily rotational, around a center of vates bone mineral density exponentially and rotation, rather than translational [8]. Sphericity increases subchondral bone stiffness, altering the of the articulation combined with the near-­ joint contact stresses with incongruent joint surfrictionless articular cartilage surface permits a faces, potentially instigating and propagating lifetime of normal joint function in most degenerative arthrosis [13]. In fact, bone mineral ­individuals. Static and/or dynamic conditions of density has shown a significant positive correlaasphericity may lead to early chondrolabral dam- tion with alpha angle, with the magnitude of age and arthrosis. Translational instability sec- deformity even more correlative than symptom ondary to dysplastic and/or versional status [12]. abnormalities may also lead to early arthritis. In In symptomatic patients that have failed nonthe endurance athlete, with tens of thousands of surgical treatments, arthroscopic hip preservation repetitive functional hip joint movements per continues to rapidly grow internationally as a day, this situation has the potential to accelerate. successful treatment of intra-articular hip patholLoss of femoral head-neck junction sphericity ogies, including those of Layer I.  Arthroscopic (cam) (Fig.  14.1a), femoral head overcoverage “normal” anatomy of the proximal femur and (pincer FAI) (Fig. 14.1b) or undercoverage (dys- acetabulum has been the subject of several high-­ plasia) (Fig. 14.1c), and extra-articular impinge- quality anatomical investigations [14, 15]. The ment (trochanteric-pelvic (Fig. 14.1d, e), superior margin of the anterior labral sulcus ischiofemoral (Fig. 14.1f), subspine impinge- (“psoas u”) has been designated as the standard ment (Fig. 14.1g, h)) all may disrupt normal joint clockface reference, denoting 3:00 on the acetabmechanics (translation in addition to rotation). ular clockface [14]. As opposed to the center of Other osseous femoral (version, neck-shaft the transverse acetabular ligament, previously angle), acetabular (version, depth), and lumbo- used as the referenced arthroscopic landmark at pelvic (pelvic incidence, sagittal, and coronal 6:00 [16, 17], the anterior labral sulcus is consisplane balance) parameters play a significant role tently and reproducibly visualized during hip in the multifactorial evaluation of normal hip and arthroscopy. Other consistently identifiable pelvis anatomy [9]. arthroscopic landmarks include the anterior infeOsseous architecture of the femoral head, rior iliac spine (1:30 to 2:30), direct and indirect neck, and peritrochanteric region demonstrates heads of rectus femoris (2:00 to 2:30 and 11:30 to compact cortical and cancellous trabecular bone. 2:00, respectively), iliocapsularis (2:00 to 2:30), Radiographically, the proximal femur can be iliopsoas (3:00 to 3:30), and lateral ascending characterized by trabecular group (compressive, vessels (11:30 to 12:00 on femur) [14]. These tensile, and greater trochanteric) and type (pri- intraoperative landmarks have been confirmed to mary, secondary) (Fig. 14.2a) [10]. During gait, be radiographically identifiable (anteroposterior a coronal plane rotatory equilibrium exists [AP] and false-profile) during surgical fluorosbetween vectors of body weight and abductor copy and during preoperative planning [18]. tension to maintain a level pelvis (Fig.  14.2b) (Table  14.1). These vectors are responsible for the designation of “compressive” and “tensile” Layer II sides of the femoral neck [10]. Proximal femoral abnormalities in bone mineral density may be Layer II is comprised of the inert, noncontractile responsible for femoral neck fractures, including soft-tissue structures in and around the hip. This both acute traumatic and chronic overuse stress includes the fibrocartilaginous acetabular labrum, fractures. which provides a joint stabilizing suction seal

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a

c

189

b

d

f

e

Fig. 14.1 (a) Dunn 45° plain radiograph of bilateral cam morphology in a 19-year-old collegiate runner, illustrating loss of anterolateral femoral head-neck offset, cortical sclerosis, and a significantly increased alpha angle. (b) Intraoperative anteroposterior (AP) fluoroscopy of far lateral and posterolateral pincer femoroacetabular impingement (FAI) overcoverage of the right hip of a 35-year-old female marathon runner. (c) Standing AP pelvis plain radiograph, illustrating bilateral acetabular dysplasia in a 25-yearold male triathlete. A reduced lateral center edge angle, increased Tönnis angle, and increased femoral head extrusion index is observed. (d) AP “splits” plain radiograph of a 19-year-old collegiate cheerleader in 90° abduction and permissive limb external rotation, illustrating bilateral posterior

trochanteric-pelvic impingement and a “vacuum” sign. (e) AP “splits” plain radiograph of a 19-year-old collegiate cheerleader (same as Fig. 14.1d) in 90° abduction and forced limb internal rotation, illustrating superior trochanteric-pelvic impingement. (f) AP pelvis plain radiograph of a 40-year-old female cyclist with increased femoral anteversion and suggestive of bilateral ischiofemoral impingement. (g) AP pelvis plain radiograph of a 45-year-old male halfmarathon runner with a type III anterior inferior iliac spine (AIIS) and subspine impingement in his right hip. He reported a history of “groin strain” as a teenage playing football. (h) False profile plain radiograph of a 45-year-old male half-marathon runner (same as Fig. 14.1g) with a type III AIIS and subspine impingement in his right hip

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g

h

Fig. 14.1 (continued)

a

b

Fig. 14.2 (a) AP plain radiograph of an 18-year-old female collegiate cross-country runner with proximal femoral primary and secondary trabeculae outlined in the right hip. GTT (greater trochanteric trabeculae); PCT (primary compressive trabeculae); PTT (primary tensile trabeculae); SCT (secondary compressive trabeculae); STT (secondary tensile trabeculae); WT (Ward’s triangle). Figure reprinted with permission from Elsevier Inc. (b) AP plain radiograph of an 18-year-old female collegiate cross-country runner (same as Fig. 14.2a) with balanced

free body diagram of force vectors outlined in the right hip. Hip center of rotation is marked with a dot and a Möse circle around the femoral head. The product of the force of the body weight and its associated moment arm equals the product of the abductor muscle force and its associated moment arm. For equilibrium, according to Newton’s third law of motion, for every action (abductor muscle tension and body weight), there is an equal and opposite reaction (joint reaction force). Figure reprinted with permission from Elsevier Inc.

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Table 14.1  Proximal femoral anatomy based on version, neck-shaft angle

Femoral version Increased Femoral version Decreased Neck-shaft angle Increased Neck-shaft angle Decreased

Increased anteversion Relative retroversion Coxa valga Coxa vara

Anatomy Greater trochanter posterior, closer to hip center Greater trochanter lateral, further from hip center Greater trochanter above center of femoral head Greater trochanter below center of femoral head

during physiologic motion [19]. This seal has been negated in subjects with FAI during flexed and rotated positions, including pivoting necessary for participation in endurance sports [20]. The labrum plays a significant role in pain generation inside the hip joint, secondary to the presence of free sensory nerve fibers and mechanoreceptors, with the highest relative concentration in the anterior zone, where most labral pathology is located [21–23]. The distribution of free nerve endings is greatest at the labral base, and decreases toward the periphery [24]. The hip capsule is composed of four discrete ligamentous structures: iliofemoral (Y-ligament of Bigelow), ischiofemoral, and pubofemoral ligaments and the zona orbicularis. The iliofemoral ligament is the strongest of the four and is transversely cut during interportal capsulotomy (anterolateral to mid-anterior) in hip arthroscopy [25]. The latter permits excellent viewing of the central compartment: labrum, acetabular rim, articular cartilage of the acetabulum and femoral head, fovea, and ligamentum teres. A “T” capsulotomy, perpendicular to the interportal capsulotomy, permits excellent viewing of the peripheral compartment: proximal femoral head-­ neck junction, zona orbicularis, lateral and medial synovial folds, and lateral ascending vessels. Several biomechanical investigations have illustrated the importance of the iliofemoral ligament for retention of normal hip kinematics: Iliofemoral ligament sectioning (unrepaired capsulotomy) leads to increased external rotation, extension, and anterior and distal translation [26–29]. Clinically, during hip arthroscopy using a “T” capsulotomy, this translates to significantly better outcomes in patients who have a complete

Coronal plane lever arm Decreased

Required abductor muscle force Increased

Increased

Decreased

Decreased

Increased

Increased

Decreased

capsular repair (Fig. 14.3a–d) versus those who have a partial repair (repaired “T” and unrepaired interportal capsulotomy) [30]. An unrepaired “T” capsulotomy may potentially leave the hip catastrophically unstable (dislocation) or prone to “microinstability” due to a disrupted “stability arc”[31–33]. The “stability arc” is a defined area of the anterior hip, defined by the medial and lateral limbs of the iliofemoral ligament as the static deep border and the iliocapsularis and rectus femoris as the dynamic superficial medial border and the gluteus minimus as the dynamic superficial lateral border [31]. In the setting of an unrepaired “T” capsulotomy, hip extension and external rotation dynamically pull the medial and lateral limbs of the iliofemoral ligament apart and evade the anterior stabilizing effect of the anterior capsule.

Layer III Layer III consists of the dynamic musculotendinous units in and around the hip and pelvis. This includes the muscles whose action is to move the hip, the lumbopelvic stabilizing girdle, and the pelvic floor. Several different extra-articular pathologies may be either the cause of the effect of intra-articular lesions, such as FAIS, dysplasia, or labral injury. In endurance athletes with FAI, increased stresses across the bony hemipelvis may result when athletes attempt to achieve supraphysiologic terminal range of motion via the hip required for participation in their sport [34]. These forces may be transmitted through the pubic symphysis (osteitis pubis), sacroiliac joint, and lumbosacral spine. Anatomical regions may

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a

b

c

d

Fig. 14.3 (a) Right hip arthroscopy of 20-year-old female collegiate gymnast. Viewing from modified mid-­ anterior portal and instrumenting from distal anterolateral accessory portal (DALA), a “T” capsulotomy has been made for improved peripheral compartment visualization of the cam morphology (following osteoplasty) and is now being repaired with a suture penetrating and passing device through the medial limb of the capsulotomy. Non-­

absorbable, #2 suture is utilized. (b) Same patient as Fig. 14.3a, the suture is being retrieved after penetrating the lateral limb of the capsulotomy. (c) Same patient as Fig. 14.3a, each limb of the capsulotomy is approximated prior to standard arthroscopic knot-tying techniques. (d) Same patient as Fig.  14.3a, three high-strength nonabsorbable sutures have been utilized for “T” capsulotomy capsular plication of the iliofemoral ligament

help categorize these subsequent tendinopathies and/or enthesopathies: anterior enthesopathy (hip flexor strain, psoas impingement); medial enthesopathy (adductor and rectus tendinopathies— “athletic pubalgia,” “core muscle injury,” “sports hernia”); posterior enthesopathy (proximal hamstring syndrome, “piriformis syndrome,” deep gluteal space syndrome, ischiofemoral impingement [greater trochanter-ischium, lesser

trochanter-­ ischium); and lateral enthesopathy (peritrochanteric pain syndrome, gluteus medius tendinopathy or tear). The iliopsoas tendon was thought to possibly instigate an atypical direct anterior labral tear (3:00) (iliopsoas impingement) [35]. However, the chicken-egg analogy may apply here—did the iliopsoas cause the labral tear, or did the labral tear cause the iliopsoas to activate more to stabi-

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lize the loss of the labral suction seal? [35]. The iliopsoas tendon has been shown to demonstrate an anterior stabilization role in the setting of hip arthroscopy. In three separate case reports with a post-arthroscopic dislocation, an iliopsoas tenotomy was performed [36, 37]. In addition, the effects of femoral version in the setting of iliopsoas tenotomy have been investigated. Significantly better outcomes have been observed in patients with femoral version less than 25° (versus greater than 25°) [38]. The posterior musculotendinous complex, primarily the proximal hamstring, short external rotators, and gluteus maximus, is frequently involved in the endurance athlete. The inferior margin of the more superficial gluteus maximus is approximately 6  cm proximal to the deeper superior aspect of the proximal hamstring origin on the ischium [39]. The inferomedial origin, the conjoined semitendinosus/long head biceps femoris tendons, is oval-shaped and larger (2.7  ±  0.5  cm from proximal to distal and 1.8  ±  0.2  cm from medial to lateral) than the crescent-­ shaped semimembranosus footprint (3.1  ±  0.3  cm from proximal to distal and 1.1 ± 0.5 cm from medial to lateral) on the superolateral ischial tuberosity [39, 40]. The most lateral aspect of the tuberosity is approximately 1  cm from the sciatic nerve [39]. However, in normal anatomy, the sciatic nerve should move, gliding past the tuberosity and hamstring origin with motion. The nerve may even contact the hamstring with a narrowed ischiofemoral space, or with extension, adduction, and external rotation (end of stance phase of gait/stride) due to the lesser trochanter, or with flexion, abduction, and external rotation (FABER position, crossing legs) due to the greater trochanter. In addition to the sciatic nerve, the more superficial, posterior, and medial posterior femoral cutaneous nerve may also be involved as a symptom source, as the nerve is typically closer to the hamstring than the sciatic nerve. Static and/or dynamic narrowing of this ischiofemoral space is typically a secondary problem, usually due to either intra-articular disorders (e.g., FAIS, dysplasia, arthritis) or peritrochanteric disorders (e.g., gluteal tendon pathology, greater trochanteric bursitis). The

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resultant abductor dysfunction leads to a weight-­ bearing pelvic dip (Trendelenburg) and subsequent narrowing of the ischiofemoral space. In runners, proximal hamstring (myotendinous junction and tuberosity origin) syndrome (Fig. 14.4a, b) is common in both short-distance sprinters and long-distance runners [41, 42]. The medial hip and abdominopelvic musculotendinous complex is variable and highly intricate, leading to an often misunderstood, under-recognized, and undertreated entity termed core muscle injury, inguinal disruption, sports hernia, or athletic pubalgia. Adductor-related pain, osteitis pubis, and core muscle injury are rarely seen in isolation, and nearly always seen in combination with intra-articular diagnoses, especially FAIS and labral injury [3]. Thus, a detailed understanding of the anatomy is paramount in timely identification and management. The anatomy centers around the pubis and pubic symphysis. The latter is a non-synovial joint stabilized by four ligaments and an intra-articular fibrocartilage disc [43]. The four ligaments conjoin the rectus abdominis, external and internal oblique, transversus abdominis, and gracilis and adductor aponeuroses. The most important ligament is the anteroinferiorly located arcuate ligament. The symphysis acts as the anterior pelvic fulcrum, around which the hip and pelvis muscle forces act. The rectus abdominis (creates a posterosuperior force) and adductor longus (creates an anteromedial force) unite anterior in a common sheath anterior to the pubis. This common aponeurosis joins the conjoint tendon (internal oblique and transversus abdominis), external oblique, pectineus (anterior), adductor brevis (posterior to adductor longus), adductor magnus (posterolateral), and gracilis (posteromedial). Core muscle injury (“sports hernia,” “athletic pubalgia”) occurs when any of these multiple structures is injured, resulting in increased stress and strain on the intact proximate structures, typically without a discrete recognizable hernia [44]. The superficial (external) inguinal ring is located just immediately lateral to the pubic aponeurosis (indirect hernia through the ring versus direct hernia through Hesselbach’s triangle). This clearly complicates the diagnostic picture, given

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a

b

Fig. 14.4 (a) Coronal, T2-weighted MRI of a 38-year-­ old female ultra-marathon runner with proximal hamstring syndrome demonstrating a partial-thickness, interstitial, insertional proximal hamstring tear with posterior hip and buttock pain at the ischial tuberosity. (b)

Same patient as Fig.  14.4a, with an axial, T2-weighted MRI demonstrating partial-thickness proximal hamstring tear. Quadratus femoris is observed without any edema (ischiofemoral impingement). This MRI was performed 2 weeks following a 50 mile ultramarathon

the close, complex, integrated anatomy and pathoanatomy in endurance athletes. The abnormal musculotendinous stress distribution may further potentiate symphyseal instability and then lead to a secondary musculotendinous injury (cyclical stress transmission). Further, especially in endurance sports, imbalances or injuries to the core muscles result in increased fatigue, decreased endurance, and injury, exacerbating the stress transmission cycle [45]. Part of the innervation of the core muscles, the iliohypogastric, ilioinguinal, and genitofemoral nerves (part of Layer IV), may also be involved via entrapment, resulting in deep anterior and/or lateral hip pain.

pelvis to the remainder of the body. Any kink in the kinetic chain may result in dysfunction. Several studies have revealed either upstream or downstream effects of hip injury and other proximal or distal structures. In the endurance athlete, this has wide implications as to the determination of the cause or effect of hip injury. Elevated alpha angle has been associated with increased risk of anterior cruciate ligament (ACL) tear (27 times greater if alpha angle greater than 60°) [46]. In patients with chronic recurrent ankle sprains, significantly delayed gluteus maximus activation during prone hip extension has been identified [47]. It is unknown if whether the ankle is the instigator for the hip, or vice versa. Similarly, patients with low back pain have consistently identified decreased hip range of motion (versus controls) [48–53]. Further, pelvic incidence (position-independent measure of lumbar lordosis and pelvis orientation) has been shown to be significantly lower in both cam and pincer FAI [9].

Layer IV Layer IV is comprised of the neurokinetic layer, the lumbosacral plexus, and lumbopelvic tissues, serving as the neural link to the hip and lower extremities. This essentially links the hip and

14  Hip Injuries and Conditions in the Endurance Athlete

History Endurance athletes should be thoroughly evaluated in a systematic fashion. The chief complaint is frequently helpful in determining the most important part of the history and physical examination: Is the source of pain coming from inside (intra-articular) or outside (extra-articular) the hip joint? Although the typical patient complains of groin pain, illustrated by a “C” sign or a “between the fingers” sign (Fig. 14.5a, b), several different locations in and around the hip may be perceived for true intra-articular hip pain [49]. Patients may complain of pain in the groin (55– 92%), lateral hip (59–67%), anterior thigh (35– 52%), buttock (29–71%), low back (23%), knee and below (22–47%), or foot (2%) [49]. The history of present illness should query several key aspects of the patient’s reason for evaluation: Onset (acute, chronic, traumatic, a

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insidious), location (right, left, bilateral; deep, superficial; anterior, lateral, posterior), character (dull, sharp, burning, aching, throbbing), duration, frequency, exacerbating and relieving factors (sitting, standing, walking, running, jumping, laying down, twisting, pivoting, putting on socks and shoes, toilet, out of bed, coughing, sneezing, Valsalva), radiation of pain (below hip, below knee, above to back), and associated symptoms (clicking, catching, popping, snapping, numbness, tingling, pins and needles, groin swelling, or bulging/hernia). Coxa saltans (snapping hip) is frequently due to one (or more) out of three potential causes: 1) external coxa saltans (snapping iliotibial band), frequently described by patients as “My hip is dislocating”; frequently this is visible (“the snapping hip you can see”); 2) internal coxa saltans (snapping iliopsoas), frequently this is audible (“the snapping hip you can hear”); 3) internal coxa saltans (labral tear), freb

Fig. 14.5 (a) Left hip “C” sign, indicative of intra-articular source of hip pain. (b) Left hip “between the fingers” sign, indicative of intra-articular source of hip pain

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quently described by patients as the snapping hip that they can feel, but you cannot see or hear. Infrequently, a “clunk” may be reported, rather than snapping, clicking, or popping, in the setting of ischiofemoral impingement due to the lesser trochanter rubbing over the hamstring origin on the ischium. Prior treatments should be thoroughly assessed (physical therapy, oral medications, injections, surgeries). Prior injections should be specified (intra-articular, peritrochanteric, ischiofemoral space, trigger point), especially regarding use of ultrasound or fluoroscopic guidance and the response to injection. In hip osteoarthritis, intra-­ articular injection has been shown to be quite accurate in determining the source of pain [54, 55]. However, for other intra-articular non-­ arthritic diagnoses, such as FAIS or labral injuries, the utility of injection is less well understood and less predictable [56]. A significant response to injection (greater than 50% pain relief) helps to rule in intra-articular pathology as the source of the patient’s symptoms [56]. However, a positive response from injection is not a strong predictor of short-term functional outcomes following arthroscopic management of FAIS and labral pathology [57]. Although the lack of a significant response (less than 50% pain relief) does not necessarily rule out intra-articular pathology [56], a negative response may be predictive of poor short-term surgical outcome [58]. The author gives all injection patients a pain diary following injection to document response to injection on a visual analog scale (0–10) at multiple time points (pre-injection; 5, 30, 60 min; 2, 3, 6, 12, 24  h; 2, 3, 7, 14  days). This helps clearly delineate the response to the local anesthetic based on typical drug pharmacokinetics. If prior surgery, the operative report and intraoperative photographs should be scrutinized. Past medical and surgical history should be critically evaluated for other potential sources of groin, hip, or pelvic pain. This especially includes general surgical, urological, colorectal, and obstetric/gynecologic. Past physical therapy notes should be evaluated to determine if high-quality, especially the avoidance of intentional terminal end of range of motion stretching, which may

worsen hip pain due to labral injury, impingement, capsular injury, among other postoperative causes like adhesions. Causes of potential unique sources of hip pathology should be elicited when indicated: Femoral head avascular necrosis (chronic corticosteroid use, alcoholism, pancreatitis, sickle cell anemia, diabetes, scuba diving decompression illness [Caisson’s disease], myeloproliferative disease, systemic lupus erythematosus, Gaucher’s disease), inflammatory arthritides (rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis), Legg-Calve-­ Perthes disease (4–14 years of age), slipped capital femoral epiphysis (8–16  years of age), and transient osteoporosis of the hip (third trimester of pregnancy, middle-aged males). For endurance athletes, a detailed athletic history is a key component of the evaluation, especially including existing risk factors: history of prior overuse injury (including stress fracture), rapid increase in training intensity or mileage, pain characterization during sport (progression with time to the point of stoppage or relieving with time), change in running shoes or equipment, pain progression from after activity, to with activity, to activities of daily living, to rest, and female athlete triad (disordered eating, amenorrhea, low bone mineral density), or tetrad (triad plus endothelial injury) [59]. Occupation and/or recreation of choice is also necessary to elicit: military service members in basic training or “boot camp,” early season workouts for individual- or team-based sports requiring a large increase in mileage after a period of relative disuse (e.g., cross-country runners early Fall season after a summer “off-season”; football players “two-a-days” after “off-season”), triathletes, marathon, or ultramarathon runners, among several others.

Physical Examination The physical examination for endurance athletes with hip pain should be an extension of the focused history of present illness. Although comprehensive and systematic, allowing for reproducibility and consistency, it should be adaptive

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as well, focused on the history elicited prior to the physical assessment. The first fundamental evaluation should be to determine if the source(s) of symptoms stems from inside or outside the joint or both. As with examination of any joint, visual inspection (especially including gait), palpation, motion, strength, and special testing is performed. Further, in order to understand if pathology is present in the involved hip or ­hemipelvis, the contralateral side should also be critically scrutinized. Extensions of the hip assessment should include a thoraco-lumbo-­ sacral spine evaluation, in addition to the distal limb. This includes coronal plane alignment, femoral version, tibial torsion, and pedal arch. Although the physical examination should focus on the presenting chief complaint, a comprehensive evaluation should also identify other abnormalities that may predispose the patient to other overuse injuries (i.e., injury prevention). Further, a caveat to the hip physical examination should be to avoid iatrogenic displacement of non-­ displaced femoral neck stress fractures with a hop test. If sufficient concern exists and radiographs are available, do not perform a hop test, as this could dramatically alter the treatment and eventual outcome.

of the tibia. This includes scrutiny for potential abductor weakness or abductor fatigue via Trendelenburg sign.

Palpation Palpation is a key component for evaluation of multiple causes of hip pain in the endurance athlete. Locations of tenderness suggestive of the source of pathology include peritrochanteric (trochanteric bursitis, abductor tendinopathy or partial tear, snapping iliotibial band), proximal hamstring (proximal hamstring tendinopathy, partial tear, ischial bursitis, ischiofemoral impingement, deep gluteal space syndrome, sciatic nerve irritation, posterior femoral cutaneous nerve irritation), sacroiliac joint (sacroiliitis, referred from FAIS and/or lumbosacral spine), lumbosacral spine (degenerative disk disease, herniated nucleus pulposus, degenerative facet arthropathy, spondylolisthesis, sacral stress fracture (Fig. 14.6), groin (direct or indirect hernia, general surgery/urologic/obstetric/gynecologic causes, core muscle injury [athletic pubalgia, inguinal disruption, sports hernia]), adductor tendon (tendinopathy, tear, core muscle injury), pubis (pubic symphysis, pubic tubercle, pubic

Inspection Thorough inspection of the hip and pelvis requires a balance between sufficient exposure and modesty. The core, hip, pelvis, and entire lower extremity should be observed. In addition to the patient him/herself, shoe wear patterns should also be assessed. Prior surgical incisions, deformity, alignment, swelling, edema, ecchymosis, and erythema should be noted. Observation of ecchymosis alone may be nearly diagnostic in certain injuries such as proximal hamstring tear, adductor tear, or gluteal tendon tear. Hip “snapping” may be observed in cases of external coxa saltans due to snapping iliotibial band. Gait evaluation by either observation in clinic or outside of clinic, on a treadmill, or via digital video analysis gives a real-time evaluation of biomechanical factors that may predispose to stress injuries

Fig. 14.6  Right sided sacral ala stress fracture in a collegiate male cross-country runner

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a

b

Fig. 14.7 (a) Three-dimensional CT scan of a 35-year-­ pelvis MRI illustrating edema in the inferior right pubic old female marathon runner with healing superior and ramus, and extra-osseous soft tissue edema, after acute inferior pubic rami stress fractures with visible fracture injury-on-chronic groin pain callus. (b) Same patient as Fig. 14.7a, axial T2-weighted

Fig. 14.8  AP pelvis plain radiograph of a 17-year-old male cross-country runner with right anterior iliac crest pain with running, illustrating an iliac crest apophysitis and stress fracture

rami for core muscle injury or stress fracture (Fig.  14.7a, b), and iliac crest (stress fracture, apophysitis (Fig. 14.8)).

Motion, Strength, and Special Testing Range of motion is an important component of the hip physical examination in endurance ath-

letes. Although different clinicians may have their own specific routine for assuring completeness and minimizing patient movement between sitting, standing, supine, lateral, and prone, it is important to ensure that a complete exam is performed and documented for every patient. It is also often helpful to examine the “normal” hip before examination of the involved hip. It is important to assess for tightness or contracture in certain muscle groups, especially the iliopsoas, iliotibial band, common adductors, and hamstring complex. The Thomas test may be utilized to assess for hip flexor tightness [60]. The Ober test may elicit iliotibial band tightness and peritrochanteric pain syndrome [61]. For the hip, it is important to normalize the pelvic position by bringing the contralateral limb up to the chest to reduce lumbar lordosis, confounding and truly isolating the magnitude of hip flexion (Fig. 14.9a). Hip flexion, internal and external rotation (Fig.  14.9b, c, respectively), abduction (Fig. 14.9d), and extension (Fig. 14.9e) should be measured and compared to the contralateral limb. Measurements may be taken using visual inspection, goniometer, digital photography, motion analysis, or imaging-based techniques (plain

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a

b

c

d

e

Fig. 14.9 (a) Digital photograph of 22-year-old female professional ballet dancer, illustrating measurement of right hip flexion. (b) Same patient as Fig. 14.9a, illustrating measurement of left hip internal rotation. (c) Same

patient as Fig. 14.9a, illustrating measurement of left hip external rotation. (d) Same patient as Fig. 14.9a, illustrating measurement of left hip abduction. (e) Same patient as Fig. 14.9a, illustrating measurement of left hip extension

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radiographs, MRI, or CT scan). Both supine and prone motion testing should be completed. This is necessary to remove the effect of cam morphology in the extended position. If the hip is flexed, as with the supine position, then either cam morphology or low femoral version may account for a loss of internal rotation. However, if the hip is extended, as with the prone position, then the cam effect is mitigated, and a loss of internal rotation may be isolated to low femoral version alone. Strength testing may be performed using the MRC (Medical Research Council) manual muscle testing system [62]. Hip flexion, extension, abduction, adduction, and internal and external rotation should be tested. Muscle strains are the most common injury in and around the hip in endurance athletes [2]. The muscles that cross both the hip and knee (two joints—eccentric contraction; rectus femoris, sartorius, tensor fascia lata) are especially at risk [63]. Further, in distance runners, iliopsoas strains have been shown to be the most common cause of groin pain [64]. The iliopsoas test, provocation of pain with resisted hip flexion in an externally rotated position, may be performed to diagnose iliopsoas strain, iliopsoas impingement, or an iliopsoas labral tear [65]. The Ludloff test is performed by passively flexing the hip greater than 90°, while supine, isolating the iliopsoas, and a positive sign is reproduction of pain with resisted hip flexion in that flexed position [66]. Impingement testing is performed in endurance athletes to assess for FAIS and labral pathology. The key with all impingement testing is to assure that, in a positive test, the reproduction of pain during the examination maneuver is the same pain location during provocative sport, the chief complaint. Although sensitive (94–99%), the anterior impingement (flexion-adduction-­ internal rotation) test demonstrates poor specificity (5–9%) [67]. It is the most common screening examination maneuver to detect intra-articular pathology. The subspine impingement maneuver is performed with straight hip flexion in the sagittal plane [68]. The lateral impingement test is performed to maximal coronal plane abduction and permissive limb external rotation [32]. Once maximal abduction is reached, the limb is then

internally rotated (trochanteric-pelvic impingement test) [32]. Posterior impingement may be tested with hip extension and external rotation [32]. The posterior impingement test may be performed supine with the patient at the side edge of the table and the leg off the side of the table or with the patient at the end of the table and the leg far off the end. It is important to assess the posterior impingement test for two possible endpoints: pain or apprehension of hip instability. The FABER (flexion-abduction-external rotation) distance test is another impingement maneuver performed in the supine position, with the affected hip flexed and externally rotated, the affected ankle on the contralateral knee, above the patella [69]. A distance greater than 3  cm (asymmetry compared to the contralateral limb) is a positive test [69]. The Stinchfield test is a supine resisted active straight-leg raise test with the knee extended and the hip flexed approximately 20° [70]. A positive Stinchfield is the most specific physical examination maneuver for intra-articular pathology [70]. In addition to the posterior impingement apprehension test, several other tests in the endurance athlete may indicate microinstability: 1) in the external rotation recoil test, a positive finding is present when release of maximal passive lower extremity external rotation, while supine, fails to demonstrate normal spring-like recoil back to the pre-external rotation position [71, 72]; 2) in the dial test, the lower extremity is maximally internally rotated, while supine, and the limb is then allowed to passively externally rotate (positive finding is indicated when greater than 45° of passive external rotation occurs and lacks a mechanical endpoint) [73]; 3) in the traction test, a positive finding occurs upon the feeling of instability or looseness with limb distraction, while supine [32, 74, 75];

Imaging Evaluation Imaging for hip pain in the endurance athlete should always begin with plain radiographs. The clinician should always remember to “treat the patient and not the x-ray.” The reason for this is

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the prevalence of abnormal radiographic findings in asymptomatic subjects [76]. In the latter large systematic review, the prevalence of asymptomatic cam and pincer FAI was 37% and 67%, respectively. Cam morphology was significantly more common in athletes (55%) than nonathletes (23%). On magnetic resonance imaging (MRI), the prevalence of asymptomatic labral tear was 68%. Weight-bearing anteroposterior (AP) pelvis and a combination of ipsilateral lateral hip views (Dunn 45°, Dunn 90°, frog-leg lateral, Lauenstein lateral, cross-table lateral, false profile) should be obtained and scrutinized for adequacy. The standing AP pelvis should demonstrate symmetry of obturator foramina, collinearity of pubic symphysis and coccyx (approximately 2 cm proximal to most superior aspect of symphysis), and an elongated femoral neck (lower extremity internal rotation). On the standing AP pelvis, acetabular coverage and version (lateral center edge angle, Tönnis angle, femoral head extrusion index, Shenton’s line, anterior wall index, crossover sign, posterior wall sign, ischial spine sign) (lateral pincer FAI versus lateral dysplasia), neck shaft angle (coxa vara, coxa valga), neck primary and secondary trabeculae (femoral neck stress fracture), alpha angle (far lateral cam), and Tönnis grade of osteoarthritis should be assessed. On the false profile view, anterior inferior iliac spine (AIIS) morphology (Type I, II, III), anterior center edge angle (anterior acetabular coverage), and inferomedial joint space narrowing and/or sclerosis may be assessed. On the Dunn, frog-leg, cross-table, and Lauenstein lateral views, measurement of head-neck offset (millimeters), head-­ neck offset ratio (unitless), and alpha angle (degrees) permits a thorough two-dimensional characterization of femoral head-neck junction asphericity (a three-dimensional issue). Femoral neck stress fractures are another common cause of hip pain in endurance athletes. Four different classifications exist to classify femoral neck stress fractures. Three of these systems may exclusively utilize plain radiographs. The most clinically relevant, easily applied, generalizable, with the highest interobserver and intra-observer reliability is the system created by Kaeding and Miller [77]. This system utilizes

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five grades, one through five. Grade 1 is a painless asymptomatic stress response visible on imaging. Grade 2 also illustrates a stress response without a fracture line. However, Grade 2 injuries are symptomatic. Grade 3 and Grade 4 injuries both have a visible fracture line. Grade 3 injuries are non-displaced and Grade 4 are displaced. Grade 5 injuries are nonunions. The Devas classification divided fractures into compression- and tension-sides [78]. The Blickenstaff and Morris classification has three types: Type 1 (callus, without fracture line); Type 2 (non-displaced fracture line); Type 3 (displaced fracture) [79]. The Fullerton and Snowdy classification also has three types: Tension-side, nondisplaced; Compression-side, nondisplaced; Displaced [80]. MRI and computed tomography (CT) offer complementary three-dimensional osseous and soft tissue information in and around the hip and pelvis. Standard series should include a combination of T1-, T2-, and proton density-weighted coronal, axial, sagittal, axial oblique, and radial series [81]. The unique three-dimensional, nearly spherical, anatomy of the hip joint makes it highly difficult to view the thin (one to two millimeters) opposing articular cartilage and labrum with standard planar series because of partial volume averaging in MRI. Radial sectioning, at 30° increments, are ideal for evaluating the curved structures of the hip. Each plane taken (13 total for 360° circumference) goes through the center of the joint. Thus, the obtained plane is perpendicular to the curvature of the curvature of the joint, providing a cross-section of the articular cartilage and labrum [81]. This reduces the partial-­volume averaging effect seen with conventional planar imaging. Axial oblique MRI had long traditionally been the gold standard reference for measurement of alpha angle, quantifying the degree of proximal femoral asphericity [82]. The images pass through the center of the femoral head parallel to the plane of the femoral neck. It essentially provides a view that corresponds to a frog-leg lateral hip radiograph (~2:45 o’clock on the femoral clockface), which is the anterior head-neck junction [83, 84]. Cam morphology is more commonly observed at the anterolateral head-neck junction, which is the Dunn 45°

