Periodization

Periodization is one structured training approach that highlights this concept. It was developed by a Russian physiologist in the 1960s but has had a significant resurgence in today’s training programs (Figure 44-1). In periodization, training is divided into defined “periods” to allow buildup of training stresses, time for rest and adaptation to training, and continual progression of fitness. These periods include macrocycles (commonly lasting 1 year), which are divided into shorter mesocycles (commonly lasting 1 month), which are then subdivided into microcycles (commonly lasting 1 week). Microcycles are generally the weekly training programs. Each mesocycle can be made up of four weekly microcycles with a gradual buildup of training frequency and intensity over the first 3 weeks and then a slight decrease in the fourth week to allow for rest and the subsequent metabolic training adaptations to occur. The athlete is then ready to enter the next 4-week mesocycle and progress through another four weekly microcycles. The amount and intensity of training occurring in each mesocycle depend on where the athlete is in relationship to the competitive season, which is how macrocycles are structured.

FIGURE 44-1 A template for a periodized training program.

(From Bachl N, Baron R, Smekal G: Principles of exercise physiology and conditioning. In Frontera WR, et al, Clinical sports medicine: medical management and rehabilitation, Philadelphia, 2007, Saunders.)

A typical year-long training program will have three macrocycles: preseason or “build-up phase,” competitive season or “maintenance and fine-tuning phase,” and finally a postseason or “recovery phase.” The preseason macrocycle is typically the longest, occurring before the competitive season. It is designed to develop fitness in anticipation of the more intense training to follow.¹⁶² During the preseason macrocycle the athlete generally focuses on higher volume and lower intensity exercise.

The competitive season macrocycle follows the preseason period. The focus of this cycle is to develop and maintain peak fitness with a focus on high-intensity training and sport-specific technique drills.¹⁶² Because of the higher intensity training, the volume must be significantly reduced.

Finally, the postseason macrocycle is a time for the athlete to recover from the previous year’s training and physically and mentally prepare for the next year of training and competition.¹⁶² The early portion of this period necessitates “active rest.” The athlete generally participates in unstructured, non–sport-specific recreational activities to allow for recovery from the stresses of the competitive season. This is an important period for the athlete to adequately recover from injuries, prevent overtraining, and take a “mental break” from the competitive season.

During the competitive season, a typical microcycle includes a tapering period just before competition. The taper is a short period of reduced training before an important competition with the goal of optimizing performance. Although it is well recognized that a reduction in training before competition improves performance, it not definitively known what is the most ideal taper strategy regarding altering training volume, intensity, and frequency.^8,77,113 A recent metaanalysis demonstrated that the most efficient strategy to maximize performance gains appears to be a 2-week taper during which training volume is exponentially reduced by 41% to 60%.¹⁹ This study found that the ideal taper for endurance athletes kept training intensity and frequency stable, with only volume being progressively reduced.

Overtraining Syndrome

An important set of symptoms to be aware of for any athlete, coach, or sports medicine physician is that related to overtraining syndrome. When prolonged, excessive training occurs concurrently with insufficient recovery, the athlete might have unexplainable performance decrements resulting in chronic maladaptations leading to overtraining syndrome.¹⁰⁹ Common symptoms of overtraining syndrome in addition to an unexplained performance decrement include generalized fatigue, mood disturbance, poor sleep, and increased rates of illness and injury. By definition, these symptoms persist despite more than 2 weeks of rest.¹⁵⁸ The treatment is rest, from weeks to months, with gradual resumption of training. Prevention, however, is the best treatment, and following a periodized training program is one method to ensure adequate rest from more intense bouts of training.

Altitude Training

Altitude/hypoxic training is a controversial area of research and sports performance. Many elite endurance athletes incorporate altitude training into their typical training program in hope of enhancing performance in competition. For those athletes who do not live in mountainous areas, there are a variety of “altitude tents” on the market that can be used to simulate living at high altitude. Some controversy arose in 2006 when the World Anti-Doping Agency (WADA) considered placing “artificially-induced hypoxic conditions” on the Prohibited List of Substances/Methods.¹⁶⁶ Another area of controversy is the uncertain primary physiologic mechanism(s) responsible for the effect of altitude training on sea-level performance. The proposed mechanisms include accelerated erythropoiesis (increased erythrocyte volume) as the primary hematologic effect, as well as nonhematologic factors such as improved muscle efficiency at the mitochondrial level, glucose transport alterations, and enhanced muscle-buffering capacity via pH regulation.⁶⁰

Most scientists agree that the most effective form of altitude/hypoxic training is the “live high–train low” method, whereby athletes “live high” to stimulate erythropoietin and subsequently increase erythrocyte volume and “train low” to train at a higher intensity with improved oxygen flux to induce beneficial metabolic and neuromuscular training adaptations.¹⁶⁷ The controversy here comes from not knowing what the optimal “dose” of altitude training truly is. So far the research suggests that for athletes to derive the most beneficial hematologic effects while using natural altitude, they need to live at an elevation of 2000 to 2500 meters for 22 hr/day for 4 weeks. For those using simulated altitude environments, 12 to 16 hours of hypoxic exposure might be necessary but at a higher elevation (2500 to 3000 meters¹⁶⁷).

Kinetic Chain Assessment

The kinetic chain model is based on the idea that each complex, athletic movement is the summation of its constituent parts. For example, a quarterback’s throwing motion is created through the action of feet on the playing surface, loading of the lower limbs, rotation of the hips and abdominal muscles, activation of the latissimus dorsi, stabilization of the glenohumeral joint by the periscapular muscles, loading of the throwing arm through the deltoid and biceps, and finally from the upper limb motion of elbow extension and wrist flexion. The upper limb acts as a “funnel” for the energy generated by the core and lower limbs.⁸⁵ Each of the “links” in the chain must function well to optimize performance and minimize potential tissue trauma.

“Catch-up” occurs when an athlete tries to compensate with one segment for a deficiency in a separate segment. This phenomenon puts higher stress on the tissues of the distal segment and predisposes it to injury.⁸⁵ For example, a runner mighty present with patellofemoral pain for a variety of these reasons. This could simply be an overtraining phenomenon, or it might be due to weak or inhibited hip musculature, abnormal foot and ankle biomechanics, or poor running technique.¹⁰⁵ Relief can be achieved through resting the athlete temporarily, but the pain might consistently return unless the causative issue is corrected. The experienced sports medicine physician will identify the tissue diagnosis and treat it appropriately, but will also identify and correct all predisposing factors. It is important that the physician is able to explain these concepts to the athlete and the treatment team to achieve optimal results.

Rather than view all similar overuse injuries as the same issue, the sports medicine physiatrist is able to break down the complex motions of the athlete into the constituent parts, identify the maladaptive pattern, and create a rehabilitation program that will prevent the injury from recurring. When examining the injured athlete, it is vital to make a biomechanical diagnosis rather than to focus exclusively on the injured tissue. Although it is easy to focus exclusively on the painful tissue, it is essential to assess the entire athlete and his or her mechanics to make appropriate tissue and biomechanical diagnoses (Table 44-1).

Table 44-1 Tissue Diagnosis and Biomechanical Diagnosis

Evaluating an injured athlete involves a thorough discussion of the current problem, previous athletic injuries in the same area, as well as potentially other seemingly unrelated injuries. Discussion of training patterns, including intensity and volume, as well as competition details is important. Proper equipment fit and technique should also be assessed. Differentiating between a slowly worsening insidious process and a more acute injury is key to creating an appropriate treatment plan. These subtle distinctions can frequently reveal the underlying cause of the current injury.

The physical examination of the athlete must be focused on finding the biomechanical culprit, rather than focusing solely on the painful tissue. The athlete must be examined in detail to fully assess the possible causes of the injury. Select upper limb tests that help determine the role of the scapula in upper limb injuries include the scapular assistance test and the scapular retraction test.⁸⁷ Core muscle function must be assessed dynamically and addressed as part of the rehabilitation plan.⁸⁸ Examples of physical examination maneuvers to evaluate core muscular function in the athlete are demonstrated in Figures 44-2 to 44-5. The kinetic chain assessment is designed to assess flexibility, strength, and functionality of the affected limb. The examination essentially assesses multiplane sports-specific dynamics rather than single-plane, solitary joint movements.

