THE ATHLETIC HEART SYNDROME
Five-Year Cardiac Evaluation of a Champion Athlete

Peter H. Gott, M.D., Harry A. Roselle, MD, Richard S. Crampton, MD

Although there has been considerable elucidation of the athletic heart syndrome in Europe, this entity has not yet become universally recognized or accepted in the United States. The athletic heart may simulate the diseased heart by exhibiting a systolic murmur, a slow pulse rate, a variety of arrhythmias and disturbances of cardiac conduction, elevation of the S-T segments, and cardiac enlargement by x-ray. Despite the history of athletic endurance, many unfortunate athletes are classified as cardiac patients and are requested to stop athletic training. For the past five years, we have observed a superbly trained athlete with chronic cardiac changes. He has had a large globular heart, an intermittent systolic ejection murmur, sinus bradycardia and arrhythmia, a wandering atrial pacemaker, occasional nodal premature beats, elevation of the S-T segments, broad peaked T waves, and the ability to meet the severe physical demands of training and competitive rowing at world championship level.

Patient Summary

A 23-year-old, single scull oarsman entered the hospital in 1963 for investigation of an enlarged heart discovered on a routine miniature chest x-ray film. He was engaged in an intensive training program preparing for the US Olympic rowing trials. His annual spring and summer training schedule demanded rowing seven days a week. He rowed 8 miles daily in one of two exercise programs. The first program was steady rowing for eight miles; the second rowing program consisted of warm-up for 2 ½ miles, then six sprints of 500 meters each interspersed with 500 meters of slower rowing. There was no history of cardiac disease, dyspnea, orthopnea, edema, rheumatic fever, chorea, syphilis, inadequate diet, anemia, hypertension, or familial cardiomegaly. He had occasionally noticed “weakness,” “faintness,” and vague “chest pressure” after particularly strenuous exercise. He was a tall, well-muscled man with blood pressure 140/80 mg Hg and weight 86.3 kg (190 lb). The heart rate varied between 40 and 50 beats per minute. The area of cardiac dullness did not extend beyond the left mid-clavicular line and right sternal edge. Physiological splitting of the second heart sound and a systolic ejection murmur which varied with postural changes were audible. No diastolic murmur or gallop were present. The rest of the examination and the blood count, sedimentation rate, protein-bound iodine, and Mazzini test were normal. A chest x-ray film showed a globular cardiac shadow with considerable fullness of the left ventricle. The cardiac thoracic ratio (17.4:35.5 cm) was normal, but the radiology department believed the heart enlarged because of an increased area of heart shadow in a man with a very wide thorax. The cardiac esophogram showed left and right ventricular prominence without atrial enlargement. An electrocardiogram showed sinus arrhythmia and bradycardia at 40 to 50 beats per minute. The P-R interval was 0.12 and the QRS complex was 0.06 second. The Q-T interval was 0.41 second (normal range 0.38 to 0.50 second). There was elevation of S-T segments in leads I, AVL, and V-2 through V-6. There was S-T depression in leads III and AVR. Broad, peaked T waves were noted in leads I, II, AVR, AVF, and V-2 through V-6. Increased QRS voltage was present. The intrinsicoid deflection in V-6 was 0.03 second. A phonocardiogram confirmed the auscultatory findings. Cardiac catheterization was performed, but atrial fibrillation began as the catheter entered the right ventricle. The arrhythmia was associated with a rise of systemic arterial pressure and an increase of ventricular rate from 40 to 50 beats per minute to 80 to 90 beats per minute which persisted for the rest of the study. Cardiac output, left ventricular stroke work, and systolic ejection rates were normal. However, the presence of transient atrial fibrillation made precise physiological measurements impracticable. During this arrhythmia, the patient reported sensations similar to those described after stopping very strenuous exercise. The heart returned spontaneously to sinus rhythm a few hours after the procedure. No intra-cardiac shunt was detected.

He left the hospital and resumed intensive rowing. A few months later, at the 1964 Olympic games in Tokyo, he won the semifinal heat with a magnificent sprint finish against the Russian world’s champion oarsman. His winter training program in 1964 to 1965 and 1965 to 1966 included five days of rowing 20 minutes in a dead water tank, followed by a steady ten-minute run, 20 chin-ups, and 50 sit-ups. He also performed a specially designed, vigorous exercise program consisting of a variety of calisthenics and weight-lifting to be completed in 18 minutes. On the days he did not row, he ran 5 miles. His spring and summer training program consisted of rowing 8 miles daily as described earlier. In 1965 an ECG showed sinus arrhythmia and bradycardia (48 per minute), one high nodal premature systole, and the same S-T segment and T wave configuration noted in 1963. A vector cardiogram was normal. In 1965 he won the Diamond Sculls at Henley-on-Thames, England. In 1966 he won the single sculls World’s Championship at Bled, Yugoslavia. For the winter seasons of 1966 to 1967 and 1967 to 1968, his training program consisted of exercise six days a week. For days a week he ran 3 to 5 miles or played one hour of squash, performed 20 chin-ups and 50 sit-ups, and ran one mile, alternating sprints with steady running. On two days, he swam a half mile or rowed 20 minutes in a dead water rowing tank, followed by ten minutes of steady running, 20 chin-ups, and 50 sit-ups. Examinations in March 1967 and March 1968 showed no murmur but were otherwise unchanged from that of 1963. The chest x-ray film showed the large globular heart unchanged from previous examinations. The EKG showed a wandering atrial pacemaker, sinus arrhythmia and bradycardia (39 to 52 beats per minute), and the same increased QRS voltage and S-T segment and T wave configurations across the precordium noted earlier.