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(~1:40) or Meyer 20° (~1:08) lateral views [83, age parameters [94]. CT is the best preoperative 84]. Thus, the Dunn 45° or Meyer 20° views are evaluation of the proximal femoral head-neck the best single lateral radiographic view to iden- junction. However, intraoperatively, CT is not tify the most common cam location, not the frog-­ routinely utilized (“O” arm). A combination of leg lateral [85, 86]. Similarly, the radial series six fluoroscopic views (AP neutral, AP in 30° MRI does a more complete head-neck junction internal rotation, AP in 30° external rotation, 50° asphericity evaluation, in that it better character- flexion view in neutral, 50° flexion view in 40° izes the more common cam apex locations external rotation, 50° flexion view in 60° external (~1:00–2:00) and provides an overall “arc of rotation) can reproducibly characterize the topogasphericity,” termed the omega angle [87]. In raphy of the cam deformity from the 11:45 to addition to the osseous and chondrolabral 2:45 position, covering the most commonly ­anatomy, MRI provides useful information on the observed maximum alpha angles [95]. Because capsule, musculotendinous units, and other extra-­ the most common reason for revision hip arthrosarticular, but relevant, structures (lumbosacral copy is residual FAI, the potential for inadequate spine [48], core muscle injury [88], and other resection should be mitigated as much as possigastrointestinal, genitourinary, obstetric-­ ble [96]. On the acetabular side, CT has shown gynecologic [89, 90]). The addition of intra-­ that normal femoral head coverage was 40% ± 2% articular gadolinium dye (magnetic resonance in an asymptomatic cohort, with the mean lateral arthrogram [MRA]) distends the joint capsule, coverage corresponding to a lateral center edge separating capsule, labrum, and articular carti- angle of 31 ± 1° [97]. lage, increasing spatial resolution for improved diagnosis of chondrolabral injury [91]. Although MRA improves the sensitivity (63–100%), speci- Differential Diagnosis Evaluation ficity (44–100%), and accuracy (65–96%), it is highly resource-intensive, requiring both fluoros- The clinician must combine the subjective hiscopy (for the arthrogram) and MRI at the same tory with the objective physical examination with time, temporal coordination of each appointment, the objective imaging studies to determine a difand direct physician performance of the arthro- ferential diagnosis (Table 14.2). The first step in gram. Further, there are risks associated with evaluation and management of hip pain in the intra-articular hip dye injection [91]. endurance athlete is determining if the pain is With reference to femoral neck stress frac- intra- or extra-articular. The magnitude and tures, if plain radiographs do not reveal a fracture potential severity of intra-articular diagnoses line or evidence of healing (periosteal thickening merits priority over most extra-articular sources and elevation, cortical sclerosis), then MRI has a (Table 14.3.). However, the clinician must always sensitivity and specificity of up to 100% [92]. be aware that these diagnoses are not mutually Technetium-99 m-labeled methylene diphospho- exclusive and frequently may coexist either as nate bone scan (Triple Phase Bone Scintigraphy) two distinct entities or one as a result of another. is a sensitive exam to detect femoral neck stress Intra-articular sources include most commonly fracture, but has poor specificity [93]. Further, FAI, labral tear, dysplasia, arthritis, and stress anatomic delineation of fracture location is poor fracture, among other less common causes. with bone scan. Computed tomography (CT) Athletes with intra-articular sources of symptoms scans are associated with significant radiation typically have a chief complaint of deep groin exposure and low sensitivity of detecting stress pain. The pain is most frequently perceived deep fracture, but do have high specificity [93]. in the hip, unable to be touched superficially. CT scan is the optimal osseous evaluation of Sitting tends to exacerbate the pain more than the hip joint, providing a patient-specific three-­ standing. Deep flexion and rotational maneuvers dimensional picture, evaluation of femoral and also exacerbate. Sports that involve high-­intensity acetabular version, and precise acetabular cover- or frequency hip flexion and rotation are frequent

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Table 14.2  Subjective and objective evaluation pearls in endurance athletes with hip pain. The clinician should be cognizant that these diagnoses are not mutually exclusive and may frequently co-exist. AIIS (anterior inferior iliac spine); CEA (center-edge angle); IR (internal rotation); ER (external rotation)

Femoral neck stress fracture

FAI, labral tear

Dysplasia

Osteoarthritis

Extra-articular impingement— AIIS

Extra-articular impingement— Ischiofemoral

Extra-articular impingement— Trochanteric-­ pelvic

Extra-articular impingement— Iliopsoas

Peritrochanteric pain syndrome

Imaging—advanced— MRI/CT Edema, discrete fracture line, 100% sensitivity, 100% specificity Cam (increased alpha Labral tear, articular Positive impingement Groin pain, worse cartilage injury, angle, loss of testing, decreased with deep flexion subchondral edema head-neck offset); and rotational sports flexion and rotation “herniation Pincer (lateral CEA pit”/“impingement >40°, crossover, posterior wall, ischial cyst” spine signs, protrusion) Labral tear Lateral CEA 25% fatigue” Articular cartilage Loss of joint space Positive impingement Groin pain, worse narrowing, subchondral (90°, “Splits” radiograph Labral tear, extra-­ Deep lateral or illustrating anterior groin pain, positive trochanteric-­ articular edema at site especially in of impingement pelvic impingement test trochanteric-pelvic impingement, vacuum hyperabducted sign, coxa vara position, either in IR or ER 3:00 labral tear, edema Increased femoral Positive anterior Groin pain, worse impingement, positive anteversion, type II or at iliopsoas-AIIS with active hip interval, increased Ludloff, iliopsoas test, III AIIS flexion, worse with femoral anteversion iliopsoas snap deep flexion and rotational sports, audible internal snapping Edema at bursa, Coxa valga, Peritrochanteric Lateral hip pain, abductor tendinopathy, calcification at tenderness, positive superficial, visible partial tear abductor insertion Ober test, abductor snapping weakness (continued) History Groin pain, rapid training increase, female athlete triad

Physical examination Pain with axial load, hop, log roll, impingement testing

Imaging—plain radiographs Compression versus tension side, frequently negative

J. D. Harris

204 Table 14.2 (continued) History Deep gluteal (aka Non-discogenic “sciatica” posterior “piriformis”) hip or buttock pain, syndrome poor sitting tolerance

Proximal hamstring syndrome Core muscle injury (aka “athletic pubalgia”) Lumbosacral spine

Posterior hip, proximal hamstring pain, worse with running Groin pain, worse with Valsalva and high intensity sport

Low back pain, sciatica

Physical examination Posterolateral hip, gluteal, retro-­ trochanteric tenderness, worse with hip rotation in flexion with knee extended, antalgic sitting position Ischial tuberosity tenderness, worse with resisted hamstring Tenderness at pubis, adductor, rectus abdominis, no direct or indirect hernia Lumbosacral tenderness, positive straight leg raise

culprits. In patients with any degree of concern for femoral neck stress fracture, every diagnostic step necessary must be taken to ensure a correct diagnosis is made, as missed diagnoses may be catastrophic with displacement of the fracture and significantly increased risk of femoral head avascular necrosis, even with timely prompt and anatomic reduction (up to 30%) [98]. These patients often complain of groin pain that begins early in the activity (e.g., running), progressively worsens during the activity, and may progress to the point of activity cessation due to pain. Endurance athletes with a previous stress fracture, females, amenorrhea, disordered eating, and low bone mineral density warrant a stress fracture evaluation. On physical examination, pain with weight-bearing, axial load, single leg stance, squat, hop, and positive impingement testing are characteristic of femoral neck stress fracture. If plain radiographs reveal no sign of fracture, then MRI is indicated. In athletes with similar symptomatology with negative stress fracture evaluation, plain radiographs frequently reveal FAI and an MRI is then indicated to evaluate for chondrolabral injury. In athletes with similar symptomatology with negative stress fracture evaluation, dysplasia may also be a cause of deep hip pain.

Imaging—plain radiographs Decreased ischiofemoral distance, ischiofemoral impingement

Imaging—advanced— MRI/CT Sciatic neural enlargement, loss of normal fascicular appearance, fibrous bands over piriformis

Prior ischial tuberosity avulsion, calcification at hamstring origin Frequent with FAI, osteitis pubis

Proximal hamstring tendinopathy, partial tear

Lumbosacral spondylosis, degenerative disk/ facet

Edema at pubis, adductor origin, conjoined tendon, rectus abdominis, labral tear Herniated nucleus pulposus, spondylolisthesis

However, frequently, this is secondary to abductor fatigue. Dysplasia induces a component of femoral head translation (in addition to rotation) with motion [32, 99]. This microinstability requires greater abductor activity to keep the femoral head center of rotation centered in the acetabulum (“abductor fatigue”). When abductor dysfunction permits pathology contralateral pelvic tilt, the ischiofemoral space narrows posteriorly and a secondary ischiofemoral impingement and proximal hamstring pain/syndrome may occur. In athletes with groin pain, loss of motion, and crepitus, plain radiographs should be critiqued for osteoarthritis (joint space narrowing, subchondral sclerosis, cysts, osteophytes). If the symptoms and examination are consistent with an extra-articular source of symptoms, then the differential diagnosis is very different from that of intra-articular sources. Extra-­ articular impingement, similar to traditional FAIS, involves a mechanical conflict that inhibits hip motion and places extra stress on tissues unequipped to handle the stress. This can occur at the AIIS in straight hip flexion with the distal anterior femoral neck contacting a prominent Type II or III AIIS [100]. Despite this being an extra-articular phenomenon, labral pathology is

14  Hip Injuries and Conditions in the Endurance Athlete

205

Table 14.3  Treatment and outcomes for endurance athletes with hip pain. NWB (non-weight bearing); NSAID (non-­ steroidal anti-inflammatory); PT (physical therapy) Femoral neck stress fracture

FAI, labral tear Dysplasia

Osteoarthritis Extra-articular impingement—AIIS Extra-articular impingement— Ischiofemoral Extra-articular impingement— Trochanteric-pelvic Extra-articular impingement—Iliopsoas Peritrochanteric pain syndrome Deep gluteal (aka “piriformis”) syndrome Proximal hamstring syndrome Core muscle injury (aka “athletic pubalgia”) Lumbosacral spine

Non-surgical treatment Compression-side, non-displaced: NWB × 6 weeks

Surgical treatment Tension-side or failed nonsurgical treatment compression side: In situ percutaneous screw fixation Displaced fracture: Anatomic reduction, screw fixation Limited evidence; Activity modification, Labral preservation, pincer oral NSAID, ± intra-articular injection, PT acetabuloplasty, cam osteoplasty Activity modification, oral NSAID, ± intra-­ Borderline dysplasia: Arthroscopic hip articular injection, PT preservation; Dysplasia: Periacetabular osteotomy Rest, activity modification, oral NSAID, Total hip arthroplasty intra-articular injection, PT, neutraceutical Limited evidence; Activity modification, Arthroscopic subspine decompression oral NSAID, ± intra-articular injection, PT osteoplasty Limited evidence; Activity modification, Endoscopic or open ischiofemoral oral NSAID, PT decompression (lesser trochanter) Limited evidence; Activity modification, oral NSAID, ± intra-articular injection, PT

Open trochanteric osteotomy advancement

Limited evidence; Activity modification, oral NSAID, ± iliopsoas tendon sheath injection, PT Rest, activity modification, oral NSAID, bursal injection, PT Rest, activity modification, oral NSAID, infiltration injection test (corticosteroid, anesthetic) Rest, activity modification, oral NSAID, PRP injection, PT (emphasize eccentric) Rest, activity modification, oral NSAID, PT (core muscle activation, strengthening)

Arthroscopic subspine decompression and/or iliopsoas tenotomy

Rest, activity modification, oral NSAID, injection, PT

frequently observed and the AIIS may be surgically treated with “intra-articular” arthroscopy [101, 102]. Further, despite being extra-articular FAI, AIIS subspine impingement symptoms are frequently perceived deep in the groin, similar to cam and pincer FAI. Straight hip flexion subspine impingement testing combined with false profile radiographs and three dimensional CT scan can reliably diagnose subspine impingement [68]. Trochanteric-pelvic impingement may be observed in high range of motion endurance sports (ballet, gymnastics, mixed martial arts, figure skating). Patients frequently complain of pain in the lateral splits (grand écart facial) and front

Endoscopic or open bursectomy and iliotibial band window, abductor repair Endoscopic or open sciatic neurolysis, lysis of fibrous adhesions Proximal hamstring repair Open repair, decompression of adductor/ rectus/conjoined tendon complex as indicated by pathology Open decompression and fusion (if indicated)

splits positions (grand écart lateral) [33]. Additionally, in dancers, “turnout” (primarily external rotation) frequently may induce lesser trochanter impingement on the lateral ischium and proximal hamstring origin or greater trochanter impingement on the lateral ischium (ischiofemoral impingement) [103]. This presents as posterior hip and buttock pain in provocative positions and maneuvers. This repetitive friction and attrition frequently causes symptoms from the ischial bursa and posterior femoral cutaneous nerve (usually burning while seated). It is important to evaluate the proximal hamstring and gluteus maximus function in this situation for

206

concurrent proximal hamstring tendinopathy or partial tearing. Iliopsoas impingement is frequently seen as an internal snapping hip, with complaints of deep groin pain with active hip flexion and rotation, inducing snapping and far anteromedial labral tears [104]. In patients with lateral hip pain, superficial tenderness is frequently diagnosed as “bursitis”[105]. However, patients with discrete abductor weakness and insignificant iliotibial band tightness warrant MRI for evaluation of abductor tendinopathy and possible tear.

Treatment Management of most conditions causing hip pain in endurance athletes is not emergent or urgent. The only potentially urgent diagnosis necessary to be made is that of potential femoral neck stress fracture and its inherent risk of displacement. In non-displaced compression-sided femoral neck stress fractures, immediate non-weight bearing is instituted with crutch-assisted ambulation for 6 weeks. If the fracture heals, the patient’s pain with weight-bearing resolves and a slow return to sport (with recognition and address of underlying risk factors) is commenced. Persistent pain warrants MRI to evaluate for fracture persistence or worsening (Fig. 14.10a). In this situation of failed nonsurgical measures, percutaneous screw fixation (Fig. 14.10b–d), followed by weight-bearing as tolerated ambulation (6  weeks) and gradual

J. D. Harris

return to sport (6–12  weeks) is commenced. In non-displaced tension-sided stress fractures, percutaneous screw fixation is indicated, as nonsurgical treatment is not indicated due to the unfavorable biomechanics of fracture location. Any stress fracture displacement requires prompt (same day) anatomic reduction (closed or open means) and fixation (percutaneous screw or plate/ screw fixation). Fracture displacement on any imaging modality is an indication to immediately cease nonsurgical treatment and anatomically reduce and fix the fracture. In patients with symptomatic FAI and labral tear, initial nonsurgical management consists of activity modification (avoidance of deep flexion and rotation), oral anti-inflammatory medications, and physical therapy (core, hip, pelvis strengthening, and flexibility; dynamic reduction in anterior impingement by improving posterior pelvic tilt). Intra-articular anesthetic and corticosteroid injections may be used both diagnostically and therapeutically. However, the clinician and patient should always be cognizant of the fact that neither medications nor injections can change the pathoanatomy of the hip morphology or heal the labral tear (Fig.  14.11a–d). Thus, nearly all of the current evidence focuses on surgical treatment of FAI and labral pathology [106]. Both arthroscopic and open techniques are successful, with a high rate of good to excellent outcomes at short- and mid-term follow-up. No long-term outcomes of either open or arthroscopic hip preservation yet exist [107].

14  Hip Injuries and Conditions in the Endurance Athlete

a

207

d

b

c

Fig. 14.10 (a) Coronal T2-weight MRI of 28-year-old female runner with a compression-sided right femoral neck fracture. This patient had failed 6 weeks of nonsurgical treatment consisting of non-weight bearing crutch-­ assisted ambulation. (b) Same patient as 10A, 1 day after the MRI, illustrating postoperative AP pelvis X-ray with three partially threaded 7.3 millimeter diameter screws traversing the femoral neck. Key surgical pearls include

avoidance of a proximal femoral stress riser effect by keeping the screw entry point on the lateral proximal femoral cortex proximal to the superior aspect of the lesser trochanter. (c) Same patient as 10a, illustrating post-­ operative Dunn 90° lateral radiograph with three partially threaded screws. (d) Same patient as 10A, illustrating postoperative false profile radiograph with three partially threaded screws

J. D. Harris

208

a

b

c

d

Fig. 14.11 (a) Arthroscopic right hip preservation surgery in 27-year-old female volleyball player. Viewing from anterolateral portal with 70° arthroscope. Probe instrumenting from mid-anterior portal pushing on acetabular labrum at 1:30 on clockface. The chondrolabral disruption is clearly visible at the chondrolabral junction. (b) Same patient as 11A after two suture anchors have been placed in the acetabular rim with a pierced vertical mattress configuration. The typical labral repair follows acetabuloplasty rim trimming to eliminate pincer impinge-

Conclusions Evaluation and management of the endurance athlete with hip pain requires a thorough knowledge of the layered structure of normal anatomy and abnormal pathoanatomy in and around the hip joint. The subjective history and objective

ment (when indicated). Two to four suture anchors are typically used. (c) Arthroscopic right hip preservation surgery in an 18-year-old female collegiate rower. Viewing from anterolateral portal with 70° arthroscope. Radiofrequency device is localizing an iliopsoas-induced acetabular labral tear at 3:00 on clockface. Erythema at the location of impingement, in addition to the chondrolabral disruption, is visible on this image. (d) Same patient as 11C after suture anchor repair in the acetabular rim with a pierced vertical mattress configuration

physical examination must be combined with any imaging to properly “treat the athlete and not the MRI.” Patients with intra-articular pathology report deep groin pain, worse with the offending sporting activity, deep flexion, and rotational maneuvers. Physical examination typically reveals a loss of hip flexion and rotation with positive impingement findings. Although FAIS

14  Hip Injuries and Conditions in the Endurance Athlete

and labral tears are the most common diagnosis in endurance athletes, risk factors for femoral neck stress fracture must be sought, evaluated, and promptly managed as this is an unmissable diagnosis. Plain radiographs are very useful in endurance athletes with hip pain. However, advanced imaging with MRI and CT has a distinct and growing role in appropriate evaluation. Sources of pain around the hip joint frequently coexist and the clinician must systematically assess all potential diagnoses, as they are not mutually exclusive.Source of FundingNone. Statement of Originality  All data, figures, tables, and text are original and previously unpublished.

Disclosures  Paid Consultant: Smith & Nephew; Research Support: Smith & Nephew, Depuy Synthes, Houston Texans, Houston Methodist Hospital; Publication royalties: SLACK, Inc., Thieme Publishers; Stock/Stock Options: PatientPop; Committees: AANA, AAOS, AOSSM, ISAKOS, ISHA, ACOEM, AOA, IADMS, ORS.

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212 the pelvis and the lower extremity. Acta Radiol. 2002;43(2):207–12. 93. Gaeta M, et al. CT and MR imaging findings in athletes with early tibial stress injuries: comparison with bone scintigraphy findings and emphasis on cortical abnormalities. Radiology. 2005;235(2):553–61. 94. Massey PA, et  al. Letter to the Editor re: “ Cam impingement: defining the presence of a cam deformity by the alpha angle Data from the CHECK cohort and Chingford cohort”. Osteoarthr Cartil. 2014;22(12):2093–4. https://doi.org/10.1016/j. joca.2014.09.023. 95. Ross JR, et  al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-­dimensional computed tomography. Am J Sports Med. 2014;42(6):1370–6. 96. Cvetanovich GL, et al. Revision hip arthroscopy: a systematic review of diagnoses, operative findings, and outcomes. Arthroscopy. 2015;31(7):1382–90. 97. Larson CM, et al. Are normal hips being labeled as pathologic? A CT-based method for defining normal acetabular coverage. Clin Orthop Relat Res. 2015;473(4):1247–54. 98. Ehlinger M, et al. Early prediction of femoral head avascular necrosis following neck fracture. Orthop Traumatol Surg Res. 2011;97(1):79–88. 99. Harris JD, et  al. Radiographic prevalence of dysplasia, cam, and pincer deformities in elite ballet. Am J Sports Med. 2015;44(1):20–7. https://doi. org/10.1177/0363546515601996. 100. Hetsroni I, et  al. Anterior inferior iliac spine morphology correlates with hip range of motion: a clas-

J. D. Harris sification system and dynamic model. Clin Orthop Relat Res. 2013;471(8):2497–503. 101. Hetsroni I, et  al. Anterior inferior iliac spine deformity as an extra-articular source for hip impingement: a series of 10 patients treated with arthroscopic decompression. Arthroscopy. 2012;28(11):1644–53. 102. Amar E, et  al. Pathological findings in patients with low anterior inferior iliac spine impingement. Surg Radiol Anat. 2016;38(5):569–75. https://doi. org/10.1007/s00276-­015-­1591-­8. 103. Gomez-Hoyos J, et  al. Femoral Neck Anteversion and Lesser Trochanteric Retroversion in Patients With Ischiofemoral Impingement: A Case-Control Magnetic Resonance Imaging Study. Arthroscopy. 2016;32(1):13–8. https://doi.org/10.1016/j. arthro.2015.06.034. 104. Domb BG, et  al. Iliopsoas impingement: a newly identified cause of labral pathology in the hip. HSS J. 2012;7(2):145–50. 105. Ho GW, Howard TM. Greater trochanteric pain syndrome: more than bursitis and iliotibial tract friction. Curr Sports Med Rep. 2012;11(5):232–8. 106. Harris JD, et  al. Treatment of femoroacetabular impingement: a systematic review. Curr Rev Musculoskelet Med. 2013;6(3):207–18. 107. Nwachukwu BU, et  al. Arthroscopic versus open treatment of femoroacetabular impingement: a systematic review of medium- to long-term outcomes. Am J Sports Med. 2015;44(4):1062–8. https://doi. org/10.1177/0363546515587719.

Common Injuries and Conditions in Rowers

15

Kristine A. Karlson and Genevra L. Stone

Introduction Rowing is a highly dynamic, highly static sport that requires both high aerobic capacity and strength. Unlike many other endurance sports, it is highly repetitive, without change in terrain that might allow changes in technique. In search of the perfect stroke, rowers repeat the same movement, altering only cadence (strokes per minute) and power per stroke. Rowers thus are at risk for significant overuse injuries [1]. Rowing is contested typically over 2000  m (the Olympic distance) in the spring and summer, and over longer distances in the fall. Winter training may be cross-training but involves significant time on the rowing ergometer (“erg”). Some athletes who row have never been in a boat and compete only on the erg, which has increasingly become part of many gyms’ fitness equipment. Rowing encompasses a wide variety of boat classes, race distances, and athletes. Boats range in size from a single (one rower) to an eight (eight rowers and one coxswain). Sculling boats include K. A. Karlson (*) Community and Family Medicine, Orthopaedics and Pediatrics, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA e-mail: [email protected] G. L. Stone Harvard Affiliated Emergency Medicine Residency at Beth-Israel Deaconess Medical Center, Boston, MA, USA e-mail: [email protected]

the single, double, and quadruple (“quad”) while sweep boats include the pair, four, and eight person discipline. In the sweep boats, “port” or “strokeside” rowers pivot around an oarlock on their right while “starboard” or “bowside” rowers pivot around an oarlock on their left. Because the sweep rowers lean toward their oarlocks and most of the force is maintained on the side of the body farthest from the oarlock, they develop physiologic asymmetries. Traditional race distances include 1000  m (mostly for “masters” rowing, which includes athletes above 26  years of age), 2000 m (interscholastic, university, and elite rowing), and “head races” of roughly three miles. The youngest rowers tend to be in middle school, and people will continue rowing into their 80 s and above. Within rowers as a general category, there are subsets of athletes. At the elite level, lightweight rowing is for those rowers under 59 kg for females and 72.5  kg for males. University racing also includes lightweight teams although the weight rules vary slightly from international competition. (Youth lightweight rowing continues to exist in some arenas, but it is being reduced out of concern for the long-term effects of weight categories on youth athletes.) Another manner of categorizing athletes is by age. Masters rowing consists of all who turn 27 years old in the calendar year. It is further broken down into categories A through K, depending on the average age of the crew (beginning with A at 27 through K at 85 or more). The last common classification system is that of para-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_15

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rowing. It is based on functional ability, and eligible rowers have a vision or functional disability. PR1 rowers use only their arms and shoulders to propel the boat while PR2 use their trunk and arms. Neither of these classes uses a sliding seat. PR3 rowers use their legs, trunk, and arms and have a sliding seat, but may have other disabilities such as below knee amputation or blindness.

Rowing Stroke Rowers face backward on rolling seats propel boats moving forward by levering the blade face(s) of the oar(s) against the water. (The rower may have one oar (“sweep”) or two oars (“scull”) in the hands.) The feet remain fixed in shoes attached to a solid footboard, providing the surface against which the power is generated before being transmitted to the hands on the handle(s) of the oar(s). The oar handle in turn provides one end of a lever arm. The other end of which is the blade face, and the pivot point is the oarlock and pin at the apex of the rigger.

The blade remains relatively stationary in the water each stroke as the boat moves past it on the segment of the stroke known as the “drive.” The drive begins at the “catch,” the moment the blade(s) enter the water, and encompasses the time when the blade is in the water before it ends with the “release,” the moment the blade(s) leave the water. During the drive, a rower extends at the knees before extending at the hips and finally flexes the elbows. The “recovery” encapsulates the portion of the stroke when the blade(s) is out of the water. During the recovery, the rower reverses the drive: first extending the elbows then flexing at the hips before the knees flex. A longer stroke is advantageous to speed; thus, at the catch the knees are flexed maximally to the point of shins perpendicular over the feet with the shoulders over the distal femurs (hips around 120° of flexion), and the arms fully straight. At the finish the knees are fully extended with the torso leaning back (hips around 60 degrees of flexion) and the elbows fully flexed so that the hands are against the abdominal wall (Fig. 15.1).

a

b

c

d

Fig. 15.1  Demonstration of the four phases of the rowing motion. (a) the catch, (b) the drive, (c) the release, and (d) the recovery

15  Common Injuries and Conditions in Rowers

Back Not only are lower back injuries common in rowing, but also rowers are one of the types of athletes most likely to complain of lower back injuries [2]. At the catch, the boat speed is at its slowest point of the stroke cycle; thus, when the rower places the blade in the water and begins exerting force on the blade with the strongest muscle groups (thigh and gluteal muscles), the load on the blade is the highest of any point of the stroke. As the rower extends the legs in the first half of the drive, much of this load is transmitted through the lower back. Like picking up a heavy box from the floor requires using the legs first and keeping the core engaged, a rower must use the legs first and keep the core engaged in order to avoid lower back injury. Rowers engage in pulling this load time and time again with each stroke, which is reflected in the chronic nature of many lower back injuries. These injuries include lumbosacral disc pathology (herniation, degeneration, bulges, annular tears), spondylosis, facet joint arthropathy, and muscle strains. Risk factors for lower back injury include a steep increase in training volume (particularly on the ergometer), reduced flexibility (anterior and posterior lower chain), and prior history of lower back pain [3]. Biomechanical data evaluating rowing technique has been analyzed to determine certain technical factors predisposing rowers to lower back injury. A general consensus is that fatigue increases risk of lower back injury [4, 5]. As fatigue leads to deterioration of technique and less use of the core stabilizing muscles, the lumbosacral spine becomes more susceptible to injury. Other more specific technical factors associated with lower back injuries include greater posterior pelvic rotation at the catch, greater hip extension at the finish, and less efficient trunk muscle activity [4]. When assessing a rower with lower back pain, in addition to the traditional musculoskeletal evaluation, it is important to ask about neurologic symptoms (including sciatica and bladder/bowel function) and to examine for neurologic signs. This consists of sensation, strength testing, and reflexes. Pain with sitting and sciatic pain (radiation down one or both leg(s)) is strongly corre-

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lated with disc pathology on imaging [6]. Keep in mind that neurologic symptoms and signs are a clue to discogenic pain, but many rowers will have disc pathology without neurologic components on examination (up to 80% of those with abnormal imaging in one study) [7]. Central disc herniation presents without sciatica and without neurologic signs on examination [6]. MRI is the preferred study for identifying discogenic pathology; however, a recent consensus statement recommends limiting MRI studies to those athletes with symptoms or signs so significant (any indication of neural compromise) or persistent that positive imaging will influence management [3]. Many episodes of rowing-­ related back pain will be self-limited. Prioritizing pain control, staying active with cross-training, and physical therapy to increase flexibility and strength [3]. If MRI is pursued, interpret the imaging with the clinical context in mind. As mentioned, many rowers will have asymptomatic disc pathology. Treatment is similar for many causes of lower back pathology, including but not limited to disc pathology, spondylosis, facet joint arthropathy, and muscle strains. The athlete should avoid rowing while symptomatic and take NSAIDs to reduce inflammation. Acetaminophen and topical lidocaine may help decrease pain. When it does not cause an increase in pain or other symptoms, the athlete should begin cross-training, stretching, and physical therapy to strengthen the core muscles as early as possible. In athletes with persistent radiculopathy or discogenic pain, imaging-­ guided steroid injection is a second-line treatment for pain relief and often improves pain enough that the athlete can begin physical therapy. The last line of therapy for discogenic pathology is surgical treatment.

Lower Extremity Hip Impingement The hip in rowing needs to tolerate a significant load in a near maximally flexed position at the catch. The hip at the finish is still in some flexion,

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extension is never required, but hip flexors are highly activated at the finish to support the trunk position, and at the initiation of the recovery. To varying degrees a sweep rower may externally rotate the outside hip (the side away from the oar). A sculler may internally rotate the hips as the athlete reaches out for the catch. Hip impingement in rowing is relatively recently recognized. This may follow increasing awareness of hip impingement in athletes in general. It may also possibly reflect increasing training volume. Rowers with hip impingement present similarly to other athletes with hip complaints. Their pain is typically experienced as deep groin pain, without palpable tenderness. Rowers will note that their pain impairs them getting all the way to the catch position, but they also have pain elsewhere in the stroke, likely due to the load placed on the hip throughout the rowing stroke. As with other athletes with suspected hip impingement, physical examination is likely to reproduce pain in the FADIR (flexion, adduction, internal rotation) position. Plain films may discover the presence of a cam or pincer deformity or both. MRI is used for further diagnosis and surgical planning. As with other sports, surgical timing is challenging because rowers compete in multiple seasons. Arthroscopic intervention to correct the impingement deformities requires multiple months of recovery. Intraarticular steroid injection may be pursued but is not typically successful long term. A group at Boston Children’s published a review of 21 cases presenting in the time frame of 2003–2010, 18 of whom went on to surgery. Of that group 56% returned to rowing but 33% did not [8]. It is useful to remember that not all hip pain is intraarticular; however, and a careful physical examination should be able to uncover whether groin pain is superficial to the hip joint. The hip flexor is highly activated at the finish of the rowing stroke as the torso goes into a layback position, and still activated at the beginning of the recovery to start the torso movement over the hips. In this case pain should be reproduced with hip flexion against resistance, whereas intraarticular pain should be more likely provoked by pas-

sive mobilization of the joint, particularly in internal rotation. Possible boat position modifications that may help with hip pain may include adjusting the height of the seat versus the feet, though there may be some limitations with trying to make those changes as they may affect other things such as back position. Though not practical for rowers pursuing racing, the recreational or noncompetitive rower may be able to avoid hip pain by limiting compression at the catch, which is known to rowers as rowing half or three quarter slide.

Knee The knee in rowing is required to tolerate a high load in a close to maximally flexed position. It then needs to tolerate that load as it goes from near maximal flexion to virtually full extension. The motion and load mimic a squat, starting in the fully flexed position. Any nuances in knee position can affect patellar tracking. Rowers may use their knee position, for example, to adjust the balance of the boat. They may deviate the knee from a biomechanically perfect line as they reach out for the catch. This is especially true as the sweep rower reaches through the legs, but also seen in the sculler who may bring the knees into an excessively valgus position due to reaching around the legs at the catch. The feet are fixed in rowing shells as the shoes are affixed in the boat. There may be some variation possible in heel rotation, but there typically is not much, and the shoe separation is not adjustable. A rower could certainly customize this, but that is rarely done, and most rowing boats are shared equipment. Patellofemoral pain is common in rowers, but it is difficult to treat due to the range of motion required of the knee in the rowing stroke. Braces typically do not work well for rowers because they do not allow the maximal flexion of the knee needed at the catch. Similarly, stiff tape such as McConnell taping may be too restrictive for knee range of motion. More flexible tape may not work well either. Suggested interventions include varying the height of the seat versus the shoes,

15  Common Injuries and Conditions in Rowers

which may be achieved with a seat pad, attention to knee tracking during the rowing stroke, and possibly altering the shoe spacing or rotation. The latter may not be possible depending on how the shoes are affixed in the boat and if the boat is shared equipment. Attention to balanced quadriceps strength with the help of a physical therapist who knows rowing is recommended. The iliotibial (IT) band may also be a location of knee pain in rowers, again due to the maximal flexion to near full extension of the rowing stroke, and possible deviations of the knee away from a biomechanically ideal line during the rowing stroke. It may be difficult to modify the rowing equipment for IT band pain, and thus physical therapy for IT band stretching with physical therapy (PT) is recommended. As with patellofemoral pain, deviation of the knee off the center line during the drive may contribute to this problem and should be considered by the athlete and coach.

Ribs and Upper Extremity Rib Stress Fracture Stress fracture of the rib has become the signature stress fracture in rowing. Though there are case reports of rib stress fractures in golf, throwing (first rib), swimming, and an assortment of other sports, stress fractures of the ribs are common in rowing, and are seen at all levels down to high school rather than being an injury seen only in elite or collegiate athletes. Prior to the early 1990s, rib stress fractures in rowers were infrequently reported. With the introduction of new oar blade shapes that increase the efficiency of the rowing stroke has unfortunately also come increased stress on this essential link in the kinetic chain. The kinetic chain of rowing includes every body part linking feet and hands. Though the exact mechanism of rib stress fractures is still debated, the interaction of the scapular stabilizers on the rib, combined with bending of the rib with deep breathing likely combine to overstress the inferior and lateral ribs [9]. Like other stress fractures these are also a result of

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training error, biomechanics, and possibly metabolic factors. Rib stress fractures can present along a continuum that includes costochondral pain and intercostal muscle pain. These both should be thought of as potential precursors to rib stress fracture and treated as such. Remembering that the anterior rib is costal cartilage and not bone should help differentiate costochonditis from stress fracture based on location. Most rib stress fractures in rowers occur in the anterior to mid-­ axillary line of ribs 4–8. Diffuse pain in this area should be assumed to be a rib stress fracture in development. Rowers should be removed from rowing and asked to cross train if these symptoms develop. Pain at that point may or may not resolve. More specifically localized pain that pinpoints to a rib and not the intercostal may also be presumed to be a rib stress fracture if there is pain reproduced with compression of the chest wall away from the area of pain yet reproducing the pain as the rib is bent. Athletes with rib stress fractures will have pain with coughing, sneezing, laughing, rolling over in bed, and protracting the scapula such as pushing open a door. If confirmation of diagnosis is desired, bone scan has been the traditional go-to imaging because it can identify stress fractures at multiple sites with an imaging study. It yields easy to interpret images (Fig. 15.2) but requires time and radiation exposure. Imaging is increasingly done with MRI as with other stress fractures. Due to the anatomy of

Fig. 15.2  Anterior to posterior image of a thoracic bone scan indicating a left seventh rib stress fracture

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the ribs it needs to be clear to the radiologist what the clinical question is and the specific location so that the MRI can be protocoled correctly. Otherwise there could be risk of missing the rib in question if image cuts are not thin enough. Due to its inability to detect bony injury without fracture, CT scan is not recommended. Like other stress fractures, time to healing is in the 6  weeks range, making it all the more important to recognize an athlete who may be in trouble early and shut down from rowing. Diagnosis and return to rowing clinical pathways have been investigated and published [10, 11].

 pper Extremity Deep Vein U Thrombosis and Thoracic Outlet Syndrome As athletes who use their upper bodies in a repetitive motion, rowers are susceptible to thoracic outlet syndrome (TOS), both neurogenic and vascular. Hypertrophy of the subclavian muscles or imbalance of the anterior/middle scalene muscles or the pectoralis minor muscle contribute to the development of neurogenic TOS [12]. Repetitive strain and compression of the veins passing through the thoracic outlet by adjacent muscles (anterior scalene, subclavian muscles) can lead to venous stasis and, in turn, formation of thrombus. This vascular TOS is also known as Paget Schroetter syndrome (PSS). Impeded venous flow results in edema distal to the thrombus and the use of collateral veins to bypass the obstruction [13]. While not as common in rowers as in swimmers and baseball/ softball players, TOS is certainly on the differential in any rower who complains of upper extremity pain, paresthesias, numbness, weakness, and swelling [12]. Paresthesia is more common in neurogenic TOS while pain and swelling are the typical presenting complaints in vascular TOS/PSS [14]. Vascular TOS/PSS should also be on the differential for any rower who complains of pleuritic pain or dyspnea on exertion as pulmonary embolus, although uncommon, is seen in 4–10% of patients with upper extremity DVT [15].