FIGURE 44-2 Single leg squat.

FIGURE 44-3 Sagittal plane evaluation.

FIGURE 44-4 Frontal plane evaluation.

FIGURE 44-5 A, Plank. B, Side plank evaluation.

Proprioception and neuromuscular control are vital, and often unrecognized, components of athletic activity, and loss of these is increasingly noted as a predisposing factor for injury. Commonly called “muscle memory,” these abilities help an athlete control the limbs throughout the full spectrum of motion. Deficits here can be subtle and difficult to assess in the typical office visit. Testing must be multiplanar and mimic the athlete’s typical motion patterns.

It is vital for the examining physician to have a thorough understanding of the motions involved in the athlete’s sport to make the appropriate changes; for example, a difference of 10 degrees in knee extension during the cocking phase of a tennis serve increases the valgus load at the elbow by 21%.⁵⁰ When necessary, this can be accomplished through discussion with the athlete, parent, coach, and/or trainer.

Prehabilitation

Prehabilitation is based on the concept that many sports injuries can be prevented if the athlete engages in an appropriate preseason “prehabilitation” program. Most of the scientific literature regarding prehabilitation programs focuses on noncontact anterior cruciate ligament tears.^73,74,97 Poor form is also linked to numerous athletic injuries. Balance perturbation, plyometric training, and stretching programs all have a role in the prehabilitation of the athlete. Ideally, some of these issues can be assessed during the preseason physical examination and corrected before the start of the season. A large proportion of sports injuries are related to overuse, and it is wise to have a discussion of these issues with athletes and coaches in the preseason. Off-season cross-training, core muscle work, and cardiovascular preparation are generally considered key to a healthy season.

Prehabilitation can be viewed as an injury prevention program. These programs are sport-specific, and often position-specific, but always address the basic components of all athletic movements and the potential “breaks” in the kinetic chain: (1) flexibility, (2) strength, and (3) endurance. These programs can be used preseason, postseason, or during the season to treat previous injury or to prevent future injuries. For example, a soccer prehabilitation program could involve daily postactivity stretching, strength and plyometric training three times per week, and cardiovascular exercise three times per week. A thrower’s prehabilitation program might involve a focus on daily postexercise range of motion (ROM), strength training two times per week, and daily technique practice, with pitch/throw volumes increasing weekly. Additional focus can be placed on any component based on the individual athlete’s needs.

Injury Phases

Rehabilitation is guided by the status of the injured tissue, so an understanding of the timing of injury and recovery is essential. Injuries can be acute, subacute, chronic, or an exacerbation of a chronic condition. A detailed history is required because athletes will present at varying points of their tissue healing, and the treatment plan will have to be created appropriately. Four general phases are typically seen in tissue injury and repair. The physician caters the treatment to the individual tissue and the timing of the injury. The first phase involves the initial injury and the subsequent inflammation, edema, and pain. This phase is typically short, lasting days, depending on the severity of the injury. The reparative phase of the injured tissue might last from 6 to 8 weeks. It involves cell proliferation, granulation tissue formation, and neovascularization. The last phase is remodeling, which occurs as the tissue matures and realigns.

Excessive inflammatory response or exuberant repair can result in poor outcomes. For example, problems experienced during the remodeling phase can result in excessive scar tissue formation and the development of recurrent/chronic injury. Many athletes return before the tissue itself is adequately healed and experience reinjury or an exacerbation of their previous symptoms. This likely occurs if the injured tissue is not fully healed or if the new tissue has not adapted to tolerate the desired motion or inherent stresses of the sport.

Stages of Rehabilitation

Rehabilitation can be viewed as a three-stage spectrum from the acute stage to the recovery stage, and then to the final functional stage through return to full play (Table 44-2).⁸⁶ Each stage has individual goals that lead to the overall goal of RTP. The acute stage of rehabilitation is focused on managing the symptoms and signs of the injury. The classic PRICE (protection, rest, ice, compression, and elevation) approach is often followed. Medications, manual therapy, and physical modalities are also used during this phase. If necessary, bracing, injection, or surgery is performed to facilitate protection and future healing. ROM, strength, and cardiovascular fitness must be maintained as much as is possible and tolerated. This can be accomplished by exercising the upper body of an athlete with a lower body injury. Passive ROM must be viewed with caution in the acute to subacute injury phase because it might injure the tissue, leading to increased pain and inflammation. Isometric strength exercises can be prescribed during this stage, if tolerated, to decrease pain, edema, and potential atrophy. The athlete can advance to the next stage of rehabilitation if adequate pain control and near-normal ROM is achieved.

Table 44-2 Typical Return-to-Play Phases

The recovery stage is often the longest part of the rehabilitation program and shifts the focus from symptom management to the restoration of strength and endurance as it applies to function. Tissue healing can continue at this time and will dictate the type of treatments recommended. Therapies move from passive to active during this stage. Flexibility, strength, symmetry, and proprioception are all addressed at this time.

Strength exercises advance from isometric to isotonic, including both concentric and eccentric movements. Open-chain exercises are ones in which the distal segment is free, whereas closed-chain exercises are ones in which the distal segment is fixed. Closed-chain activities are designed to stabilize an injured segment or to decrease the force passing across a joint. They also allow for a stepwise approach to kinetic chain rehabilitation. The rehabilitation program should typically focus on correcting erroneous movement patterns rather than creating completely new patterns for the athlete to learn.

In the case of an athlete with a shoulder injury, the rehabilitation program moves from predominantly closed-chain exercises, to axial-loaded exercises, to open kinetic chain exercises, to full sport-specific rehabilitation.¹⁰⁸ Kinetic chain rehabilitation is modified to the individual athlete’s symptoms and dysfunction. Rather than view this type of rehabilitation as a series of discrete steps, the physiatrist should consider it as a transition from dysfunction to function and adjust the treatment plan and timing accordingly.¹⁰⁸

The parameters of the strength training program (repetitions, resistance, speed, multijoint movements) can be adapted during this time, depending on the clinical scenario. Preexisting kinetic chain issues or tissue overload issues from the current injury are addressed at this time as well. As the rehabilitation program continues, increasingly athletic maneuvers (running, jumping, cutting) are used. Neuromuscular control (NMC) involves proprioception, muscle control, and the interplay between the two. Without sufficient NMC, the athlete might continue to be predisposed to future injury. This recovery phase is the most variable and has the highest potential for reinjury, as the tissue is actively remodeling. The athlete must be reevaluated frequently during this phase because setbacks are common and can require modification of the rehabilitation plan. The athlete can advance to the final stage once pain-free ROM is achieved and strength is 75% to 80% or greater (compared with the noninjured side).

During the final functional stage of rehabilitation, the focus remains on kinetic chain issues and technique errors. Strength balance, power, endurance, functional ROM, and NMC are aggressively addressed. Sport-specific drills are used during this stage and advanced to include practice. Full RTP is achieved when the injury is no longer painful; when there is normal flexibility, strength, and proprioception; and when appropriate sport-specific mechanics and sport-specific skills are achieved and reproducible. In many cases, this rehabilitation phase becomes the maintenance program.⁵⁶

Throwing

Pitching a baseball is a classic example of the body acting as a kinetic chain of motion where foot placement and ankle ROM will affect how the pitcher uses his or her shoulder girdle and subsequently throws the ball. If there is a “weak link” in the pitcher’s kinetic chain, there can be a predisposition to injury because of the repetitive nature of pitching. Whole body activity is involved in transferring momentum from the body to the ball. The momentum begins with a drive from the large leg muscles and rotation at the hips, progressing through segmental rotation of the trunk and shoulder girdle, transferring energy through elbow extension, next through the small forearm and hand muscles, and finally to the ball. This transfer of momentum and subsequent energy is related to a series of body segment accelerations and decelerations. When an initial segment of the body (e.g., trunk) accelerates, the next segment (e.g., arm) within the kinetic chain is left behind. When the trunk decelerates, the momentum is transferred to the arm with an increased velocity of the arm that is accentuated by the forces acting on the shoulder/arm. This motion and the forces are ultimately transferred to the ball.

