Chapter 36. The Athlete and the Heart

• The patient has an extensive history of exercise training
• There may be profound sinus bradycardia, sinus arrhythmias, or atrioventricular conduction delays at rest that disappear with exertion.
• The athlete's heart may demonstrate four-chamber enlargement and mild left ventricular hypertrophy, but normal diastolic function and B-natriuretic peptide levels. The diastolic wall-to-volume ratio should be < 0.15 mm/m2/mL by magnetic resonance imaging.
• Morphologic changes reverse with detraining.

The salutary physiologic effects of exercise training on the cardiovascular system have been studied extensively, but intense exercise training can produce cardiac adaptations that mimic pathological conditions. Consequently, clinicians should be aware of the normal cardiac structural and functional responses to exercise training in order to distinguish these changes from clinical disease that could also affect athletes.

Physiology of Exercise Training

The “athlete's heart” refers to the normal structural and physiologic cardiac adaptations to exercise training. Clinical characteristics of the athlete's heart include resting sinus bradycardia (occasionally profound), sinus arrhythmia, atrioventricular (AV) conduction delays, systolic flow murmurs, four-chamber enlargement, and an increase in cardiac mass, but usually normal or augmented ventricular systolic function.

The magnitude of these cardiac changes depends on a variety of factors including the duration and intensity of the exercise training, the body size of the athlete, the sport, and the physiologic demands of the exercise used to train for that sport. Sports can be roughly classified according to the type and intensity of the exercise performed and the degree of static and dynamic exercise required, but such classifications are innately flawed because they do not consider exercises used in training. Dynamic (isotonic) exercise and sports primarily involve changes in muscle length and joint movement with rhythmic contractions and small intramuscular force. Static (isometric) exercise and sports mainly involve large intramuscular force with little or no change in muscle length or joint movement. Most sports require elements of both.

The acute cardiovascular response to dynamic (aerobic) exercise includes a decrease in peripheral vascular resistance and increases in heart rate, stroke volume, cardiac output, systolic blood pressure, the arteriovenous oxygen difference, and oxygen consumption. Endurance exercise training increases maximal exercise capacity as measured by maximal oxygen uptake. This increase in exercise capacity is produced by increases in the arteriovenous oxygen difference and cardiac output due to increased stroke volume.

Endurance (aerobic) sports, such as long-distance running, and their required training produce the greatest reductions in heart rate and the largest increases in maximum oxygen consumption, cardiac output, stroke volume, and cardiac chamber dimensions. Endurance exercise predominantly produces a volume load on the left and right ventricles. Static or strength sports, such as weight lifting, in contrast, produce only small increases in oxygen consumption and minimal changes in cavity size, but may be associated with mild to modest increases in wall thickness, some of which may be due to increased body mass in such athletes. These changes in wall thickness with little change in chamber dimensions mimic the changes produced by pressure load.

Chamber Morphologic Adaptations to Endurance Training

The morphologic adaptations to endurance training have been characterized by echocardiography and magnetic resonance imaging. Cardiac remodeling occurs in approximately one-half of trained athletes. It consists of increases in left and right ventricular and left atrial cavity dimensions and volumes almost always associated with normal systolic and diastolic function (Figure 36–1). Few studies have examined right atrial size, but this may also be increased.

There can be overlap between the athlete's heart and mild forms of cardiac disease such as hypertrophic cardiomyopathy (Figure 36–2). The morphologic features of the athlete's heart are reversible with cessation of training so that cessation of exercise can help distinguish these two conditions. Many athletes resist the idea of detraining, however, so other approaches are often required.

Sudden Cardiac Death in Athletes

Clinicians require knowledge of the athlete's heart primarily because vigorous exertion increases the risk of sudden cardiac death during exercise in individuals with known or occult heart disease. Consequently, clinicians need to know what cardiac findings in athletes are normal and how to advise individuals with diagnosed cardiac disease concerning exercise.

The frequency of sudden cardiac death (SCD) in young athletes is not clearly defined, although the largest registry of such events estimates a rate in the United States of only 66 deaths per year. Other estimates have ranged from 1 in 23,000 to 1 in 300, 000 deaths in athletes per year. This variance is likely attributable to collection bias, incomplete identification of cases, and an imprecise denominator. A study of SCD in a defined population of American collegiate athletes suggested an incidence of SCD as high as 1 in 43,000 athletes.