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When identifying neurogenic TOS, a critical component of the physical examination is the Roos test (or the elevated arm stress test), which involves placing both arms in the 90° abducted position with elbows flexed at 90° then opening and closing the hands for 3 min. Patients with TOS typically have severe pain with this test to the extent they may not be able to complete the 3  min [14]. Neurogenic TOS can be confirmed with neurophysiologic studies such as nerve conduction velocity and electromyography [14]. The physical examination is an unreliable method of diagnosing vascular TOS; rather, ultrasound is the recommend initial diagnostic modality as it has a high sensitivity and specificity to evaluate for thrombus [15]. If not conclusive, recommendations are to proceed with CT venogram or MR venogram [13]. Initial treatment of neurogenic TOS is physical therapy consisting of range of motion exercises and tendon and nerve gliding techniques in addition to anti-inflammatories and possibly botulinum injections and/or nerve stimulation [14]. Second-line treatment of neurogenic TOS is surgical decompression of the thoracic outlet. Treatment of vascular TOS/PSS begins with anticoagulation therapy and potential thrombolysis before definitive surgical management to decompress the thoracic outlet, typically a first rib resection with potential supplementary procedures. Anticoagulation should be continued for three to 6 months [13].

Shoulder Instability and Dislocation Shoulder instability and dislocations are most commonly seen in young people, and many young people are rowers, suggesting that there should be a fairly high incidence of shoulder issues in rowers. The shoulder, unless well stabilized, is vulnerable at the catch, and especially vulnerable during a racing start, where the highest load per stroke is experienced. Fortunately shoulder dislocation is a rare occurrence in rowers. Perhaps rowing training is effective for strengthening of the rotator cuff and scapular sta-

15  Common Injuries and Conditions in Rowers

bilizers. If/when shoulder dislocation happens during a race that athlete and their whole boat would be immediately forced to stop. It is strongly recommended that rotator cuff strengthening exercise be included in any rowing specific weight training regimen. The rotator cuff sees a high load with rowing and may be a weak link in the kinetic chain. Particular attention to a strong rotator cuff and scapular stabilizers is recommended. Rowers also need to avoid the rotator cuff dominant and relatively unstable position of overreaching, versus a more stable and latissimus engaged position at the catch.

Forearm Compartment Syndrome Exertional compartment syndrome is most commonly seen in the lower leg [16]. Though rare, it has been seen in forearms in rowing [17]. The mechanism of this is likely lack of relaxing the forearms in the recovery portion of the stroke. Rowers are taught to relax their grip on the recovery, but in rough water conditions or with less experienced rowers this may not be the case. On the rowing ergometer one cannot loosen grip nearly as much because of the return mechanism, which is a bungee cord. Forearm compartment syndrome may be more likely therefore on the ergometer. This could potentially be avoided by the use of lifting straps while on the erg. Lifting straps are not recommended for rowing on the water because it could be dangerous to be unable to let go of the oar in the case of an emergency. Similar to compartment syndrome in the lower leg in other sports, compartment syndrome in the forearm is characterized by exertional pain that escalates in severity, described as burning pain similar to anaerobic effort-related pain. This dissipates quickly with cessation of effort. If this occurs on the water, options are to consider changing grip size, either larger or smaller, and focus on looser grip on the recovery. Rarely this could go on to compartment release if the athlete is determined to continue rowing and has exhausted all other options [17].

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Intersection Syndrome As a rower feathers the oar in sweep rowing, the hand closest to the oar (“inside hand”) cocks the wrist to roll the oar. Done repetitively this puts the forearm at risk for intersection syndrome. This can also happen with sculling, but the experienced sculler rolls the handles out into the fingers rather than cocking the wrists so the wrists should be less vulnerable. In the dorsal wrist, the first compartment crosses over the second compartment. This is an area of possible friction and the source of crepitus when palpating the dorsal wrist of an affected athlete while asking the athlete to extend and flex the wrist. Intersection syndrome may be treated with steroid injection, depending on the severity, though first-line treatment is time off rowing and wrist splinting.

Skin There are four primary contact points of the rowing athlete in the boat – hands, buttocks, calves, and feet – and three of these are potential locations for skin breakdown or potential infections. Clearly the most obvious is the hands on the oar or oars. Blisters and calluses are painful, and common especially early in seasons or after time away from rowing. There are many approaches that have been attempted to mitigate these, not always successfully. Many rowers feel that using gloves diminishes their feel of the oar in the hand, though this may be primarily a concern more deeply rooted in rowing culture rather than true reality. Taping the hands typically yields a sticky mess and is not advisable. Leaving blisters intact is ideal but not usually practical when the next practice is within the next 24  h. Care of open wounds is critical to ability to continue rowing; infected blisters necessitate time off the water. Liquid bandage preparations are used relatively commonly, and other folk remedies to dry up blisters periodically circulate among rowing teams. Two other contact points with the boat are less obvious. Chafing can be a significant concern between the buttocks as the rower leans back at

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the finish, known to rowers as “seat bites,” and not all seats fit rowers’ buttocks perfectly, similar to but not as much of a problem as bicycle saddles. Seat fit can be altered to some degree with buttock pads, but there are few alternate seat options. Typically these chafing areas can be lubricated before rowing, or can be covered with Tegaderm or similar dressings if they become more open wounds. The other contact point is the back of the lower legs. Depending on the width of the sliding seat tracks, at the finish the calves may contact the tracks repeatedly, yielding “track bites.” These posterior calf wounds are another potential chafing location. Choosing a different boat manufacturer with different spaced seat tracks is not usually a viable option since rowing shells are expensive, and rowers will commonly protect this area with long socks or calf sleeves. As with the hands, taping may be attempted but is not reliable for this problem.

References 1. Smoljanovic T, Bohacek I, Hannafin JA, Terborg O, Hren D, Pecina M, et  al. Acute and chronic injuries among senior international rowers: a cross-sectional study. Int Orthop. 2015;39(8):1623–30. 2. Trompeter K, Fett D, Platen P.  Prevalence of Back pain in sports: a systematic review of the literature. Sports Med. 2017;47(6):1183–207. 3. Wilson F, Thornton JS, Wilkie K, Hartvigsen J, Vinther A, Ackerman KE, et al. 2021 consensus statement for preventing and managing low back pain in elite and subelite adult rowers. Br J Sports Med. 2021;55(16):893–9. 4. Nugent FJ, Vinther A, McGregor A, Thornton JS, Wilkie K, Wilson F.  The relationship between rowing-­ related low back pain and rowing biomechanics: a systematic review. Br J Sports Med. 2021; bjsports-2020-102533. 5. Wilson F, Gissane C, McGregor A. Ergometer training volume and previous injury predict back pain in

K. A. Karlson and G. L. Stone rowing; strategies for injury prevention and rehabilitation. Br J Sports Med. 2014;48(21):1534–7. 6. Hosea T: Aetiology of low back pain in young athletes:… - Google Scholar [Internet]. [cited 2021 Nov 2]. https://scholar.google.com/scholar_lookup?journa l=Br+J+Sports+Med&title=Etiology+of+low+back+ pain+in+athletes;+role+of+sport+type&author=T+H osea&author=J+Hannafin&author=J+Bran&author= D+O%E2%80%99Hara&author=P+Seufert&volume =45&publication_year=2011&pages=352&. 7. Maurer M, Soder RB, Baldisserotto M.  Spine abnormalities depicted by magnetic resonance imaging in adolescent rowers. Am J Sports Med. 2011;39(2):392–7. 8. Boykin RE, McFeely ED, Ackerman KE, Yen Y-M, Nasreddine A, Kocher MS. Labral injuries of the hip in rowers. Clin Orthop Relat Res. 2013;471(8):2517–22. 9. Warden SJ, Gutschlag FR, Wajswelner H, Crossley KM. Aetiology of rib stress fractures in rowers. Sports Med. 2002;32(13):819–36. 10. Evans G, Redgrave A.  Great Britain rowing team guideline for diagnosis and management of rib stress injury: part 1. Br J Sports Med. 2016;50(5):266–9. 11. Hooper I, Blanch P, Sternfeldt J. The development of a clinical management pathway for chest wall pain in elite rowers. J Sci Med Sport. 2011;1(14):e104. 12. Chandra V, Little C, Lee JT.  Thoracic outlet syndrome in high-performance athletes. J Vasc Surg. 2014;60(4):1012–8. 13. Saleem T, Baril DT.  Paget schroetter syndrome. In: StatPearls [internet]. Treasure Island (FL): StatPearls Publishing; 2021; [cited 2021 Nov 13]. http://www. ncbi.nlm.nih.gov/books/NBK482416/. 14. Kuhn JE, Lebus GFV, Bible JE. Thoracic outlet syndrome. J Am Acad Orthop Surg. 2015;23(4):222–32. 15. Mustafa J, Asher I, Sthoeger Z. Upper extremity deep vein thrombosis: symptoms, diagnosis, and treatment. Isr Med Assoc J. 2018;20(1):53–7. 16. Rowden GA.  Chronic exertional compartment syndrome: background, anatomy, pathophysiology. 2021; [cited 2021 Nov 13]. https://emedicine.medscape. com/article/88014-­overview. 17. Harrison JWK, Thomas P, Aster A, Wilkes G, Hayton MJ. Chronic exertional compartment syndrome of the forearm in elite rowers: a technique for mini-open fasciotomy and a report of six cases. Hand (N Y). 2013;8(4):450–3.

Common Injuries and Conditions in Crossfit Participation

16

Brian D. Giordano and Mina Botros

Introduction

training sessions require less time and leaves more time for sports specific training sessions Crossfit is a conditioning program known for its [4]. The rising popularity of Crossfit is not surfocus on successive ballistic motions that build prising given the positive response that exercise strength and endurance. Crossfit workout ses- participants have exhibited with interval training sions use a wide variety of exercises, ranging and the social support associated with joining a from running and rowing, to Olympic lifting Crossfit gym [5, 6]. (snatch, clean, and jerk), powerlifting (squat, Crossfit endorses a business model unlike that dead lift, bench), and gymnastic movements of other commercial gyms. Gyms are required to (pull-ups, toes to bar, muscle ups, ring dips, rope pay an initial and annual fee to use the Crossfit climbs, push-ups, pistols, handstand push-ups). name. The requirement to open a gym or be a These exercises are combined into high-intensity trainer is to have a Level 1 Crossfit certification, workouts that are performed in rapid succession, which can be obtained in a weekend at a seminar. with limited to no recovery time. It has been Crossfit headquarters allow its credentialed ownadopted in both military and civilian populations ers to develop their own within the parameters of with widespread anecdotal reports of impressive, the business model. They believe that the market sustained fitness gains. These findings parallel will select for the best gyms and those that do not existing literature demonstrating that high-­ provide adequate services will fail. Therefore, intensity, single modal exercise is an effective there can be a wide variation in quality between and efficient means of enhancing physical perfor- Crossfit gyms based on the experience of the mance without a large time investment [1–3]. owner and coaches. Young athletes participating in high-intensity Injury rates among Crossfit participants have interval training (HIIT) exercises tend to have an been investigated in several observational studimprovement in their aerobic and anaerobic exer- ies. Hak et al. 2013 collected 132 responses from cise performance; they even sustained an Crossfit participants and established an injury improvement of their endurance, compared to rate of 3.1 per 1000 h trained, with 9 of the 186 alternative training protocols. Therefore, young injuries requiring surgical intervention. Similar athletes may benefit from HIIT programs as findings were also reported by Toledo et al. 2021 with an injury rate of 3.4 per 1000 h, with 83% joint injuries and/or muscles injuries 45% [7]. B. D. Giordano (*) · M. Botros Department of Orthopeadic Surgery, University of Weisenthal and colleagues collected 386 Rochester Medical Center, Rochester, NY, USA responses with an injury rate of 2.4 per 1000  h e-mail: [email protected]; trained. This is comparable to long-distance [email protected] © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_16

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ning, training periods for triathletes, weightlifting, powerlifting, and gymnastics [8, 9]. The risk factors associated with injuries are older age, male sex, higher body mass index (BMI), existence of a previous injury, the lack of supervision by coaching, and experience with Crossfit. Further, among published studies, the mean percentage of injuries that required surgery were 8.7% [10]. Additionally, the reported injury rate is lower than that associated with competitive contact sports such as rugby [11]. Although the reported injury rates have been routinely low as popularity, access, and involvement in Crossfit increase, physicians will likely begin to encounter injuries due to Crossfit in their clinic [12]. As such, it is important that physicians are aware of the movements and potential risk they pose for injury in Crossfit workouts. Injuries in Crossfit occur via several common training faults. Poor form is a commonly cited cause of concern [11]. There is a decrease in the injury rate when training coaches educating participants on their form and guide them through the workout [6]. In essence there are two situations that could contribute to poor form: inadequate initial education on the movement or deterioration of good form due to fatigue. Overtraining is another cause of injury, with overuse-related tendonitis occurring primarily in the shoulder and knee [13]. This can result from programming that focuses on one area of the body and does not adequately distribute the stress of exercising [14]. As well, athletes who have a clinically silent preexisting tendonitis are likely to unmask this injury over the course of the strenuous nature of Crossfit workouts. In addition, injuries can occur as a direct consequence of the riskier activities in Crossfit. Examples of these are an athlete falling from the bar during toes to bar, a barbell dropping on the back following a missed snatch, or hyperextending the elbow in a wide overhead grip (such as the snatch or overhead squat). Further, exertional rhabdomyolysis, which is induced in CrossFit practitioners after intense training session, have been reported in literature [15–17]. Mainstream media have expressed significant interest in the sport of Crossfit, its phi-

B. D. Giordano and M. Botros

losophies, and some of the more dramatic injuries that have been documented. When a physician evaluates a Crossfit athlete, it is important to define a general training fault, the specific movement that caused or exacerbates their pain, and several aspects of their training and athletic history. In order to learn exactly what the athlete is doing, the physician has to understand the mechanisms and language of the exercises. The majority of injuries in Crossfit are mild and most likely will not require surgery [8, 11]. Further, in these cases, athletes are often aware of a specific movement that caused their pain and can even pinpoint a specific time. This helps to define the general mechanism of injury and the potential etiology. It is important to determine whether this occurred as the result of inadequate education on the movement prior to initiating the workout or was a result of breakdown in form due to fatigue. If the athlete reports a more insidious onset, then their training frequency, type, previous athletic interests, and prior injuries should be explored in more detail. In both cases, this information will help to determine the proper treatment for the athlete’s injury and identify any faults that may exist in their training program to prevent further injuries. For example, it has been reported that only 5% of Crossfit athletes with hand or wrist injury reported seeking medical attention after their injury; these trainees are returning to unmodified training too early following their injury, which leaves them susceptible to the development of further injury [18]. Therefore, it is essential that physicians identify the underlying case of injury to prevent its recurrence. In this chapter, we explore the important philosophies, training methods, and themes of Crossfit that will help the treating physician evaluate injuries that occur among these athletes. We will review the exercises associated with injury in each subset of movements within Crossfit. Since there are limited studies examining injuries incurred specifically during Crossfit, we will review existing literature related to sports or activities that utilize each separate subset of movements. Lastly, we will discuss specific concerns related to Crossfit athletes with regard to the combination of these distinct movements.

16  Common Injuries and Conditions in Crossfit Participation

Weightlifting Weightlifting in Crossfit is divided into two primary categories: Olympic lifting and powerlifting. The classic powerlifting exercises are the dead lift, back squat, and bench press. Olympic lifting exercises include the snatch, clean, and jerk. In competitive weightlifting, the goal of each of these is to lift as much weight as possible in a single attempt. In Crossfit, the incorporation of these movements is intended to achieve two separate objectives: (1) to improve strength, by using a high weight for low repetitions, and (2) to facilitate and optimize metabolic conditioning, when a low weight is used for many repetitions. In the dead lift, the athlete begins in a hip width stance with the barbell positioned over the midfoot and extends the hip and knees until the weight is at waist level with the back in full extension. In the back squat, the athlete begins with a loaded barbell across the upper back and shoulders and then flexes at the hip and knees until the thighs are below parallel with the floor and then presses the weight back up [14]. In both of these exercises, the extensors of the spine, hip, knee, and ankle keep the body from collapsing

Fig. 16.1 Snatch

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under the load. For the bench press, the athlete is supine with the barbell over their chest with the arms extended, and the bar is lifted off a rack and brought to the chest and pushed back up again. In this exercise, the shoulder muscles (pectoralis major and minor, deltoids, core muscles, and anterior rotator cuff) provide the primary support for the motion of the barbell. In the snatch, an athlete initiates the lift with the barbell on the ground. Using a wide grip, the athlete lifts the bar rapidly up and over his or her head in one smooth motion. In the clean, the athlete starts with the barbell on the ground with a grip similar to the dead lift and then lifts the bar quickly onto the front of his or her shoulders in one motion. Finally, in the jerk, the barbell is initially rested on the shoulders, and the athlete then explosively pushes the bar upward, using a small dip to initiate the motion. As the bar is raised, the arms are extended, and the bar is caught with the arms extended over the athlete’s head (Fig. 16.1) [13, 19]. Crossfit athletes frequently report that injuries incurred are acute in onset, with the majority experiencing no history of discomfort in that body region prior to the injury. Most of these

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injuries are fairly mild, with sprain/strain being relatively common [8]. Studies examining weightlifters corroborate this finding, with muscular strains and ligamentous sprains accounting for 40–60% of the acute injuries. Training time missed is usually less than 1 day in about 90.5% of the injuries [14, 20]. It is reported that the incidence of weightlifting injuries among athletes participating in extreme conditioning programs (ECP), such as Crossfit, is 2.71 per 1000 h. The most affected regions have been reported at the shoulder and upper arm. ECP participants with previous shoulder injury are eight times more likely to sustain shoulder injury, compared to athletes with healthy shoulders. It is reported that 20% of injuries from ECP, were secondary to improper technique and 35% was due to overexertion. The incidence of weightlifting injury was 2.5 times greater among athletes with less than 6 months of experience, compared to more experienced participants [21]. More emergent acute injuries, such as tendon ruptures, joint dislocations, and muscular tears, are uncommon among Crossfit athletes and in weightlifters [8, 14]. The incidence of injuries among CrossFit participants were comparable, or even lower, to rates of injuries in those participating in distance running, Olympic weightlifting, rugby, track and field, or gymnastics [22]. Fisker et al. evaluated changes within the tendon after a period of high-intensity Crossfit exercise, where they reported that there is a significant increase in the thickness of the Achilles and the patellar tendons after a period of intense CrossFit workout sessions. This is significant as chronically overloaded tendons tend to thicken. However, significant tendon thickening has also been found post-workout, which is a physiologic response to high stress placed on these tendons during the workout sessions [23]. Chronic injuries tend to be due to repetitive stress with insufficient recovery time. In weightlifting, this occurs in entry-level athletes who increase their training too quickly or in high-level athletes focused on performance [14]. With the intense nature of Crossfit, and the use of high repetitions at lower weight, combined with gymnastic movements, chronic injuries of attrition are far more likely. Tendonitis/tendinopathy is the most com-

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mon chronic injury accounting for 12–25% of all strength-training injuries. Most commonly, overuse tendonitis afflicts the shoulder and knee. Stress fractures occurring at sites of repetitive loads are less common, but more worrisome, as they can destabilize with improper attention and potentially lead to overt fractures in rare cases. Scapula and humeral stress fracture have been reported, where the athlete was treated conservatively [24, 25]. It is important to note that in both these case studies the authors reported that identifying stress fractures was made possible by high suspicion and advance imaging modalities (Fig. 16.2). The lumbar spine is particularly at risk due to repetitive loaded flexion and extension and potential development of spondylolysis [14]. In Crossfit, the push press and jerk are often used in the metabolic conditioning portions of the class. As the athletes fatigue, they tend to assume a more lordotic posture through the lumbar spine and place themselves at risk for stress reaction or fracture in the pars interarticularis [26]. Crossfit athletes frequently report injuring their lower back with these movements [8, 11]. A Swedish study of elite level Olympic and powerlifters demonstrated an injury rate of 2.6 injuries per 1000 h, with the lumbar spine reportedly as the common injury location [13]. Most occurrences of low back pain in athletes are self-limited sprains or strains [14, 20]. However, when an athlete succumbs to fatigue due to repetitive lifting, as commonly seen in Crossfit workouts, there is less knee and hip range of motion and a greater spine peak flexion, which may place increased pressure on the intervertebral disks [27]. In addition, squatting and dead lifting can increase both compressive and shear force across the lumbar spine [28]. Therefore, persistent pain should prompt concern for disk herniation or exacerbation of preexisting degenerative lumbar disk disease [29]. Therefore, radicular complaints were the most commonly reported symptom among athletes reporting back pain; approximately, 32% of these athletes had a positive finding on the neurological exam [26]. Furthermore, lumbar hyperextension during bench and overhead press represents a failure of form and is commonly seen in Crossfit in the setting of fatigue as a stra-

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Fig. 16.2 Clean

tegic adaptation to accomplish the lifting task [19]. In the pathologic state, this maladaptation can result in clinically significant spondylolytic stress reaction or fracture [29]. In addition to stress fractures, an underlying spondylolisthesis or spondylolysis could put an individual at increased risk of injury (Fig. 16.3) [19]. Crossfit athletes report a higher prevalence of shoulder injuries when compared to elite and competitive Olympic weightlifters [11, 13, 14, 19, 28]. Crossfit workouts tend to use lighter weights for higher repetitions and incorporate gymnastics into their workouts, both of which increase stress on the shoulder girdle. The rate of weightlifting shoulder injuries presenting to the emergency room is increasing annually in a linear regression [30]. The current literature indicates that the incidence of shoulder injury secondary to Crossfit participation is 2.71–3.3 per 1000  h, which is similar to published rates among triathletes (2.5–5.4 per 1000  h), recreational tennis (1.6–3.0 per 1000  h), and traditional weightlifters (2.7–5.5 per 1000  h). However, CrossFit participants are 1.3 times more likely to develop weightlifting shoulder

injury and 1.8 times more likely to seek treatment, compared to traditional weightlifters [31]. It is important to note that 38.6% of athletes with shoulder injury reported that their “new” injury is an exacerbation of a shoulder injury that occurred prior to their Crossfit training. Therefore, rate of all shoulder injuries, among Crossfit athletes, is 1.94 per 1000  h; however, the rate of “new” shoulder injuries is 1.18 per 1000  h [32]. This highlights the importance of identifying whether the shoulder injury was present prior to training, or whether it is “new.” A cross-sectional study of weightlifters demonstrated considerable soft tissue damage involving the rotator cuff, biceps tendon, and capsular and ligamentous insertions [19]. The authors postulated that the demands on the shoulder and motions involved (extreme overhead position, as in the overhead press or jerk) increased the risk of injury to the rotator cuff, acromioclavicular joint, and glenohumeral capsule. In addition, an athlete must drop a missed snatch behind themselves, which can result in extreme external rotation and extension of the shoulders [20]. It is reported that 100% of Crossfit athletes that underwent arthroscopic

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Fig. 16.3  Dead lift

repair of supraspinatus tear associated with SLAP lesion return to their Crossfit program and 90% of subjects returning to competitions in 24 months [33, 34]. In addition, osteolysis of the distal clavicle has been reported to occur in powerlifters, and presumably Crossfit athletes would be subject to similar risks, although peak loads are somewhat smaller [13, 14]. Knee injuries are more commonly reported in Olympic weightlifting versus powerlifting [14, 28]. In Olympic lifting, there is more emphasis on an upright position in the squat and the ability to squat deeper than parallel, requiring deep loaded knee flexion. This position enables the athlete to more effectively catch a heavy clean or snatch. However, it causes increased anterior displacement of the center of gravity, augmenting patellofemoral joint reactive forces, which can potentially result in patellofemoral pain and patellar tendonitis [19]. It has been reported that the knee injury rate among Crossfit athletes is between 0.74 and3.3 per 1000 h, which is lower than traditional weightlifting. Athletes who previously participated in another sport are more likely to report significantly higher proportion of knee pain [35]. For an athlete with persistent pain, chronic inflammatory problems from persistent tendinitis is the likely diagnosis [20]. Traumatic

cruciate and collateral ligament injuries, common in cutting and pivoting sports, are rare in the sport of weightlifting (Figs. 16.4 and 16.5). Other rare injuries can occur during weightlifting, which are not directly related to repetitive stresses on the body. Dropping weights is a rare but potentially catastrophic event. In a Crossfit competition in California in 2014, an athlete missed a heavy snatch, and the barbell came into contact with his lower thoracic spine causing a traumatic spinal cord injury, resulting in paraplegia. Unfortunately, this pattern of injury has been previously reported during weightlifting [14, 19]. Elbow dislocations can occur in the snatch, due to the wide grip and aggressive rotation or over rotation of the shoulders [14]. Compartment syndrome, primarily of the forearm, has been described as a consequence of aggressively gripping a barbell during a workout [13, 36]. Callous tears are very common in Crossfit and weightlifting. Rectal prolapse has occurred among powerlifters due to the heavy loads incurred during their lifts, this has been reported in Crossfit athletes with highest occurrence among female athletes [14, 37–39]. It is important to note that female athletes, particularly parous women, have a higher prevalence of pelvic organ prolapse and anal incontinence than those participating in Crossfit [40].

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Fig. 16.4 Squat

Fig. 16.5 Squat

Endurance Running and indoor rowing on the ergometer are the two most common endurance exercises in Crossfit. Typical distances used in metabolic condition portions of classes range from 150 to 2000  m in rowing and 200–1600  m in running.

These distances are performed several times in a workout and are combined with gymnastic and weightlifting movements. Crossfit Endurance is a program within Crossfit that focuses almost entirely on high-intensity interval distances of these two specific exercises. It is commonly used as a supplement to the traditional Crossfit classes in the athletes who wish to improve their cardio-

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vascular workload. Crossfit athletes are less likely to be injured in either of these two movements compared with typical endurance athletes, as their mileage is far less. The risk to Crossfit athletes, however, is when stresses from these exercises are combined with weightlifting and gymnastics, and when fatigue becomes a factor, overall potential for injury increases. Indoor rowing on the ergometer is used in metabolic conditioning portions of the Crossfit classes. In colder climates, it is used more frequently in the winter, when running is no longer an attractive option. As many rowing injuries are overuse injuries due to changes in training volume, this is concerning [41]. In rowers, the knee and back are the two most commonly injured body areas, both of which are at risk in a number of other movements in Crossfit [42, 43]. In rowing, there is constant flexion and extension of the knee under loaded conditions. Patellofemoral chondromalacia patella and iliotibial band syndrome are common sequelae of this mechanism. In rowing, the lower back functions as a braced cantilever during each stroke, which enables the transfer of power from the legs to the flywheel. As the erector spina muscles fatigue, there is increased lumbar flexion. The spine is well suited to handle compression; however, the shear load created by the lumbar flexion makes the intervertebral disks susceptible to injury. Willwacher et  al. 2021 reported that there is an increase in thoracic spine curvature secondary to back muscle fatigue, especially the trapezius descendens, which leads to the unbalance loading of the intervertebral discs [44]. This finding is important because it highlights that strenuous activities, such as rowing, combined with high loading activities over the spine, such as weightlifting, can lead to impaired spinal stabilization and increases risk of injury. Disk herniation on MRI was demonstrated by 95.2% of male rowers and 78.9% of females; however, only 27% of females and 15% of males had neurologic signs or symptoms. In addition to discogenic pain, strains, sprains, spondylosis, and facet joint arthropathy are potential sequel of the long-term repetitive stresses of rowing [45]. Stress fractures of the ribs are a concern for rowers; however, the mile-

age of Crossfit rowers is significantly less, and therefore they are at a reduced risk for this to occur. Running does not usually cause injuries in the Crossfit athlete unless preexisting pathology is present and is exacerbated by the demands of the exercises. The predominant site of injury related to running is the knee. Common overuse injuries of the knee include patellofemoral pain syndrome, iliotibial band syndrome, and medial tibial stress syndrome. When running is combined with a heavy squat routine or intense Olympic weightlifting, then patellofemoral pain may manifest. Achilles tendinopathy is a common cause of calf pain in runners [46]. This is worrisome, as high repetition box jumps are often used in the conditioning portion of Crossfit, and this motion places strain on the gastrocnemius-soleus and Achilles tendon complex. There have been anecdotal reports of Achilles tendon ruptures with high repetition box jumps. Muscle strains and tendonitis are the most common etiologies of hip pain due to running. Bursitis, exacerbation of hip osteoarthritis, stress fractures, snapping hip syndrome, and acetabular labral tears are all potential etiologies [47]. It is reported in a case series that Crossfit athletes with hip or groin pain and injuries tend to be females with the majority having insidious onset; the most common diagnosis were femoral-acetabular impingement syndrome (FAIS), which is reported in 34%, following by hamstring strain 11%. Majority of these injuries that required physical therapy and surgery occurred in 24%. The greatest predictor of surgery were patients presenting primarily with anterior hip or groin pain [48]. Postoperatively Crossfit athletes that underwent hip arthroscopic surgery for the treatment of FAIS had 88% return to their Crossfit programs, with 96% returning at the same level or better than before their surgery [49].

Gymnastics Gymnastics movements are a common component of Crossfit workouts and are the most frequently reported cause of shoulder injuries [8].

16  Common Injuries and Conditions in Crossfit Participation

While gymnastics encompasses a wide range of activities, there are some movements that are used more frequently and put the participant at greater risk for injury. These include pull-ups, toes to bar, handstand push-ups, ring dips, muscle ups, push-ups, and pistols (one-legged squats). Large numbers of pull-ups are often incorporated into Crossfit workouts. The muscles used for a strict pull-up fatigue quickly. Therefore, athletes compensate with a “kipping” motion, meaning they use momentum from the lower body to generate an explosive force to complete the repetition [11]. A similar-type kipping motion is used in toes to bar, where an athlete generates a force in their lower body in order to touch their feet to the bar. Handstand push-ups can be programmed in large numbers. In this exercise, athletes assume a handstand position against a wall with their arms extended and then flex at the elbow until their head reaches the ground and then press back up again. Muscle ups require an athlete to hang from the rings and pull him or herself into a ring-­ dip position, with the arm flexed to 90°, and then push him or herself up until the arms are fully extended (Figs. 16.6 and 16.7). Studies of male gymnasts correspond with data from Crossfit, demonstrating that the shoulder is the most commonly injured joint in these movements [8, 50]. Kipping, both in the pull-up Fig. 16.6 Kipping pull-up

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and toes to bar, places the shoulder in a position of hyperflexion, internal rotation, and abduction at the bottom of the hang [11]. Handstand push-­ ups place the shoulder in a position of extreme loaded hyperflexion, which imparts stress upon the rotator cuff and shoulder capsule. Both the push-up and burpee tax the anterior shoulder musculature, as in the bench press. Lastly, in ring dips and muscle ups, the athlete is required to press up and to stabilize the rings. This means that they can fall forward, which may lead to anterior translation of the humerus and an increased risk of shoulder dislocation (Fig. 16.8). The wrist and lower back are sites of frequent injury in gymnastics. The wrist is the most commonly injured area in female gymnasts and the second most commonly injured area in male gymnasts [50]. Approximately a third of all reported injuries in Crossfit are specific to the hand or wrist; with the majorities of hand or wrist injuries occurring in the first year of starting a Crossfit training. These athletes are prone to reinjuring their hand or wrist if they return too early following their injury without identifying the underlying cause [18]. This is most likely due to movements such as the handstand, which subjects the wrist to a combination of axial compression in extreme hyperextension [51]. Injuries to the spine/trunk

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Fig. 16.7  Muscle up

compromise 13.7–24% of gymnastic injuries, with the lumbar spine representing the most frequently injured region [50, 52]. The handstand position, as seen in the press and jerk, can cause an athlete to assume a hyper-­lordotic posture through the lumbar spine. This can result in

stress fractures of the pars interarticularis and eventually spondylolysis. In addition, pistols (one-legged squats) are commonly programmed into lower extremity Crossfit workouts, which place strain on the lower back. Athletes are encouraged to squat below parallel on one leg.

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Fig. 16.8  Ring dip

It is difficult to maintain balance with an upright chest in this position, so athletes compensate with lumbar flexion and anterior drift of the knee. This puts increased shear force on the vertebral bodies. Lastly, athletes often perform many handstand push-ups in a row without a

break. This may lead to fatigue of periscapular musculature and inability to resist gravity in the eccentric portion of the motion. As a result, athletes may place a considerable axial load on the head and cervical spine as they impact the ground (Fig. 16.9).

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Fig. 16.9 Handstand push-up

Other There are several exercises and injuries related to Crossfit that do not fit into a general category. Box jumps, often conducted at a height of 20 or 24 inches, have anecdotally been associated with Achilles tendon rupture, although the exact mechanism is unclear. This could be the result of an acutely overloaded tendon or an overuse condition [53]. Kettlebells are frequently used in Crossfit workouts. There have been reports of extensor pollicis brevis tendon damage presenting as de Quervain’s disease with kettlebell training [54]. Occasionally, athletes fall off the bar in toes to bar. This poses a significant risk, as it usually occurs when the athlete is raising his or her feet toward bar and, therefore, is unable to slow the descent. Lastly, rope climbs, usually to 15 feet, are incorporated into Crossfit workouts. If an athlete fatigues, or does not appreciate the appropriate means of descent, they can fall from that distance.

Another concern with Crossfit athletes is the development of rhabdomyolysis. This is a serious condition that requires immediate hospitalization and intravenous fluid administration to prevent further complications. Suspicion should be raised in an individual who presents with muscle stiffness in the days following a period of exercise, as well as swelling, and pain out of proportion to the expected fatigue post exercise. It is confirmed clinically by myoglobinuria and an elevated serum creatinine phosphokinase. It should be readily identified and treated to prevent acute renal failure [55]. The most commonly reported symptom is dark urine followed by upper extremity pain; symptoms duration and hospitalization tend to be 3 days. Only 82% of patients presented initially to the ED after development of symptoms for evaluation [56]. While this is a concern for Crossfit athletes, it has been reported very infrequently in single cases [15].