Approximately 50% of the velocity of a pitch results from the step and body rotation (from the potential energy stored in the large leg and trunk musculature).¹⁵⁴ The other 50% comes from the smaller muscles of the shoulder, elbow, wrist, and hand. When forward stride is not allowed, the peak velocity of a pitched ball decreases to 84%. When the lower body is restricted, it decreases to 64%. Peak velocities in water polo are approximately 50% that of baseball because of the lack of a ground reaction force.

The baseball pitch is composed of six phases (Figure 44-6). Understanding these phases is critical to understanding, diagnosing, preventing, and treating throwing sports’ injuries.

FIGURE 44-6 The six phases of the baseball pitch.

Windup begins when the pitcher initiates motion and ends with maximum knee lift of the lead leg when the ball is removed from the glove. Push off of the stride leg allows the center of gravity of the body to move forward. Few injuries occur in this early phase because the shoulder musculature is relatively inactive and most forces arise in the lower half of the body.

Early cocking is next and is often called the stride phase.¹¹⁰ The stride leg extends toward the batter, as does the knee and hip of the pivot leg, propelling the body forward into the stride. As the hips rotate forward, the trunk follows and subsequently, the throwing shoulder abducts, extends, and externally rotates, leaving the shoulder in a “semicocked” position. Again, in this early phase, there is less risk of injury because most forces are still being generated in the trunk and lower limbs; however, shoulder activity does become more evident. The trapezius and serratus anterior demonstrate moderate to high activity to protract and upwardly rotate the scapula. The middle deltoid generates the abduction force, and the supraspinatus fine-tunes humeral head positioning within the glenoid.

The next phase is late cocking. The hallmark of this phase is when maximal shoulder external rotation is obtained. The shoulder begins this phase in approximately 50 degrees of external rotation and ends in about 175 degrees at maximal external rotation. This extreme amount of rotation allows the greatest accelerating force to the ball over the greatest possible distance. The amount of external rotation obtained correlates with the speed of the pitched ball. A majority of injuries occur in the late cocking and deceleration phases of throwing (Box 44-2).¹²¹ For late cocking, this is due to the forces needed to stabilize the shoulder in this extreme ROM. The dynamic stabilizers of the anterior shoulder (long head of the biceps, subscapularis, and pectoralis major) are very active in this phase. The static stabilizers (glenohumeral ligaments, capsule, and labrum) are active as well. The glenohumeral ligaments and capsule increase in laxity because of the extreme ROM in the overhead athlete. This laxity is necessary for performance; however, overstretching these ligaments enhances the work of the dynamic stabilizers with a resultant potential for injury to them.

During the acceleration phase, the shoulder is powerfully internally rotated from 175 degrees of external rotation to 90 to 100 degrees at ball release. Shoulder abduction is relatively fixed in all throwers at 90 degrees. Trunk lateral flexion (and not shoulder abduction) generally determines what position the arm is in relative to the vertical plane. “Over the top” throwers have a greater amount of contralateral trunk flexion, and “sidearm” throwers have less contralateral trunk flexion. If there is less than 90 degrees of abduction as a result of fatigue, weakness, or just poor form, the common observation is a “dropped elbow.” “Hanging” or dropping the elbow results in a reduced pitch velocity and an increased risk of injury to the shoulder (rotator cuff) and the elbow (ulnar collateral ligament injury). Another common injury from the acceleration phase, particularly in older pitchers, is due to subacromial impingement as they internally rotate and adduct the abducted arm during acceleration.

The deceleration phase is manifested by large eccentric muscular forces of the posterior shoulder girdle to decelerate that rapid internal rotation of the acceleration phase.²⁰ Deceleration begins after ball release and ends when the arm reaches 0 degrees of internal rotation. The posterior shoulder girdle is active in this phase, including the scapular muscles, rotator cuff external rotators (particularly the teres minor), and the posterior deltoid. Because of these large eccentric contractions, injury is common in this phase (Box 44-3).

The final phase of pitching is the follow-through phase. This is a “passive” phase where the body is merely catching up with the throwing arm. Low-grade eccentric loading of the shoulder musculature and little risk of injury are noted during this phase.

Because of the high risk of overuse injury in the young pitcher’s throwing arm, U.S. baseball has developed age-based pitch count guidelines to decrease this risk (Table 44-3).⁸³ For similar reasons, curve balls and sliders should not be pitched until the athlete reaches puberty. It is also recommended that young pitchers not compete in baseball more than 9 months per year. During those 3 “off” months, they should not compete in other overhead arm sports, such as competitive swimming or javelin throwing.

Running

Notable differences are observed between a walking gait cycle (see Chapter 5) and a running gait cycle.¹²⁰ One in particular is a third phase in running called the float phase. Float is a period when neither foot is in contact with the ground. It occurs at the beginning of initial swing and the end of terminal swing (Figure 44-7).

FIGURE 44-7 A comparison of the walking (A) and running (B) gait cycles.

(Modified from Ounpuu s: The biomechanics of walking and running, Clin Sports Med 13(4): 843-863, 1994.)

The walking gait cycle has a period of double limb support, which is not present in running, that occurs in the first and last 10% of the stance phase. The stance phase of gait is decreased from 60% while walking to 30% while running and 20% while sprinting. Consequently, as speed increases, the stance phase decreases. As speed increases, the velocity and range of lower limb motion increases, which in turn serve to minimize vertical displacement and improve efficiency. The body lowers its center of gravity by increasing hip flexion, knee flexion, and ankle dorsiflexion; consequently, the major kinematic difference between walking and running occurs in the sagittal plane of motion.

Faster running also changes foot contact.¹⁶⁸ In slower running and walking, contact is typically heel to toe. As running speed increases, foot strike occurs with the forefoot and heel simultaneously, or the forefoot strikes initially followed by the heel lowering to the ground. In sprinting, the athlete maintains weight-bearing on the forefoot from loading response to toe-off.

The angle of gait is different between walking and running. This is the angle between the longitudinal bisection of the foot and the line of progression. This angle is 10 degrees in walking. In running, this angle approaches 0 degrees as foot strike is on the line of progression to allow more efficient locomotion by limiting deviation of the center of gravity.

Swimming

Four competitive strokes are used in swimming: freestyle (crawl), backstroke, butterfly, and breaststroke. Four phases of the swim stroke are common to freestyle, backstroke, and butterfly. The first phase is the entry or catch. This encompasses hand entry into the water until the beginning of its backward movement. The propulsive phase is divided into two separate phases: pull and push. The pull phase ends as the hand arrives in the vertical plane of the shoulder. During the push phase, the hand is positioned below the shoulder and pushes through the water until its exit from the water historically at the level of the greater trochanter. The final phase is the recovery phase, which entails the aerial return of the hand.

During the propulsive phases of swimming, the arm is moved through adduction and internal rotation starting from a stretched position of abduction and external rotation. The pectoralis major and latissimus dorsi are the major contributors to this motion; however, the serratus anterior and the internal rotator function of the subscapularis and teres major assist.¹⁵⁶

During the recovery phase, scapular retraction is provided by the rhomboids and middle trapezius, whereby shoulder external rotation is provided by the posterior deltoid, teres minor, and infraspinatus. In preparation for hand entry during midrecovery, the serratus anterior and upper trapezius upwardly rotate the scapula for shoulder stabilization.

Kick patterns are also an important part of swimming mechanics. In the flutter kick for the freestyle stroke, the knees should flex only about 30 to 40 degrees, and hip flexion should be minimal. The breaststroke kick is a whip-kick that creates a significant valgus moment at the knee. Because of this increased knee valgus, medial knee injuries in breaststrokers are common. The pain can be from a medial collateral ligament sprain or a medial plica/synovitis.

General rehabilitation and prehabilitation principles have been established for swimmers with shoulder pain with which all sports medicine clinicians should be familiar. The overarching principle is that most shoulder pain in swimmers (impingement and rotator cuff tendinopathy) is due to dynamic muscle imbalances, weakness, and biomechanical faults, and not hard anatomic factors. A major tenet of shoulder rehabilitation for the swimmer is scapular stabilization, with a prime focus on endurance training of the serratus anterior and lower trapezius. The serratus anterior is a muscle of particular focus because it has been demonstrated to function at 75% of its maximum test ability in swimming and is active throughout the swim stroke cycle.¹⁴³ Other tenets of shoulder rehabilitation in swimmers include stretching the internal rotators and posterior capsule and cervical and thoracic mobilization.