The most common cause of SCD in athletes younger than 35 years of age in the United States is hypertrophic cardiomyopathy (HCM), accounting for up to one-third of sport-related deaths. Other frequent causes include congenital coronary artery anomalies, myocarditis, and aortic rupture, and less commonly, arrhythmogenic right ventricular cardiomyopathy, coronary artery disease, and conduction system abnormalities. In contrast, the most common cause of exertion-related SCD in the Veneto region of Italy is arrhythmogenic right ventricular cardiomyopathy, either because mandatory Italian screening has detected and eliminated athletes with HCM or because of population differences in the prevalence of disease. In contrast to young athletes, SCD in athletes over the age of 35 years is most frequently due to occult coronary artery disease (CAD), and multiple studies have documented an increase in acute myocardial infarction (MI) and SCD among older adults during vigorous exertion.

Medical History & Physical Examination

As with all of medicine, the most important element of evaluating athletes and their clinical findings is the medical history, and in the medical history, the most important element is what prompted the athlete to obtain medical evaluation. Abnormalities found on screening examinations in an asymptomatic athlete have far less import than abnormalities found during the evaluation of a symptomatic individual. In our clinical experience, most clinical abnormalities found during screening ultimately turn out to be normal variants of the athlete's heart syndrome. Consequently, dividing athletes into those with and without symptoms is an important initial approach to their evaluation.

The other key elements of the history are the athlete's exercise training history and his or her exercise performance. Marked changes in cardiac dimensions require considerable amounts of exercise training so that cardiac findings in an athlete with a short or low-level training history are of more concern than similar findings in an athlete with high volumes of training. It is also extremely useful to be able to assess the athlete's level of performance. Excellent endurance exercise performance requires a large cardiac stoke volume, so that excellent exercise capacity is reassuring but does not absolutely exclude important disease. Family history of cardiac disease or unexpected or unexplained sudden death (including drowning, unexplained car accidents, or sudden infant death syndrome) is also useful in evaluating young athletes since most conditions causing SCD during exercise in this group are congenital or inherited.

The evaluation of both symptomatic and asymptomatic athletes should include a thorough physical examination. Vital signs are usually notable for training bradycardia with a resting heart rate as low as 30 bpm in highly trained aerobic athletes. Asymptomatic adolescent athletes with heart rates in this range can participate without further evaluation. Athletes may also have an S3 and S4 gallop. Athletes frequently have classical flow murmurs related to their slower heart rates and concomitant increased stroke volume. These functional murmurs typically are systolic and less than IV/VI in intensity. They are typically present supine because of enhanced venous return in this position and absent with the athlete upright; they have no diastolic component and are associated with a normal physiologic split of the second heart sound. Because HCM is the most frequent cause of SCD in young athletes, auscultation during the Valsalva maneuver or after arising from the squatting position, either of which should decrease cardiac dimensions and increase the murmur of HCM, is useful.

Syncope is a common problem among athletes and a frequent reason for referral to a cardiologist. Syncopal events are significant if judged to be not neurocardiogenic (vasovagal) and if they occur during exercise. Postexertional syncope is a common phenomenon in athletes. It is usually benign and does not require further workup. Under normal circumstances, exercise increases cardiac output and decreases peripheral vascular resistance due to vasodilation. Syncope after exercise can occur because the increases in cardiac output and heart rate decrease more rapidly than does the peripheral vasodilation. The net effect when the individual stops exercising is an increase in vasodilation without the compensatory increase in heart rate and cardiac output, thus explaining postexertional syncope. In contrast, syncope during exercise usually suggests a cardiac origin, such as anomalous coronary artery anatomy or cardiac arrhythmias.

The American Heart Association (AHA) position on screening athletes before competition recommends a 12-point evaluation (Table 36–1). The historical elements are important, but young athletes often respond positively to many of these queries, again highlighting the importance of separating the evaluation of athletes with abnormalities found on screening from those presenting with symptoms.