16  Common Injuries and Conditions in Crossfit Participation

Conclusion Crossfit is an extreme conditioning program that utilizes successive ballistic motions to build strength and endurance. Injuries related to Crossfit present the treating physician with certain challenges. Despite significant overlap between body areas stressed by the demands of Crossfit exercises, injury rates are relatively low and in concordance with established injury rates for the various components of the workout (i.e., weightlifting, running, gymnastics, etc.). Nevertheless, Crossfit owners continue to pursue training strategies that optimize safety in their gyms. This contention is further supported by evidence that suggests that the degree trainer involvement directly correlates with injury rate [8]. Crossfit is a rapidly growing sport. While its injury rate is comparable to most adult fitness activities such as gym/fitness club training, running, and triathlon training, physicians are ­ likely to interact more frequently with Crossfit participants as the sport grows in popularity [7–9, 11]. It is important to recognize that quality control may vary from gym to gym and depends heavily on the coach operating and maintaining the gym. Therefore, the risk of injury is dependent upon factors related to the quality of the gym and athlete-­dependent factors. Both of these issues should be addressed to treat the current injury and prevent further injuries. The key to defining the etiology of a Crossfit injury is to understand the different exercises and their related mechanisms. By doing so, a physician can adequately counsel the athlete on their course of recovery. By recognizing larger faults in their training, such as poor form or programming, the physician can help the athlete decide if exercise modification or even participation at a different gym may help them achieve their athletic training objectives and promote optimal wellness.

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234 17. Adhikari P, Hari A, Morel L, Bueno Y.  Exertional rhabdomyolysis after CrossFit exercise. Cureus. 2021;13(1):e12630. 18. Tawfik A, Katt BM, Sirch F, et al. A study on the incidence of hand or wrist injuries in CrossFit athletes. Cureus. 2021;13(3):e13818. 19. Basford JR.  Weightlifting, weight training and injuries. Orthopedics. 1985;8(8):1051–6. 20. Calhoon G, Fry AC.  Injury rates and profiles of elite competitive weightlifters. J Athl Train. 1999;34(3):232–8. 21. Aune KT, Powers JM.  Injuries in an extreme conditioning program. Sports Health. 2017;9(1):52–8. https://doi.org/10.1177/1941738116674895. 22. Klimek C, Ashbeck C, Brook AJ, Durall C. Are injuries more common with CrossFit training than other forms of exercise? J Sport Rehabil. 2018;27(3):295–9. 23. Fisker FY, Kildegaard S, Thygesen M, Grosen K, Pfeiffer-Jensen M.  Acute tendon changes in intense CrossFit workout: an observational cohort study. Scand J Med Sci Sports. 2017;27(11):1258–62. 24. Rodrigues C, Claro R.  Unusual stress fracture in a Crossfit athlete: a case report. JBJS Case Connect. 2021;11(1):e20.00135. 25. Godoy IRB, Malavolta EA, Lundberg JS, da Silva JJ, Skaf A. Humeral stress fracture in a female Crossfit athlete: a case report. [published correction appears in BMC Musculoskelet Disord. 2019 Jun 18;20(1):289]. BMC Musculoskelet Disord. 2019;20(1):150. 26. Hopkins BS, Cloney MB, Kesavabhotla K, et  al. Impact of CrossFit-related spinal injuries. Clin J Sport Med. 2019;29(6):482–5. 27. Sparto PJ, Parnianpour M, Reinsel TE, Simon S. The effect of fatigue on multijoint kinematics, coordination, and postural stability during a repetitive lifting test. J Orthop Sports Phys Ther. 1997;25(1):3–12. 28. Keogh J, Hume PA, Pearson S. Retrospective injury epidemiology of one hundred one competitive Oceania power lifters: the effects of age, body mass, competitive standard, and gender. J Strength Cond Res. 2006;20(3):672–81. 29. Bono CM.  Low-back pain in athletes. J Bone Joint Surg Am. 2004;86-A(2):382–96. 30. Pirruccio K, Kelly JD. Weightlifting shoulder injuries presenting to U.S. emergency departments: 2000-­ 2030. Int J Sports Med. 2019;40(8):528–34. 31. Elkin JL, Kammerman JS, Kunselman AR, Gallo RA.  Likelihood of injury and medical care between Crossfit and traditional weightlifting participants. [published correction appears in Orthop J Sports Med. 2020 Jan 24;8(1):2325967119895027]. Orthop J Sports Med. 2019;7(5):2325967119843348. 32. Summitt RJ, Cotton RA, Kays AC, Slaven EJ.  Shoulder injuries in individuals who participate in CrossFit training. Sports Health. 2016;8(6):541–6. 33. Carbone S, Candela V, Gumina S.  High rate of return to Crossfit training after arthroscopic management of rotator cuff tear. [published correction appears in Orthop J Sports Med. 2020 May 30;8(5):2325967120928365]. Orthop J Sports Med. 2020;8(4):2325967120911039.

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Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation

17

Kathryn Thomas

Abbreviations ABP ACL APTA

Arterial blood pressure Anterior cruciate ligament American physical therapy association ART Active release technique BFR Blood flow restriction CK Creatine kinase CNS Central nervous system CRP C-reactive protein CWI Cold water immersion CWT Contrast water therapy DN Dry needling DOMS Delayed onset muscle soreness DVT Deep vein thrombosis FR Foam rolling GTO Golgi tendon organ HL High load IASTM Instrument assisted soft tissue mobilisation IGF-1 Insulin-like growth factor LBP Lower back pain LEF Lower extremity function LL Low load MET Muscle energy technique MTrP Myofascial trigger points MVC Maximum voluntary contraction NCS Neurocryostimulation PFP Patellofemoral pain K. Thomas (*) Co-Kinetic, Centor Publishing, London, UK

PNF

Proprioceptive neuromuscular facilitation RCT Randomised controlled trial REPS Repetitions RM Repetition maximum ROM Range of motion ROS Reactive oxygen species TKA Total Knee arthroplasty VAS Visual analog scale VFR Vibrating foam roller VJH Vertical jump height WBC Whole body cryotherapy

Introduction In recent years sport specialization has become the norm, resulting in an increase in sport training specificity, frequency, and intensity that can place the athlete at risk for overtraining, and injury. Endurance sports athletes are at especially high risk. Appropriate training schedules, with dedicated time for recovery, rest, and optimal nutrition can help prevent problems in the endurance athlete. Demanding training and competition schedules has resulted in a focus on recovery, between sessions and competitions, to maximize potential and performance. This may be especially relevant in multiday stage events like ultramarathons and cycling, adventure racing, and other sports that require high level performance

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_17

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in consecutive sessions including swimming and CrossFit. Improving physical performance through effectual training strategies have been identified over the past decades. Maximizing performance capacity of an athlete is not simply a matter of training, but a fine balance between training, competing, and recovery. The accumulated physiological and psychological stresses induced by the training load can result in maladaptation if that balance is not achieved. Recovery is multifaceted including both physiological and psychological components. It is defined as “a component of sports training that through the targeted use of physiological effects means to restore the homeostasis of the body to pre-competition or training level; not only attaining that level, but to a superior one (overcompensation) which represents optimization time for restoration” [1]. Recovery may involve passive methods (the application of external methods, i.e., massage), active recovery (i.e., cooldown jogging), and proactive recovery (i.e., social activities, which requires a high level of self-­ discipline by choosing activities customized to individual needs and preferences). Cryotherapy and manual therapy techniques, including massage, foam rolling, and massage devices, are all beneficial in aiding the athletes’ recovery. Multiple forms of “hands-on” manual therapy techniques exist including massage, ischemic compression, trigger point therapy, strain/ counter-­strain techniques, muscle energy techniques, joint mobilization and manipulation, transverse friction massage, and other soft tissue mobilization techniques to name a few. These therapeutic strategies are used to treat and prevent sports pathologies and dysfunction associated with overuse and biomechanical deficits. These techniques are applied to alleviate hypersensitivity in myofascial tissues, promote tissue healing, decrease pain, release scar tissues and adhesions, improve joint range of motion (ROM) and functional performance, reduce delayed-­ onset muscle soreness (DOMS), and accelerate recovery. Exercise therapy is synonymous with rehabilitation and is an integral tool in preventing and managing sports injuries. Blood flow restric-

tion (BFR) training has recently and quickly gained interest as a resistance training technique that could be a revolutionary tool to decrease the time to return to sport post-injury/postoperatively, for general rehabilitation, strength training, and prehabilitation. Our understanding of pain as a complex biopsychosocial problem has been broadened with contemporary pain science. Applying pain neuroscience education will allow athletes to gain better understanding of their pain, including the role of neurophysiology (e.g., central nervous system sensitization) and the relevance of psychological, social, and environmental influences combined with biomedical factors. Education typically decreases the threat value of pain, diminishes catastrophizing, and facilitates a more active coping strategy. An approach with education, goal setting, and therapeutic treatment will go a long way to having successful outcomes in managing an endurance athlete through their rehabilitation. This chapter reviews the effectiveness of BFR training for general rehabilitation, strength training, and prehabilitation relevant to the athlete. Innovations, new, modified, and “retrieved from the archives,” will be discussed, evaluating their role in sports injury prevention, rehabilitation and recovery. These modalities include dry needling, cryotherapy, foam rolling, massage with the use of devices (percussive massage and instrument assisted), muscle energy and active release techniques, as well as cupping therapy.

Blood Flow Restriction Strength training is used to increase an athlete’s performance, prevent and rehabilitate injuries. During a period of reduced activity or inactivity due to a sports injury, pain, instability, and/or immobilization following a fracture or surgery, loss of muscle mass and function results. This in turn can increase the risk of reinjury and prolong recovery time, a concern for both clinicians and athletes. Musculoskeletal dysfunction has its challenges. Pain and dysfunction in damaged muscle or connective tissue can affect muscle strength, range of motion (ROM) and neuromus-

17  Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation

cular control, leading to persistent impairment and deficiencies in functional ability. Muscle weakness is a primary contributor to functional impairment. Treatment goals should be to stimulate muscle hypertrophy and subsequent strength gains [2]. Resistance training has been demonstrated to be highly effective in combating loss of muscle mass and function; it is often contraindicated for postoperative or injured patients because of elevated risk of injury or exacerbating existing injury sites, by overloading healing tissues. Hence the need for low-intensity exercises that are interesting, dynamic, and most importantly effective. Beneficial anabolic and functional responses in skeletal muscle can be elicited with low-intensity resistance exercise [60% of 1RM). Unfortunately, for the average individual rehabilitating an injury using high-load (HL) strengthening programs may not

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be feasible. Following muscle or ligament tears, tendon strain, or surgical procedures, patients are frequently restricted in their ability to perform activities with high loads in an attempt to protect the tissues’ integrity. Increasing muscle strength and size would be advantageous for most, if not all, athletes especially when heavy lifting (>60% of 1RM) is contraindicated for painful conditions, postoperatively or until the latter stages of rehabilitation [3, 4]. A mounting body of evidence indicates positive muscle adaptations at low intensities using BFR training [2, 4–9], and “attenuation of muscle atrophy during periods of disuse” [4]. Individualized BFR training may provide a comparable surrogate for HL training while minimizing pain during training [2].

Mechanism As skeletal muscle fibers fatigue, additional fibers are recruited to facilitate the activity. These surplus fibers require a higher stimulatory threshold [4]. Oxygen restriction and intramuscular metabolite accumulation generated during BFR is thought to drive fatigue and the recruitment of additional muscle fibers. Skeletal muscle hypertrophy is principally controlled by the total volume of mechanical work performed (sets × repetitions × resistance) and the number of muscle fibers used to perform that work [2]. LL-BFR training may mimic high-volume/HL training in a setting that minimizes resistance and reduces risk [4]. It is hypothesized that the mechanics of BFR cause an ischemic and hypoxic muscle environment, which results in elevated levels of metabolic stress together with mechanical tension when BFR is used in tandem with exercise. “Primary hypertrophy factors” is the term used to describe both the metabolic stress and mechanical tension that are thought to activate other mechanisms for the induction of muscle growth [4]. A hypothetical theory proposed for BFR mechanism includes elevated systemic hormone production, cellular swelling, production of reac-

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tive oxygen species (ROS), intramuscular anabolic/anticatabolic signaling pathways, increased fast-twitch fiber recruitment, and satellite cell activity [2, 4]. These proposed mechanisms are not fully understood or researched as yet (Fig. 17.1). Research by Christiansen et  al. (2018) [11] provides convincing evidence that BFR exercise can augment skeletal muscle signaling responses, particularly those related to the physiological mechanisms associated with fatigue resistance and mitochondrial capacity [11]. In well-trained athletes phenotypic adaptations to exercise training are more difficult to elicit, particularly in those who already have the necessary physiology to be competitive in their chosen discipline [5]. Reduced plasticity of skeletal muscle and a blunting of the adaptive capacity in trained individuals or in response to exercise training is reflected at a molecular level [5]. Where Christiansen et  al. (2018) [11] used participants of “trained” status, their results suggest that regardless of exercise modality or intensity, BFR may overcome the blunted nature of the acute signaling response to exercise and act as a potent stimulus in enhancing a broad range of adaptive processes [11]. Improvements in muscle physiological processes and morphological adaptations could result in an enhanced performance capacity, particularly at high exercise intensities where limits of exercise tolerance or task failure have been reached [5].

A primary goal in training elite athletes is to maximize the magnitude of event-specific performance adaptation. BFR exercise may augment well-conditioned athletes’ training, providing those small elusive gains they need or facilitating athletes who have plateaued [5]. A greater understanding of the potential benefits and mechanisms of BFR training might provide the incentive for integration into training practice. Research has demonstrated that 6  weeks of LL-BFR training resulted in significant gains in muscle size and strength, with no significant changes in peripheral or central neuromuscular function, yet moderate-to-large effect sizes in central activation and evoked torque. This suggests that further research on the neuromuscular variables with BFR training is necessary [12].

Clinical Application The application of BFR training for enhanced rehabilitation or for modifying effects to exercise programs is gaining momentum in the sports medicine and athletic communities [2, 4–8, 13]. Many studies have focused on knee-extension exercises, using healthy subjects, showing significant increases in quadriceps strength and thigh girth in the BFR groups, especially when usual resistance training was augmented with BFR (Fig. 17.2) (Table 17.1) [16–18].

Fig. 17.1  Proposed mechanism of action of BFR (reproduced with permission from Pignanelli et al. [10])

17  Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation

a

241

b

Fig. 17.2  Examples of blood flow restriction exercise training. (a) non-weight-bearing, such as seated knee extension, (b) weight-bearing, such as partial squatting (reproduced with permission from Barber-Westin et al. [14])

Table 17.1  Model of exercise prescription for BFR resistance exercise [15] Guidelines Frequency Load Restriction time Type Sets Cuff

2–3 times a week (>3 weeks) or 1–2 times a days (1–3 weeks) 20–40% 1RM 5–10 min per exercise, re-perfusion between exercises Small and large muscle groups (arms, legs, uni or bilateral) 2–4 5 cm (small), 10 or 12 cm (medium), 17 or 18 cm (large) (75 reps)—30 × 15 × 15 × 15, or sets to failure 40–80% AOPa 30–60 s

Repetitions and pressure Rest between sets Restriction form Continuous or intermittent Execution speed 1–2 s (concentric and eccentric) Execution Until concentric failure or completion of planned rep. scheme AOP arterial occlusion pressure

a

Postoperative rehabilitation can require prolonged treatment to achieve pre-injury muscle strength and some surgical interventions require delays in high-intensity training to allow healing of repaired or reconstructed joints. This is a clinically relevant time where BFR training may com-

bat some of the negative effects of deconditioning following injury or surgery. Outcomes following knee ligament reconstruction are often plagued with weakness and dysfunction. One of the greatest impairments following surgery is quadriceps weakness. Decreased function and increased probability of delayed or unsuccessful return to sport can result from insufficiency of the knee extensor complex. A long-term complication could involve the development of osteoarthritis later in life [2]. Studies have shown that low-level isometric exercises with BFR, early after ACL reconstruction surgery, can improve muscle activation. And, for those with limited weight-bearing status, positive benefits can be expected using BFR combined with low-level isometric and open-chain activities to prevent muscle atrophy before returning to full weight-bearing [2]. As tolerance and weight-­ bearing status progress, functional activities with BFR (using lower loads at high repetitions) can be used with positive outcomes [2]. BFR training on postoperative ACL reconstruction patients have shown significant decreases in postoperative extensor muscle atrophy; similarly in postoperative arthroscopic knee patients [19]. Those performing BFR exercises

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showed significant increases in thigh cross-­ sectional area, greater improvements in timed stair ascents, and patient reported outcome measures significantly improved as did extension and flexion knee strength [2–6, 8, 9, 20, 21]. Following total knee arthroplasty (TKA) individuals risk losing up to 80% of their knee-­ extension strength in the first few days [2]. Although, most individuals are allowed to bear weight early after TKA, typically HL or impact-­ related activities are restricted. Incorporating BFR training early on for these patients would seem beneficial and could result in faster recovery times [21], owing to reduced muscle loss and improved strength and function [2]. Case reports have shown that BFR training incorporated into a rehabilitation program may be a beneficial treatment option for patients with Achilles tendon injuries [22]. Following surgical repair for Achilles tendon rupture a program using BFR training showed plantarflexion peak torque improvements of 522% and 108.9% and power gains of 4475% and 211% at 60°/s and 120°/s, respectively. Similarly, Achilles tendon rupture without surgical repair benefited from BFR training experiencing plantarflexion strength improvements of 55.8% and 47.1% and power gains of 68.8% and 78.7% at 60°/s and 120°/s, respectively. Incorporating BFR training with rehabilitation programs can significantly improve strength, endurance, and function after Achilles tendon injury [22]. Quadriceps strengthening is considered a cornerstone of rehabilitation in patellofemoral pain (PFP), one of the most common conditions among active individuals. The use of LL-BFR is a solution to loading the joint without aggravating the patient’s symptoms. LL-BFR for PFP may be used in two stages: (1) pain reduction immediately after a treatment session to encourage compliance, and (2) improved quadriceps strength combined with chronic reduction in pain. Research has shown that BFR training in PFP subjects had a 93% greater reduction in pain with activities of daily living compared to standard treatment [23]. When performing BFR on upper body musculature, it should be noted that the smaller limb

K. Thomas

circumference and girth in this region may require alterations in BFR application. There is gross heterogeneity across upper extremity BFR studies [2, 19]. From the data available, exercise repetition schemes may be performed as with the lower extremity; however greater number of repetitions (up to 165) may be required to achieve comparable improvement [2, 24]. Benefits of low load strengthening have been shown for musculature in the back, chest, shoulders, and arms [24]. Using BFR during rehabilitation for ligament injury, fracture, or tendinosis in the upper extremity is hypothesized to improve function. Benefits of BFR for specific upper extremity injuries are largely unknown at this point and provide an intriguing paradigm for future research [2]. The proven benefit of BFR training in increasing muscle strength and cross-sectional area makes it an ideal tool for rehabilitation following muscle strain [25]. The application of eccentric exercises to the injured muscle group is a common intervention to rehabilitate and prevent muscle and tendon injuries. Unfortunately, many individuals cannot tolerate the eccentric load after injury, nor the muscle soreness associated with eccentric training. BFR training can be incorporated into eccentric loading, although this can result in muscle soreness [25]. The effectiveness of BFR training only on the eccentric portion of the exercise is currently limited. The majority of the studies suggest that _concentric-only BFR exercise was capable of increasing muscle size and strength, yet this was not observed with _eccentric-only BFR exercise [25]. Since BFR training requires the use of a tourniquet-­like cuff to be applied proximal to the portion of the limb/muscle to be trained, it would be assumed that a cuff could not be applied to isolate muscles proximal to the limbs, i.e., closer to the trunk than the axilla or groin. However, Dankel et al. (2016) found several instances of proximal gains in muscle strength and size while applying BFR to the limbs [24]. BFR training is able to increase muscle strength in the shoulders and back but may require greater volume of exercise than muscles distal to the cuff [24]. The suggested mechanism for this phenomenon may be the high number of repetitions (upward of 75 total repeti-

17  Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation

tions per exercise) used with BFR. Alternatively as distal muscles fatigue a synergistic effect of proximal muscles and higher recruitment of type II muscle fibers and muscle cell swelling during BFR may be responsible [2, 4, 9]. Muscle strength and hypertrophy can be enhanced with LL-BFR in well-trained athletes who would not normally benefit from using light loads. For healthy athletes an additional stimulus may come from combining LL-BFR training in conjunction with normal HL training. As LL-BFR exercise does not appear to cause measurable muscle damage, supplementing normal HL training with this novel technique may elicit beneficial muscular responses in healthy athletes [20]. However, some studies have shown that 8  weeks of lower-body BFR training at 50% occlusion does not appear to have an added effect on measures of muscle strength or body composition in resistance-trained females [26]. This may relate back to the challenges of phenotypic alterations in trained individuals (mentioned earlier) and possibly even technique of BFR application. A greater occlusion pressure of 60%, as used in most clinical trials, may be necessary to show benefit. Current evidence suggests that the addition of BFR to dynamic exercise training is effective, with consistent changes for both resistance training and aerobically based exercise [7] (Table 17.2). Although BFR resistance training is well studied, its effects on hemodynamic and cardiorespiratory responses during aerobic exercise are not fully established. During aerobic exercise testing, when compared to normal conditions, BFR results in significantly increased cardiac work, myocardial oxygen consumption, ventilation, ratings of discomfort/pain, perceived exertion, numbness/tingling, and soreness as well as significantly decreased total test time and predicted VO2 max [27]. Although benefits have been shown with performance in BFR walking and treadmill running, one may need to judge the intensity of the aerobic activity and the individual as to whether BFR training used in an aerobic activity will be beneficial [27]. Faster recovery programs mostly focusing on perioperative pain management or early mobili-

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Table 17.2  Model of exercise prescription for BFR aerobic exercise [15] Guidelines Frequency Intensity Restriction time Type Sets and pressure Cuff Exercise mode

2–3 times a week (> 3 weeks) or 1–2 times a day (1–3 weeks) < 50% VO2max or HRRa 5–10 min per exercise Small and large muscle groups (arms, legs, uni or bilateral) Continuous or intervals 40–80% AOPb 5 cm (small), 10 or 12 cm (medium), 17 or 18 cm (large) Cycling or walking

HRR heart rate recovery reserve AOP arterial occlusion pressure

a

b

zation may benefit an athlete eager to return to sport. Preoperative strengthening exercise using BFR has shown promising improvements in strength before TKA, a positive outcome for BFR to be incorporated in prehabilitation [2, 28]. Shifting from a mechanical to a more metabolically challenging exercise regime, BFR may have prehabilitation benefits. The molecular adaptations associated with gains in muscle mass and strength preoperatively; BFR has the potential to counteract postsurgery side effects, theoretically reducing length of hospital stay and altering patients’ postoperative subjective feeling [28]. BFR training has a positive effect on bone metabolism, formation, and resorption [29]. Research has shown that LL-BFR training, compared with HL training, increases the expression of bone formation markers (e.g., bone-specific alkaline phosphatase) and decreases bone resorption markers (e.g., the amino-terminal telopeptides of type I collagen) after both aerobic and anaerobic exercise across several populations. So, BFR may not only be a safe technique for the osteoporotic patient but may actually have physiological benefits for their condition too. Passive BFR is another strategy that involves applying the cuffs to limbs without undertaking exercise. This approach has not received substantial research; however the available data indicates that intermittent application of passive BFR may offset muscle atrophy and strength loss during

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periods of bed rest or immobilization. Periods of ischemia followed by periods of reperfusion can mitigate this decline. Theoretically this could provide benefit to an athlete following surgery or immobilization [15]. Passive BFR can enhance local skeletal muscle oxidative capacity and cardiovascular improvements [15] (Table 17.3). BFR combined with electrical stimulation has been shown to increase muscle thickness and strength. Muscle adaptation appears to be a dose– response relationship; with significant strength gains witnessed when maximal tolerable stimulation is used. Similarly positive associations between training intensity and increase in strength, as well as cross-sectional area of both fast and slow twitch fibers is observed [15, 30]. While both passive BFR and BFR with electrical stimulation are interesting new treatment avenues, more research is needed. A proposed model for progression using BFR from early rehabilitation through to HL resistance training incorporates a four-step approach: (1) During periods of bed rest, passive BFR; (2) BFR combined with low-workload, for example, walking exercise; (3) BFR combined with LL resistance exercise, and (4) LL-BFR training in combination with HL exercise [31]. This type of progressive model may provide an effective rehabilitation tool from early ambulation to return to full recovery [4]. Table 17.3  Model of exercise prescription for passive BFR [26] Guidelines Frequency Restriction Time Type Sets Cuff Pressure Rest between sets Restriction form

1–2 times a day for duration of bed rest/immobilization 5-min intervals Small and large muscle groups (arms, legs, uni or bilateral) 3–5 5 cm (small), 10 or 12 cm (medium), 17 or 18 cm (large) Uncertain, higher pressures may be needed 70–100% AOPa 3–5 min Continuous

AOP arterial occlusion pressure

a

Safety and Side Effects A pressure-controlled tourniquet must be applied to the most proximal portion of the limb being trained during exercise with BFR. The cuff should be placed around the proximal thigh, just distal to the inguinal crease, for lower extremity exercise. In the case of the upper extremity, a cuff would be placed around the upper arm, just distal to the axilla. The tourniquet or cuff should preferentially be used over regions with higher mass and limb width in order to prevent complications due to pressure over a peripheral nerve (neurapraxia). Some concerns exist over venous occlusion, although no complications have been reported in studies to date, granted many had small sample sizes. Subjects with a previous history of deep venous thrombosis and/or presence of varicosities were excluded from studies, potentially a reason why no venous thrombotic events have been reported [20]. Endothelial damage and the effects on the coagulation cascade with venous stasis in the extremities may be concerning. Contrary to this some research has shown significant decreases in von Willebrand factor and improvements in vascular endothelial function and peripheral blood flow [2]. Other safety evaluations have assessed the effects of LL-BFR on plasma volume reduction, which was significantly greater after BFR exercise, suggesting that in healthy patient populations, BFR does not activate the coagulation system [2]. BFR does not increase myocardium load or have an effect on coronary vascular function [32]. Partial blood flow restriction during exercise can affect blood pressure in an ambiguous way. Systolic arterial blood pressure (ABP) values continue to be higher, while diastolic ABP changes are not expressed. There is no additional strain on cardiac function during BFR training [32]. Rare cases of rhabdomyolysis after BFR have been reported with an incidence of 0.008% [2]. There is a low occurrence of adverse effects other than skin bruising [4]. It remains unknown what effect BFR training has on tendon strength. The possibility of connective tissue injuries related to increased muscle strength without concurrent tendon conditioning remains to be seen. Despite

17  Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation

concerns of ischemic reperfusion injury and disturbed hemodynamics, indepth review of BFR training has confirmed that with correct implementation there is no greater risk than traditional exercise modes [2–9, 20, 21]. Many risks can be mitigated by accounting for correct cuff width, cuff type, and the individual to which the pressure is being applied. The pressure should be relative to the cuff used (wider cuff, lower pressure) and to the individual (larger limb circumference, greater pressure) rather than applying the same absolute pressure to each individual [4, 25].

Conclusion Maximum muscle strength and hypertrophy may be optimized by specific training methods; both HL resistance training and BFR training seem equally effective in increasing muscle mass. BFR training is an effective approach for increasing muscle strength in a wide spectrum of ages and physical capacities. As a safe method to begin strength training at earlier stages of rehabilitation and to augment standard exercise therapy, BFR has promising influences in the goal to achieve accelerated function and recovery. As an adjunct to standard strength training, athletes driven to better performance or patients who have plateaued in their progress with traditional rehabilitation may benefit from the addition of BFR training. Large-scale clinical trials are needed to obtain better understanding of BFR physiology, complications, side effects, and standardized treatment protocols.

Dry Needling Several needling techniques are proposed for the management of myofascial pain syndromes. The “modern” Western medicine techniques are those called dry needling (DN) and are defined below. This is different from acupuncture that is embedded in traditional Chinese medicine and uses specific acupuncture points to treat a variety of medical conditions.

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The American Physical Therapy Association (APTA) defines dry needling (DN) as: “a skilled intervention using a thin filiform needle to penetrate the skin that stimulates myofascial trigger points (MTrPs), musculature and connective tissue for the management of neuromusculoskeletal disorders, pain and movement impairments. DN is a technique used to treat dysfunctions in skeletal muscle, fascia, connective tissue and diminish persistent peripheral nociceptive input, and reduce or restore impairments of body structure and function leading to improved activity and participation” [33]. The Australian Society of Acupuncture Physiotherapists describe dry needling (DN) as: rapid, short term needling to altered or dysfunctional tissues in order to improve or restore function. This may include needling of MTrPs, periosteum, and connective tissues. It may be performed with an acupuncture needle or any needle without the injection of a fluid [34].

Mechanism The mechanisms by which DN exerts a therapeutic effect is not fully understood. An integrated hypothesis of both mechanical and neurophysiological mechanisms has been proposed. Dry needling creates an analgesic effect in the musculature around the point of insertion, through inhibition of the descending central nervous system (CNS) pathways. Stimulation of alpha-delta nerve fibers aids the release of endogenous endorphins and enkephalins. This results in an increase in pain pressure threshold and a decrease in muscle tone [35]. DN activates large myelinated fibers within the MTrP; this hypoalgesia cascade results in decreased metabolic and chemical mediators and increased local microcirculation [36]. Peripheral, spinal, and supraspinal mechanisms underpin DN’s efficacy [37]. Mechanical effects include (i) disruption of dysfunctional end plates to increase sarcomere length and to reduce the overlapping between actin and myosin filaments, (ii) decrease in the amplitude and frequency of end plate noise and end plate spike, decreasing the acetylcholine lev-

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els and the neuromuscular junction response, (iii) an increase in muscle blood flow and oxygenation supporting a reduction of sarcomere contracture [37]. By removing the source of peripheral nociception DN may reduce both peripheral and central sensitization. Neurophysiological effects include (i) modulating spinal dorsal horn activity, and activating central inhibitory pain pathways; (ii) reduction in the peripheral concentrations of neurotransmitters, several cytokines, and interleukins within the extracellular fluid of the MTrP after needle insertion; (iii) increase in β-endorphin and TNF-α levels; (iv) activate cortical brain areas involved in sensorimotor processing [37].

Clinical Application Studies on dry needling have focused on the management myofascial pain, specifically the cervical spine, lumbar back, knee, shoulder, and foot [36]. Dry Needling can be effective for improving pain-related disability and pain intensity in individuals with neck pain symptoms associated with MTrPs. Dry needling is more effective than placebo, sham, or simply waiting. However it may not influence cervical range of motion [38]. Dry needling should be considered for the treatment of headache, including tension-type and cervicogenic, and may be applied either alone or in combination with traditional treatments [39]. Spine-related disorders that are not due to serious pathology have four major pain originators comprising disc derangement, radiculopathy, joint dysfunction, and myofascial trigger points. Dry needling improves outcomes, including pain scores, pain pressure thresholds and range of movement, regardless of diagnosis or treatment parameters [40]. Compared with other treatments, DN of MTrPs is more effective in relieving the intensity of lower back pain (LBP) and functional disability. However, the combined effects of dry needling plus other standard treatments (manual and exercise therapy) on pain intensity could be superior to DN alone when managing LBP [41, 42].

There is low quality evidence to support the use of DN in the shoulder region for treating patients with upper extremity dysfunction and pain [43]. Nevertheless, dry needling for lateral epicondylalgia is effective in reducing pain and disability, increasing pain pressure thresholds and grip strength. The most significant effect was in the short term [44]. Dry needling is an effective treatment for patellofemoral pain (PFP), but not knee osteoarthritis or postsurgical knee pain [45]. The positive effects of DN on PFP are heightened when combined with other treatment modalities including manual therapy and exercise. This is clinically relevant as most clinicians should consider a multimodal approach to pain management. Muscles receiving needling intervention for PFP included the hip (e.g., gluteus medium, iliopsoas) and/or knee (e.g., vastus medialis, hamstrings, adductors) [45]. Tendon dry needling (percutaneous needle tenotomy) involves repeated fenestration of the affected tendon (passing the needle in and out of the tendon between 20 and 50 times). The technique is thought to disrupt the chronic degenerative process and encourage localized bleeding and fibroblastic proliferation. Although there is vast diversity regarding the needling technique (using ultrasound guidance and additional treatments), studies have reported statistically significant improvement in patient-reported symptom scores across common tendinosis sites including wrist extensors, patellar and Achilles tendon, hip trochanter, and rotator cuff. Future investigations are needed to provide high-quality evidence for the effect of tendon needling on tendinopathy [46].

Safety and Side Effects The clinician should firstly identify the MTrP area before inserting the needle and then envision the needle as an extension of their finger. It is critical to have thorough knowledge of human anatomy and the patient’s clinical status for minimizing adverse events [37]. The risk of ­ adverse events is small, the most significant doc-

17  Blood Flow Restriction and Other Innovations in Musculoskeletal Rehabilitation

umented adverse events include pneumothorax, epidural hematoma, puncturing the stomach, cardiac tamponade, hemiplegia, and infection [37]. It is advised, where muscles are deep or in close proximity to neurovascular structures, ultrasound-­ guided needle intervention be employed. The most common minor adverse event reported includes post-needling-induced pain or tenderness. This can result in a reluctance of individuals to receive further needling therapy, possibly generating patient dissatisfaction and poor adherence to treatment. Neuromuscular micro-­ damage generated by consecutive needling insertions into the muscle is thought to be the cause of post-needling soreness [37]. This soreness lasts for approximately 48–72  h, but can be reduced with stretching, ischemic compression, low-load eccentric exercise, therapeutic exercise, posture correction, and education [37]. When properly applied, needling therapies seem to be safe; however it cannot be assumed there is no risk of potentially serious complications [37].

Conclusion Low to moderate quality evidence exists for DN. Dry Needling is as effective as other treatments, and more effective than sham or no treatment, in reducing pain and increasing pain pressure threshold in the short term. Greater research into musculoskeletal and sports injuries, as well as long-term efficacy is needed.