Jumping and Landing

The biomechanics of jumping and landing in sports is particularly well researched in the setting of noncontact anterior cruciate ligament (ACL) injuries of the knee. Noncontact ACL injuries occur more frequently with the knee in less flexion.¹⁷² In this position there are greater knee extensor loads with greater forces creating anterior tibial translation and subsequent ACL injury. A well-defined gender difference is observed in jumping and landing mechanics that is likely one reason for the higher rate of noncontact ACL injuries in female athletes.²⁹ Female athletes land more erect with less knee and hip flexion. They land with less hip external rotation and abduction. They also generally have an imbalance of increased quadriceps to hamstrings activation ratio, creating greater knee extension and lesser knee flexion forces. One goal of ACL injury prevention programs is to improve jumping and landing technique by increasing knee and hip flexion during landing and balancing the quadriceps to hamstring activation ratio.

Therapeutic Drugs

Performance-Enhancing Drugs

Creatine

According to one source, 90% of weightlifters and bodybuilders in the United States are regular users of creatine (Cr). They tend to be male, have an average age of 32 years, attended college, and have a substantial income.¹²⁷ In a survey of NFL trainers and team physicians, all teams had players actively taking the supplement, with estimated usage 33% to 90%.¹⁵²

Cr, a naturally occurring compound made from amino acids glycine, arginine, and methionine, is the most popular nutritional supplement on the market.^94,152 It is proposed that Cr phosphate supplementation benefits short-duration, high-intensity, repetitive exercise by enhancing adenosine triphosphate regeneration.^94,125

Cr appears to be most effective for activities that involve repeated short bouts of high-intensity physical activity,^63,152 such as jumping, sprinting, and cycling.¹² When maximal force or strength is the outcome measure, Cr has consistently been found to significantly impact force production regardless of sport, sex, or age.¹⁵²

Common side effects of Cr include muscle cramping and gastrointestinal distress.¹²⁷ A number of cases of renal failure have been reversed with withdrawal of Cr supplementation.^94,152 It is notable that most studies in the literature were short term with healthy subjects. Also, there are insufficient data on the possible effects of Cr on other Cr-containing tissues, such as the brain, cardiac muscle, or the testes.¹⁵²

Because it is not classified as a drug, Cr is not under direct regulation by the FDA and is widely available over the counter.¹⁵² The NCAA does not allow member teams to provide Cr to its players. According to one survey, 40% of NFL teams provided Cr for their players.¹⁵²

For a summary of drugs and supplements used in sports, see Table 44-5.

Clearance to Play

The lead physician must make the determination to clear the athlete without restrictions or with recommendations for further evaluation or treatment. Alternatively, athletes might not be cleared for participation in certain sports or might not be cleared for participation in any sport.

Cardiovascular Screening

Sudden cardiac death (SCD) is a rare and devastating condition seen at all levels of sport. The American Heart Association’s (AHA) recommendations for cardiovascular screening include specific questions regarding family history, personal history, and a thorough physical examination (Box 44-5). Controversy exists in sports medicine regarding screening electrocardiograms (ECG) and echocardiography. The AHA currently does not recommend screening 12-lead ECG, echocardiograms, or exercise stress testing for athletes without risk factors.¹⁰² The IOC and the European Society of Cardiology recommend screening ECG as part of the PPE, in part because of different etiologies of SCD between the United States and Europe.³⁸ The AHA decision not to recommend this extra screening is based on the low prevalence of SCD, limited resources, impracticality of mass screening, and the lack of a physician base to interpret the ECG, as well as the consequences of false-positive test results.^38,102 Hypertrophic cardiomyopathy (HCM) is the most common cause of SCD in American athletes. It is an autosomal dominant disease, and detailed family history might detect premature cardiac death and lead to further diagnostic testing in the athlete. Echocardiography is the most effective way of diagnosing HCM but would require the screening of 200,000 athletes before finding one with the condition.⁵¹

Medicolegal Aspects of the Preparticipation Evaluation

The majority of the responsibilities of a volunteer team physician are covered by Good Samaritan laws. The PPE is a notable exception. A physician might be held liable for malpractice if an athlete is cleared to play despite the presence of a medically contraindicated condition. Liability waivers and similar documentation are not acceptable in the presence of medically contraindicated conditions. Athletes can legally challenge physician nonclearance decisions and have occasionally won the right to participate despite medical judgment. In the presence of a life-threatening condition, physicians are advised to follow their medical judgment and not clear the athlete for play.

Sudden Cardiac Arrest in Athletes

The leading cause of death in young athletes is sudden cardiac arrest (SCA), typically as a result of a structural cardiac abnormality. In a cohort of 387 young athletes, HCM was the most common cause of SCA, accounting for 26% of deaths; commotio cordis was second at 20%; and coronary artery anomalies was the third most common cause at 14%.¹⁰⁰ Coronary artery anomalies are the most common cause of SCA in young female athletes. In athletes over the age of 35, coronary artery disease is by far the most common cause of SCA at 75%. Nonstructural causes, such as inherited arrhythmia syndromes and ion channel disorders, are much less common sources of SCA in young athletes, making up only 2% of deaths in that cohort.

The incidence of SCA in high school–aged athletes is 1:100,000 to 1:200,000, and in college-aged athletes it is 1:65,000 to 1:69,000. A higher incidence is seen in males (5:1, males/females). Vigorous exercise appears to be a trigger for lethal arrhythmias because 90% of SCA occurs during training or competition. It is unfortunately very difficult to prevent, given that most athletes are asymptomatic until the fatal event. Most patients with SCA are found in asystole of pulseless electrical activity (PEA), both nonshockable rhythms. The next most common are ventricular fibrillation (VF) and ventricular tachycardia (VT) (both shockable rhythms). It is likely that most victims start in VF or rapid VT at the time of collapse, but the rhythm has already deteriorated to asystole or PEA before the first rhythm analysis. The probability of successful defibrillation from VF decreases rapidly over time, with survival rates declining 7% to 10% for every minute defibrillation is delayed, which emphasizes the importance of AEDs and a well-rehearsed EAP.

Survival after SCA is dismal. In a cohort of 486 young athletes (ages 5 to 22), the survival rate was only 11%.⁴⁶ Besides the inherently poor prognosis, another factor affecting survival in SCA is delayed early recognition and consequently delayed defibrillation. Three main factors are known to delay treatment in SCA that all medical personnel need to understand. The first is agonal or occasional gasping mistaken for breathing. Second, many lay rescuers falsely identify the presence of a pulse; consequently the updated CPR guidelines eliminate lay rescuer assessment of the pulse and recommend cardiac arrest be assumed if the victim does not demonstrate normal breathing. Finally, the third factor is myoclonic activity falsely identified as seizure and not cardiac arrest. Seizure activity is present in approximately 20% of patients with cardiogenic collapse.⁴⁷

Cervical Spine

Cervical spinal cord injuries are one of the most catastrophic injuries in all of sports medicine. They have the potential to occur in any sport but are predominantly seen in football, gymnastics, and ice hockey. The data are most robust for high school and collegiate football, and the annual incidence of cervical spinal cord injury is 6:100,000 and 4:100,000, respectively.¹¹² Advances in helmet technology have decreased the incidence of intracranial hemorrhage but paradoxically increased the incidence of cervical spine injury. Rule changes, including the banning of spear-tackling, have been effective at decreasing this rise. The risk of injury can never be fully avoided in contact sports, but the minutes that follow the injury itself are vital to prevent secondary neurologic or cardiopulmonary sequelae.^17,153

As with all injuries, the athlete should be assessed for the need of basic life support (BLS). If BLS will be needed, emergency personnel should be contacted and the EAP activated. Any athlete who is unconscious or unable to move must be treated as having a spinal cord injury or unstable fracture until proven otherwise. The athlete should not be moved unless absolutely essential to maintain the airway, breathing, or circulation. If the athlete must be moved, the spine should be kept in a neutral position, and the athlete should be placed supine. Athletes found prone must be moved safely into a supine position by a minimum of four trained individuals. These transfers are stressful, not intuitive, and must be practiced by the team physician and training staff to be performed safely and correctly.

