The athlete’s heart or the athletic heart syndrome is a constellation of clinical findings including sinus bradycardia, systolic flow murmurs, and cardiac chamber enlargement with normal or augmented function. All four cardiac chambers may be enlarged. Chamber enlargement may rarely exceed the upper limits of normal, but marked enlargement of the right ventricle or either atrium suggests a pathologic process. Clinical findings of the athletic heart syndrome are limited to athletes whose sports and training require a large aerobic or endurance exercise component. The left ventricular wall can be slightly thickened, but this thickening is generally restricted to athletes with left ventricular chamber enlargement and rarely reaches the thickness of pathologic, states such as hypertrophic cardiomyopathy (HCM). Physicians are often required to evaluate asymptomatic athletes prior to participation and to evaluate symptomatic athletes before permitting their return to vigorous exercise training. In these situations, the athletic heart syndrome must be differentiated from pathologic conditions associated with cardiac complications during exercise. These include HCM, coronary artery anomalies, aortic stenosis, and right or left ventricular cardiomyopathy in young athletes and coronary artery disease in adults.

The athlete’s heart presently refers to normal cardiac adaptations that occur with prolonged, primarily endurance, exercise training, but the history of the athlete’s heart reflects the historical debate about the risks and benefits of vigorous exercise training and competition (1). Vigorous sports competition in the pre-Victorian era was largely an activity of the laboring class who competed in rowing, bicycling, and running events to test the skills required in their employment. There was little interest in such intense competition among the aristocracy and therefore little concern about its health risks. This changed during the Victorian era, when interest in competitive athletics increased, in part because sports were believed to develop what has been called the “most prized of Victorian virtues,
character” (2). The athlete’s heart in this period was primarily a moral concept referring to the character developed from athletic competition (2). Concern about the possible health risk of extreme exertion increased with growing sports participation among the aristocracy, and the appearance of such events as the Oxford–Cambridge boat race, first held in 1829 (2). In 1867, the “mechanic clause” was added to the rules of the British Amateur Athletic Club to exclude competitors whose work required physical labor. This made amateur athletic competition an activity for the elite (3). Articles on the dangers of the rower’s, runner’s and bicyclist’s heart soon followed (1). These concerns are understandable given the cardiac diagnostic techniques of the day, primarily by palpation of the pulse, percussion of the precordium for heart size, and auscultation for murmurs. The clinical characteristics of the athlete’s heart including sinus bradycardia, cardiac enlargement, and pulmonic and aortic flow murmurs were interpreted as heart block, cardiomyopathy, and valvular obstruction, respectively, conditions with poor prognoses until the later half of the twentieth century. Indeed, it was not until 1942 that the famed Boston cardiologist, Paul Dudley White, reported four cases of marked bradycardia in endurance athletes and concluded that this could be normal in endurance athletes (4).

The term athlete’s heart appears to have been coined by a Swedish physician, S. Henschen in 1899 (5). He percussed cardiac size in cross-country skiers before and after a ski race and concluded that skiing produce a physiologic cardiac enlargement, which enabled the heart to perform more work than the heart of an untrained individual. He also noted that both the right and left sides of the heart were enlarged. Subsequent studies using roentgenographic, echocardiographic, computed tomographic, and magnetic resonance imaging techniques have only confirmed Henschen’s conclusion that exercise training produces a generalized cardiac enlargement.

How could Henschen, using only the “educated finger” for chest percussion, have reached such accurate conclusions? In sum, he picked the right athletes, and this fact highlights several clinical characteristics of the athletic heart syndrome. First, Henschen studied endurance trained athletes. Strength trained athletes, such as weight lifters, have increased cardiac dimensions, but their enlargement is related to body size and muscle mass (6). Only endurance trained athletes, or athletes training with both endurance and strength modalities, develop the athletic heart syndrome. Second, Henschen selected cross-country skiers, endurance athletes whose exercise uses both arm and leg muscles. Cardiac dimensions and stroke volume are greatest in those athletes whose training requires the use of the most muscle mass. This chapter summarizes the clinical principles of the athlete’s heart developed since Henschen’s report 100 years ago.