Cryotherapy For decades icing has been ingrained in acute injury management. Recently, however, the application of cold/ice therapy has become extremely controversial in sports medicine and acute soft tissue injury rehabilitation. This therapy is often used for its immediate analgesic effects following acute injury. Cold therapy is generally used to lessen the inflammatory response to trauma, reduce edema, reduce hematoma formation, reduce muscle spasm, decrease tissue metabolism, and reduce enzymatic activ-

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ity. It can also reduce nerve conduction velocity, vascular permeability, and cause vasoconstriction [47]. Understandably these physiological effects are questionable when considering what is needed for tissue healing and recovery. The evidence for the use of cryotherapy is relatively low, with significant heterogeneity across studies and a limited number of randomized controlled trials (RCT) [47, 48]. Since the process of inflammation is an essential component to recovery, anything that reduces inflammation may also delay healing. If the goal is to limit the extent of the edema (e.g., severe joint sprain), then cold therapy could be a useful option, as too much or prolonged swelling has been proven to hinder the healing process during the recovery period. However, when the edema level is less severe (e.g., muscle strain), cold therapy may in fact act as a barrier to recovery [47]. When injured the body signals inflammatory cells, macrophages, which release the hormone insulin-­ like-­growth factor (IGF-1), which in turn initiates the healing process. However, when ice is applied topically, the vasoconstriction may impede the transport of inflammatory chemicals to injured cells thereby delaying the initiation of the healing process [49]. The historical acronym of acute injury management, originating with ICE (ice, compression, and elevation) continues to evolve. The term RICE (rest, ice, compression, and elevation) was entrenched for nearly 20 years before they added “protection” altering it to PRICE.  In 2019, the latest and most inclusive acronym: PEACE & LOVE (protection, elevation, avoid anti-­ inflammatory drugs, compression, and education & load, optimism, vascularization, and exercise) was published [48]. With that, localized conventional cryotherapy (the application of ice, cold packs, or cold sprays) was removed from the acute management of soft tissue injury guidelines as it has the potential to cause serious side effects such as nerve injury, delayed healing, neuromuscular impairment, and skin burn. Recently, research has prioritized optimal recovery strategies for elite athletes, based on the premise that suboptimal recovery can lead to fatigue, reduced quality of subsequent training

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sessions and/or competitive performances, increased risk of injury, and potential hampering of adaptive processes [50]. In the absence of acute injury, cooling the body results in a generalized decrease in training-induced muscle damage and inflammatory markers, thereby accelerating recovery [47, 50–52]. The cryotherapy techniques mentioned below have the potential to positively affect human physiological and psychological conditions, thereby aiding sports recovery and performance. For this a few cryotherapy techniques exist: (1) cold-water immersion (CWI) involves submersing a part of or the whole body except the head in a cold-water bath (95% limb asymmetry correlated with 6.5 × increased risk for a lower extremity injury [165, 166]. A study by Ambegaonkar et al. [123] found an association in collegiate female athletes who had better YBT-LQ score were correlated with hip flexor, extensor, and abductor strength rather than core strength [123]. It can be extrapolated that the use of the YBT-LQ screen can be a useful tool to measure injury risk and performance in the swimming athlete as well. One final return to sport consideration is the short but not insignificant amount of time spent utilizing the racing blocks. This is the only time that normal gravitational forces need to be considered in their natural context in this sport. After injury, clinicians and coaches need to consider return to the starting platform (aka “block”) for racing in freestyle, butterfly, and breaststroke events. For strengthening and power considerations [167]:

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Table 20.9  Freestyle drills Sculling Can have pull buoy between thighs or lightly kick legs With your arms in front of you, push your arms back and forth while turning your palms toward the direction of motion of your hands Can be done with arms extended forward, with arms flexed to 90°, or with arms extended behind you Done to focus on the catch phase of stroke at various points throughout the stroke 6 kick 3 s Start with arm above head with body rolled onto its side Kick six times on side before taking three normal freestyle strokes Then kick six times on opposite side Repeat Purpose of drill: improve bilateral breathing, functional rolling during stroke Ride the side/zipper Swim freestyle With each stroke, bring thumb up your side into your armpit Focus on high elbow during stroke recovery Focus on high elbow during stroke recovery Focus on high elbow during stroke recovery Catch-up drill Swim freestyle Each stroke tap hands in front of body and switch arm strokes Start with one hand in front of body and take stroke with opposite arm Each stroke tap hands in front of body and switch arm strokes Focus of drill: focus on form during recovery, focus on appropriate hand placement without excessive cross over Single arm freestyle Keep one arm in front of body while taking strokes with opposite arm Take breaths to the side of the arm taking strokes Focus on strong kick and full roll to side while breathing Focus of drill: improve body positioning, rolling, and form with arm pull Shark fin drill Swim freestyle Each time your arm reaches head level, pause for 1 s in high elbow position Purpose of drill: to improve elbow positioning during recovery ensuring hand entry prior to elbow entry Fists Swim freestyle normally but keep your hands in a fist throughout the stroke Focus on using forearms for propulsion throughout stroke Done to emphasize use of forearms and to emphasize maintaining high elbows with pull through phase of stroke Paddle grab Swim freestyle while holding paddles in fists Instead of attaching paddles to the hand, have handgrab paddles throughout stroke Done to emphasize using hands to propel body with open hand and strong push

• Shoulder joint extension torque (symmetrically applied with bilateral upper extremities). • Front side lower limb (FSLL): –– Before: hands off the block, supports the weight of the swimmer vertically. –– After: hands off the block, ankle plantarflexion and knee extension torques increase.

• Rear side lower limb (RSLL): –– Hip joint extension forces were the largest, followed by ankle plantarflexion torque, and then knee extension torque was the smallest [167]. Understanding the relationship between these limb kinetics can help focus return to sport considerations for the injured swimmer.

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Swimming Injury and Rehabilitation Conclusion Regardless of the injury, treatment should begin with relative rest, ice, compression, and elevation during the acute phase to reduce inflammation. Conservative rehabilitation should focus on technique correction during the swim stroke and improving muscle asymmetries found upon evaluation. Corticosteroid injections have been suggested if pain is consistent and hinders rehabilitation [25]. The final option, if 3–6 months of conservative treatment has been unsuccessful, is surgery. However, research on overhead athletes with arthroscopy and subacromial decompressions includes few swimmers and suggests a low rate of return to prior level of competitive swimming (56%) [25]. However, the return rate for posteroinferior capsular shift has been found to be 70%, with a low recurrence rate of multidirectional instability [25]. Literature supporting postoperative return to swimming is still lacking for the knee, spine, hip, and ankle.

Return to Swimming Protocol There exists a large percentage of injuries, especially to the shoulder, of the swimming athlete during his/her career. These injuries are often caused by strength asymmetries, improper stroke technique, swim practice duration, and high yardage. Dryland rehabilitation can assist with the correction of the typical “swimmers’ posture” including forward-head and forwardshoulder position, scapular stabilization,

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shoulder and scapular neurological rehabilitation, and core strengthening [11]. However, dryland training does not appropriately activate the muscles in the same way that swimming does. Therefore, return to swimming protocols (RTSP) are critical. Spigelman et  al. created a list of drills to improve the swimmer’s stroke mechanics [11]. Additionally, Hamman created a RTSP for the pediatric swimmer while Spigelman created a RTSP for the adult swimmer. Both programs were created to address progression of yardage safely and create a guideline to assist clinicians’ ability to communicate effectively with coaches and swimmers regarding appropriate return to sport advancement [11, 44]. For example, utilizing RTSPs can assist with recovery from tendon inflammation by providing guidance on intensity and volume, based on the individual needs of the swimmer (Figs.  20.12, 20.13, 20.14 and 20.15 [11] and Figs. 20.16 and 20.17 [11, 13, 44]). As mentioned above, Hamman offers a clinical commentary with regard to a RTSP specific to the pediatric swimmer. He provides three phases for return to swimming for the nonoperative swimmer after injury but could also fit other swimmers’ needs on a case-by-case basis. Hamman not only emphasizes progressive return to normal practice distance but also progresses swimmer’s exertion level [44]. The phases were not created to be used in a linear fashion, so pre-­ organization of individualized swimmer needs and circumstances will dictate where to begin and end for the athlete’s full return to sport (Table 20.10 [44]).

20  Clinical Application of Swim Stroke Analysis Freestyle Drills Sculling

Can have pullbuoy between thighs or lightly kick legs With your arms in front of you push your arms back and forth while turning your palms toward the direction of motion of your hands Can be done with arms extended forward, with arms flexed to 90 degrees, or with arms extended behind you Done to focus on the catch phase of stroke at various points throughout the stroke

6 kick 3s

Start with arm above head with body rolled onto its side Kick 6 times on side before taking three normal freestyle strokes Then kick 6 times on opposite side Repeat

Ride the side/zipper

Purpose of drill- improve bilateral breathing, functional rolling during stroke Swim freestyle With each stroke bring thumb up your side into your armpit Focus on high elbow during stroke recovery Purpose of drill- improve arm position during recovery with hand entering water before elbow

Catch up drill

Swim Freestyle Start with one hand in front of body and take stroke with opposite arm Each stroke tap hands in front of body and switch arm strokes Focus of drill: focus on form during recovery, focus on appropriate hand placement without excessive cross over

Single arm freestyle

Keep one arm in front of body while taking strokes with opposite arm Take breaths to the side of the arm taking strokes Focus on strong kick and full roll to side while breathing Focus of drill: improve body positioning, rolling, and form with arm pull

Shark fin drill

Swim freestyle Each time your arm reaches head level pause for one second in high elbow position Purpose of drill: to improve elbow positioning during recovery ensuring hand entry prior to elbow entry

Fists

Swim freestyle normally but keep your hands in a fist throughout the stroke Focus on using forearms for propulsion throughout stroke Done to emphasize use of forearms and to emphasize maintaining high elbows with pull through phase of stroke

Paddlegrab

Swim freestyle while holding paddles in fists Instead of attaching paddles to hand have hand grab paddles throughout stroke Done to emphasize using hands to propel body with open hand and strong push

Fig. 20.12  Drills for return to swimming progression, freestyle [11]

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332 Backstroke Drills Single arm

Swim backstroke with one arm overhead while the other arm goes through the stroke Focus on rolling onto your side with each stroke and on appropriate stroke technique with single arm Repeat with each UE Purpose: improving form by isolating individual UE and focusing on appropriate technique, facilitate appropriate body roll

6 kick 3s

Start with arm above head with body rolled onto its side Kick 6 times on side before taking three normal backstroke stroke Then kick 6 times on opposite side Repeat Purpose of drill- functional rolling during stroke with increased fluidity

Pause backstroke

Start by swimming backstroke normally Each stroke when your arm reaches 90 degrees of flexion (hand is over eyes) pause for 2 seconds with arm in the air Then continue stroke as usual

Fists

Swim backstroke normally but keep your hands in a fist throughout the stroke Focus on using forearms for propulsion throughout stroke Done to emphasize use of forearms and to emphasize maintaining elbows position with pull through phase of stroke

Paddlegrab

Swim backststroke while holding paddles in fists Instead of attaching paddles to hand have hand grab paddles throughout stroke Done to emphasize using hands to propel body with open hand and strong push

Fig. 20.13  Drills for return to swimming progression, backstroke [11]

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Breaststroke Drills Single arm

Start by swimming breaststroke as you normally would Following the breaststroke pull and breath kick a single breaststroke kick and bring your arms into a streamline Kick two more kicks while in streamline before starting a second arm pull Purpose: focus on breaststroke kick and timing

Breaststroke pull/butterfly kick

Begin breaststroke pull as you typically would As your head comes up to breath and your arms insweep together initiate a single, powerful butterfly kick Continue swimming this way with a dolphin kick replacing a breaststroke kick Purpose: improve timing of breaststroke and facilitate appropriate hip motion during stroke

Sculling

Can perform with pullbuoy between knees or without With your arms in front of you push your arms back and forth while turning your palms toward the direction of motion of your hands Purpose: to focus on the insweep portion of the breaststroke stroke to improve arm pull

Pull,kick,& extended glide

Begin by initiating arm pull and breathing as you typically would As you initiate your kick bring your arms into a streamline position following insweep Maintain glide in streamline following kick for 2–3 seconds prior to initiating next stroke Purpose: timing of breaststroke, focus on power of kick

3 size underwater circles breaststroke kick

Start by initiating pull as you typically would to begin stroke With initial pull use very small arm stroke with very small elbow bend With second pull slightly increase pull while keeping arms extended in front of body With third pull use full, normal breaststroke pull Repeat Purpose: to improve form with breaststroke pull, emphasize forward body position

Fig. 20.14  Drills for return to swimming progression, breaststroke [11]

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334 Butterfly Drills Single arm

Keep one arm in front of body throughout stroke With other arm swim butterfly normally Breathe to the side of the arm that is moving every other stroke Focus on rhythm of kick and appropriate UE movement Purpose: improve timing of kick and appropriate movement of upper extremity during butterfly

Alternating

Done in a similar way to single arm butterfly First perform two strokes with your R arm, Then perform two strokes with your L arm, then perform two strokes with both arms Repeat Done to improve timing during butterfly and progress toward appropriate performance of full butterfly stroke

Head down butterfly

Swim butterfly as you normally would As you breathe keep your head down facing the water rather than looking forward Focus on staying close to the water while still breaking the surface allowing you to breathe Purpose: improving head positioning during butterfly drill to avoid cervical hyperextension

Fig. 20.15  Drills for return to swimming progression, butterfly [11]

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20  Clinical Application of Swim Stroke Analysis Fig. 20.16  Return to swim protocol for swimmers deactivated for 6 weeks or greater [11, 13, 44]

Return to Swim Protocol for Swimmers Deactivated for 6 Weeks or Greater Athlete's Pain/ Soreness Scale throughout protocol:

White Zone

Yellow Zone

0

•

Orange Zone

Red Zone

10

White Zone (0 – 3): Normal level Fatigue and soreness during and post-workout, may last 2–4 hours Pain levels resolve by next morning Monitor mechanic breakdown from fatigue, do not swim with compensation Progress to next level after one week in white zone

•

Yellow Zone (4 – 5): Heads-Up Fatigue and soreness during and post-workout, may last 4–8 hours Pain levels are not resolved by next morning but are in white zone Reduce speed in practice, focus on good form May use fins to unload shoulder if no knee pain Stay at level until one successful week in white zone

•

Orange Zone (6 – 8): Fatigue and pain are not resolved to white zone by next practice 2 days off, drop 1 level or stay at lowest level for full week If pain continues, refer to sports medicine staff member

•

Red Zone (9 – 10): Stop swimming and refer to a sports medicine staff member

Phase I (No Organized Practice): • • • • • • •

Perform each practice 3 times with at least full day off in-between Progress to next practice after one week in white zone Freestyle only throughout Phase I Backstroke, breaststroke, and fly begin in Phase II No pull buoys or paddles (for upper extremity and neck injuries) until Phase II No Kickboard or fins (for low back or lower extremity injuries) until Phase II Progress to Phase II once practice 3 is completed in white zone for one week

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336 Fig. 20.17  Return to swim protocol for swimmers deactivated for less than 6 weeks [11, 13, 44]

Return to Swim Protocol for Swimmers Deactivated for less than 6 Weeks Athlete's Pain/ Soreness Scale throughout protocol:

White Zone

Yellow Zone

Orange Zone

0

Red Zone

10

•

White Zone (0–3): Normal level

•

Yellow Zone (4–5): Heads-Up

•

Orange Zone (6–8):

Fatigue and soreness during and post-workout, may last 2– 4 hours Pain levels resolve by next morning Monitor mechanic breakdown from fatigue, do not swim with compensation Progress to next level after one week in white zone Fatigue and soreness during and post-workout, may last 4 – 8 hours Pain levels are not resolved by next morning but are in white zone Reduce speed in practice, focus on good form May use fins to unload shoulder if no knee pain Stay at level until one successful week in white zone

Fatigue and pain are not resolved to white zone by next practice 2 days off, drop 1 level or stay at lowest level for full week If pain continues, refer to sports medicine staff member

•

Red Zone (9–10): Stop swimming and refer to a sports medicine staff member

Phase II Organized Practice: Practice Yardage Stage 1

60%

Stage 2

70%

Stage 3

80%

Stage 4

90%

Stage 5

100%

Short Course Intensity/Pace 100 pace time divided by 4, then add 2 sec 100 pace time divided by 4, then add 1.5 sec 100 pace time divided by 4, then add 1 sec

Long Course Intensity/ Pace 100 pace time divided by 4, then add 4 sec 100 pace time divided by 4, then add 3 sec 100 pace time divided by 4, then add 2 sec

100 pace time divided 100 pace time divided by 4, then add 0.5 sec by 4, then add 1 sec Full Participation Full Participation

Example Stage 1 Short Course with 100 pace of 1:20: 25 no faster than 0:22; 50 no faster than 0:44; 100 no faster than 1:28; 200 no faster than 2:56

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Table 20.10  Return to swimming criteria [44] Phase 1: reintroduction 1. Used if the swimmer has been removed from sport for greater than or equal to 6 weeks to water. Focus is on due to injury normalizing stroke 2. No participation in formalized practice to prohibit competition and refocus on stroke mechanics technique 3. Only freestyle performed as it comprises more than half of their training volume regardless of stroke specialization 4. Rest involved body part (a) Neck, upper extremity injuries: swimmers are to perform on their back in a streamline position and kick (b) Low back, lower extremity injuries: swimmers use the pull buoy Phase 2: Emphasis on 1. Used if the swimmer has been removed from sport for less than 6 weeks or has already technique restoration completed phase 1 2. Return to organized swim practice with team 3. Yardage and pacing restrictions outlined for safe progression to prior level of function Phase 3: Multiple 1. Dictates to follow practice guidelines normally during first practice of day practices in 1 day 2. Restricts second practice of day to follow the guidelines outlined in phase 2 3. During second practice, allow for relative rest of involved body part(s): (until phase 2, stage 3) (a) Neck, upper extremity injuries: no pull buoy or paddle use (b) Low back, lower extremity injuries: no use of kickboard or fins

Training Considerations Equipment Evidence-based research is still needed to inform appropriate progression back to utilizing swimming equipment. Literature currently supports the use of in-water resistance training as it can improve maximal swimming force, power, and velocity. One example is the assisted elastic band which was found to enhance technical skills including decreasing stroke rate while decreasing stroke depth [168, 169]. Safety Concerns • Barbosa et al. raises concern for the selection of paddle size by age group or for rehabilitation as their results showed an increase in paddle size had a significant effect on increasing peak force, average force, minimum force,

time to peak force, stroke duration, rate of force development, and impulse [170]. • Utilization of fins, kick boards, and pull buoys have been found to produce excessive hyperextension of the lumbar spine [170]. • Fins have been associated with ankle injuries as the foot requires more energy and torque which has been found to affect the body position during the kick [11, 129]. Therapeutic Uses/Rehabilitation • Wanivenhaus et al. discuss the therapeutic use of fins to decrease upper body stress while swimming as well as a pull buoy to reduce drag and stress on the shoulder [14]. • Evidence is lacking to support the use of a swim bench for rehabilitation [162]. Spigelman et  al. [11] highlights additional use and considerations of equipment here: Fig. 20.18 [11].

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Swimming Equipment Indiciaitons & Contraindications Equipment Name Indications

Contraindicaitons

Kickboard Focus on kick if able to hold overhard without shoulder or back pain

Shoulder Injuries & (spondylolysis)

Pull Bouy Focus on stroke only; offloads the legs

Shoulder overuse (tendiitis/tendonsis) elbow or forearm injues

back injuries

Zoomers & Fins

Increase length length & strength

Ankle, Knee and Hip Injuries

Paddles

Variety of sizes increase surface area of the hand to increase pull strength

Shouder Injury & improper technique

Parachute, Varies resistances to increase arm resistance and leg strength cord & tower Technique training of freestyle, Snorkle breast and butterfly: Removing the breathe and errors that occur when breathing

Shoulder, back, hip, knee, and ankle injurires

Backstroke & cardiopulmonary issues

Fig. 20.18  Swimming equipment—uses and contraindications [11]

Coach/Teacher/Trainer Safety Awareness Communication with coaches, physical education (PE) teachers, and strength training instructors is critical in assessment of benefits versus barriers to swimmer health. If the athlete is not adequately educated on appropriate resistance training and safe mechanics, they may sustain injuries and create unsafe training regimens for themselves. McGladrey et  al. [171] investigated coach and teacher awareness of safe resistance training practices to assess knowledge of the instructors. This group evaluated 287 strength coaches and PE

teachers and 140 university PE teacher education students with a 90-question examination covering safety, training regimen and prescription, as well as mechanics. It was found that coaches who instructed athletes in resistance training had a pass rate of 9.5%, the university PE education students had a pass rate of 16%, and coaches and those that had a resistance training certification (CSCS, USAW) passed at 50% [171]. A concerning find was that the lowest scores occurred in the “safety knowledge” section. Knowledge of safe practices and mechanics as well as communication with other care providers are crucial to the safety of athletes.

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When training, there are several factors the instructor/therapist/coach and the swimmer should consider. First, once an injury or risk of injury has been accurately identified, it is important that the swimmer focus on the activation of individual muscles in order to best increase/ improve activation of targeted muscles [92]. Athletes often use commonly practiced motor activation patterns, which may usurp the activation of the desired muscle groups—thus perpetuating the muscle imbalance cycle.

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training has been the routine with athletes swimming anywhere from 4000 to 10,000 yards per high school or club swim practice for competitive events that range in completion time between 20  s and 15  min (50 yards through 1500  m). However, recent studies have experimented with bouts of high-intensity, low-volume training finding success with swimmer competitive performance [174–177]. And due to the high level of overuse injuries in swimmers, especially of the shoulder complex, lower volume may be beneficial to injury prevention in swimmers which makes investigation into this topic even more Efficacy of Dryland Strength important. Training In a study by Faude et al. [174], ten high-level teenage swimmers altered their normal training Dryland training has historically been utilized to routine to perform two different 4-week training improve swimming performance and prevent periods, both followed by one identical taper injuries. In a study by Gatta et al. [172], swim- week. The athletes continued to be coached by mers performed either dryland training in addi- their home coach, but during the high-volume tion to swim practice or performed additional training trial, their total training volume increased swimming drills before swim practice for 30% above normal. During the swimmers’ high-­ 6 weeks [172]. It was found that power increased intensity training, the training volume decreased in the dryland strength training group and not the 40% below their normal level. After 4 weeks of swim training group using high-intensity, lower training, both the high-volume and high-intensity repetition dryland training [172]. Therefore, it is trials increased the individual anaerobic ­threshold recommended to use high-intensity, lower-­ to higher than pre-training values. Additionally, repetition dryland training to increase power and the high-intensity group increased their maximal performance in swimmers. blood lactate concentration. Swimmer 100 m and Another group studied the effects of eccentric 400 m performance times were not significantly strengthening. During rehabilitation, restoration different between groups between the 4-week of function is a top priority, and the focus is com- training trials [174]. Overall, this study found no monly the involved/injured side. However, significant differences in performance, heart rate Lepley and his co-authors found that eccentri- with maximal and submaximal swim speeds. cally strengthening the uninjured side carries Lastly, there was no difference between trials in over to the injured side and therefore should be subject “Profile of Mood States” (POMS) quesused in addition to focused strengthening of the tionnaire which assesses possible overtraining by injured side. The resultant effects can be useful measuring changes in vigor, fatigue, depression, both for injury prevention and rehabilitation and anger [174]. strategies for swim training [173]. These results are in agreement with those found by Kilen et  al. [175]. Kilen and his co-­ authors studied 41 elite swimmers (average Efficacy of Swim Training Regimen age  =  20  years) and assigned them to a control group or high-intensity training group. The high-­ The perfect prescription of training volume, intensity group (HIT) reduced their training volintensity, and frequency to result in optimal exer- ume to 50% of their normal volume and increased cise performance has yet to be discovered in the intensity to 50% more than normal. After sport. In swimming, historically, high-volume 12 weeks of training, these authors found no sig-

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nificant difference between the high-intensity training and the control groups with regard to swimming performance, swim-specific VO2max, body composition, blood metabolic markers, and swimming economy. However, it was found that VO2max normalized to body weight decreased in the high-intensity group only and did not change in the control group [175]. It has been found in other studies that younger swimmers (average age  =  10) demonstrated improved swimming performance with high-­ intensity training [178]. This could signify that the age of the participant has a different effect on training results. It is also possible that there exists an upper limit to how much exposure to high-­ intensity, low-volume training is present as the elite swimmers in the Kilen study had performed high-intensity and low-volume training as part of their normal regimen for several years [175]. Pugliese studied the high-intensity training effect on ten male masters swimmers (average age  =  32  years) [177]. Pugliese et  al. put his swimmers through both a high-volume, low-­ intensity training regimen for 6 weeks and then a high-intensity, low-volume training regimen for the next 6  weeks [177]. These swimmers responded with improved peak oxygen consumption and improvements in the 400 m and 2000 m swim performance after the high-volume, ­low-­intensity training. After the subsequent high-­ intensity, low-volume training, these same swimmers did not demonstrate changes in their peak oxygen consumption nor changes in their 400 m and 2000  m time from their post high-­volume, low-intensity training. They did, however, improve their individual anaerobic threshold and their 100 m swim performance [177]. In a similar study, Laursen [176] split groups of cyclists/triathletes into three different groups for three different kinds of high-intensity, low-­ volume training [176] • Group 1 completed eight intervals at VO2peak power output for a duration equal to time to exhaustion as calculated from a progressive exercise test with a recovery ratio of 1:2. • Group 2 completed eight intervals at VO2peak power output for a duration equal to time to

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exhaustion as calculated from a progressive exercise test with a recovery time as long as needed to allow the body to return to 65% of max heart rate. • Group 3 completed 12 × 30 s bouts of 175% peak power outlet with a 4.5 min recovery in between bouts. • The control group did not alter their normal training regimen. Their results demonstrated that Groups 1 and 2 demonstrated the biggest improvement in endurance performance (40 km time trial), peak power output, and VO2peak. Laursen reported that this could be that time to exhaustion intervals could be more rigorous than other study protocols. Additionally, effort adjustments in protocol training were made after reassessments were performed to monitor cyclist progress throughout the trial. These effort adjustments also increased the rigor of the training [176]. It is important to note that while the above studies do not demonstrate improved performance with high-intensity, low-volume training, the subjects did not note a decrease in performance which means that both methods, as understood so far, produce similar results. Perhaps high-intensity, low-volume training can reduce the risk of overuse injuries by reducing training time and allowing longer recovery time between training sessions. Current training programs incorporate variations of intensity, volume, and frequency in their routine, but the exact proportions required to produce the best and safest performance have yet to be determined. Laursen [179] recommends a mixture of both high-­ volume, low-intensity and highintensity, low-­ volume regimens into a highly trained athletes’ plan. Laursen [179] also suggests that because the metabolic adaptations occur with both training strategies overlap significantly, but the molecular events are different, both should be incorporated. Laursen [179] suggests a ratio of approximately 75% high-volume, low-intensity training, and 10–15% of the training regimen should be high-intensity, low-volume training [179]. One study conducted found that sprint performance is enhanced after plyometric exercise pro-

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vided adequate recovery time. Post-activation potentiation (PAP) is a form of high-intensity exercise that induces fatigue and potentially increases the muscle’s capacity to generate high forces in a short period of time [37]. PAP has shown beneficial effects on performance, maximum voluntary contractions, sprint running, and sprinting and jumping; however, data on the effects of PAP in swimming performance are lacking. Therefore, it may be an interesting tool to use in between a swimming warm-up and a race to enhance performance. The 50-m freestyle is predominately an anaerobic-­ based performance due to the short duration and intense effort and power through the arm pull in elite swimmers. Abbes et al. investigated the use of a PAP protocol in a 50-m swimming time trial and found no significant improvement in performance and biomechanical, physiological, and psychophysiological variables before, during, and after the time trial. Tethered swimming (TS) is a frequently used, in-water resistance training and used to measure swimming force. It has been found to improve lactate production and could potentially be a method to enhance sprint performance in training and in competitions. Another study by Abbes et al. investigated TS at the end of a warm-up had an ergogenic effect on the 50-m sprint performance. The study found that TS warm-up had no significant effect on 50-m performance, post-­ exercise rating of perceived exertion, or stroke length.

 raining Effort and Communication T with Coaches Communication between athletes and coaches is very important to ensure the status of goal achievement, training plan compliance, and athlete safety. Barroso published two articles regarding communication between swimmers and coaches. Barroso et  al.’s group (2014 and 2015 studies) defined communication during one training workout as “session rating of perceived exertion” (SRPE). The authors studied 160 swimmers of different age categories (11–12-year-olds,

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13–14-year-olds, and 15–16-year-olds) and different competitive swimming experience and 9 coaches. The coaches rated the SRPE before the training session as falling within these three categories: easy (SRPE 5). The SRPE was indicated by the swimmers 30 min after the end of the session. Barroso et al. [180] found that increased age and competitive swimming experience improved coach and athlete SRPE agreement. It was found that younger swimmers (ages 11–14) rated training intensity differently from coaches in all three categories. The 15–16-year-old swimmers demonstrated agreement with the easy and moderate SRPE but differed in the SRPE difficult category [180]. Additionally, in a follow-up study, Barroso et al. [181] investigated SRPE and how training volume and intensity may affect agreement between swimmers and coaches. Using the three SRPE categories defined above, coaches recorded the desired SRPE levels before the session and swimmers recorded their response 30  min after the training concluded. In 13 moderately trained swimmers (average 21  years  ±  1.1  years), they were given different swim volumes (10 × 100m, 20  ×  100m, 10  ×  200m, and 5  ×  400m) at the same relative intensity. Athlete and coach SRPE differed in 10 × 200m and 5 × 400m. Therefore SRPE is affected by intensity, volume, and distance. It is recommended that coaches ensure thorough communication with swimmers especially with increased volume, longer distance, and higher intensity to ensure desired training effort is applied by the athletes and to prevent injuries [180, 181].

Injury Prevention Schlueter’s (2021) systematic review demonstrated that limited evidence exists to draw specific correlations between clinical objective measures and the development of pain and/or injury in elite swimmers [182]. Grouping the best and most appropriate clinical outcomes into the following constructs may allow clinicians to begin to account for the dynamic interactions

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between modifiable and non-modifiable risk factors in the development of pain/injury in elite swimmers (mobility, strength/endurance, static/ dynamic postures, and patient reported outcomes) at the shoulder, knee, and spine (Table 20.11 [182]). In 2021, Feijen et al. described an injury prediction model for youth swimmers. The following risk factors should be considered: 1. Workload ratio: acute distance swum in the previous week divided by the distance that had been swum as a rolling average (incorporating the previous week). If volume increases by 1, odds for pain increased by a factor of 4.3.

Table 20.11  Relevant predictors of injury [182] Evaluation Strength

ROM

Outcome reports

Relevant findings Shoulder IR/ER muscle imbalance → watch for mid- to post-season changes (Batalha 2013) (Bak 1997) Knee flexion/extension muscle asymmetry > 10% (Secchi 2011) Shoulder  • Pec muscle length: ≥0.53 cm rest; ≥0.68 cm stretch (Harrington 2014)  • Forward shoulder posture (Hibberd 2016)  • Shoulder pain higher with joint hypermobility (Ozcaldiran 2002)  • Scapulohumeral rhythm → ≤55° of scap rotation at 135° humeral elevation (Su 2004)  • Shoulder ER ROM → ≤93° or ≥ 100° [66].  • Decreased shoulder IR/ER AROM mid-season and/or increased scapular upward rotation at 90° abduction [78] Knee  • Decreased hip IR → ≤37° (better if ≤46°) [101]  • Kick initiation hip abduction angle → ≤37° or ≤ 41° [102] Spine  • Higher risk (by 2.5x) if female; kyphosis plumbline ≥90 mm; lordosis plumbline ≥60 mm (Zaina 2015) KJOC Kerlan-Jobe Orthopedic Clinic Overhead Athlete Shoulder and Elbow Questionnaire (Wymore, 2015) SFPS Swimmer’s Functional Pain Scale (Drake, 2015)

2. Competitive level: younger, regional swimmer’s higher risk than national, international, club. 3. Shoulder flexion ROM: limitations can be a risk factor. 4. Posterior shoulder muscle endurance: for posterior shoulder strength that increases by 1 unit, odds for pain decrease by 5%. 5. Hand entry and recovery stroke technique errors [183]. Pre-, mid-, and post-season screens should be completed to help understand risk factors that may increase pain/injury risk. A recent study found that shoulder extension strength less than 13.5% of body mass had a fair chance (0.7) of developing shoulder pain within the 24  months follow-up period [184]. Additionally, Flex: Ext strength values of 0.71 and 0.72 were fair predictive value for male swimmers in the 24-month follow-up period. All subjects were pain-free during testing [184].

Video Swim Stroke Analysis Along with focused strengthening and stabilization techniques used inside and outside of the pool, poor or abnormal stroke biomechanics are risk factors for developing pain and pathology [24, 185]. Video swim stroke analysis (VSSA) can be a useful tool to provide the swimmer with technique feedback to address current abnormal movement patterns and also reduce future injury risk. Refer to the “Common Stroke Technique Errors” section at the beginning of this chapter for common biomechanical stroke errors that can be improvable with use of video analysis.

Feedback The ability to communicate between coaches and swimmers is inhibited by the aquatic environment. In other sports, coaches and clinicians can easily provide verbal simultaneous feedback to athletes to convey comments/critiques on mechanics and form. However, due to the nature

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of water, both swimmers hearing and vision are diminished which limits coaches’ ability to communicate. Zaton and Szczepan [186] studied the effectiveness of immediate verbal feedback (IVF) in swimmers. The goal was to modify stroke length in freestyle. The authors communicated with the swimmers in the experimental group so the swimmer could hear feedback immediately while swimming. The control group received no feedback at all but understood the goal of the exercise was to lengthen the stroke to improve freestyle speed. The authors utilized two different methods to measure stroke length: [37] the SIMI 2D movement analysis software and [38] the Hay method [187] which describes stroke length as the number of stroke cycles completed within a fixed distance. Between both measurements, the experimental group increased stroke rate between 5 and 7% improving speed and efficiency, while the control group did not create significant change in performance [186]. The authors found that IVF had the ability to correct misperceptions of coach’s information immediately to redirect the swimmer to more desirable swimming mechanics [188, 189] and also increased athlete interest in making these corrections [190]. Therefore, it would benefit coaches to utilize technology to provide more immediate feedback to athletes.

Injury Screening Preseason injury screens use common clinical tools to assess injury risk with the goal of decreasing and preventing athlete injury in season. While swimming is a bilateral overhead sport where both arms are frequently (and ideally) performing symmetrical repetitive movements through symmetrical ranges of motion,

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strength and range of motion normative values in the pain-free athlete are not yet established. For screening purposes, it can be expected that younger athletes will have greater ROM availability (even through high school age) especially in the composite IR and total arc of motion ranges [68]. And again, the dominant arm will likely have greater ER AROM while the nondominant arm will have greater IR AROM [68]. The goals of these screens are to help identify individuals at higher risk for injury allowing targeted treatment to be appropriated to promote healthier, safer, and pain-free performance in sport.

A Proposed Dynamic Warm-Up The Federation Internationale de Football Association (FIFA) has an injury prevention program created to help prevent soccer sports injury. Characteristics of the program include core stability, proprioception, dynamic stability, plyometrics, minimal equipment needed, and less than 15  min to complete. Barengo et  al. [191] performed a systematic review investigating the effectiveness of the use of the FIFA 11+ injury prevention program [191]. From the review, it was found that the FIFA 11+ injury prevention program reduces the injury incidence and improves athlete sport performance. It is recommended that a coach administer the program to ensure athlete “buy-in” and compliance. Additionally, the review concluded that increased compliance frequency improved injury prevention [191]. The authors of this textbook chapter propose a swim-specific version of the FIFA 11+ Injury Prevention Program to decrease injury risk in swimmers. Appendix 1, 2 and 3 [191, 192].

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 ppendix 1: Part 1—Dynamic A Shoulder, Spine, Hip, Knee, and Ankle Warm-Up (all 2 × 15 reps) ([191]; Edelman 2015) Diaphragmatic breathing

Supine

Standing

Start

Finish

Start

Finish

Start

Finish

Start

Finish

Start

Finish

Start

Finish

Start

Finish

Shoulder ER to IR

Scapular squeezes

90/90 abduction to adduction

90/90 ER to IR

Scapular squeezes to streamline

Hip IN and OUTs

Dynamic ankle and knee

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 ppendix 2: Part 2—Strength/ A Plyometric/Balance/Reaction Time Progression [191] Plank progression

TrA activation hold, 2 × 20–30 s

Alt LE lift for 2 s holds, 2 × 40–60 s

Alt LE lift for 20–30 s, 2 × 20–30 s

Side plank hold, 2 × 20–30 s

With hip ABD reps for time, 2 × 20–30 s

With hip ABD reps for time, 2 × 20–30 s

Slowly lower, 1 × 3–5 reps

Slowly lower, 1 × 7–10 reps Slowly lower, 1 × 12–15reps

All three prone, 2 × 15 reps

All three prone with All in quadruped with perturbations, 2 × 30 s each perturbations, 2 × 30 s each side side

No weight 2 × 3–5 repetitions on each side

Water bottle in hand 2 × 3–5 on each side

5 s partner perturbations at each phase, 2 × 3–5

Reaction starts squat jump with 5 s holds, 2 × 5

Split squat jump with 5 s holds 1 × 5 on each side

Relay start squat jump, double leg step with 5 s hold, 2 × 5

Side plank progression

Eccentric hamstring drop progression

T, A, and W’s progression

Turkish get-up progression (see figure # for mechanics)

Reaction jump progression (take your mark, go!)