Removal of the facemask must be done as soon as is prudent to ensure access to the airway, regardless of the patient’s current respiratory status. Current recommendations advise against removal of an athlete’s helmet or shoulder pads in an uncontrolled environment because of the amount of cervical movement that is created.⁹⁰

Any athlete having significant spine pain, neurologic deficit, or diminished level of consciousness should be transported in the appropriate manner for further observation and testing. A written plan must be established for the care and transfer to a medical facility of a potentially spinal cord–injured athlete. Coaches and athletic trainers should have BLS skills and should be active participants in preparing a plan for the stabilization of an injured player. The athlete’s equipment must be properly maintained, and the medical personnel that will assess players on the field must have the ability, skill, and tools necessary to remove the athlete’s equipment if necessary.

Exercise-Associated Collapse in Athletic Endurance Events

Exercise-associated collapse (EAC) in the endurance athlete has a broad differential diagnosis (Box 44-6). Given space constraints, this section focuses on benign EAC, exercise-associated hyponatremia, cardiogenic collapse, and heat-related illnesses. In general, when an athlete collapses before the finish line in a race while still running, the diagnosis is more ominous. The assessment of a collapsed athlete starts with assessing the level of responsiveness and checking airway, breathing, and circulation (ABCs). Depending on the severity of the presentation, specific symptoms, and vital signs, a diagnostic workup can include an assessment of cardiac rhythm, rectal temperature, and blood glucose and sodium levels.

The most common cause of collapse in a marathon runner after crossing the finish line is benign EAC. This is generally considered a form of postural hypotension. While running, the leg muscles act as a venous pump to improve blood flow return to the central circulation. When the athlete stops running, venous pooling of blood in the legs can occur, resulting in a decrease in blood pressure and a subsequent collapse. This is exacerbated in warm environments because blood flow is shunted from the core to the skin to facilitate cooling. It is important to keep the athlete walking after crossing the finish line to keep the muscular venous pump engaged. Treating EAC means treating the primary cause of collapse and providing supportive care. If the underlying cause of the collapse is determined to be benign EAC, oral rehydration and lying the athlete down on a stretcher with legs and pelvis elevated above heart level are typically all that is needed. If the athlete does not improve within 15 to 30 minutes, a search for a more ominous cause of collapse should be undertaken, including orthostatics, if possible, and an electrolyte assessment, followed potentially by administration of intravenous fluids. It is rare to definitively need intravenous fluids after running a marathon.

Exercise-associated hyponatremia (EAH) was first reported in the 1981 Comrades Run (90-km ultramarathon) in South Africa; however, national and international media attention publicized it after the death of a 28-year-old female runner in the 2002 Boston Marathon. It is a hypervolemic hyponatremia causing early symptoms of lightheadedness, a nauseated feeling, later a progressive headache, vomiting, confusion, and finally obtundation, seizures, and death. The pathophysiology is fluid shifts from low osmotic pressure in the blood causing cerebral edema and then neurogenic pulmonary edema. The early symptoms are nonspecific, so medical providers must have an index of suspicion in any marathoner who is not feeling well after the race. Risk factors for EAH include weight gain during the race, marathon race time more than 4 hours, and body mass index extremes.² Those at risk are runners who ingest too many fluids on the race course and subsequently gain weight. Slower runners have more of an opportunity to drink excessively, and smaller runners generally need less fluid to dilute their serum sodium levels.

Once the diagnosis is made, treatment is indicated according to the severity of presentation and serum sodium level. For those runners who are fluid overloaded with low serum sodium but have minimal symptoms, close observation and fluid restriction are indicated as a natural diuresis occurs. If the sodium level is low or is not reversing, observation in the hospital might be indicated. If the same athlete has progressive encephalopathic symptoms, treatment would include high flow oxygen, a bolus of hypertonic saline (3% NaCl), and quick transport to an emergency facility.

Prevention of EAH should be the ultimate goal for any medical director of an endurance athletic event such as a marathon. Prevention starts with educating athletes about the risk of overdrinking on the course and teaching athletes to use their training in the months before the event to determine their individual fluid needs. Emphasizing individual differences and reminding the athletes to replace what they need (sweat losses) and not necessarily more is appropriate (Box 44-7). The mantra “drink when you are thirsty” is generally safe for slower and at-risk runners. Only if the athlete is a very salty sweater or if the competition lasts more than 6 hours should sodium or electrolyte replacement be necessary. Spacing the water/aid stations on the course about every 1.5 miles is another way to limit excessive drinking and potentially prevent EAH.

Given the continued popularity of marathons and other mass participation endurance events, the lay press commonly reports on deaths in these races. With more events and more press coverage, there is an appearance of an increase in marathon-related deaths. The often-quoted risk of SCA in a marathon is 1:50,000. This is an old statistic that came from a study evaluating cardiac-related deaths in the Twin Cities Marathon and Marine Corp Marathon from 1976 to 1994.¹⁰¹ These marathons presented follow-up data from 1995 to 2004, demonstrating a new rate of cardiac-related deaths of 1:220,000.¹³⁴ The London Marathon also published its rate of 1:80,000 from 1981 to 2006.¹⁵⁷ Even though there are more marathons and marathoners, the rate of SCA has improved during the past 10 to 15 years. This could be related to earlier recognition, better preparation, and AED use.

Heat-related illness is another etiology of EAC. Heat exhaustion is the inability to continue to exercise in the heat but is not related to body temperature. It represents the failure of the cardiovascular response to workload, high environmental temperatures, and dehydration. No chronic or harmful effects are known. In contrast, heat stroke is a medical emergency. Heat stroke is defined as multiorgan system failure secondary to hyperthermia. The rectal core temperature in an athlete with heat stroke is generally more than 39°C. Treatment is immediate total body cooling. Disagreement exists on which cooling method is most efficient. Ice bath/cold water immersion, the “taco method” using wet sheets and ice, and finally administering ice to the head, neck, axilla, and groin are all common cooling methods used in the field (at races and in the military). Whatever method is used, it should be simple and safe, provide adequate cooling, and not restrict other forms of treatment, including CPR, defibrillation, and intravenous cannulation.²⁶ The mortality rate and organ damage in athletes with heat stroke are proportional to the length of time between core temperature elevation and the onset of cooling therapy. Finally, it is important to note that heat stroke can occur in cool environments and might be more of a genetic predisposition to excessive endothermy (i.e., endogenous heat production) and not just a factor of extreme environmental conditions.¹²⁹

Sports Concussion

Concussions are mild traumatic brain injuries sustained as a result of direct blows to the head or forces transmitted through the head and neck. The Centers for Disease Control and Prevention estimates 1.6 to 3.8 million sports- and recreation-related traumatic brain injuries occur each year. They occur in all sports but are most common in contact and collision sports. Concussions can result in symptoms, physical signs, behavioral changes, cognitive impairment, and sleep disturbance (Box 44-8). These symptoms are typically due to a functional disturbance of the brain rather than a true structural injury. It is vital to recognize that concussions rarely result in a loss of consciousness. Concussion symptoms are generally transient, although chronic sequelae might occur.

Pathophysiologically the concussed brain exhibits increased metabolic needs combined with decreased cerebral blood flow.¹⁴ This mismatch of “supply and demand” creates a state of tissue vulnerability. Second-impact syndrome is a rare and catastrophic outcome of concussion that might be due to this mismatch. This phenomenon is seen when a youth athlete receives a second impact before the symptoms of the first concussion have subsided. These rare injuries have only been reported in youth athletes and result in severe brain injury and even death from malignant cerebral swelling.

The most vital component of concussion care is the prompt recognition of the injury itself. Athletes, coaches, trainers, and family members should have some degree of education regarding the most common signs and symptoms. An athlete with a suspected concussion should be removed from play immediately and evaluated on the sideline. The Standardized Assessment of Concussion, pocket Sport Concussion Assessment Tool 2, and Maddocks’ questions are commonly used sideline tools. These screening tools do not replace the value of a more thorough assessment that can detect more subtle abnormalities.¹⁰⁷ Current consensus recommends that athletes less than 18 years of age should not RTP on the same day as a concussion. In certain professional athletic settings, adult athletes can RTP on the same day.¹⁰⁷

Imaging is initially reserved for situations in which an intracranial abnormality is suspected, including prolonged loss of consciousness, focal neurologic deficit, or progressive decline in neurologic status. In athletes with prolonged or severe symptoms, magnetic resonance imaging (MRI) can be used to evaluate for other intracranial abnormalities. Newer imaging protocols, such as functional and diffusion-weighted MRI, positron emission tomography, and diffusion tensor imaging, are emerging but have yet to be a part of current concussion management.