Diagnostic Studies

Electrocardiogram

Many clinical and electrocardiographic (ECG) findings of concern in the general population are normal for athletes. The accuracy of the ECG interpretation is particularly difficult in young athletes due to ECG evolutionary changes that are related to age. Furthermore, there are inconsistencies in the definitions of ECG abnormalities and definite criteria for the diagnosis of several diseases. While the routine use of ECG for preparticipation screening remains controversial in young adults, its use remains a cornerstone of any cardiac evaluation in athletes with cardiac complaints. It is recommended as part of a routine evaluation for all masters athletes > 40 years of age since it occasionally identifies a prior MI.

Sinus bradycardia as low as 30 bpm, sinus arrhythmia, prolonged PR interval up to 300 ms, sinoatrial block, junction rhythms, and Wenckebach phenomenon are common in athletes due to a high resting parasympathetic tone and should not prompt further workup if the athlete is asymptomatic and has good exercise capacity and the abnormalities disappear during exercise.

QRS axis varies with age, but in athletes, mild right or left axis deviations should not trigger further evaluation unless there is history of pulmonary disease or systemic hypertension. An acceptable rage is between –30 and +115 degrees.

Incomplete right bundle branch block is extremely common in athletes. In contrast, complete block of either bundle, even in asymptomatic athletes, should prompt further investigation. Increased QRS amplitude is present in up to 80% of the athletes, but if the increased voltage is not accompanied by axis changes, repolarization changes, atrial abnormalities, or increased QRS width, it does not warrant further evaluation.

Small q waves may be present in athletes. The ECG in patients with HCM may also show q waves, but these “septal q's” are often seen in the inferior and/or lateral leads and suggest HCM if they are > 3 mm in depth and/or > 40 ms duration in at least two leads. Athletes with pathologic Q waves should be referred for further evaluation to exclude HCM (Table 36–2).

Early repolarization in V3–V6 with an elevated J point and peaked upright T waves is common in athletes and especially in those of African descent. The repolarization pattern may also include a domed ST segment followed by a biphasic or inverted T wave. These benign repolarization changes must be distinguished from the Brugada ECG pattern commonly present in leads V1–V2.

Other Noninvasive Cardiovascular Evaluations

ECG and echocardiography are indicated when clinical, historical, or physical findings suggest the possibility of structural heart disease (valvular disease, HCM, arrhythmogenic right ventricular cardiomyopathy, or prior MI). Tilt table testing is often positive in athletes because of their resting bradycardia and large venous capacitance and thus should not be used or should be used cautiously in athletes to evaluate lightheadedness, syncope, or presyncope.

Echocardiography in highly trained endurance athletes may show evidence of four-chamber cardiac enlargement. Left ventricular end-diastolic dimensions can exceed 60 mm in 15% of athletes. Left ventricular wall thickness can occasionally exceed the upper normal limit of 12 mm. Values of 13–15 mm may be seen in normal athletes, although marked enlargement of > 16 mm is unusual, and the ratio of the septal to posterior wall thickness does not exceed 1.2. The left ventricular cavity in HCM typically has asymmetric wall thickening, although symmetric wall enlargement may occur and the cavity dimensions are usually small and < 45 mm. In contrast, the athlete's heart typically has symmetric mild increases in left ventricular wall thickness and an increase in left ventricular chamber size of 55 mm or greater.

Left atrial enlargement in athletes is also common, and anterior-posterior diameters > 40 mm, the upper limit of normal, exist in 20% of high-performance athletes. This increased atrial size may contribute to the observation that atrial fibrillation is more common in older athletes than in age-matched nonathletes.

Left ventricular diastolic function measured by tissue Doppler is normal in athletes despite the hypertrophy, and normal diastolic function can help distinguish the athlete's heart from pathologic hypertrophy. The systolic anterior motion (SAM) of the mitral valve and mitral leaflet elongation can help with the diagnosis of HCM. These changes could happen in HCM even when the walls are not severely thickened. Stress echocardiography could provoke SAM and can provide more information than at rest.

Cardiac MRI can also help distinguish athlete's heart from HCM. A left ventricular diastolic wall thickness–to–cavity volume ratio of < 0.15 mm/m2/mL is useful in diagnosing athlete's heart. In HCM, intravenous gadolinium used in contrast-enhanced MRI is taken up by areas of myocardium with extra expanded cellular space indicating areas of fibrosis and scarring, also referred to as “late gadolinium enhancement” (LGE). LGE is not typical of the athlete's heart, especially in young athletes, but has been observed in older athletes with a history of life-long, intense exercise training.