Successful endurance athletes, compared to the general population, have a higher ability to perform maximal dynamic exercise, which can be measured as maximal oxygen uptake (VO₂ max) (7). VO₂ max is physiologically limited by the ability of the cardiopulmonary system to deliver, and the ability of the exercising muscles to use, oxygen. Rearranging the Fick equation for cardiac output (cardiac output = VO₂/A – VO₂ difference) demonstrates that VO₂ max is the product of maximal cardiac output and the maximal arteriovenous O₂ difference (7). Maximal cardiac output is the product of maximal heart rate and stroke volume. Because maximal heart rate among healthy individuals varies primarily by age and because the ability to increase the A – VO₂ difference is limited, the major factor responsible for the higher VO₂ max among endurance athletes is an increased stroke volume (7). The clinical findings typical of the athlete’s heart are generally manifestations of this increased stroke volume.

Although higher VO₂ max values distinguish endurance athletes from sedentary individuals, among endurance athletes, VO₂ max is not a good discriminator of superior athletic performance because VO₂ max does not measure an individual’s ability to maintain exertion over a long period of time (7). Other factors including the athlete’s mechanical efficiency and the athlete’s anaerobic threshold or onset of blood lactate accumulation (OBLA) contribute to submaximal work capacity and are better discriminators of competitive exercise performance among athletes (7). Enhanced mechanical efficiency means that an athlete can perform a physical task while consuming less oxygen than a less efficient athlete. A higher OBLA means that the athlete can perform more mechanical work without producing lactate. OBLA is associated with a higher respiratory rate stimulated by the production of carbon dioxide from buffering lactic acid (HLactate + HCO₃^– → H₂CO₃ + lactate^– → H₂O + CO₂). In addition, the lactate production indicates a level of exertion requiring glycogen catabolism and glycogen depletion is one potential limiting factor in endurance performance. Finally, lactic acid itself contributes to fatigue.

The increase in heart rate early during exercise is due primarily to withdrawal of resting vagal tone. At approximately 50% of maximal heart rate, additional acceleration of heart rate is associated with increased sympathetic activity (8). Peak heart rate is estimated as 220—age with a standard deviation of the estimate of ±11 to 22 beats per minute (BPM) (9) and 95% confidence limits of ±22 to 44 BPM. This emphasizes the problem of estimating heart rate by age. The increase in A – VO₂ diff in produced by redistribution of blood from nonexercising tissue to the exercising musculature, increased extraction of O₂ over the exercising muscle bed, and hemoconcentration (8). A change in any component of this system can affect exercise capacity. Cardiologists focus on changes in maximum heart rate and stroke volume, but changes in hemoglobin concentration, the ability to fully oxygenate the red cells, the capacity to shunt blood to exercising muscle, and the ability of the muscles to extract oxygen can affect exercise performance. All should be considered in evaluating athletes for problems with exercise performance.

Athletes frequently present for cardiac consultation because of palpitations. This is often sinus tachycardia, among the more
nervous subjects, or premature atrial or ventricular depolarizations (PVDs) detected by heart rate monitoring or palpation during athletic training. Occasional PVDs may be more frequent in athletes because the prolonged diastole provides extra time for such beats to occur. Premature beats are best treated with reassurance alone, but some athletes may require β-adrenergic blocking or other agents for symptomatic relief. Physicians should avoid β-blockers in elite athletes because they may affect athletic performance and are prohibited in sports such as archery and shooting because they prolong diastole and thereby reduce body movement produced by cardiac contraction.

Habitual endurance exercise produces a global cardiac enlargement that may affect both the right and left atria and ventricles. The most consistent enlargement is seen in the left ventricular chambers where intracavity dimensions, and rarely wall thickness, can be large enough to raise the suspicion of cardiac disease. Mild enlargement of both atria and the right ventricle can occur, but marked enlargement of these structures suggests a disease process and is not observed in the athletic heart syndrome.