Neuropsychologic (NP) testing is a useful component in the management of concussions. Cognitive and somatic symptoms typically improve in parallel but often completely resolve at different times. As such, NP testing can give added information that cannot be gained in a typical clinical setting. Neuropsychologists are best suited to interpret these data, but in situations where no neuropsychologist is available, other medical professionals can be trained to perform the interpretation.⁴⁹ NP testing is only one component of concussion management, however, and the decision to RTP is ultimately a medical one.

Athletes with concussions are managed with both physical and mental rest. This includes the limitation of activities that require concentration and attention such as scholastic activity, video games, computer usage, text messaging, etc. These activities often exacerbate the athlete’s symptoms and can prolong the final resolution of symptoms. Youth athletes might require individualized schoolwork adaptations and the cooperation of school administration (e.g., extended test-taking time, tutors, limited class schedules). Section 504 of the Americans with Disabilities Act is part of a federal law that protects students with disabilities and is often used to create plans to help concussed athletes continue to participate in school.

Prognosis after concussion is typically excellent with 80% to 90% of athletes free of symptoms within 7 to 10 days.¹⁰⁶ Children and adolescents are a notable exception and might exhibit a longer recovery time.¹⁰⁷ RTP decisions can be challenging and must be made by practitioners familiar with concussion management. No athlete should RTP until all the symptoms of the concussion have resolved. Once the athlete is asymptomatic at rest, a stepwise approach RTP protocol must be completed before competition is resumed (Table 44-7). The athlete will be asked to have a 24-hour symptom-free period before advancing to the next step in the protocol. No athlete should be returned to competition while still symptomatic.

Table 44-7 Return-to-Play Protocol

Modified from McCrory P, Meeuwisse W, Johnston K, et al: Consensus statement on concussion in sport—The 3rd international conference on concussion in sport held in Zurich, November 2008. Phys Med Rehabil 1(5):406-420, 2009.

Athletes with repeated concussions must be evaluated on an individual basis. These athletes typically have a prolonged recovery course and might have higher symptom severity.^36,37,39,147 An increasing body of literature suggests concussions are an independent risk factor for long-term deficits in executive function and processing speed.^37,65 The phenomenon of athletes suffering increasingly severe concussions with decreasing impact severity should raise significant concerns for the physician. These athletes might need to consider giving up contact sports and might not be cleared to participate.²³

Physiatrists have a unique expertise in brain injury, sports medicine, and the complexities of managing the expectations of the multiple involved parties in the care of a concussed athlete. Emerging recognition has been noted of concussion as a significant public health concern that can result in significant long-term deficits in a young, vulnerable patient population. The Zackery Lystedt Law is the first concussion management law, passed by the state of Washington in 2009, stating that all youth athletes with suspected concussion must be removed from play, evaluated, and cleared by a medical professional before returning to play.

Stingers

The stinger, or sometimes termed a burner, is probably one of the most common but least understood peripheral nerve injuries that occur in sports. Stingers are nerve injuries that occur within the peripheral neural axis at a specific but variable point from the nerve root to the brachial plexus. The true incidence of stingers is unknown; however, it is estimated that more than 50% of collegiate football players sustain a stinger each year.³⁴

A great deal of controversy exists regarding the pathophysiology of stingers. The symptoms can result from a tensile (stretch) or compressive injury to the cervical nerve root or brachial plexus. Of the two, the cervical nerve root appears to be at greater risk for both tensile and compressive injury than the brachial plexus. However, the literature slightly favors brachial plexus tensile overload^∗ over nerve root stretch,^32,103,149 nerve root compression,^126,138,163 and direct brachial plexus compression^44,99 as the primary mechanism of injury in stingers. The pathomechanics of each injury vary by the age and experience of the athlete as well as by specific sport. Tensile injuries typically occur in younger athletes with less experience who have weaker neck and shoulder girdle musculature, leaving them vulnerable to forceful contralateral neck lateral bending with ipsilateral shoulder and arm depression. Cervical root compression is likely to occur in the older, stronger, and more experienced athlete during forceful cervical extension and rotation, narrowing the neuroforamen. This scenario is more commonly seen in professional football defensive backs and offensive lineman. Least commonly, a compressive blow to the brachial plexus can result from equipment issues such as padding.

The patient with a stinger classically presents with sudden onset of a lancinating, burning pain in one upper limb after a traumatic event. The symptoms typically follow a single dermatomal distribution, most commonly in a C5, C6, or C7 pattern. The pain usually lasts seconds to minutes, with the sensory disturbance usually resolving quickly, whereas weakness can be more persistent. Simultaneous, bilateral stingers are very uncommon; therefore any athlete with bilateral upper limb paresthesias or dysesthesias should be evaluated for a spinal cord injury. With the first occurrence of a stinger, symptoms generally resolve quickly and no medical attention is sought. With each subsequent recurrence, more distinct neurologic sequelae might result, including persistent motor weakness. Motor impairment (particularly in the deltoid and biceps, i.e., C5 myotome) is the more common residual neurologic symptom of an athlete with a stinger.⁶⁸

The initial sideline evaluation includes determining the specific mechanism of injury and the precise distribution and duration of symptoms. The sideline physical examination includes cervical active range of motion (AROM) to assess pain provocation and rigidity, palpation for tenderness, and a detailed neurologic examination with close attention to the C5–C7 myotomes.

The duration of any given episode can vary from seconds to hours, much less commonly lasting for days or longer. Serial assessments are critical for RTP and management decisions. If symptoms progressively worsen over the first few days or if weakness persists more than 10 to 14 days, additional ancillary testing and specialty consultation would be indicated to precisely determine the site of injury and the degree of axonal damage.

If the athlete’s symptoms resolve very quickly (within seconds to minutes) and physical examination demonstrates no abnormality (including full pain-free cervical ROM), then no additional testing might be necessary. Persistent symptoms or signs and recurrent stingers are indications for further workup.

Although plain radiographs of the cervical spine provide limited information in this setting, they can reveal clues to pathoanatomy contributing to the symptoms. A higher incidence of degenerative changes (creating central canal and neuroforaminal stenosis concomitantly) is noted in more experienced athletes who sustain stingers.⁹⁵ Levitz et al.⁹⁵ studied a cohort of football players with chronic stingers and demonstrated that 93% of these players had significant cervical disk disease or neural foraminal narrowing.

Advanced imaging with MRI or computed tomography is indicated if the athlete experiences severe, unrelenting pain, persistent symptoms, or abnormal neurologic findings on examination. Electrodiagnostic testing (EDX) is complementary to imaging studies. EDX can provide quantification of neural dysfunction and can help to determine the site of nerve injury. EDX is most useful in the athlete with persistent or progressive weakness beyond 2 weeks postinjury or in the setting of recurrent stingers. As with other nerve injuries, 7 to 10 days might be required for the axonal damage to manifest on electromyography (EMG), so this is not a test used immediately postinjury.