Finally, detraining is another approach that could help to distinguish the athlete's heart from HCM. Three months of detraining should be sufficient to reverse the left ventricular hypertrophy of the athlete's heart and to distinguish this condition from HCM, although some studies suggest 6 months may be required. A decrease of > 2 mm in left ventricular wall thickness with detraining relative to peak training is more consistent with athlete's heart since patients with HCM should not demonstrate a change with deconditioning.

Evaluating athletes, just like evaluating any patient, requires a careful integration of all aspects of the history, physical examination, and imaging findings. Clinicians should be careful of overreacting to borderline abnormalities found in asymptomatic athletes during screening. These often lead to “diagnostic creep” in which one borderline abnormality, such as a flow murmur, leads to other borderline abnormalities, with no clinician willing to diagnose normalcy. Such cases often are best handled by clinicians who have extensive experience dealing with athletes.

Preparticipation Screening

To prevent SCD in athletes, Italy has mandated by law the screening of all athletes ages 12 through 35 prior to participation in organized competitive sport. This is a state-subsidized national program that includes a history and physical, an ECG, and a 3-minute step test. The evaluation is performed by accredited sports medicine doctors specifically trained for this task. Further testing is done for abnormal findings or if there is a family history of sudden death or MI or a personal history of syncope or palpitations. The incidence of SCDs in 12- to 35-year-old athletes in one region of Italy, Veneto, has decreased since the implementation of this law due to decreases in deaths from arrhythmogenic right ventricular hypertrophy. No changes in the nonathlete population mortality rate occurred over the same period of time.

Based on this single-center data, the European Society of Cardiology (ESC) and the International Olympic Committee (IOC) recommended the addition of an ECG to preparticipation screening. In contrast to the Italian experience, mandated preparticipation ECG and exercise testing in Israel has had no effect on the incidence of SCD in athletes. The AHA has also proposed guidelines for screening athletes prior to participation, but the AHA guidelines do not recommend routine ECG screening. Consequently, whether or not athletes require a routine ECG prior to athletic participation is controversial, and preparticipation ECG is not presently recommended in the United States. Clinicians should perform such ECG screening in individual athletes when the clinical situation warrants such testing or to reassure anxious parents. In such screening, however, the clinician should be wary of the diagnostic creep noted earlier.

In 2001, the AHA also published recommendations for preparticipation medical evaluations for master athletes. These are individuals over the age of 35 who are involved in masters sports training programs and participate in organized competitions designed for older athletes. Exercise testing is recommended for masters athletes who have a moderate-to-high cardiovascular risk profile for coronary heart disease; this risk profile includes men > 40 years old and women > 50 years old (or postmenopausal) with one or more independent coronary risk factors (hypercholesterolemia or dyslipidemia, hypertension, current or recent cigarette smoking, diabetes mellitus, or a history of MI or sudden death in a first-degree relative < 60 years old). An exercise test is also recommended for masters athletes of any age with symptoms suggestive of coronary heart disease or those ≥ 65 years of age even in the absence of risk factors or symptoms. A positive test requires further evaluation to determine the coronary anatomy. Although these are the current AHA guidelines, we also regard the recommendation for routine exercise testing in asymptomatic individuals as controversial since athletes frequently have false-positive ECG responses to exercise testing and there is limited clinical evidence to justify the routine revascularization of asymptomatic individuals, especially those with excellent exercise tolerance.

Recommendations for Sport Participation

Based on the routine history and physical examination prior to sport participation, the athlete should be either given clearance for participation, clearance to participate with activity limitations, or exclusion from participation pending further evaluation. If a cardiac diagnosis is made, limitations or exclusion might be warranted. The American College of Cardiology convened a consensus panel in 2005 to evaluate eligibility recommendations that are helpful once a diagnosis is made. This document summarizes experts' opinion regarding the type of sports the athlete is allowed to perform based on the cardiac pathology. Guidelines for sports participation for children with medical conditions have also been published and can assist in determining the level of sport recommended. Decisions should be individualized for each athlete since there are no definite data to determine the exercise risk for every cardiac condition, and guidelines are necessarily restrictive since they will be used by clinicians of varying ability. The decision to restrict sports participation should involve the athlete, the parents, and the coach.