Comment

This oarsman’s athletic capacity and achievement during a five-year period provided strong evidence for normal cardiac function. No stigmata of the syndrome of the “hyperkinetic” heart such as ventricular or arterial thrusting, increased systolic ejection rate, electrocardiographic evidence of ventricular hypertrophy, or congestive failure with passage of time were present during a five-year follow-up. In our opinion, his athletic endurance in the presence of a variable systolic ejection murmur, slow heart rate, electrocardiographic changes, and cardiomegaly is compatible with the athletic heart syndrome.

There is evidence that strenuous physical training does produce remarkable alterations in the anatomy of the heart. At autopsy, the hearts of athletes have shown a general increase in size, increased volume of individual chambers, and microscopic hypertrophy of ventricular muscle. An athletic heart has shown marked increase in the diameter of the coronary arteries. Athletic training also modifies the physiological behavior of the heart. The commonest characteristic of the athletic heart is bradycardia. In one study, racing cyclists in the resting, recumbent state had a greater average stroke volume, cardiac output, left ventricular stroke work, and heart size than did sedentary individuals at comparable heart rates. During and immediately after exercise, athletes also have a greater stroke volume. Estimation of heart size by electrokymography and x-ray studies had shown a larger systolic and diastolic heart size in athletes both before and after exercise. Other features distinguishing the athletic heart from the hearts of sedentary individuals include a greater increase of right ventricular filling pressure and pulmonary arterial pressure during exercise, a greater increase of cardiac output during exercise, and less fall of right ventricular filling pressure upon change from the supine to the sitting position.

Disturbances in conduction and rhythm as well as other electrocardiographic changes are frequently seen in trained athletes. These include slow atrial, atroventricular, and ventricular conduction; right axis deviation, increased magnitude of QRS and T vector loops with a shift of the horizontal angle to the right; splintering, notching and widening of the S wave in lead VI; elevation of the S-T segment, increased T wave voltage, bifid T waves, and T wave inversion in the precordial leads, paroxysmal atrial flutter and fibrillation at rest and after exercise; and post-exercise ventricular and nodal premature systoles and nodal rhythm. Of 21 marathon runners in the 1962 Commonwealth Games, 5 had incomplete right bundle branch block (RBBB) and 16 had increased QRS voltage suggesting left ventricular hypertrophy. In another analysis, incomplete RBBB was found in 19.1% of 413 athletes; in those with the largest hearts, 46% had incomplete RBBB. Seven percent of 92 former athletes showed incomplete RBBB; of 20 athletes with RBBB, 10 developed normal conduction after stopping regular sports activity.

It may be difficult to distinguish clinically between a diseased heart and an athletic heart since both may show bradycardia, a systolic murmur, a loud and often palpable third sound, a large globular silhouette, and a variety of electrocardiographic alterations. Usually the history of athletic endurance, cardiac examination before and after exercise, chest x-ray film, and ECG provide adequate information to evaluate the athlete. Difficulties arise from clinical interpretation of the systolic ejection murmur, the enlarged heart, and the electrocardiographic variations. Systolic ejection murmurs occur in up to 40% of young athletes and do not signify cardiac disease in spite of the astonishing suggestion that such persons be put on the “doubtful” list for competitive sports. The suggestion that a diastolic murmur must disqualify an athlete from competition seems superficially reasonable. However, apical diastolic murmurs from increased flow across the mitral valve have been found in normal individuals. The chest x-ray film may demonstrate ventricular enlargement in both diseased and athletic hearts. However, interpretations of chest x-ray films as well as cardiac murmurs and ECGs are usually considered in terms of the sedentary individual and may be misleading in evaluating the well-trained athlete. In the sportsman, the greater chance of recording the cardiac silhouette during diastole in the slowly beating, large athletic heart with an increased end diastolic volume enhances the larger globular configuration on x-ray. Electrokymography and routine chest radiograms synchronized with the cardiac cycle have been used to estimate systolic and diastolic heart size before and after exercise. The diseased heart enlarges during exercise; athletic and normal hearts show a decrease in size and an increase in output during physical activity. Following periods of intensive athletic training when the individual is no longer active, the heart returns to its former size. Electrocardiographic changes may also disappear when the athlete stops training. The criteria for diagnosis of the athletic heart syndrome include a history of athletic endurance; biventricular cardiac enlargement; systolic ejection murmur; third heart sound; increased stroke volume, left ventricular stroke work, and cardiac output; bradycardia and sinus arrhythmia; recurrent atrial and ventricular arrhythmias; cardiac conduction defects; S-T segment elevation; and T wave alterations.

Cineradiography of the heart, as yet unreported in normal individuals or athletes, might be used to show the systolic and diastolic size and contour of the slowly beating heart before, during, and after and after exercise. The resulting standardization of heart size should be useful in evaluating athletic as well as sedentary hearts. In addition, a technique of indirect estimation of left ventricular contractility has been suggested and might be tried in order to assess myocardial function without resorting to cardiac catheterization.

In Summary

During a five-year observation of a superbly trained champion athlete, the constellation of a large globular heart, an intermittent ejection murmur, a variety of arrhythmias, and S-T and T wave alterations suggested the presence of an athletic heart syndrome resulting from anatomical and physiological adjustments to strenuous training.

In distinguishing the athletic heart from the diseased or normal sedentary heart, the use of criteria derived from sedentary individuals is misleading.