Treatment of stingers includes pain control, antiinflammatories, strengthening, and rehabilitation of postural faults and muscle imbalances that might have contributed to the athlete’s risk of sustaining the stinger. Persistent symptoms can be treated with fluoroscopically guided epidural steroid injections, surgical decompression of neuroforaminal stenosis, or even anterior cervical diskectomy and fusion. Equipment modifications should be considered for prevention of recurrent injury, although research is lacking to support their effectiveness.⁶⁸

Well-established return to competition guidelines do not exist for stingers. The following is an approach based on a combination of clinical experience, neurophysiologic principles, and extrapolation of information from other peripheral nerve injuries. After an initial stinger, if full recovery is demonstrated within 15 minutes, return to same game competition is allowed. If full recovery occurs within 1 week after the initial stinger, then return to competition that next week is allowed. A limited rehabilitation program to address postural dysfunction and relative weaknesses should be prescribed during the in-season strength and conditioning program and definitely in a more comprehensive fashion in the off-season. If the athlete has sustained recurrent stingers, a general rule is to hold the player from competition for the number of weeks that corresponds to the number of stingers sustained in a given season (e.g., 2 weeks for a second stinger). If more than three stingers occur in a season, ending the season should be considered, especially if there is significant weakness, axonopathy on EMG, or focal disk herniation or foraminal stenosis noted on MRI.⁶⁷

Exercise-Induced Bronchospasm

EIB describes airway narrowing that occurs in association with exercise. EIB can be present with chronic asthma but generally is a separate entity. The prevalence of EIB is significantly higher in athletes than the general population. A diagnosis based solely on clinical symptoms is often inaccurate, and pulmonary function testing and consultation with an asthma specialist is important to definitively diagnose and optimally treat EIB.¹³⁹

Symptoms can include breathlessness with or without coughing and wheezing or even solely the vaguer symptom of decreased performance during vigorous endurance training or competition. Cross-country skiers and other winter sport athletes are most common to present with EIB, although runners are not far behind. EIB is much less common in swimmers. Cold, dry air is much more likely than warm, humid air to precipitate symptoms.

The mechanism of EIB is not fully understood but is certainly different than that of chronic asthma, which is caused by inflammation resulting from overly reactive airways to inhaled stimulants. EIB is thought to result from water loss and cooling in the airway that occurs with hyperventilation, which subsequently triggers bronchoconstriction.²⁴

A variety of diagnostic testing options are available for those in whom EIB is suspected by history but the physical examination is normal (Box 44-9).²⁴ Once a diagnosis of EIB is made, treatment is multifaceted. An adequate warm-up has been demonstrated to reduce the severity of EIB. Some recommend inducing a refractory period by briefly precipitating symptoms with short, vigorous bursts of exercise lasting 15 to 20 minutes before the competitive endurance event. The mainstay of pharmacologic therapy is a short-acting β-agonist 15 minutes before exercise. If this is ineffective, adding cromolyn, a mast cell stabilizer, is indicated first, then inhaled corticosteroids for the final addition to preexercise therapy. If EIB is refractory to the aforementioned treatment, daily chronic asthma therapy should be added to the regimen. This includes inhaled corticosteroids first, and then long-acting β-agonists and leukotriene receptor antagonists can be added.²⁵

BOX 44-9 Diagnostic Testing for Exercise-Induced Bronchospasm

• Spirometry

• Formal PFTs

• Challenge testing

• Eucapnic voluntary hyperventilation challenge

Breathing in 4.5% CO₂ for eucapnia, then measure FEV₁

Any decrease in FEV₁ is diagnostic for EIB

• Exercise challenge in the field or laboratory

Useful because it simulates the sport-specific temperature/environment

• Methacholine challenge

Good to classify the severity of asthma

Not specific for EIB

EIB, Exercise-induced bronchospasm; FEV₁, forced expiratory volume in 1 second; PFT, pulmonary function test.

Anemia

The three most common causes of anemia in the athlete are iron-deficiency anemia (IDA), physiologic anemia or pseudoanemia, and foot-strike hemolysis.

IDA is most common in menstruating women, and female athletes can be more prone to developing it. The etiology is either blood loss or poor iron intake. Many athletes consume restrictive diets that can have too little iron to meet daily needs. A complete history and physical examination are still important, however, to evaluate for “nonathletic” causes such as significant gastrointestinal or genitourinary blood losses. Usually a serologic workup is diagnostic and includes complete blood count (CBC), serum ferritin, and total iron binding capacity (TIBC). The CBC will show a microcytic anemia.⁸⁹ Serum ferritin levels that are less than 30 ng/mL in athletes are considered suggestive of IDA.⁵³ The TIBC will be elevated. If IDA is diagnosed, a trial of oral iron supplementation (typically ferrous sulfate or ferrous gluconate, 325 mg three times daily) is undertaken.³⁵ Iron is best absorbed in an acidic environment, so it is concomitantly administered with vitamin C, usually for a 2- to 3-month course.

Physiologic anemia is considered a pseudoanemia seen commonly in endurance athletes. Endurance athletes tend to have a lower hemoglobin concentration than the general population because of an expansion of plasma volume with a dilutional effect. It is an adaptation to exercise and is not considered to inhibit athletic performance. It generally normalizes with training cessation of 3 to 5 days. If IDA is ruled out, there is no necessary treatment.

Foot-strike hemolysis refers to red blood cell destruction in the feet from running impact. However, intravascular hemolysis is seen in swimmers, cyclists, and runners, and whether actual mechanical red blood cell trauma is the source is questionable. Possible reasons are intramuscular destruction, osmotic stress, and membrane lipid peroxidation caused by free radicals released by activated leukocytes. Intravascular hemolysis can even be regarded as a physiologic means to provide heme and proteins for muscle growth in athletes.¹³⁷ Generally the hemolysis is mild, and treatment is rarely required.

Women in Sports

Until puberty, boys and girls are similar in body size, shape, and physiology.¹⁸ On average, women have a larger surface area-to-mass ratio, lower bone mass, and a wider, shallower pelvis than men. Because of these differences, women might tolerate heat better than men, might be more prone to osteoporosis, and might develop knee problems more frequently.¹⁸ The following discussion highlights one issue unique to the female athlete: the female athlete triad.

The Female Athlete Triad

The female athlete triad is a constellation of interrelated findings of inadequate eating, menstrual abnormalities, and skeletal demineralization.¹¹⁹ The definition of the triad does not require the simultaneous occurrence of all three components. Each facet, in isolation or combination, needs to be considered and treated.¹¹⁷

Inadequate eating describes women who eat insufficient calories for the amount of calories burned, as well as women with frank anorexia or bulimia (Box 44-10). Diminished athletic performance often results, and a vicious cycle develops in which psychologic distress and depression can develop.¹¹⁶ A higher incidence of eating disorders has been reported in female athletes compared with the general population.^18,64 Female athletes are also more likely to have disordered eating than their male counterparts.⁶⁴ A higher rate of eating disorders has been reported among athletes in sports emphasizing leanness, such as gymnastics, figure skating, dancers, distance runners, divers, and swimmers.^9,18,116,117

BOX 44-10 Diagnostic and Statistical Manual of Mental Disorders–IV Definitions of Anorexia, Bulimia Nervosa, and Eating Disorders Not Otherwise Specified⁶

Anorexia

• Body weight 15% below expected

• Morbid fear of fatness

• Feeling fat when thin

• Amenorrhea

Bulimia nervosa

• Binge eating twice per week for at least 3 months

• Loss of control overeating

• Purging behavior

• Overconcern with body shape

Eating disorders not otherwise specified

• All criteria for anorexia nervosa are met except amenorrhea, or the individual’s current weight is within the normal range

• All criteria for bulimia nervosa are met except that binge and purge cycles occur at a frequency less than twice a week for a duration of <3 months

• An individual of normal body weight uses purging behaviors after eating small amounts of food

• An individual repeatedly chews and spits out, but does not swallow, large amounts of food

Athletic women are 3 times as likely to develop primary or secondary amenorrhea as their nonathletic counterparts.¹²⁸ Menstrual irregularities range from reduction in luteal phase length and suppression of luteal function to amenorrhea.¹⁸ Women with athletic amenorrhea present with a reduction in luteinizing hormone pulse frequencies, which depend on energy availability.¹¹⁶ Dietary supplementation (i.e., providing adequate energy sources) can prevent or eliminate menstrual disturbances.^18,64

Skeletal demineralization is the third component of the triad and can lead to premature osteoporosis. The prevalence of osteopenia in female athletes has been reported to be 22% to 50%, whereas the prevalence of osteoporosis remains relatively low.⁸⁴ Bone undergoes continual resorption and formation, a process called remodeling. Hormonal status, weight-bearing physical activity, and dietary intake (particularly calcium) influence remodeling. Stress fractures pose a health risk to amenorrheic athletes as a result of reduced bone mass. The relative risk for stress fractures is 2 to 4 times greater for amenorrheic athletes compared with those with regular menses.¹¹⁷