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 ppendix 3: Part 3—Aquatic A Swimming-Specific Drills ([191]; Edelman 2015) Out of water, streamline with core hallowing 2 × 20 s on, 10 s off

In water streamline from: Block × 1 and wall × 1 2 × max distance with easy swim

Prone sculling, catch 2 × 25 yards

Prone sculling, mid-pull 2 × 25 yards

Supine sculling, finish 2 × 25 yards

Six kick strokes with 180° rotation 2 × 25 yards

Corkscrew swimming, alternating direction by 25 2 × 25 yards

Speed work × 1 fast between walls and flags and ×1 fast between flags 2 × 25 yards

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352 143. Wells GD, Plyley M, Thomas S, Goodman L, Duffin J.  Effects of concurrent inspiratory and expiratory muscle training on respiratory and exercise performance in competitive swimmers. Eur J Appl Physiol. 2005;94:527–40. 144. Kilding AE, Brown S, McConnell AK.  Inspiratory muscle training improves 100 and 200 m swimming performance. Eur J Appl Physiol. 2010;108:505–11. 145. Schagatay E, van Kampen M, Emanuelsson S, Holm B. Effects of physical and apnea training on apneic time and the diving response in humans. Eur J Appl Physiol. 2000;82(3):161–9. 146. Lemaître F, Seifert L, Polin D, Juge J, Tourny-­ Chollet C, Chollet D.  Apnea training effects on swimming coordination. J Strength Cond Res. 2009;23(6):1909–14. 147. Joulia F, Steinberg JG, Faucher M, Jamin T, Ulmer C, Kipson N, Jammes Y.  Breath-hold training of humans reduces oxidative stress and blood acidosis after static and dynamic apnea. Respir Physiol Neurobiol. 2003;137(1):19–27. 148. Joulia F, Steinberg JG, Wolff F, Gavarry O, Jammes Y. Reduced oxidative stress and blood lactic acidosis in trained breath-hold human divers. Respir Physiol Neurobiol. 2002;133(1–2):121–30. 149. Boyd C, Levy A, McProud T, Huang L, Raneses E, Olson C. Centers for Disease Control and Prevention (CDC). Fatal and nonfatal drowning outcomes related to dangerous underwater breath-holding behaviors—New York state, 1988–2011. MMWR Morb Mortal Wkly Rep. 2015;64(19):518–21. 150. Barlow HB, MacIntosh F. Shallow water black-out. Royal naval physiological laboratory report R N P 44/125 UPS 48(a). 151. Lanphier EH.  Breath-hold and ascent blackout. Presented at: the physiology of breath-hold diving. Buffalo, NY: Undersea and Hyperbaric Medical Society Workshop; 1985. p. 28–9. 152. Sergienko S, Kalichman L.  Myofascial origin of shoulder pain: a literature review. J Bodyw Mov Ther. 2015;19(1):91–101. 153. Laudner K, Compton BD, McLoda TA, Walters CM. Acute effects of instrument assisted soft tissue mobilization for improving posterior shoulder range of motion in collegiate baseball players. Int J Sports Phys Ther. 2014;9(1):1–7. 154. Jay K, Sundstrup E, Søndergaard SD, et al. Specific and crossover effects of massage for muscle soreness: randomized controlled trial. Int J Sports Phys Ther. 2014;9(1):82–91. 155. Mohr AR, Long BC, Goad CL. Effect of foam rolling and static stretching on passive hip-flexion range of motion. J Sport Rehabil. 2014;23(4):296–9. 156. Škarabot J, Beardsley C, Štirn I.  Comparing the effects of self-myofascial release with static ­stretching on ankle range-of-motion in adolescent athletes. Int J Sports Phys Ther. 2015;10(2):203–12. 157. Lim EC, Tay MG. Kinesio taping in musculoskeletal pain and disability that lasts for more than 4 weeks: is it time to peel off the tape and throw it out with

K. Wayman et al. the sweat? A systematic review with meta-analysis focused on pain and also methods of tape application. Br J Sports Med. 2015;49(24):1558–66. 158. Dawood RS, Kattabei OM, Nasef SA, et  al. Effectiveness of Kinesio taping versus cervical traction on mechanical neck pain dysfunction. Int J Ther Rehabil Res. 2014;2:1–5. 159. Simsek HH, Balki S, Kekik SS, et al. Does Kinesio taping in addition to exercise therapy improve outcomes in subacromial impingement? A randomized, double-blinded, controlled clinical trial. Acta Orthop Traumatol Turc. 2013;47:104–10. 160. Sallis RE, Jones K, Sunshine S, Smith G, Simon L. Comparing sports injuries in men and women. Int J Sports Med. 2001;22(6):420–3. 161. Butler R, Arms J, Reiman M, Plisky P, Kiesel K, Taylor D, Queen R.  Sex differences in dynamic closed kinetic chain upper quarter function in collegiate swimmers. J Athl Train. 2014;49(4):442–6. 162. Aspenes ST, Karlsen T.  Exercise-training intervention studies in competitive swimming. Sports Med. 2012;42(6):527–43. 163. Gorman PP, Butler RJ, Plisky PJ, Kiesel KB. Upper quarter y balance test: reliability and performance comparison between gender in active adults. J Strength Cond Res. 2012;26(11):3043–8. 164. Roush JR, Kitamura J, Waits MC. Reference values for the closed kinetic chain upper extremity stability test (CKCUEST) for collegiate baseball players. N Am J Sports Phys Ther. 2007;2(3):159–63. 165. Plisky PJ, et  al. Star excursion balance test as a predictor of lower extremity injury in high school basketball players. J Orthop Sports Phys Ther. 2006;36(12):911–9. 166. Vrbanić TS, Ravlić-Gulan J, Gulan G, Matovinović D.  Balance index score as a predictive factor for lower sports results or anterior cruciate ligament knee injuries in Croatian female athletes–preliminary study. Coll Antropol. 2007;31(1):253–8. 167. Sakai S, Koike S, Takeda T, Sengoku Y, Homma M, Takagi H.  Kinetics of four limb joints during kick-start motion in competitive swimming. [published online ahead of print, 2021 Aug 23]. Sports Biomech. 2021:1–19. https://doi.org/10.1080/14763 141.2021.1963465. 168. Girold S, Maurin D, Dugué B, Chatard JC, Millet G.  Effects of dry-land vs. resisted-and assisted-­ sprint exercises on swimming sprint performances. J Strength Cond Res. 2007;21(2):599–605. 169. Gourgoulis V, Antoniou P, Aggeloussis N, Mavridis G, Kasimatis P, Vezos N, Boli A, Mavromatis G. Kinematic characteristics of the stroke and orientation of the hand during front crawl resisted swimming. J Sports Sci. 2010;28(11):1165–73. 170. Barbosa AC, Castro Fde S, Dopsaj M, Cunha SA, Andries O Jr. Acute responses of biomechanical parameters to different sizes of hand paddles in front-­ crawl stroke. J Sports Sci. 2013;31(9):1015–23. 171. McGladrey BW, Hannon JC, Faigenbaum AD, Shultz BB, Shaw JM. High school physical educa-

20  Clinical Application of Swim Stroke Analysis tors’ and sport coaches’ knowledge of resistance training principles and methods. J Strength Cond Res. 2014;28(5):1433–42. 172. Gatta G, Leban B, Paderi M, Padulo J, Migliaccio GM, Pau M. The development of swimming power. Muscles Ligaments Tendons J. 2014;4(4):438–45. 173. Lepley LK, Palmieri-Smith RM.  Cross-education strength and activation after eccentric exercise. J Athl Train. 2014;49(5):582–9. 174. Faude O, Meyer T, Scharhag J, Weins F, Urhausen A, Kindermann W. Volume vs. intensity in the training of competitive swimmers. Int J Sports Med. 2008;29(11):906–12. 175. Kilen A, Larsson TH, Jørgensen M, Johansen L, Jørgensen S, Nordsborg NB.  Effects of 12 weeks high-intensity & reduced-volume training in elite athletes. PLoS One. 2014;9(4):e95025. 176. Laursen PB, Jenkins DG.  The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes. Sports Med. 2002;32(1):53–73. 177. Pugliese L, Porcelli S, Bonato M, Pavei G, La Torre A, Maggioni MA, Bellistri G, Marzorati M. Effects of manipulating volume and intensity training in masters swimmers. Int J Sports Physiol Perform. 2015;10(7):907–12. 178. Sperlich B, Zinner C, Heilemann I, Kjendlie PL, Holmberg HC, Mester J.  High-intensity interval training improves VO(2peak), maximal lactate accumulation, time trial and competition performance in 9-11-year-old swimmers. Eur J Appl Physiol. 2010;110(5):1029–36. 179. Laursen PB.  Training for intense exercise performance: high-intensity or high-volume training? Scand J Med Sci Sports. 2010;20(Suppl 2):1–10. 180. Barroso R, Cardoso RK, do Carmo EC, Tricoli V.  Perceived exertion in coaches and young swimmers with different training experience. Int J Sports Physiol Perform. 2014;9(2):212–6. 181. Barroso R, Salgueiro DF, do Carmo EC, Nakamura FY.  Training volume and repetition distance affect session rating of perceived exertion and internal

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21

Joshua F. Feuerbacher and Moritz Schumann

Physiological and Neuromuscular Determinants of Endurance Performance By definition, endurance performance is multifaceted, varies in distance and duration, and is, thus, related to a variety of physiological and neuromuscular characteristics [1, 2]. Endurance is defined as the ability of an individual to sustain continuous repeated muscle contractions for an extended period of time in order to maintain the highest possible velocity or power [1]. These continuous repeated muscle contractions can last from several minutes to competitions that last between 2 and 8  h [3] or even up to multiple days during ultra-marathon events [4]. In order to sustain muscular power and to account for the constant need of oxygen to convert substrates into energy and, hence, delay the onset of muscle fatigue, athletes are required to maximize their aerobic capacity. An overview on the most important determinants of endurance performance is provided in Fig.  21.1. Among the most important determinants of aerobic capacity is the maximal oxygen consumption (VO2max), which refers to the highest energy demand that can be covered aerobically [5]. It

has been repeatedly illustrated that the VO2max is strongly associated with endurance performance [6] and accordingly numerous studies have targeted the optimization of training regimens in order to increase VO2max [7]. Consequently, well-trained endurance athletes typically have a higher VO2max than sedentary or recreationally active individuals. Additionally, endurance athletes do not merely achieve a greater VO2max but are also able to sustain the time spent at VO2max for longer durations than less trained individuals [8, 9]. The elementary physiological factors that influence the VO2max are collectively embedded within the Fick equation: VO2 = CO × a – v O2 difference, where VO2 is the oxygen consumption, CO is the cardiac output, and a – v O2 difference refers to the arterial–venous oxygen difference. CO, in turn, is the product of stroke volume (SV) and heart rate (HR). Accordingly, improvements in VO2 uptake are related to both enhanced O2 transport via the cardiovascular system and O2 extraction within the muscles. Key factors that drive the O2 transport capacity are the plasma volume, red blood cell volume, absolute hemoglobin mass,

J. F. Feuerbacher · M. Schumann (*) Department of Molecular and Cellular Sports Medicine, Institute of Cardiovascular Research and Sports Medicine, German Sport University, Cologne, Germany e-mail: [email protected]; m.schumann@ dshs-koeln.de © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_21

355

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356 Fig. 21.1 Schematic overview of selected physiological and neuromuscular factors that determine endurance performance

• Ventilation • Perfusion • Diffusion

Pulmonary capacity

Cardiac output

Endurance performance

Oxygen delivery

Skeletal muscle

Neuromuscular capacity

• Stroke volume • Ventricular compliance • Ventricular dimensions

• Red blood cell volume • Total haemoglobin mass • Vascular function

• Mitochondrial volume density and oxidative capacity • Fiber distribution • Capillarisation

• Fibre recruitment • Musculotendinous stiffness • Inter/intermuscular coordination • Morpholigical factors

and stroke volume [10].1 Especially elite endurance athletes often show superior cardiac adaptations, such as an enhanced capacity of ventricular filling that results in an elevated end-diastolic volume [11]. Thus, it seems that the cardiovascular adaptations limit the aerobic capacity and that the adaptations of the O2 extraction are more of a secondary nature that contribute to the improvements in aerobic capacity [10, 12, 13]. Nevertheless, adaptations within the muscle fibers are observed following endurance training as well, and it has been reported that endurance athletes also show a higher mitochondria volume and/or content compared to less trained individuals [14]. Apart from VO2max, the fractional utilization of VO2max and the movement/work economy2 1  For further dissection of the contributors to the VO2max, the reader is referred to a review by Lundby, Montero, and Joyner, Acta Physiol 2017, 220, 218–228. 2  N.B. “economy” and “efficiency” are often used synonymously. Nonetheless, economy refers to the relationship

(often expressed in mL(O2)/min/kg or mL(O2)/ km) have a direct impact on endurance performance [15]. It has been shown that a high fractional utilization of VO2max is a prerequisite for high-level endurance performance, especially when comparing endurance athletes with a homogenous VO2max [9]. Hence, it is apparent that an improved movement economy further aids improvements in endurance performance, since an economization of the movement reduces the need for oxygen at a given velocity/ power and by that improves endurance performance [16–18]. It has been reported that the cost of locomotion in elite runners is significantly lower compared to untrained runners [19]. For this reason, numerous studies have addressed the training-­ induced changes of the movement economy and between oxygen consumption and movement speed/ power, while efficiency circumscribes the ratio between the mechanical energy and the energy cost of exercise (Hackney, 2018).

21  High-Intensity Interval Training and Resistance Training for Endurance Athletes

gross efficiency in order to improve endurance performance [20–22]. Improved movement economy in runners [23] and gross efficiency in cyclist [24] have been associated with the number of type I fibers within the muscle, increasing the ability to generate chemical energy more efficiently than less efficient type II fibers. As a consequence, prolonged endurance training might improve the oxidative capacity through an increased type I fiber content [25–27]. These morphological adaptations are accompanied by increases in capillary/fiber and capillary/area ratios that improve the O2 distribution within the muscle [28]. Another factor that has been associated with elite endurance performance is the increased fat oxidation at a given intensity. Enhanced fat oxidation corresponds to increases in endurance performance [29] since intramyofibrillar glycogen depletion has been linked to excitation–contraction coupling and Ca2+ release from the sarcoplasmic reticulum, affecting muscle contractility and thereby inducing fatigue [30]. Accordingly, the fat oxidation rates in endurance athletes are positively related to mitochondrial volume density, suggesting that increases in mitochondrial content might be a contributing and limiting factor for fat oxidation in endurance trained individuals [31]. In addition to primarily physiological determinants, endurance performance may also be limited or at least compromised by neuromuscular fatigue [32]. Repetitive muscular contractions lead to an increased descending drive [33], elevated ATP demand [34], and a high Ca2+ oscillation [35]. As the duration or intensity of endurance exercise progresses, also the magnitude of neuromuscular fatigue may increase. This is reflected in a reduction of maximal voluntary force, maximal voluntary shortening velocity, or power output [36], all of which is required to sustain muscle contractions for an extended period of time (i.e., see definition of endurance above). Depending on the exercise modality, intensity and duration reductions in the force generating capacity may result in increased metabolic demands, thereby limiting endurance performance [37].

357

Training Principles and Periodization for Endurance Performance Enhancement In order to maximize training adaptations in well-trained and elite athletes and, thereby, improve endurance performance, the manipulation of training intensity, duration, and frequency are key factors in endurance training programming. Endurance training is primarily performed within an intensity of 50–100% of VO2max [38]. Over the past decade, the training intensity distribution (TID) of endurance athletes has been analyzed in depth [39–44]. A common traditional intensity scale to classify training intensities based on physiological parameters is a model that employs three intensity zones [38]. These zones are separated using ventilatory (VT) and/or lactate thresholds (LT). Hence, low-intensity training (LIT) commonly refers to training that is performed below the VT1/LT1, while threshold training or training at moderate intensities (MIT) relates to training between VT1/LT1 and VT2/ LT2, and training above the maximum lactate steady state (MLSS) is classified as high-­intensity training (HIT). The ongoing research on periodization concepts indicates that including HIT to high volumes of LIT (LIT + HIT) elicits superior adaptations compared to LIT only or additional MIT (LIT + MIT). This periodization model is known as polarized training. Polarized training comprises of high volumes of LIT supplemented by HIT, while little to no training is performed in zone 2 [44]. However, this does not mean that training at moderate intensities is not used by successful endurance athletes. For example, cross-country skiers may employ up to 7% in the threshold/MIT zone within their training, while only performing 5% within the HIT zone [45]. This has also been observed in elite rowers [46] and cyclist [47], who performed up to 15–20% of the training in zone 2. This type of periodization is known as pyramidal periodization, where most of the training is performed in zone 1 and a decreasing proportion of training in zones 2 and 3. In practice, training intensities are monitored using heart rate, velocity/power, and/or ratings of

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358

perceived exertion (RPE) which are then translated into respective training zones using several different methods (e.g., time in zone, session goal3) [48]. Accordingly, the TID varies depending on the method used, and methodological inconsistencies yield dissimilar results, making comparisons difficult. Beside these obvious limitations, in the past it was shown that the TID of endurance athletes seems to favor high volumes of LIT (80%) complemented by training at higher intensities (20%) around and above the lactate threshold [38]. However, current evidence on this topic is largely inconsistent and suggests that optimal TID cannot be summarized simplified by an “80/20 scheme.” It much rather appears that the optimal TID is dependent on various factors, such as type of sport, training status as well as length of competition, and, therefore, the metabolic demands, raising the question of whether there is an optimal TID at all [44]. Elite cross-country skiers and biathletes, for example, performed 90% of endurance training in zone 1 and 10% of the training in zones 2 and 3, while the general training intensity was increased from the preparation phase to the competition phase [49]. The training characteristics of the world’s most successful female cross-­ country skier indicated a similar TID [50]. Here, the overall endurance training time consisted of 92.3% LIT, 2.9% MIT, and 4.8% HIT.  Interestingly, evidence can be found for both approaches. A recently published study showed that while there were no differences in the adaptations between low- and moderate-­ intensity training, the number of athletes with large performance improvements (i.e. high responders)  was higher in the high-intensity group [51]. However, there seems to be discrepancies between retrospective TID used as “best practice” by athletes compared to controlled studies. Interestingly, recently it was also shown that high-intensity training of a much shorter duration

(i.e., speed or sprint interval training [SIT]) may be an effective way of improving endurance performance [52]. These HIT approaches refer to an intensity above the maximal aerobic velocity/ power (e.g., >120% vVO2max), translating into short all-out performances with durations of 1, whereas SIT comprises of all-out performances between 15 and 30 seconds with a work-to-rest ratio of 90% VO2max being a good predictor of a successful training stimulus [78]. One of the first studies that analyzed the interplay between interval duration and intensity of work and relief intervals was a study performed by Seiler and Sjursen [79]. In this study, 12 well-­ trained runners performed several self-paced interval sessions consisting of 24  ×  1, 12  ×  2, 6  ×  4, or 4  ×  6-min running bouts with a 1:1 work-to-rest (e.g., 1-min work vs. 1-min rest) interval, accumulating to a total session duration of 48 min. The authors showed that blood lactate and rate of perceived exertion (RPE) throughout each session were identical, but 6 out of 12 athletes reached their highest VO2 during the 4-min intervals. Therefore, the authors concluded that 3–5  min might be an optimal load to improve physiological adaptations to HIT.  Several years later, however, Seiler and colleagues [80] compared 4 × 4 min, 4 × 8 min, and 4 × 16 min effort-­ matched intervals showing that 4 × 8 min yielded the greatest improvements, indicating that the relationship between work intensity and duration mediates physiological adaptations and that the adaptations to interval training are highly individual. It has been shown that not only longer continuous intervals but also shorter intermittent exercises lead to a maximized time spent near VO2max [77]. In a study performed by Billat and colleagues [81], intermittent runs of 30 s alternating between 100% and 50% vVO2max were found to maximize time at VO2max compared to continuous running between threshold velocity and vVO2max. However, within the same study, it was shown that responses to the training stimulus were highly individual. However, for both long and shorter intervals, a work intensity of 100% and a relief intensity of 50–60% of vVO2max were found to be optimal for maximizing time at VO2max with 2:1 and 1:1 being the most frequent ratios of work and relief intervals [78]. The importance of work interval duration has been further investigated by Rønnestad and

J. F. Feuerbacher and M. Schumann

Hansen [82]. They compared short intervals of 30 s with a rest period of 15 s to longer intervals (approximately 3–5 min) and showed that shorter intervals allowed the athletes to perform longer periods above >90% VO2max and >  90% HR. Furthermore, 30-s work intervals induced a longer time  ≥  90% of peak stroke volume. However, the intensities in this study were fixed and were set at the minimal power that elicits VO2max. In a “follow-up” study, Rønnestad and colleagues [83] aimed to investigate the adaptations of effort-matched short intervals compared to longer intervals in a 10-week training study using well-trained cyclists. While the shortinterval group performed 3 series of 13 x 30-s work intervals with 15s recovery (total work per series: 9.5 min), the long-interval group completed 4 × 5 min interspersed by 2.5 min recovery. Hence, the total time in the work interval was 19.5 and 20 min for the short and long intervals, respectively. The authors showed that the athletes in the short intervals had a larger increase in VO2max and tended to show greater improvements in power output at 4 mmol/L [La−] compared to the long-interval group. They concluded that the 2:1 work-to-rest ratio and the total work of each set (9.5  min) seem to be predominant factors that might improve performance, whereas comparable studies failed to show increases in performance after 4 [56, 84] or 8 weeks [65] of training. In the study performed by Stepto et al. [56], 30-s work intervals were used as well with an intensity of 175% of power at VO2max. These intervals were, however, interspersed with 4.5 min of rest, while another group performed 4  min of work with 1.5  min of recovery and showed this to be more effective. These effects might be explained by the unfavorable work-torest ratio in the short-­interval group (i.e., 1:9), which is more comparable to  SIT.  It has been shown that in longer recovery periods, the VO2 drops to a greater extent compared to shorter recovery periods (e.g., 4.5 min vs. 15 s). Where the VO2 remains almost unchanged. Accordingly, it is possible to perform the exercise for an extended period at the desired intensity [82]. In general, it can be speculated that a longer time under tension might compensate for the lower

21  High-Intensity Interval Training and Resistance Training for Endurance Athletes

intensity in the HIIT session (when compared to SIT), so that stimuli on both the cardiovascular system and the local muscle oxygen potential can be optimized [83]. This was supported by another study in elite cyclists (VO2max 73 ± 4 mL min−1 kg−1) performing effort-­matched short and long intervals of the same configuration, showing greater improvements in peak aerobic power output and mean power output during a 20-min test in favor of the short-­interval group [85]. In addition, it has been shown that short intervals lead to longer exercise post-­ oxygen consumption that might further result in an ameliorated stimulus after short intervals [55]. Another way to modify longer intervals and therefore optimize the time  >90%  VO2max  is to incorporate a fast start. Eleven well-trained cross-­ country skiers performed either the traditional 5 × 5 protocol, or each 5-min interval was optimized by 1.5  min of 100% maximal aerobic speed, followed by 3.5 min at 85%. Interestingly, the optimization of the intervals led to an elevated mean oxygen uptake accompanied by a lower RPE [86]. This has been also shown by kayakers performing either traditional HIIT or HIIT using an all-out start [87]. Thus, implementing intervals using a fast start improves VO2 kinetics and enhances mean oxygen uptake. In addition to acute variables that can be manipulated with HIT, also the arrangement of HIT sessions over a micro- or mesocycle can be modified. Most commonly, studies have looked at block periodization approaches which were initially introduced to focus on improving distinct abilities, while others are maintained [88]. In endurance athletes, block periodization of HIT has been shown to improve performance more effectively than a traditional approach [89, 90]. In a traditional approach, HIIT sessions are equally distributed across a cycle (e.g., 4 weeks), whereas in a block periodization, key sessions are grouped within a shorter cycle (e.g., 1 week), followed by sessions that are conducted to preserve the previously elicited adaptations the remaining weeks. In a study by Rønnestad and colleagues [91], well-trained cyclist performed either 12 weeks of traditional (two sessions per week for 4 weeks) or block periodization (five sessions in the first

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week, followed by one weekly session during the subsequent 3 weeks). The results after the intervention period indicated improvements in VO2max and a tendency towards superior increases in power output at 2 mmol/L [La−] in favor of the block periodization. These findings were supported by a recently published meta-analysis revealing favorable effects for VO2max and maximal aerobic power following training organized in a block periodization. Below we provide a short list of key recommendations that should be considered during HIIT programming: –– HIT intervals should comprise of four to six sets of 4–8  min of training in the HIT zone (preferably near or at VO2max). –– A work-to-rest ratio of 2:1 is preferred, with work intensities of 90% and relief intensities of 50–60% of power/velocity at VO2max. –– Total work length should be 16–30 min (e.g., four times, 4 min; six times, 5 min). –– Short intervals offer a sound alternative to long intervals (e.g., 3 sets of 13 times 30/15 s with 3-min rest after each set) compared to long intervals. –– We recommend using different configurations of intervals in order to maximize the training stimulus. A progression in intensity to an event is recommended (e.g., long to short, progression in work-interval volume). –– Block periodization may be used to increase the HIT stimulus, although coaches and athletes should be cautious to avoid possible overtraining. We therefore recommend this type of programming only in well-trained athletes.

Effects of Strength Training on Endurance Performance The previous section clearly outlined the achievements that can be expected by programming endurance training sessions. Whether strength training incorporated into the training routine of endurance athletes also affects endurance performance has long been a matter of debate. In a textbook entitled Peak Performance published

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around 2000, the authors highlighted that modern training studies at that time did not support the use of strength training to improve performance of highly trained athletes [92]. While it is indisputable that untrained individuals will eventually improve especially short-term endurance performance irrespective of the type of training [93], it remained unknown at that time whether improvements in neuromuscular performance will lead to improved endurance performance in well-trained endurance athletes. However, already ~10 years later, the first indications were provided for strength training-induced improvements in endurance performance, especially in performances that require fast-twitch fiber recruitment [94]. The first substantial evidence for associations of strength training-induced improvements in neuromuscular function and indices of endurance performance originating from controlled studies was provided in 1999 [95, 96]. In a Finnish study, it was shown that 5000 m running performance as well as running economy and the maximal anaerobic running velocity improved to a larger extent when 30% of the endurance training volume were replaced by explosive strength exercises (such as 20–100  m sprints; countermovement, hurdle, and drop jumps; as well as leg press and knee extensor/flexor exercise with low load and high velocity) for a duration of 9 weeks. These superior changes in running performance were independent of changes in VO2max but accompanied by a significant reduction in ground contact times, hinting towards a link between changes in neuromuscular characteristics and running performance. To date, numerous review papers have summarized an abundance of positive effects of strength training for selected performance determinants of endurance runners [97–103], swimmers [104, 105], and cyclists [98, 106] of any level. These beneficial effects of strength training typically occur independent of changes in the VO2max but may be mediated by changes in exercise economy, maximal work capacity, and/or delayed fatigue [98]. However, the magnitude by which strength training aids development of endurance performance depends on a majority of factors such as the type of sport, the competiti-

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tion duration and format, as well as the strength training experience of the athletes. For example, while the beneficial effects of strength training have been well documented for endurance running and cycling and evidence in swimming is emerging especially over the past few years, rather controversial data are available for cross-­ country skiing [107]. Interestingly, looking at skiing performance, it appears that large effects were especially present for studies that were published between 1999 and 2002 using double-­ poling ergometer tests, while the majority of more recent studies has actually shown these effects to be marginal when testing more specific and technically demanding movements, such as roller skiing outdoors [107]. On the one hand, these findings imply that the effects of sole strength capacities may actually not translate easily into sport-specific settings. On the other hand, during the time these early studies were published, strength training may have not been an integral part of the regular training routine of most cross-country skiers, leading to large effects when a novel training stimulus was added. Since strength training gained popularity in cross-­ country skiing throughout the past two decades also due to the introduction of new competition formats (e.g., sprint races), significant effects in scientific settings are more difficult to observe since athletes involved in these studies will already be strength training-experienced. These findings not only highlight the need for long-term implementation of strength training but also imply that the absolute measurable performance effects induced by strength training may be the largest in novice athletes. A schematic overview on the endurance performance determinants that may be affected by distinct strength training programs is presented in Fig.  21.2. According to previous research, endurance performance may generally be enhanced through factors such as an improved neuromuscular efficiency [98], induced by increased maximal strength [109] and an increased muscle–tendon stiffness [110–112], a delayed recruitment of type II muscle fibers [113], a fiber shift from type IIx fibers to more efficient type IIa fibers [114], and improvements in the rate of force develop-

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Endurance performance

Energy availability

Exercise economy

Performance VO2

Anaerobic capacity

VO2max

Ground contact times

Utilization of the SS Cycle

PO of type I fibers

RFD

Type llx

Type lla

Explosive strength & plyometric training

Fractional utilization of VO2max

Peak force earlier during contraction

Maximal strength

Mitochondria sharing PO

Muscle mass for shared PO

Mitochondrial content

Heavy & Maximal strength training

Fig. 21.2  Flowchart highlighting the effects by which different types of strength training affect endurance performance. Explosive strength training improves the rate of force development that, in turn, will help to achieve peak force earlier during a given movement or stroke, leading to a longer relaxation phase and consequently improved performance capacity. Plyometric training improves the utilization of the stretch-shortening cycling, leading to a reduction in ground contact times during running and ultimately an improved exercise economy. Heavy and maximal strength training may improve exercise economy

through an increased power output of type I fibers as well as a shift from type IIx to type IIa fibers. In addition, maximal strength training may improve the muscle mass shared to sustain a given power output, thereby increasing the fractional utilization of VO2max. Increased muscle mass may also directly affect anaerobic capacity. Figure and descriptions are modified from [108]. Dashed boxes indicate theoretical effects. PO, power output; RFD, rate of force development; SS, stretch shortening; VO2max, maximal oxygen consumption; ↔ indicate no effect; ↑ indicate increases; ↓ indicate reductions

ment [95]. Moreover, increases in muscle mass have been associated with an improved fractional utilization of VO2max in female cyclists [115]. Very recently, links were also made between changes in pennation angle and fascicle length along with variations in the training load of both aerobic and strength training in elite rowers, highlighting that other factors may account for improved endurance performance as well [116]. However, as this specific study was not designed to specifically assess the morphological effects of combined strength and endurance training versus endurance training alone, future studies should urgently aim at elucidating further mechanisms that may underlie improved endurance performance following strength training. Notably, the type of strength training required will depend on the type of sport as well as the exercise mode and performance determinant that

should be improved. As such, improvements in maximal strength and to certain extent in muscle mass should be a target for cyclists [108], while endurance runners may benefit from a mix of maximal and explosive and/or plyometric type of strength training due to a larger utilization of the stretch-shortening cycle during running [99, 117]. However, the choice of strength training becomes even more complex for swimmers where maximal and explosive strength training will primarily target start and to a certain extent also turn performance, while the scientific evidence for strength training-induced effects on the free-swimming phase remains scarce [118]. In this context, we showed a strong correlation between improvements in lower (i.e., squat performance) but not upper body (i.e., bench press) strength performance and the 400  m swimming time as well as the swim speed at a fixed blood

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lactate concentration of 4 mmol/L in well-trained adolescent swimmers [119]. Importantly, these findings were independent of whether heavy or combined maximal and explosive strength training was performed, indicating that especially in adolescent athletes improving maximal strength is important irrespective of how this is achieved. In this context, it was interesting to note that it was actually the lower body strength training that was associated with improved swimming performance, even though the role of the upper body appears to be more significant for front crawling performance [120]. However, the swimmers included in this study were initially much stronger in the upper compared to the lower body, allowing for a larger potential for improvements through lower body squat training. This finding also underlines the importance of training experience when assessing the absolute effects of strength training interventions in endurance athletes. Interestingly, while strength training has indeed been shown to increase both leg and vertical stiffness in recreational endurance runners, no changes were observed in running kinematics [121]. Similarly, in a recent meta-analysis including 25 studies with endurance runners at any level, it was concluded that strength training may improve the force-generating capacities of the muscles associated with forward locomotion (i.e., ankle plantar flexors, quadriceps, hamstrings, and gluteal muscles), but no evidence was found for these effects being transferred into running [102]. However, while the reasons for this may be manifold, it needs to be acknowledged that these findings may largely be related to a paucity in data available to directly assess the effects of strength training on both running mechanics and indicators of running performance. This relates especially to stride parameters such as stride length, stride frequency, and ground contact times, which were assessed by only very few studies [96, 122, 123]. In this context, it is also  important to mention that even though Paavolainen and colleagues [96] indeed showed reductions in ground contact times concomitantly with changes in running performance, in this study no mediation analysis was per-

J. F. Feuerbacher and M. Schumann

formed, and this study was not included in the aforementioned  meta-analysis due to a lack of reporting. Thus, while it was shown that strength training does superiorly affect endurance performance (or at least determinants associated with endurance performance) of distance runners, to date  the mechanisms underlying these effects remain unclear. Besides beneficial adaptations, also possible adverse effects of strength training need to be considered. Among the biggest concerns typically brought up by athletes and coaches alike is the fear of gaining excessive body (muscle) mass that may especially be disadvantageous in weight-bearing disciplines, such as running and cross-country skiing. However, changes in muscle hypertrophy in endurance athletes performing a much higher endurance compared to the strength training volume are typically expected to be small (i.e., ~3–6%) over a period of 12 weeks [107, 114, 124]. Moreover, at least in strength-­ trained athletes it was nicely shown that the changes in limb girth are related the overall endurance training volume, being as low as 1% after 6 weeks of training with three weekly endurance training sessions as compared to ~2% after only one concomitant endurance training session for the same muscle group [125]. Thus, muscle mass may be well controlled if hypertrophic strength training is performed for muscles that are also included in the sport-specific movement, and may be preferred over hypertrophic training targeting non-functional muscle groups [126]. In addition to muscle mass, concerns have also been raised as to whether strength training may impair cardiovascular adaptations, such as exercise economy and VO2max, but to date there is no evidence for such maladaptation in top athletes [114]. Moreover, rather mechanistically driven studies have failed to show impaired oxidative enzyme activities after periods of strength training in endurance athletes [94, 127]. However, from a programming point of view, blunted shortor long-term performance may theoretically arise from residual fatigue induced by strength and endurance sessions that are performed in close proximity. In a recent review [37], possible causes for what was called sub-optimal endur-

21  High-Intensity Interval Training and Resistance Training for Endurance Athletes

ance development may be induced by prior strength training through (a) acutely impaired neural recruitment patterns; (b) acutely reduced movement efficiency due to alteration in kinematics during endurance exercise and an increased energy expenditure; (c) acutely increased muscle soreness; and (d) acutely reduced muscle glycogen. In this review, assumptions were also made that endurance training sessions that are consistently compromised due to residual fatigue will eventually hinder optimal long-term adaptations. However, while indeed a number of studies have shown short-term impaired endurance performance and/or exercise economy following single sessions [128, 129] or microcycles with repeated strength and endurance training sessions [130], these short-term impairments do not translate into compromised long-term adaptations, with literally no study showing impaired endurance performance following the inclusion of supplemental strength training. Consequently, the worst-case athletes and coaches can expect by implementing regular strength training are improvements in endurance performance that are similar to sole endurance training but additional improvements in force generating capacities [131] that may be advantageous at a later point in time (e.g., in terms of injury prevention [132]).