Peak bone mass is achieved during the first 3 decades of life, with Tanner stages II and III (early to mid puberty) as the maturational stage in which physical activity has the strongest impact on bone.¹¹⁷ Young athletes with primary amenorrhea might be unable to build bone during formative years, with the end result being that peak bone mass might never be achieved.¹⁸

Dual-energy x-ray absorptiometry is the most widely used and validated technique to assess bone mineral density (BMD).^82,117 The World Health Organization defines osteoporosis as a BMD greater than 2.5 standard deviations (SD) below the youthful mean (T-score less than or equal to −2.5 SD).⁸² Osteopenia is defined as a BMD between 1.0 and 2.5 SDs below the youthful mean (T-score 1.0 to 2.5) (Table 44-8).⁸² Notably, normative data for adolescent girls are not available to definitively define pathologic bone loss in this group; hence Z-scores are best used in the skeletally immature athlete because the Z-score is age matched and the T-score is compared with a 35 year old.^9,18

Table 44-8 Current Recommendations for the Diagnosis of Low Bone Mineral Density and Osteoporosis in Premenopausal and Postmenopausal Women and Young Athletes

Randomized controlled trials have shown that oral contraceptive pills might increase lumbar and total body BMD in patients with hypothalamic amenorrhea.^71,161 In addition, 1200 to 1500 mg of calcium and 400 to 800 international units of vitamin D supplementation per day are recommended (see Chapter 41).⁶⁴More recently, attention has turned to the cardiovascular risks associated with the hypoestrogenic state in women with hypothalamic amenorrhea. Estrogen has cardioprotective effects, such as increasing high-density lipoprotein and decreasing low-density lipoprotein cholesterol.¹⁵⁹ Estrogens also stimulate the production of nitric oxide (NO), a potent vasodilator and inhibitor of platelet aggregation, leukocyte adhesion, and vascular smooth muscle proliferation and migration, all of which are part of the atherosclerotic process. Flow-mediated vasodilatation (FMD) results from NO release in response to shear stress and increased blood flow.⁷⁶ Athletic amenorrhea is associated with decreased endothelium-dependent dilation of the brachial artery (a measure of FMD)^131,173 and unfavorable lipid profile.¹³¹ Treatment with oral contraceptive pills has been associated with improved FMD.¹³²

Female athletes presenting with features of the female athlete triad require appropriate workup and referrals (Figure 44-9). Although referrals to a nutritionist, psychologist/therapist, and other medical specialists, such as endocrinologists, cardiologists, and gastroenterologists, might be necessary, a primary treatment focus should be to restore energy balance by improving caloric intake and potentially decreasing energy expenditure (limiting aerobic exercise). Finally, pregnancy should be excluded in any amenorrheic female of childbearing age.

FIGURE 44-9 Overview of the management of the female athlete triad. HRT, Hormone-replacement therapy.

(Modified from Borg-Stein J, Dugan SA, Solomon JL: Special considerations in the female athlete. In Frontera WR, Micheli LJ, Herring SA, et al, editors: Clinical sports medicine: medical management and rehabilitation, Philadelphia, 2007, Elsevier.)

The Pediatric and Adolescent Athlete

According to one estimate, 30 million children and adolescents participate in organized sports activities in the United States.^1,70 As athletic involvement increases, the incidence of sports-related injuries also increases.^91,148

Physically active adults had better standardized fitness scores as children,⁴² suggesting that an active lifestyle as a child promotes continued lifelong physical fitness. Physical activity in children and adolescents prevents osteoporosis, improves self-esteem, and reduces anxiety and depression.^15,28 Furthermore, there is a positive relationship between physical fitness and academic achievement in English and mathematics.³¹ High school athletes are more likely to engage in positive health behaviors and less likely to engage in negative health behaviors compared with nonathletes.¹²³

When advising pediatric athletes in their training program, the physiologic and anatomic differences between children and adults must be considered. Strength training has been historically discouraged in the pediatric population because of concerns of growth disturbance and potential for other injuries.⁹¹ According to a position statement by the American Academy of Pediatrics Committee on Sports Medicine, “short-term programs in which prepubescent athletes are trained and supervised by knowledgeable adults can increase strength without significant injury risk.”⁵ Although growth plate disturbances have been reported, these have been attributed to poor lifting techniques, lifting maximal weights, and lack of adult supervision.⁶⁶

Training programs for pediatric athletes should include stretching routines. Children tend to lose flexibility with age, with the greatest losses occurring at puberty because of muscle–tendon imbalances that occur with rapid growth.⁹² Loss of flexibility can make the athlete vulnerable to acute and overuse injuries involving the low back, pelvis, and knee.¹¹¹ Excessive flexibility, however, is associated with increased risk of sports-related injury, especially in sports that necessitate rapid change of direction or acceleration.¹¹¹

The pediatric skeletal system is distinguished from that of adults by the presence of the active growth plate, or physis. The physis is situated between the epiphysis and metaphysis. Two types of epiphyses exist: traction and pressure.²¹ The traction epiphysis, also known as the apophysis, is the point of attachment of a tendon to bone.¹ Because apophyses contribute to bone shape, but not bone length, acute or chronic injuries involving apophyses are not usually associated with growth disturbance. Osgood-Schlatter disease, Sever’s disease, and medial epicondylopathy are examples.^1,21

Pressure epiphyses are found at the end of long bones such as the distal femur and proximal tibia (Figure 44-10). In contrast to apophyseal injuries, injuries to active pressure epiphysis can result in limb-length discrepancies or angular deformities.^21,146 The most common cause of injury to the pressure epiphysis acutely is a fall. Acute physeal injuries are widely described using the system described by Salter and Harris (Figure 44-11). Chronic injuries result from ongoing stress to the physis, as is seen in distal radial injuries in young gymnasts (Figure 44-12).²¹

FIGURE 44-10 Physes of the distal femur and proximal tibia.

(Modified from Caine D, DiFiori J, Maffulli N: Physeal injuries in children’s and youth sports: reasons for concern? Br J Sports Med 40[9]:749-760, 2006.)

FIGURE 44-11 Growth plate injuries as described by Salter and Harris.¹⁴²

(Modified from Caine D, DiFiori J, Maffulli N: Physeal injuries in children’s and youth sports: reasons for concern? Br J Sports Med 40[9]:749-760, 2006.)

FIGURE 44-12 Radiograph of a chronic distal radius injury resulting from ongoing stress to the physis.

Older Athlete

According to the Healthy People 2000 report, 60% of adults 65 and older engage in leisure-time physical activity.⁷⁵ Popular activities among seniors include gardening, dancing, golf, hunting, fishing, woodworking, tennis, bowling, biking, and swimming. Masters athletes have achieved impressive improvements in peak exercise performance. In fact, athletes more than 70 years of age have surpassed the winning time at the first modern Olympic Games held in Athens in running events from 100 meters to the marathon.¹⁵¹

Athletes With Disabilities

Physiatrists are uniquely equipped to treat athletes with disabilities, given their training in disabling diseases and musculoskeletal problems. Organized athletic competition among disabled persons dates back to 1944, when Sir Ludwig Guttmann formally introduced sporting activities as part of a rehabilitation program at Stoke Mandeville Hospital in England. He believed that “by restoring activity of mind and body—by instilling self respect, self discipline, a competitive spirit and comradeship—sport develops mental attitudes that are essential for social reintegration.”¹⁶⁴

The Paralympic Games provide opportunities for thousands of elite athletes with various disabilities to compete. The first games took place in Rome in 1960.⁴⁰ Currently people with spinal cord injuries, amputations, cerebral palsy, and visual impairments compete in the Paralympic Games. People with other disabilities participate as well, in a group collectively known as Les Autres (“the others”). This group includes those athletes with multiple sclerosis, muscular dystrophy, Friedreich’s ataxia, arthrogryposis, osteogenesis imperfecta, and Ehlers-Danlos syndrome.⁴⁰

Organized competitions use a classification system to ensure that training and skill provide the advantage, not level of disability. Various classification schemes are based on medical, disability-specific, combined, or functional/sport-specific models. Table 44-9 is one example of such a system.

Table 44-9 Classification System for Training the Disabled Athlete