Considerations for Strength Training Programming In order to avoid carryover effects of subsequent strength and endurance training sessions and to optimize long-term adaptations, strength training programming requires careful consideration. Since endurance athletes and coaches are typically concerned about possible endurance performance-­ related maladaptation originating from strength training, naturally much attention is given to the optimized scheduling of endurance training sessions. However, inferentially this bears the risk that less priority is given to strength training sessions and, consequently, the full potential of the strength training program may not be utilized. This is especially true, since high

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volumes of endurance training have previously been shown to impair indices of strength performance. In a recent meta-analysis, we provided convincing evidence that especially explosive strength development will be compromised when concomitantly performing both endurance and strength training [133]. Since this may be the case even with an already very low training volume (i.e., two weekly endurance and strength training sessions) [134] but at the same time explosive strength development may be required, e.g., for endurance runners and swimmers, coming up with training programs that account for these interferences is indispensable. Importantly, the aim of incorporating strength training into the endurance training routine would rarely be to achieve similar absolute improvements in neuromuscular performance as strength athletes. In this sense, accepting muscular interference induced by high endurance training volumes may to some extent be acceptable but, e.g., well-trained cyclists commencing with heavy strength training twice weekly for 8–12  weeks can still expect improvements in maximal strength of ~25% [135]. However, the aim of training programming should be to incorporate phases of prioritized training based on specific aims. For example, in recreational endurance runners, we have previously shown that the neuromuscular adaptations as reflected by maximal strength, muscle cross-sectional area, electromyography, and voluntary activation of the lower limbs were maintained (but not improved!) over a period of 24  weeks when the strength training performed twice weekly was carried out always immediately after an exhausting endurance training session [127, 136]. Moreover, endurance performance assessed by 1000 m all-out performance during an incremental 6 × 1000 m field test was similarly improved as after endurance training alone. Thus, the strength training did not induce any apparent or desired effects on the performance of these athletes, and the resources invested in this could likely have been used for improving other capacities. It appears that strength training programming is an integral part of the training prescription and performing strength training in a fatigued stated

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should be avoided. However, short-term studies in individuals that were not specifically trained for endurance have also shown that explosive [137, 138] but not maximal strength development [139] is impaired when endurance training is performed immediately after a plyometric strength training session. Since this effect is likely to depend on endurance training intensity and/or volume, it is advisable to separate strenuous endurance (i.e., high-intensity and prolonged continuous low-intensity training) and strength training sessions whenever possible. In order to avoid interference, fatigue between subsequent endurance and strength training sessions should be monitored, and load adjustments should be made whenever acute performance decrements are observed. Unfortunately, studies specifically addressing strength training periodization in well-trained or elite endurance athletes are scarce. Early recommendations for strength training periodization were provided in a review published in 2014 [98]. According to these guidelines, maximal strength development of important muscles (i.e., ideally those that are recruited throughout the sport-­ specific movement) should be targeted during the preparatory period, performing two weekly sessions. Since muscle fibers are recruited based on the size principle [140] and especially low-­ intensity endurance training primarily recruits low-threshold motor units including mainly type I fibers, loads between 4–10 RM are typically sufficient and may be performed in linear (novice athletes) or undulating (strength training experienced athletes) programs. Since maximal strength is considered a prerequisite for explosive strength development [141], focusing on maximal strength development will ultimately improve explosive strength performance as well. However, endurance runners are advised to add additional plyometric training, such as countermovement, hurdle, and drop jumps. During the competition period, the strength training frequency may be reduced to one weekly session without compromising overall endurance and strength performance [142]. Importantly, however,  ceasing strength training entirely will induce rapid decre-

J. F. Feuerbacher and M. Schumann

ments in strength performance back to pre-­ training levels both after 6 weeks in recreational endurance runners [143] and 8  weeks in well-­ trained cyclists [144] and should be avoided. Much rather should strength training be incorporated into the weekly training routine and periodized throughout the year. In that sense blocks with a specific focus on strength vs. endurance capacities could help to develop both endurance and strength simultaneously. We have provided detailed recommendations for scheduling strength and endurance training sessions in a recent review paper [145]. This paper also provides a set of flowcharts that can be applied to athletic training settings. To summarize the current evidence and to provide ready-to-­ use recommendations, below we provide a short list of key factors that should be considered during strength training programming: –– Focus on sport-specific muscle groups and avoid excessive training of nonfunctional muscles (especially if body mass is of concern). –– Maximal and explosive strength training should be considered supplementary to other training routines, including also core stability training. –– Whenever possible, focus on an anticipated maximal movement velocity throughout the concentric phase. Currently no data exist for the effects of accentuated eccentric training in endurance athletes. –– Use heavy weights of 4–10 RM with two to three sets and 2–3  min recovery; maximal weights (i.e., 1RM) are not ultimately necessary and may increase the risk of injuries. –– For novice athletes, allow for a preparatory period with reduced endurance training volume and/or intensity in which the focus is on learning the correct technique. –– Beware that especially during the early phases of the strength training muscle soreness may hinder the performance of strenuous endurance training sessions. This should be accounted for with reduced endurance training volume and/or intensity. –– For novice athletes, apply a linear periodization progressing from light to heavy loads; for

21  High-Intensity Interval Training and Resistance Training for Endurance Athletes

experienced athletes, incorporate a daily undulating periodization. –– Whenever possible, separate endurance and strength training sessions. Otherwise, reduce the intensity and/or volume depending on the focus of this specific session. –– For strength maintenance, one session every 7–10  days is sufficient for durations of 6–8  weeks  (i.e. throughout the competition period). Thereafter, increase the strength training volume again.

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372 omy in recreational marathon runners. J Strength Cond Res. 2010;24:2770–8. https://doi.org/10.1519/ JSC.0b013e3181d64e9c. 123. Saunders PU, Telford RD, Pyne DB, et  al. Short-­ term plyometric training improves running economy in highly trained middle and long distance runners. J Strength Cond Res. 2006;20:947–54. https://doi. org/10.1519/R-­18235.1. 124. Schumann M, Pelttari P, Doma K, et  al. Neuromuscular adaptations to same-session combined endurance and strength training in recreational endurance runners. Int J Sports Med. 2016;37:1136– 43. https://doi.org/10.1055/s-­0042-­112592. 125. Jones TW, Howatson G, Russell M, French DN. Performance and neuromuscular adaptations following differing ratios of concurrent strength and endurance training. J Strength Cond Res. 2013;27(12):3342–51. https://doi.org/10.1519/ JSC.0b013e3181b2cf39. PMID: 24270456. 126. Sandbakk Ø. Long-term effects of strength training on aerobic capacity and endurance performance. In: Concurrent Aerobic and Strength Training; 2019. p. 325–31. 127. Bishop D, Jenkins DG, Mackinnon LT, et  al. The effects of strength training on endurance performance and muscle characteristics. Med Sci Sports Exerc. 1999;31:886–91. https://doi. org/10.1097/00005768-­199906000-­00018. 128. Doma K, Deakin GB. The acute effects intensity and volume of strength training on running performance. Eur J Sport Sci. 2014;14:107–15. https://doi.org/10. 1080/17461391.2012.726653. 129. Palmer CD, Sleivert GG.  Running economy is impaired following a single bout of resistance exercise. J Sci Med Sport. 2001;4:447–59. https://doi. org/10.1016/s1440-­2440(01)80053-­0. 130. Doma K, Deakin G. The acute effect of concurrent training on running performance over 6 days. Res Q Exerc Sport. 2015;86:387–96. https://doi.org/10.108 0/02701367.2015.1053104. 131. Ache-Dias J, Dellagrana RA, Teixeira AS, et  al. Effect of jumping interval training on neuromuscular and physiological parameters: a randomized controlled study. Appl Physiol Nutr Metab = Physiol Appl. Nutr Metab. 2016;41:20–5. https:// doi.org/10.1139/apnm-­2015-­0368. 132. Lauersen JB, Bertelsen DM, Andersen LB.  The effectiveness of exercise interventions to prevent sports injuries: a systematic review and meta-­ analysis of randomised controlled trials. Br J Sports Med. 2014;48:871–7. https://doi.org/10.1136/ bjsports-­2013-­092538. 133. Schumann M, Feuerbacher JF, Sünkeler M, et  al. An updated systematic review and meta-analysis on the compatibility of concurrent aerobic and strength training for skeletal muscle size and function. Preprint. 2021. 134. Häkkinen K, Alen M, Kraemer WJ, et  al. Neuromuscular adaptations during concurrent

J. F. Feuerbacher and M. Schumann strength and endurance training versus strength training. Eur J Appl Physiol. 2003;89:42–52. https:// doi.org/10.1007/s00421-­002-­0751-­9. 135. Rønnestad BR.  Strength Training for Endurance Cyclists. In: Concurrent Aerobic and Strength Training. Cham: Springer International Publishing; 2019. p. 333–40. 136. Schumann M, Mykkänen O-P, Doma K, et al. Effects of endurance training only versus same-session combined endurance and strength training on physical performance and serum hormone concentrations in recreational endurance runners. Appl Physiol Nutr Metab = Physiol Appl Nutr Metab. 2015;40:28–36. https://doi.org/10.1139/apnm-­2014-­0262. 137. Spiliopoulou P, Zaras N, Methenitis S, et al. Effect of concurrent power training and high-intensity interval cycling on muscle morphology and performance. J Strength Cond Res. 2021;35:2464–71. https://doi. org/10.1519/JSC.0000000000003172. 138. Terzis G, Spengos K, Methenitis S, et  al. Early phase interference between low-intensity running and power training in moderately trained females. Eur J Appl Physiol. 2016;116:1063–73. https://doi. org/10.1007/s00421-­016-­3369-­z. 139. Tsitkanou S, Spengos K, Stasinaki AN, et al. Effects of high-intensity interval cycling performed after resistance training on muscle strength and hypertrophy. Scand J Med Sci Sports. 2017;27(11):1317–27. https://doi.org/10.1111/sms.12751. 140. Henneman E.  The size-principle: a deterministic output emerges from a set of probabilistic connections. J Exp Biol. 1985;115:105–12. https://doi. org/10.1242/jeb.115.1.105. 141. Cormie P, McGuigan MR, Newton RU.  Influence of strength on magnitude and mechanisms of adaptation to power training. Med Sci Sports Exerc. 2010;42:1566–81. https://doi.org/10.1249/ MSS.0b013e3181cf818d. 142. Rønnestad BR, Hansen EA, Raastad T.  In-season strength maintenance training increases well-­ trained cyclists’ performance. Eur J Appl Physiol. 2010;110:1269–82. https://doi.org/10.1007/ s00421-­010-­1622-­4. 143. Karsten B, Larumb-Zabala E, Kandemir G, et  al. The effects of a 6-week strength training on critical velocity, anaerobic running distance, 30-M sprint and Yo-Yo intermittent running test performances in male soccer players. PLoS One. 2016;11(3):e0151448. https://doi.org/10.1371/journal.pone.0151448. 144. Rønnestad BR, Hansen J, Hollan I, et al. Impairment of Performance Variables After In-Season Strength-­ Training Cessation in Elite Cyclists. Int J Sports Physiol Perform. 2016;11:727–35. https://doi. org/10.1123/ijspp.2015-­0372. 145. Doma K, Deakin GB, Schumann M, Bentley DJ.  Training considerations for optimising endurance development: an alternate concurrent training perspective. Sports Med. 2019;49:669–82.

Mental Skills Training for Endurance Sports

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Jennifer E. Carter and Joshua L. Norman

Introduction

country skier battling icy wind, a cyclist trying to avoid a crash while flying down a steep decline, Ask athletes the percentage of sport performance or a runner trudging through mile 20 of a marathat is mental and they will often give estimates thon. Endurance sports often present such stressaround 75%. Next, ask what percentage of their ful, demanding conditions, and athletes who are training is mental. Zero is the common response. mentally prepared will be the ones to thrive. While sport psychologists and psychiatrists do Mental skills training has positive effects on not advocate for athletes to substitute a 50-mile endurance sport performance, according to one bike ride with a 3-h imagery session, we do rec- literature review [2]. In particular, goal setting, ommend supplementing physical training with self-talk, focus, and imagery show consistent mental training. Sport psychologists assist ath- effectiveness for mental toughness and endurletes with mental health and mental skills train- ance sport performance [3]. More research is ing to improve their sport performance and needed to learn how and for whom these mental recovery from injury. In addition to mental skills skills work. training, sports psychiatrists assist athletes with Mental training interventions occur individuthe medical management of mental health condi- ally or in packages. Individually, mental skills tions often through psychotropic medications. In include motivation, goal setting, arousal or this chapter, we focus on mental skills training energy management, self-talk, focus, imagery, for endurance sports and considerations regard- routines, mindfulness, and team building. Sport ing the medical management of mental health psychologists commonly teach several mental conditions within athletes. skills in combination, and packages including Mental skills training can “…enhance ath- goal setting, energy management, imagery, and letes’ chances of performing at their highest level self-talk have improved triathlon performance [4] under very demanding, stressful, and sometimes and 1600 meter running performance [5]. even hostile conditions” [1]. Imagine a cross-­ Get ready to psych up for endurance sports! Because it takes inordinate discipline to excel as an endurance athlete, we start with a discussion about motivation. Then we dive into specific mental skills to train your mind as well as your J. E. Carter (*) ·J. L. Norman body. We finish the chapter with a discussion of Psychiatry and Behavioral Health, Jameson Crane Sports Medicine Institute, Ohio State University finding balance in exercise and a review of mediWexner Medical Center, Columbus, OH, USA cation considerations for athletes. Here is the e-mail: [email protected]; order of topics in this chapter: [email protected] © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_22

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Motivation Goal setting Energy management Self-talk Focus Imagery Performance routines Mindfulness Exercise balance Medication considerations

Motivation Motivation is likely one of the most important psychological constructs in sport, especially within endurance sport. The ongoing energy required for endurance athletes to persist in repetitive high-quality, grueling training sessions, even in the face of adversity and other life demands, exemplifies motivation as a foundational requirement for high performance and achievement. As such, it is no surprise that trainers, coaches, organizations, and athletes alike all have vested interest in understanding, developing, and maintaining motivation. Motivation is a crucial factor in human behavior because it influences the initiation, direction, intensity, and persistence of specific goal-directed behavior [6]. Self-determination theory (SDT) focuses on the strength of athletes’ motivation to perform and has been increasingly applied to sport [7]. SDT focuses on the factors that influence athletes’ decisions to perform and persist in sport. One such factor is the goals or motives that athletes cite for engaging in their sport [7]. Specifically, a distinction is made between intrinsic (i.e., establishing meaningful relationships, feeling a sense of community, gaining knowledge, finding stimulation, and achieving personal growth) and extrinsic goals or motives (i.e., winning, seeking fame, obtaining an appealing appearance, and achieving financial success) [6]. Within self-determination theory, goal type has implications for personal and relational functioning. Intrinsic goals focus on developing personal interests, values, and potential and are inherently satisfying to pursue [7]. According to

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SDT, the pursuit of intrinsic goals will lead to both sustained engagement in the behavior and more positive psychological outcomes (e.g., well-being, self-esteem) [8]. In contrast, extrinsic goals are more outwardly oriented, directed towards external indicators of worth, leading to the less inherent satisfaction and human development [8]. While the desire to win to prove something to others can be motivating, athletes must be careful in their utilization of extrinsic motives for they may undermine the development of intrinsic motivation. Relying solely on extrinsic motives might limit the ability for endurance athletes to sustain training requirements for the long haul and decrease their enjoyment of the process. Strategies for increasing intrinsic motivation include preparation, positive reinforcement, variety in training, building on past success, and athlete contribution to training [9]. Adequate preparation is essential for endurance athletes. Slowly progressing through a training protocol will be more motivating than going for a long distance without sufficient training. Rewards that are contingent with performance can be beneficial, whether those originate from the athlete or others. For example, Bill has been gunning for a particular pace on a training run, and once he reaches it, he rewards himself with his favorite meal. Motivational self-talk has also been shown to improve performance in whole body endurance activity [2]. Further, verbal and nonverbal praise from athletes and coaches can provide positive feedback that helps increase motivation. Mixing up the training process by varying drill sequences or activity days can keep training stimulating and more motivating. Successful experiences increase perceived intrinsic ability and strengthen personal competence. For example, athletes experience success by setting small goals and reaching them. Finally, allowing athletes to have a say in training or other decisions can increase autonomy and intrinsic motivation. Understanding the need for increasing and maintaining higher motivation levels is critical for athletic success in endurance sport. Appropriately tapping into intrinsic and extrinsic motivation is essential to developing this performance fuel.

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Goal Setting

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Within endurance sport, goal setting has been shown to improve performance. In particular, A goal is a target, specific standard, or accom- using goals helped high school runners improve plishment that one strives to attain, usually within their 2.3 km times and non-athletes cycle for lona specified period [10]. Goal setting has been ger durations during an incremental test [2]. shown to consistently facilitate sport perfor- Further, in a gymnasium sprint triathlon, outmance [11]. Objective goals are those that are come, performance, and process goals all posimeasurable, such as “I want to run a half-­ tively impacted race day performance [4]. These marathon in under 2 hours” [12]. Subjective endurance sport data, combined with many years goals, on the other hand, are more general state- of goal setting research in other sport performents of intent, such as wanting to do well at the mance domains, yield clear and consistent results race [12]. for goal setting as a performance-enhancing Goals have commonly been further divided strategy. based on whether the intention of the goal is outThere are guidelines which improve the effeccome, performance, or process driven [12]. An tiveness of goal setting [11]. Set specific goals in outcome goal usually focuses on the result of an measurable and behavioral terms, which makes it event, such as winning a race, qualifying for a easier to detect progress. Set moderately difficult championship, or earning a medal. Performance but realistic goals to remain challenged enough to goals focus on achieving objectives that are in be motivated, instead of frustrated from repeated comparison to one’s own previous performance failure. Set short-range and long-range goals to rather than the performance of competitors. For stay focused on the path and experience small instance, striving for a personal record in a mara- successes along the way. As noted above, outthon and lowering one’s swim time during a tri- come, performance, and process goals all offer athlon are examples of performance goals. benefits to enhancing performance when used Finally, process goals focus on executing con- appropriately. Set goals in both practice and comcrete actions to perform well [12]. For instance, petition to enhance performance. Set positive focusing on spearing the hand into the water dur- goals instead of negative goals, which allows athing each swim stroke and pushing and pulling letes to focus on what they want to accomplish, with each pedal revolution are pertinent process not reminding themselves of what they do not goals. When used systematically, goals help ath- want to accomplish. For example, instead of, letes plan, evaluate, and manage their behavior “Don’t bonk,” repeat, “Fight through it.” Identify and thoughts [11]. targets for goal attainment to improve focus and In general, when compared to no goals or promote a sense of urgency, such as completing a vague “do your best” goals, specific goal setting half marathon within 4  months. Finally, write has been shown to enhance athletes’ performance goals down and frequently evaluate them to stay [10]. Outcome goals, though uncontrollable, are on the path towards success. attractive and exciting—useful in enhancing the motivation needed for the physical and mental grind of training. Performance goals offer more Energy Management control and flexibility, thus allowing athletes the opportunity to raise and lower their goal diffi- Too high or too low? Some athletes experience culty to remain challenged and excited [10]. excessive anxious energy prior to competition, Athletes use process goals in immediate situa- causing tense muscles and wasted energy. Others tions to enable focus on specific task demands in feel too flat or tired to perform well. Athletes productive ways. Considered collectively, setting have an optimal zone of energy (also known as outcome, performance, and process goals offers arousal or emotion) in which they perform best, unique benefits to maximizing performance. and mental training helps them find that ideal energy.

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Following the tenet of “moderation in all things,” it appears a moderate level of energy works well for most athletes [13, 14]. But due to the complexity of behavior, researchers have theorized more multifaceted relationships between energy and performance. Hanin proposes that individuals vary in the amount of energy they need to succeed in sport, depending on their personality and sport event [15]. For example, sensation-­ seeker Shannon swims faster in shorter events like the 200 Freestyle when she has high energy, whereas anxiety-prone Sean rows best in the longer single sculls event when he’s more relaxed. Individual interpretation of energy level is also important, according to reversal theory [16]. Shannon views her fast heartbeat as excitement and a sign she’s ready to swim fast. Sean, however, interprets the butterflies in his stomach as unpleasant anxiety—a feeling of dread. McGonigal found that stress can be good for us if we reframe a thumping heartbeat and butterflies flitting about in the stomach as a sign our bodies are preparing to rise to the challenge [17]. When athletes have too much energy or anxiety, relaxation strategies are often helpful [18]. A key skill is diaphragmatic breathing, also known as belly breathing. To practice diaphragmatic breathing:

Table 22.1  Energy management strategies

–– Place one hand on your chest and one hand on your belly (below belly button). –– Inhale through your nose; exhale through your mouth. –– When you inhale, keep the hand on your chest still while pushing out the hand on your belly with air (the opposite of “sucking it in”). –– When you exhale, pull your belly button into your spine. –– The diaphragm is the muscle beneath your lungs; you’ll feel that drop or push down as you inhale, which allows your lungs to expand down into your chest cavity.

Self-Talk

Another calming breathing strategy is paced breathing which involves a shorter inhale and a longer exhale [19]. For example, breathe in to a count of two, and breathe out to a count of four. Paced breathing has been shown to reduce heart rate.

Too nervous? chill out Take diaphragmatic breaths, paced breaths Repeat cue word like “just do my best” Focus on the process, the controllables Re-experience your best performance Get perspective—it’s just a sport! Listen to happy music, a comedy routine Talk to a friend about your stress Hold a power pose for 2 min

Too flat? pump up Take fast, shallow breaths Move your body. Jump up and down Alternate contracting and relaxing muscles Review your most important goal Walk and talk quickly. Act as if you’re energized Listen to pump up music Repeat an affirmation “I’ve got great stamina” Watch a psych-up sports video

When athletes are too low in energy, they often feel tired and flat and may suffer a “let down” [20]. Strategies to increase energy include quick, shallow breaths and jumping up and down. According to Cuddy, holding the body in a “power pose” for 2 min decreases cortisol (stress) and increases testosterone (feelings of energy and power) [21]. See Table 22.1 for more “chill-­ out” and “pump-up” strategies [18, 20–22].

“Push harder.” “I can’t keep up.” “Why the hell am I doing this?” Sound familiar? Self-talk is what athletes say to themselves before, during, and after training and competition. Cognitive behavioral theory, which challenges unbalanced self-talk, is a cornerstone of mental training for sports. Cognitive theories espouse that our reactions do not stem from the events that happen to us, but rather from how we interpret those events. For example, Amy and Sienna both swallow water during the swim of a triathlon. Amy thinks, “Oh, no! Why does this always happen to me? I suck at swimming. My race is ruined.” In contrast, Sienna thinks, “Yuck. This happens to lots of swimmers. I swallowed water in my last race and still got a PR. Breathe. One stroke at a time.” Both Amy and

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Sienna experience the negative event of swallowing water, but Sienna reacts more effectively due to her evidence-based self-talk. Cognitive behavioral therapy teaches skills to challenge unbalanced thoughts like overgeneralization [23]. Athletes who overgeneralize interpret one negative event as a never-ending pattern, making broad conclusions about themselves and others. While training for a tramping event in New Zealand, Daniel’s old knee injury acts up, and he must cut one practice short. If he thinks, “I’ll never be ready for this event. I screw up everything,” he is overgeneralizing. One abbreviated training session doesn’t mean that he will be ill prepared for the race, nor does it imply that he fails at everything in his life. Such unrealistic thoughts can lead to feelings of anxiety, hopelessness, and irritability, which can then impair training and sport performance [1]. Another classic unbalanced thinking style is “should” statements. When thoughts like “I should’ve known better” or “I should beat that athlete” pop up, athletes often become too tense or angry to perform well. Ellis advises us to stop “shoulding” all over ourselves [24]. Instead, use words like “prefer,” or acknowledge the facts, such as “Just because I have a better ranking doesn’t mean I should beat that athlete. Rankings are meaningless on any given day.” Do self-talk interventions improve sport performance? In a 2011 meta-analysis, Hatzigeorgiadis et al. reported a moderate positive effect size [25]. For instructional self-talk such as “Follow through,” fine motor skills like golf-putting benefit more than gross motor skills like running. Motivational self-talk (“Just keep swimming”) may be more useful for gross motor skills used in endurance sports. Anticipation of positive consequences like “I’ll feel amazing crossing the finish line!” is a type of motivational self-talk helpful in endurance events [26]. Regarding endurance sports, studies find that self-talk interventions have improved performance in swimming [27] and marathon running [26]. Hamilton, Scott, and McDougall found that positive self-talk improved cycling performance, particularly when audio of positive messages reinforced the cyclists’ self-talk [28]. The authors

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also found that negative self-talk slightly improved performance for some athletes. They explained that athletes may perceive negative statements like “You can’t keep up this pace” as surprisingly motivating. This study highlights the unique responses of athletes to mental training interventions, as well as the fact that effective self-talk is balanced, not necessarily positive. Self-talk interventions do not focus only on challenging unbalanced self-talk but also on brief self-coaching instructions prior to performance. Intelligent athletes may tend to overthink, which can cause muscular tension, hesitation, poor focus, and mental fatigue. Decreased athletic performance may result. Their internal dialogue may sound something like this: “I really want to PR today. Why does that athlete have to be in this race? So annoying. Are my water bottles full? Coach told me to get after the third mile. Ooh, I like that guy’s bike. How does he afford that? I hope my quad doesn’t cramp up. Crap, that work deadline’s approaching. What if I don’t finish? That’d be awful. Is it going to rain? Remember to pick up milk on the way home. C’mon, focus. PR, baby.” Such rambling self-talk impairs concentration. For increased focus, sport psychologists often teach “cue words”: words or phrases under the athlete’s control, about the task at hand, that focus on one thing at a time [29]. Behind the blocks, swimmers might use cue words like “Fast and loose,” “Hop on the fourth one-hundred,” or “Do my best.” In the above example, Sienna uses cue words like “Breathe” and “One stroke at a time” to refocus after swallowing water during a swim.

Concentration Concentration is the ability to focus attention on the task at hand without distraction from irrelevant external or internal stimuli. It is a learned skill of limiting reactions and distractions to unimportant information, which has a profound effect on athletic performance [1, 2]. When athletes concentrate well, they respond to changing performance demands, control emotion and performance state, and release muscular tension

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[30]. Attentional focus has been theorized to reside on two dimensions: width (broad or narrow) and direction (external or internal) [31]. A broad attentional focus allows a person to perceive several stimuli simultaneously, such as scanning the weather conditions of the ski course. Narrow attentional focus occurs when an athlete only focuses on one or two cues, like a competitor’s tire when making a pass on the bike. An external attentional focus directs attention outward to an object, such as biking towards your specific transition spot. Finally, an internal attentional focus is directed inward to thoughts and feelings, like working through the heavy legs after a bike. Another important quality of focus is whether athletes associate, i.e., focus on bodily sensations or performance-specific cues, or dissociate, i.e., focus on external stimuli as a means of distracting themselves. Early studies suggested that elite athletes gravitate towards associative strategies and non-elite athletes favor dissociative strategies, but 35  years of subsequent research has resulted in equivocal findings regarding the best attentional focus for peak performance [32]. Brick et al. recommended future research break down associative strategies into active self-­ regulation and internal sensory monitoring and dissociative strategies into active distraction and involuntary distraction [32]. Additional support for the value of concentration comes from Moran [33]. He contends that a focused state of mind requires deliberate mental effort and intentionality. Although skilled athletes can divide their attention between two or more concurrent actions, they can focus consciously on only thought at a time. (Focusing on only one thing is also known as the one-mindful mindfulness skill.) During peak performance states, athletes’ minds are so focused that there is no difference between what they are thinking and what they are doing. Athletes tend to lose their concentration when they pay attention to events and experiences that are in the future, in the past, out of their control, or otherwise irrelevant to the task. Excessive anxiety can also undermine optimal performance by leading performers focus on inappropriate cues, as well as focus too much on

conscious, instead of automatic, control of movement. Considered collectively, concentration is a worthwhile mental skill that needs to be trained and sharpened. Fortunately, there are many supported strategies for improving concentration. Simulating competitive demands in practice can aid with concentration on event day [34]. Simulation offers the opportunity to learn how to cope effectively with distractions and practice strategies for refocusing the mind. Self-talk, especially cue words, can be used to cue an identified response. Using nonjudgmental thinking about performance also helps athletes stay in the present moment and not be distracted by past or future performances. (See the section on “Mindfulness” for more details.) Performance routines allow athletes to focus on what is under their control and reduce distractions that may come up on race day, as well as ready the mind for reaching the zone. Plans for competitions also offer athletes a way to remain focused during the event by reminding themselves of strategies, goals, and techniques. Finally, another strategy to enhance concentration is to overlearn the skills required to perform. Cyclists focus better on race strategy if they aren’t overly concerned about how to effectively engage the pedal stroke. A well-learned stroke will be automatic, thus allowing cyclists to focus on other elements necessary for great performance.

Imagery Imagery is using all senses to create an experience in the mind [34]. Imagery, visualization, mental rehearsal, mental blueprint, and mental practice all refer to the process of recalling from memory pieces of information stored from experience and shaping these pieces into meaningful images [35]. It is an act of simulation that occurs internally within the mind. Anyone can use imagery, in any setting, to learn and practice skills and performance strategies, correct mistakes, prepare a mental focus for competition, automate pre-­ performance routines, build and enhance mental skills, and aid in the recovery from injuries [34].

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How does imagery work? When engaging in visualization, similar neural impulses occur in the brain and muscles, mimicking those fired when physically performing the action [35]. For example, picturing yourself biking up a tough hill will fire neurons in your brain and body that are responsible for moving your quads and hamstrings. Imagery also facilitates performance by helping athletes blueprint the movements or strategies necessary for success, so they become more automatic [35]. For instance, picturing a technically sound swimming stroke increases the likelihood of performing a perfect stroke. Athletes are also able to develop coping responses to potential stressful situations [35]. As such, a rower can image clean blade entry into choppy water. Finally, imagery allows athletes to create the optimal levels of energy and concentration required for their performance endeavor [36]. A marathoner who is nervous before a race might picture a beach scene to relax her mind and body. Evidence supporting the use of imagery in endurance performance has been well documented. For example, non-athletes using pre-­ performance imagery of skill execution and successful performance outcomes showed improvement in a 1.5-mile run [2]. In a small group of competitive youth swimmers, imagery training and listening to an imagery script improved performance in a 1000-yard practice set [2]. Another study of a small group of indoor gymnasium triathlon participants showed that imagery helped in the tolerance of pain, increased motivation and confidence, and improved race strategy [4]. These examples, as well as supplemental research involving participants in varying levels of ability and sport type, offer support for the use of mental imagery in enhancing performance. To set up an effective imagery training program and maximize the potential overlap in neural activation between real and imaged behaviors, it has been suggested to use the pettlep model [37]. The pettlep model outlines seven elements (physical, environment, task, timing, learning, emotion, and perspective) that amplify the relatedness between the imaged and actual performance [37]. For instance, the physical element

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suggests imaging in a similar physical environment (i.e., imaging the swim while standing in the pool or floating in the water). The timing element suggests imaging the performance in real time (note: obviously this may be difficult when imaging endurance sport, though picturing a swimming stroke or run cadence in real time would be ideal). Hence, engaging in imagery in ways that best utilize and approximate the elements of the pettlep model would offer the greatest benefit [37]. Further, it is essential to assess which aspect of performance that will be imaged [34]. For instance, does the athlete need to focus on technique, dealing with a flat tire, or picturing strength while running up a muddy hill? All require a different type of imagery. Another obvious key to imagery includes being able to control the image [34]. If athletes have difficulty creating the image they want, backtracking to individual behaviors and building from what they can controllably image are appropriate.

Performance Routines Throughout this chapter we have introduced mental skills to enhance athletic endurance performance. Though helpful in isolation, these mental skills can serve additional purpose when combined in unison before, during, and after competition. Such deliberate packaging of mental skills to ready the mind and body for a successful performance is known as performance routines. Performance routines are a sequence of task-relevant thoughts and actions systematically engaged in prior to performing a specific sport skill [38]. Though commonly used in closed sport situations such as golf putting or free throw shooting, routines also have a place in longer repetitive activities such as endurance sport. In this case, routines would be utilized the night before, the day of, and immediately before competition to prime the athlete for a ready state to perform. In addition, athletes may employ routines after performance to aid in their mental and physical recovery. Performance routines can aid in building confidence, composure, and concentration. For

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instance, with confidence, every night before a race, a triathlete might eat the same dinner, take time visualizing herself feeling strong the entire race, double-check her gear bag, and write effective self-talk statements in her journal. Doing this the night before each race builds confidence for a successful race. An athlete who is prone to performance anxiety or is participating in high stakes races might use performance routines to calm his nerves. He may begin the day of an ultramarathon with a deep breathing exercise prior to leaving for the race venue. He may sit quietly after his aid stations and support crew are organized. Picturing a calm mind and body throughout the race allows him to maintain composure up until the race begins. Finally, pre-­ performance routines allow athletes to automate their behaviors leading up to race day and start. As such, they can focus solely on the race, rather than irrelevant information such as gear, navigating the venue, etc. All the potential stress and mental chatter has been silenced by developing a routine that effectively addresses these areas in an automated manner. Routines have received substantial support in the empirical literature in a variety of sporting domains [30]. Although routines often occur before or between competitive performances, it is optimal to use them systematically during training, so they are learned and easily transferable to competition. It is also helpful to identify strategies to shrink or stretch the routine depending on unanticipated late arrivals or competition delays. Developing appropriate and effective pre-race routines may take some time. It is important to use mental skills and routine strategies in a way that fits with the individual. This is not a one-­ size-­fits-all approach. It is necessary to assess what athletes need on race day. Which would they like from the routine—confidence, composure, concentration, or all three? What mental skills do the athletes tend to use the most and with the greatest amount of success? Include these skills in the routine. Developing a routine takes time and may require some trial and error. Stay patient and be flexible. Make sure that the

components of the routine help enhance performance and not distract from it.

Mindfulness Mindfulness is experiencing the moment without reacting to the moment [39]. Jon Kabat-Zinn described mindfulness as “the awareness that emerges through paying attention on purpose and nonjudgmentally to the unfolding of experience moment by moment” [40]. It is “affective, compassionate, and nonreactive.” Mindfulness is at the heart of Buddha’s teachings and has been incorporated in clinical treatments like dialectical behavior therapy [39]. Significant improvements in anxiety, depression, and emotionality have been linked to mindfulness training [41]. Mindfulness develops an accepting relationship with one’s inner experience, instead of trying to control thoughts and feelings like in traditional cognitive behavioral approaches [42]. Cognitive models attempt to replace unrealistic thoughts with evidence-based thoughts. In contrast, mindful approaches notice the thoughts without reacting to them. For example, athletes might think, “I’m a failure.” Cognitive interventions encourage the athlete to challenge that belief with evidence like “I didn’t pace the race well but that doesn’t mean I’m a failure in all things—I did succeed by managing my nutrition effectively.” Mindfulness training encourages responses like “I notice the thought ‘I’m a failure’. I’m aware of a tightness in my chest; a feeling of insecurity.” Then, athletes gently refocus their attention to their breath [40]. Interest in mindfulness interventions in sport has increased recently [1, 43]. Control isn’t all it’s cracked up to be, especially when attempts to control backfire. Strategies designed to suppress or replace negative thoughts may paradoxically increase those thoughts [44]. Gardner and Moore argue that traditional mental skills training has reduced negative mental states in some studies but has not translated into consistent ­improvement in sport performance [42]. Because some athletes

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struggle to achieve control over their cognitive processes via traditional skills training, acceptance approaches like mindfulness offer promise for the future. Kabat-Zinn first applied mindfulness to endurance sport performance by studying mindfulness meditation and rowers [45]. More recently, soccer players who trained in mindfulness reported feeling calmer and less reactive to negative emotional states [46]. Thompson et al. found that mindfulness training improved runners’ mile times and feelings of relaxation [47]. The mindfulness training was also associated with decreased anxiety and irrelevant thoughts. One unique study explored the usefulness of mindfulness for recovering from burnout in sport [48]. Mindfulness increases awareness of all things, including experiences of confidence and mastery, which may enhance feelings of flow. Peak athletic performance is known as being in the zone or in a state of “flow”: the optimal zone where skill meets challenge [49]. Pineau et  al. studied mindfulness in rowers and found an association between mindfulness, efficacy, and flow [50]. The authors theorized that mindfulness increased awareness of mastery experiences, thereby increasing feelings of efficacy and flow. To practice mindfulness skills, endurance athletes might start with observing nonjudgmentally [39]. The observe skill involves noticing the present moment without reacting. Athletes may feel stuck in the past when they berate themselves for mistakes or stuck in the future when they worry about the outcome of a race. They can become more anchored in the present by observing with their five senses: “I see the red buoy. I hear the splash of water. I feel coolness on my skin. I notice my breathing is shallow.” The nonjudgmental skill is noticing facts without evaluating them as good or bad. Athletes who judge themselves with thoughts like “I shouldn’t get angry” can practice the nonjudgmental skill by listing five facts about the situation (“I am angry,” “Everyone feels anger,” “Anger is different from aggression,” etc.) and/or asking what a supportive person in their life would say (e.g., “It’s okay to be angry”).

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A skill that bridges self-talk and mindful nonjudgment is self-compassion, or kindness and understanding directed inward when experiencing emotional pain. There are three components of self-compassion: kindness, common humanity, and mindfulness [51]. Endurance athletes who are hard on themselves can benefit from learning to speak to themselves as they would to friends. A rower who chides himself, “I can’t believe you caught a crab and ruined the race for your crew, you loser,” might consider how he would talk to a teammate in a similar situation. He could instead practice self-talk like, “Of course you’re devastated—you care a lot about your teammates and performing well. I’m sorry this happened. You’re new to this sport and still learning technique. Everyone makes mistakes.” One study found an association between athletes with less self-judgment and higher athletic performance [52]. There are interventions to train athletes in self-compassion to cope more effectively with negative events in sport [53].

Balanced Exercise Exercise has countless physical, mental, and emotional benefits, and endurance athletes know these benefits well. But many people do not exercise at all, and most don’t get enough exercise [54]. There are fewer who get too much exercise [55]. Endurance athletes are more at risk for excessive exercise [56], thereby increasing their risk for developing eating disorders and physical injuries [57]. Finding the balance between too little and too much exercise is important for health [54]. Various terms for excessive exercise include compulsive exercise, obligatory exercise, exercise addiction, exercise dependence, and exercise abuse. To manage psychological distress, exercise joins food restriction, binge eating, substance use, gambling, and other addictive behaviors as a potential means to escape or numb painful emotion. Like other compulsive behaviors, excessive exercise provides short-term relief of negative emotional states but often adds to distress in the

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long run. It can be difficult to detect excessive exercise, particularly in competitive athletes. Think about athletes who run the extra mile or train multiple times a day—others often applaud their unparalleled discipline. For this reason, it may be a challenge to recognize exercise as an addictive, potentially harmful behavior. How do athletes know if they are overexercising? Powers and Thompson recommend determining if exercise has a negative impact on physical, emotional, or psychological health, as well as interfere with daily activities like school, work, or relationships [54]. Exercise is also problematic if it occurs at inappropriate times or settings or continues despite injury. Examples include the compulsion to take a long bike ride in lieu of attending to family needs. The American College of Sports Medicine recommends taking at least 1 day off exercise per week [58, 59]. The quality of exercise may be more important that the quantity [54]. Qualities to consider include motivation for exercise and level of control over exercise. What motivates athletes to exercise? If the motivation is solely to burn calories, punish themselves, give permission to eat, or compensate for calories eaten, exercise may represent an eating disorder symptom. More balanced motivations include health, training for sport, stress reduction, fun, and mind-body connection. It’s also helpful to gauge the level of control individuals feel over exercise. If exercise feels compulsive or obligatory, the athlete’s health may be compromised. For instance, cyclists with uncontrollable urges to go on long bike rides experienced more internal conflict [60]. Individuals who are concerned about inadequate or excessive exercise will find The Exercise Balance by Pauline Powers and Ron Thompson to be a helpful resource [54] (Table 22.2). Intuitive eating is a balanced, flexible approach to nutrition that jettisons diet rules and honors physical and emotional needs, including hunger and fullness [61]. An exciting recent direction for implementing balanced exercise is intuitive exercise [62]. Intuitive exercise is about listening to inner wisdom—how one’s body feels while exercising, cues for starting and stopping exercise,

Table 22.2  Signs of balanced and unbalanced exercise Signs of balanced exercise Improved physical and mental health Supported by adequate nutrition Increased sensation and awareness of body Exercise as one of many coping skills for stress Exercise that you like, not exercise that you dislike Balance of cardiovascular, strength, and flexibility exercise Being able to stop when injured Including leisure activities like hiking

Signs of unbalanced exercise Avoidance of all exercise Exercising without fueling your body Obsession with weight and calories burned Exercising to allow yourself to eat Skipping work, class, or social plans for exercise Not taking a day off (even when sick or injured) Exercising to compensate for calories eaten Judging a day as good or bad depending on how much you exercise

and embracing a variety of activities and intensities [63]. When an athlete’s body tells her that she’s too sore and tired to crank out speed training on the track one day, it’s often more effective for her to take a rest day or a light walk instead. Her next day of training will likely be even stronger when she listens to her body’s needs.

Medication Considerations Sports psychiatrists must consider several important factors when prescribing psychiatric medications to athletes. In addition to the usual considerations when prescribing any psychiatric medication to the general population, physicians must consider several factors when providing treatment to athletes. Psychiatrists must remain vigilant for potential performanceenhancing effects, negative impacts on athletic performance, and safety risks unique to an athletic population. Physicians must also remain acutely aware of medications that are monitored or banned by athletic governing bodies including the National Collegiate Athletic Association (NCAA) and the World Anti-Doping Agency (WADA) [64].

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Medication safety is paramount when considering treatment options for any patient, and ­athletes present unique concerns for prescribers. Certain psychiatric medications, including tricyclic antidepressants and lithium, have the potential to reach toxic serum concentrations particularly in athletes who sweat heavily. Stimulant medications have the potential to decrease an athlete’s ability to detect thermal stress during exercise, theoretically increasing risk for cardiovascular complications, heat exhaustion, and physical injury [64]. When considering the potential for negative impact on sport performance, prescribers must be aware that “one one-hundredth of a second slower of a race time for a high-level athlete can mean the difference between top achievement in sport, with attendant fame and financial benefit, and a second-place performance to which no one pays heed” [64]. Physicians must also consider that any degree of tremor or other movement side effects, potential for weight changes, or opportunity for an altered level of alertness may be unacceptable when prescribing to an athletic population [64]. The potential for performance-enhancing effects from medications certainly present ethical considerations in addition to potential for safety concerns. Many sports governing bodies, including the NCAA and WADA, ban medications that have been found to have ergogenic effects. Some examples of banned medications include stimulants and beta-blockers that are prohibited in sports requiring fine motor control. A complete list of banned or monitored medications by the NCAA and WADA can be found at each organization’s respective website. Ethical issues notwithstanding athletes can obtain a therapeutic use exemption (TUE) for a banned substance through WADA should the medication be deemed medically necessary by a physician. Collegiate athletes may be prescribed a substance banned by the NCAA if they have certain documentation of an approved indication and an ongoing prescription for the medication on file within their collegiate institution [64].

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Conclusion The mind of an athlete is a terrible thing to waste. This chapter provides an introduction into the mental world of endurance athletes and how to make the most of what is between the ears to achieve greater performance. Much like the physical and technical training necessary for endurance sport success, systematic training of mental skills can be difficult and requires tremendous self-discipline. We encourage you to identify the mental skills that interest you most (perhaps imagery, energy management, goal setting, and/ or mindfulness) and practice these skills until they become part of you. Start small and have fun along the way!

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Performance-Based Nutrition for Endurance Training

23

Steven Liu, Shawn Hueglin, Jacque Scaramella, and Kenneth Vitale

Introduction Endurance event participation has been continuously growing, with 2.5 million triathletes as of 2015 in the USA and 3.1 million globally [1]. As our society continues to grow, people discover new interests and find different avenues to endurance participation compared to traditional jogging and running events such as 5 K races, half marathons, and marathons. Furthermore, athletes are now attempting other styles of races, such as mud runs, color runs, and obstacle course runs [1]. There are also ultra-endurance events that have been gaining momentum in recent years. While endurance events (according to nutritional fueling strategies) are typically considered events lasting at least 60–90 min [2–4], ultra-endurance races are typically defined as events lasting 4–6 h (or longer); they have been shown to cause extreme fatigue, suboptimal nutrition, and energy S. Liu Department of Internal Medicine, Providence Portland Medical Center, Portland, OR, USA S. Hueglin Sports Performance, United States Olympic and Paralympic Committee, Chula, CA, USA e-mail: [email protected] J. Scaramella Sports Dietitian, San Diego, CA, USA

deficit if not properly supported by adequate sports nutrition [5, 6]. Because of these challenges, there has been more interest in research on potential complications that can occur during endurance and ultra-endurance events and the need to develop an approach for proper athlete nutrition and hydration during a competition [5, 6]. With the increasing number of participants in both endurance and ultra-endurance events, there is a growing need to provide more education on defining appropriate nutritional intake athletes require to not only perform at a high standard but also maintain their health and safety. Over the years, the understanding of nutritional requirements for athletes, specifically endurance athletes, has evolved and shown significant advances. However, despite all the information existing in the literature, there are still gaps that make the science of nutrition a complex topic. Registered dietitians, sports scientists, physicians, and other healthcare professionals often debate about the ideal diet for athletes. This chapter will explore key nutrients vital for endurance performance. Specifically, major macronutrient requirements including carbohydrate (CHO), protein, fat, and hydration are discussed while also reviewing specific micronutrients, electrolytes, and dietary supplements/ergogenic aids, such as sodium, caffeine, nitrates, and iron supplementation.

K. Vitale (*) Department of Orthopedic Surgery, University of California San Diego, La Jolla, CA, USA e-mail: [email protected] © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. L. Miller (ed.), Endurance Sports Medicine, https://doi.org/10.1007/978-3-031-26600-3_23

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Carbohydrate Carbohydrate is perhaps the most discussed macronutrient among endurance athletes and critical to improve energy levels and endurance performance. Historically there has been dispute regarding the amount and timing of CHO intake before and during a race. While many condone traditional carbohydrate loading, in recent years some ultra-endurance athletes are embracing the concept of a low-carbohydrate and high-fat diet. The most recent recommended guidelines for CHO fueling will be discussed. The Academy of Nutrition and Dietetics (AND), Dietitians of Canada (DC), and the American College of Sports Medicine (ACSM) have released a joint position statement on recommendations based on exercise intensity. For moderate exercise (1 h/day), intake of 5–7 g per kilogram of body weight per day (g/kg/day) is recommended, while moderate- to high-intensity exercise (1–3  h/day) mandates 6–10  g/kg/day. Ultra-endurance athletes who do 4–5 h of moderate to high intensity of exercise every day may need upwards of 8–12 g/kg/day [7]. Other major clinical sports nutrition resources and texts echo these recommendations [8]. Table  23.1 summarizes recommendations on CHO requirements according to exercise duration. When compared to fat, carbohydrates are utilized more heavily and more efficiently at higher intensities than fat (of note, intramuscular triglycerides provide a local and efficient fuel source to support carb during endurance exercise) [10]. As a result, they are traditionally the primary source of energy for endurance athletes. However, when CHO stores are depleted, fatigue, reduced work, impaired concentration, and

reduced performance occur [1, 6, 10], colloquially termed “hitting the wall.” Therefore, strategies exist to combat this through fueling before (“preloading” or “loading”) and during races/ events [9].

Pre-Competition: “Loading” Before a race, athlete may choose to boost their carbohydrate intake before an event in attempt to help improve their performance. This preloading or “carb loading” strategy and the amount of CHO recommended are based on several factors, including the length of time of the event, ability to ingest adequate fuel in the days leading up to the event, and access to fuel sources throughout the event. If the race is no more than 90 min, a simple “topping off” of glycogen stores to replenish muscle and liver glycogen lost from the previous day and overnight fast is recommended [6, 10]. And if the athlete can simply “top off” pre-­ event and has access to fuel sources throughout the race, the athlete does not necessarily need to carbo load pre-race. In events >90 min, a glycogen supercompensation “carbo loading” occurring up to 36–48  h before an event can improve an athlete’s results [1]. A carbohydrate-rich diet consisting of 6 g/kg [10] and up to 7–12  g/kg [6] in a 24-h period before a performance has been shown to maximize CHO stores. There are recent studies showing a short high-intensity (3 min at >100%VO2max) exercise bout, or even complete physical inactivity, 1 day before high CHO intake (10–12 g/kg/ day) result in similar glycogen supercompensation [1, 11] compared to traditional methods without exposing the athlete to a particularly

Table 23.1  Key recommendations for carbohydrate according to exercise duration, listed in parentheses (adapted with permission from: [9]) Daily Nutrient requirements Carbohydrate 5–7 g/kg/day (1 h/day) 6–10 g/kg/day (1–3 h/day) 8–12 g/kg/day (4 ≥ h/day)

Pre-exercise 6 g/kg/day ( 90 min) + 1–4 g/kg (1–4 h prior to event)

During exercise 30–60 g/h (2.5 h) 90 g/h (>2.5 h, if tolerable)

Post-exercise 1.0–1.2 g/kg/h (first 3–5 h) Or 0.8 g/kg/h + protein (0.3 mg/kg/h) or caffeine (3 mg/kg)

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draining long high-intensity exercise sessions that may risk injury immediately prior to a race. And on the same day in the last 1–4 h before an event, a final intake of 1–4  g/kg CHO is often recommended to maximize complete glycogen storage by repleting CHO loss after the overnight fast [6].

During Competition: “Fueling” When endurance events occur for less than 60  min, athletes do not need additional exogenous CHO during the event [2, 6] as glycogen stores remain adequate. However, in events over 60–90  min, athletes need to commence in-race CHO fueling to maintain glucose availability. In events that last 1–2.5 h, 30–60 g/h of CHO in a 6–8% CHO solution (often in smaller amounts every 10–15  min) [2, 6] is a common recommended range for CHO intake during exercise. For events over 2.5  h, high CHO intake with a minimum of 60–70  g/h, up to a maximum of 90 g/h, can improve athlete performance [6]. When reaching these higher levels of CHO intake, exogenous CHO oxidation peaks at a CHO ingestion rate of 1.0–1.1 g/min [1, 12]. This is primarily due to the maximal gastrointestinal (GI) absorption at this rate; athletes can increase their oxidation up to 1.2–1.3  g/min by adding multiple CHO sources (glucose/fructose mixtures) at higher intakes (1.8 g/min) [1, 6, 10, 12, 13]. This glucose/fructose combination can improve GI tolerance (and allow for increased oxidation) due to alternative intestinal CHO transport mechanisms [1, 6, 10, 12, 13]. From a practical perspective, these extreme high levels of CHO intake, e.g., 90 g/h, can represent a significant barrier to athletes due to GI distress. If considering a high CHO intake during an event, athletes are recommended to determine what CHO diet is tolerable and implement a plan to refuel glycogen during training. The type of sport and nature of competition can impact the opportunity for athletes to refuel throughout their event (e.g., halftime or time-­ outs, type of venue/course, access to hydration at the ready vs. on the course). For example, run-

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ners and cyclists may be able to carry hydration and food with them; however, swimmers essentially cannot refuel in certain competitions (of note, some open water races actually have fueling opportunities during the race as feed stations on a boat; however, it is not ad libitum and only at available intervals). Some sporting events allow athletes refuel at their leisure, whereas others have to wait until a designated aid station. It is highly recommended athletes practice their CHO fueling plan at the same timing, same intensity, and with the same accessibility as the events in which they will participate. This is often referred to as “training the gut” and can be a valuable training tool for the endurance athlete to become more aware of sometimes overlooked practical considerations such as how to physically transport their fuel during the race, timing of fueling, and overall tolerance. As the body may have reduced GI tolerability due to the increased stress response of race time and sympathetic/parasympathetic imbalance, closely mimicking race conditions may prove advantageous [9]. Furthermore, athletes exhibit reduced CHO oxidation rates in hot environments and should consider implementing cooling strategies in addition to decreasing their CHO intake by 10% in these conditions to avoid GI distress [1, 9]. Training the gut and practicing a fueling strategy in race-like conditions are keys to implementing an effective carbohydrate fueling plan and avoiding unwanted race day GI distress. Similarly, an athlete may need to train the gut to tolerate more CHO (and total caloric) intake if exercising in the cold and/or at altitude when appetite can be decreased, but CHO needs are increased [14]; this is further discussed in the following section, “Environmental Considerations.”

Post-Competition: “Repleting” Depending on initial glycogen stores, CHO consumption during competition, and the intensity/ duration of the exercise, athletes may have depleted glycogen stores post-exercise. In situations of endurance exercise >60–90 min, at high intensities, if there are multiple training sessions

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in the same day, and/or if there are back-to-back competitions (e.g., multiple day tournaments), it is important for athletes to replete glycogen stores for future competition or training sessions [15, 16]. In the time immediately following glycogen depletion, glycogen synthase activity increases, insulin sensitivity increases, and membrane permeability to glucose increases, all leading to glycogen resynthesis given ample exogenous CHO supply [17, 18]. As a result, the well-known “metabolic window of opportunity” (higher glycogen synthesis when CHO consumption occurs within 2 h post-exercise compared to >2 h [19]) is traditionally an ideal time for athletes to replete glycogen stores. Initially, guidelines had recommended at least 50 g (1 g/kg body mass) of CHO during the first 2 h of recovery to optimize glycogen repletion [16]. However, recent studies report a similar 30–50% increase in glycogen stores with small, spaced out meals rich in CHO (>1  g/kg body mass) over the 4–24 hr. period post-exercise [16]. As a result, if the athlete does not have another exercise bout planned within 24  h, they may opt for a high CHO diet distributed over time. However, for athletes who engage in more than one endurance exercise session per day, it is important to replete glycogen storage as quick as possible [16]. For athletes that have another event with 2 h Adjust intake according to individual athlete variations (sweat rates, sweat sodium content, exercise intensity, body temperature, ambient temperature, bodyweight, kidney function)

Suggested recommendations post-exercise Continue pre-­ exercise plan Improved water repletion observed with >60 mmol/L sodium content (~1380 mg/L)

with, e.g., dehydration and hyponatremia which may indirectly help the athlete (by preventing medical conditions that would otherwise slow the athlete down), the literature is unclear on a direct and conclusive connection between sodium intake and endurance performance as an ergogenic aid [52]. Continued research is needed on the effects of sodium intake on endurance performance and to better quantify both sodium loss and sodium repletion strategies for athletes.

Caffeine There has been keen interest in better understanding the ergogenic effects caffeine can have on athletes and their performance. Although caffeine may have effects at other body locations, research shows it has the most benefit to the CNS [56]. Caffeine works as a CNS stimulant by blocking adenosine receptors to increase neurotransmitter release [57, 58]. Adenosine is a major homeostatic regulator and neuromodulator, causing decreased concentration of many neurotransmitters including serotonin, dopamine, acetylcholine, norepinephrine, and glutamate [59–61]. Adenosine receptor blockade allows increased

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concentrations of these neurotransmitters and ultimately leads to benefit in mood, vigilance, focus, and alertness [62, 63]. Caffeine also increases Na+/K+ pump activity, which can boost the excitation-contraction coupling for muscle contraction [62]. In addition, caffeine increases motor unit recruitment and helps mobilize calcium to increase muscle contraction [63–66]; by this mechanism, caffeine may also attenuate feelings of fatigue due to reduced calcium release [65, 67]. Systemically, caffeine assists in fatty acid mobilization for energy usage (thereby decreasing dependence on glycogen) and increases thermogenesis [57]. Caffeine has high bioavailability that reaches near 100% for area under the plasma concentration-­time curve (AUC) [68]. When caffeine is consumed orally and absorbed through the GI tract, it can appear in the bloodstream within minutes and reach peak plasma concentrations at around 30–120 min post-ingestion [68– 71]. The way caffeine is consumed may also affect its pharmacokinetics [69, 72–74]. One study showed capsules had a peak caffeine concentration at around 30 min while cola and chocolate had a later peak (90–120  min) and lower peak concentrations [69]. However, there appears to be no impact of temperature that caffeine is ingested (e.g., iced coffee vs. hot) as the evidence for any changes in pharmacokinetics are minuscule [70]. Caffeine gum and strips are also popular forms with a much quicker oral absorption through the buccal mucosa (5–15  min) [75]. Interestingly, mouth rinsing with caffeine may additionally stimulate nerves with direct links to the brain, separate from caffeine absorption in the mouth; however, caffeine mouth rinsing does not appear to have significant effects on cognitive performance [75]. There are even caffeine aerosol mouth and nasal spray routes of administration which can also stimulate nerves with direct brain connections and get absorbed via mucosal and pulmonary pathways, but little support exists for this method as being effective [75]. Caffeine is widely consumed by athletes on the national and international level. The International Olympic Committee (IOC) has recognized caffeine as a substance athletes use for

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performance enhancing or ergogenic effects [76]. In 1984, the IOC initially added caffeine as a banned substance and was followed by the World Anti-Doping Agency (WADA) in 2000 [77]. It was determined that if an athlete had a urinary caffeine concentration greater than 15 ug/mL, then it would be considered doping; that threshold was later reduced to 12 ug/mL (and defined by excluding a casual amount of caffeine ingested in a daily diet and social coffee drinking patterns, versus levels needed for performance improvement) [78]. Later in 2004, the IOC and WADA then removed caffeine as a controlled substance (due to its ubiquitous nature in food and beverages and its variability in metabolism and urinary concentrations among individuals) [79], leading to renewed interest in athletes for performance benefits [80, 81]. However, the National Collegiate Athletic Association (NCAA) still categorizes caffeine as a banned substance if urinary concentration exceeds 15 ug/mL (equivalent to roughly 500 mg, estimated at ~6 cups of brewed coffee for a 154 lb. individual) [82–84]. Regarding performance improvement, meta-­ analyses and reviews suggest that a moderate dose of 3–6 mg/kg of caffeine 30–90 min before exercise can maximize its effect and may lead to endurance performance improvements by up to 2–4% [57, 58, 85–88]. Additionally, a systematic review determined that caffeine had a small (2.9%) but significant impact in power output during time trial performance [87]. Among sports studied, caffeine has been shown to improve performance in endurance sports such cycling, running, cross-country skiing, and swimming [82–84, 86, 89–92]. As high-level Olympic endurance competitors exhibit an overall difference in speed of sometimes less than 1% [93], a small 2–4% improvement may have a significant impact on outcomes. Caffeine and carbohydrates are often taken together in endurance sports, and there appears to be a synergistic effect with caffeine and carbohydrates [9, 94]. In a famous but dated study, cyclists taking both caffeine and CHO together showed a 7.4% improved work production and a very significant (31%) increase in fat oxidation as opposed to when the two were taken

individually [94]. A systematic review of 21 studies in 2011 demonstrated co-ingestion of carbohydrates with caffeine results in a small but significantly improved endurance performance when compared to taking CHO alone [95]. However, several other studies both before and after this review have produced inconsistent results [90]. Interestingly, the magnitude of improvement of synergistic caffeine (i.e., caffeine + CHO vs. caffeine alone) is less when added to CHO than when caffeine is taken alone versus placebo [96]. Caffeine may have additional benefits for athletes during prolonged exercise as well. In a 2 h cycling time trial at 60% VO2max interspersed with bouts of high-intensity (82% VO2max) exercise [97], athletes were given low-dose (~100 mg, 1.5 mg/kg) or moderate-dose (~200 mg, 2.9 mg/ kg) caffeine. Both caffeine groups had faster time trial completion compared to placebo, and the moderate-dose group was better than the low-­ dose group [97]. This suggests that a “topping up” of caffeine periodically during prolonged exercise may be beneficial; this strategy may particularly be helpful in ultra-endurance events [9]. Table  23.6 provides pre-, during, and post-­ exercise caffeine recommendations. There has been a long-held theory that regular caffeine intake may blunt the ergogenic effects of a single pre-exercise caffeine dose. Athletes taking low-dose (3 mg/kg) caffeine on a daily basis for 15–18 days exhibit a decrease in the benefits of pre-exercise caffeine on peak cycling power performances (Wingate and incremental cycling exercise tests) [98]. After 4  weeks of this daily Table 23.6  Key recommendations for caffeine (adapted with permission from: [9]) Suggested recommendations for daily, pre-exercise, and Nutrient during exercise Caffeine 1–6 mg/kg taken 30–90 min prior to exercise ≤3 mg/kg can also be ergogenic without side effects compared to higher doses

Suggested recommendations post-exercise 3 mg/kg with carbohydrate may enhance glycogen repletion

23  Performance-Based Nutrition for Endurance Training

intake, the performance benefits of pre-exercise caffeine were no longer apparent [99]. However, athletes can still show improvements in cycling time-trial performance with a higher (6  mg/kg) pre-exercise caffeine dose [100]. Additionally, some athletes find it useful to cycle intake of caffeine, with periods of abstaining during lower-­ intensity training and/or prior to races and then resuming at race time or during high-intensity training. A caffeine “washout period” of lower (or no) caffeine intake may take about 14 days for adenosine receptor upregulation to return to “caffeine novice” levels; timing the resumption prior to a race is equally as important as performance benefits decline at 15–18  days after resuming [101]. Like any other supplement, caffeine may have adverse effects. The most common reported side effects are tachycardia, heart palpitations, anxiety, headaches, insomnia, and decreased sleep quality [102–105]. Although these side effects may be unpleasant, caffeine does not appear to result in serious side effects or complications such as water-electrolyte imbalances, dehydration, hyperthermia, or reduced exerciseheat intolerance according to one review [106]. However, higher caffeine doses (7–9 mg/kg) not only fail to show further performance improvement but also have additional undesirable side effects, such as GI distress, nervousness, confusion, and further disturbed sleep [57, 71, 80]. Due to these side effects, athletes should determine whether caffeine may help or be detrimental to their performance according to the nature of their sport. For example, athletes in high precision sports such as archery and shooting may benefit from avoiding excess caffeine or caffeine altogether, while athletes in strength and endurance sports, such as football and cycling, may benefit from caffeine [93]. Lower doses of caffeine (less than 3 mg/kg) can still have a similar positive impact on endurance performance; improve vigilance, mood, and cognitive function; and do not appear to result in any major side effects [80]. Athletes are encouraged to utilize the lowest effective dose that provides a performance benefit without unnecessary side effects.

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Nitrates Dietary nitrates have been used for years in general medical conditions such as cardiovascular disease and hypertension (1109). After the landmark study by Larsen in 2007 which demonstrated decreased oxygen cost for a given submaximal exercise workload (1110), nitrate attention has shifted towards the endurance athlete population. Inorganic nitrate (NO3-) exists at high levels in certain vegetables such as beets and beet juice (also known as beetroot juice), arugula, spinach, and celery [9]. Once consumed, NO3- is converted by oral bacteria to NO2- and then in the gut to nitric oxide (NO) [107, 108]. Nitric oxide results in systemic effects including modulation of blood flow (vasodilation), O2 regulation in working muscle, mitochondrial respiration and biogenesis, glucose uptake, and muscle contraction/relaxation [107–109]. These effects collectively improve muscle economy and efficiency, mitigate fatigue, impact cardiorespiratory performance by decreasing effort at submaximal workloads, and may improve time trial performance [10, 107, 108, 110]. One particular dietary source of nitrate studied in endurance athletes is beet juice. A review showed athletes consuming beet juice 2–3 h prior to endurance exercise led to reduced oxygen cost during exercise, improved time to exhaustion, and improved cardiorespiratory performance at anaerobic threshold and VO2max [47]. However, other studies have shown mixed results. In a subsequent review, studies that showed positive effects had only ten or fewer subjects in each study, and there were less benefits (or no benefit at all) noted in elite training athletes [10, 110]. The authors concluded this was likely due to elite athletes’ diet already containing adequate dietary nitrate, and/or already optimized metabolic efficiency from training adaptations (to the point that additional nitrate did not further increase NO). There may be variability in nitrate levels with single-day dosing. Multiday nitrate intake can result in higher nitrate levels and is also studied in endurance athletes [9]. Six days of a high nitrate diet (8.2  mmol/day, from vegetables and fruits) compared to a control diet of 2.9  ­mmol/

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day caused a significant rise in plasma nitrate Table 23.7  Key recommendations for nitrates (adapted [111]. Athletes taking this high dose showed with permission from: [9]) reduced oxygen cost during moderate-intensity Nutrient Suggested recommendations cycling, higher muscle work during high-­ Nitrates 300–600 mg of nitrate (up to 10 mg/kg or 0.1 mmol/kg) or 500 mL beet juice or 3–6 intensity leg exercise, and improved performance whole beets within 90 min of exercise onset in repeated sprints [111]. This may help further Consider multiday dosing, e.g., 6 days of a high-nitrate diet prior to event explain the variability in results with acute single-­ day supplementation and help an athlete target healthy nitrate intake levels [9]. Nitrate supplementation dosing, measurement fordable for some. If athletes can eat sufficient method, and route of administration also highly amounts of high nitrate vegetables including vary from study to study and may further contrib- beets in a healthy diet, this should in theory proute to confusion in dosing and obtaining appro- vide nitrite levels similar to nitrate supplementapriate plasma level. Recommendations have tion (of note, the nitrate content in soils may also ranged from a standard dose of 300–600 mg of a vary and may need to be taken into account nitrate supplement up to 10 mg/kg bodyweight, regarding geographic source of vegetables). In 0.1 mmol/kg (minimum 6–8 mmol), 500 mL of the above Larsen study, the daily nitrate dose beet juice (of note is over two cups of juice), or used were considered amounts achievable 3–6 whole beets [36, 52, 107]. Along with dosing through a diet rich in vegetables, specifically “the variability, timing varies in studies. Some amount normally found in 150–250g of a nitrate-­ research has studied beet supplementation 2–3 h rich vegetable such as spinach, beetroot, or letprior to exercise, as NO levels peak at 2–3 h post-­ tuce” [114]. If an athlete chooses to supplement consumption [107, 112, 113]. However, recent or change their diet to high-nitrate foods (if predata shows beet juice consumption should be viously low), they should be aware that nitrates consumed only 90 min before exercise; although can mildly lower diastolic and mean arterial NO levels may peak at 2–3 h post-ingestion, they blood pressure. This can be an issue for athletes then sharply decline leaving athletes only in peak with low blood pressure, orthostasis, or risk for NO levels at the start of a race and in a subopti- hypotension [115]. Finally, on a practical note, mal state for the rest of the event [107, 112, 113]. athletes should be aware of the possibility of beeFurthermore, the method of nitrate ingestion turia and red bowel movements, which is considshould be considered. Reduced oral contact time ered normal [108]. with oral bacteria (drinking quickly) or regular use of mouth rinse or oral antiseptics, especially immediately prior to nitrate consumption, can Iron limit the NO3- to NO2- conversion [10, 32, 107]. Lastly, athletes should take into account possible Iron is an important mineral for the body with GI distress from beet juice pre-race. The above significance to athletes due to its role in oxygen 500  ml recommendation of beet juice (almost transport and energy metabolism [116]. There are 17 oz.) can certainly result in GI discomfort and two important iron-dependent metabolic pathimpact the athletes’ hydration plan. Newer alter- ways relevant to the athlete: oxygen transport via natives include beet juice concentrate, powders, hemoglobin (Hb) and myoglobin to exercising and “shots” that have been commercially devel- skeletal muscle and the oxidative production of oped [9]. Refer to Table 23.7 for endurance ath- adenosine triphosphate (ATP) in the electron lete nitrate recommendations. transport chain via non-heme iron (sulfur When considering nitrate supplementation, enzymes) and heme-containing cytochromes athletes should understand the costs. Commercial [117, 118]. As endurance athletes have a high nitrate or beet supplements like any other sport demand for aerobic metabolism, iron plays an supplement can be expensive and may be unaf- important role in the metabolic pathway for

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­athletes [119]. Despite its importance for athletes, iron deficiency is widely common in the athlete population; that can be from multiple etiologies including GI blood loss, hemolysis, hematuria, sweat loss, intense exercise, foot strike hemolysis, thermohemolysis, or lack of dietary intake or absorption [120, 121]. Iron deficiency is documented in around 15–35% of female and 3–11% of male athletes, including collegiate and even elite athletes [122–125]. Iron deficiency can cause symptoms such as lethargy, fatigue, negative mood swings, and decreased work capacity, all of which may affect athletes’ training and performance [126–130]. It has been debated what levels specifically define iron deficiency, such as serum iron, total iron binding capacity, and others. Current evidence on assessment of iron deficiency utilizes blood markers including ferritin, hemoglobin concentration, and transferrin saturation [117]. Furthermore, there are limitations with each biomarker to accurately define iron deficiency. Ferritin is an acute phase protein and is increased during states of inflammation and even after intensive exercise, resulting in possible falsely high levels in an iron-deficient athlete [131]. Hemoglobin can also be affected by hydration, plasma volume shifts, and hypervolemia that can occur with exercise, leading to possible pseudo-­ anemia [132–134]. To avoid misdiagnosing iron concentration and red blood cell markers, an athlete’s hydration status and level of exercise should be taken to account, with no high-­intensity exercise 2–3  days prior to a blood assessment [135, 136]. There are three proposed stages of iron deficiency in the athlete population. Stage 1 iron deficiency presents as depleted iron stores primarily in the bone marrow, liver, and spleen (as defined by serum ferritin   115  g/L, and transferrin saturation  >  16%) [137]. Stage 2 is iron deficiency non-anemia when iron supply for the erythroid marrow decreases causing erythropoiesis to diminish, manifesting as low transferrin saturation, lower ferritin levels, but still normal Hb (ferritin115 g/L, transferrin saturation  90.0

American College of Sports Medicine (ACSM) guidelines for training or non-continuous activities.

b WBGT

Risks/Impacts

65.1–72.0

Risk of heat stress and other heat illnesses begin to rise. High risk individuals should be monitored or not compete

72.1–78.0

Risk for all competitors is increased

78.1–82.0

Risk of unfit, non-acclimatized individuals is high

82.1–86.0

Cancel activity/competition

American College of Sports Medicine (ACSM) guidelines for continuous activities or competitions

Fig. 24.3 (a) ACSM’s guideline summary chart for noncontinuous activities. (b) ACSM’s guideline summary chart for continuous activities [3]

young athletes will understand how to pace themselves during activity in a hot and humid environment. Youth athletes do not tolerate the heat as well as adults and are at greater risk for heat collapse than adults. This is due to the combination of a greater surface area-to-mass ratio, which causes them to retain proportionally more heat in a hot environment and the fact that they have less efficient body temperature

control regulation. As such they produce less sweat than adults. A separate plan for lightning hazard should be developed and documented. The current recommendations are to stop the event for flash-to-bang times under 30 s and not to resume activity until 30 min after the last sighted lightning. Shelter for competitors in case of dangerous weather needs to be identified ahead of time.

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Work/Rest and Water Consumption Table Applies to average sized, heat-acclimated Soldier wearing ACU, hot weather. (See TB MED 507 for further guidance.) Easy work • Weapon Maintenance • Walking Hard Surface at 2.5 mph,