Intensive, prolonged endurance and strength training causes many physiologic adaptations. Volume and pressure loads in the left ventricle (LV) increase, which, over time, increase LV muscle mass, wall thickness, and chamber size. Maximal stroke volume and cardiac output increase, contributing to a lower resting heart rate and longer diastolic filling time. Lower heart rate results primarily from increased vagal tone, but decreased sympathetic activation and other nonautonomic factors that decrease intrinsic sinus node activity may play a role. Bradycardia decreases myocardial oxygen demand; at the same time, increases in total hemoglobin and blood volume enhance oxygen transport. Despite these changes, systolic function and diastolic function remain normal. Structural changes in women are typically less than those in men of the same age, body size, and level of training.
Symptoms and Signs of Athlete’s Heart
There are no symptoms. Signs vary but may include bradycardia; an LV impulse that is laterally displaced, enlarged, and increased in amplitude; a systolic ejection (flow) murmur at the left lower sternal border; a 3rd heart sound (S3) due to early, rapid diastolic ventricular filling; a 4th heart sound (S4), heard best during resting bradycardia because diastolic filling time is increased; and hyperdynamic carotid pulses. These signs reflect structural cardiac changes that are adaptive for intense exercise.
Diagnosis of Athlete’s Heart
Rarely, cardiac magnetic resonance imaging
Rarely, stress testing
Findings are typically detected during routine screening or during evaluation of unrelated symptoms. Most athletes do not require extensive testing, although ECG is often warranted. If symptoms suggest a cardiac disorder (eg, palpitations, chest pain), ECG, echocardiography, and exercise stress testing are done.
Athlete's heart is a diagnosis of exclusion; it must be distinguished from disorders that cause similar findings but are life threatening (eg, hypertrophic cardiomyopathy Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy is a congenital or acquired disorder characterized by marked ventricular hypertrophy with diastolic dysfunction but without increased afterload (eg, due to valvular... read more , dilated cardiomyopathy Dilated Cardiomyopathy Dilated cardiomyopathy is myocardial dysfunction causing heart failure in which ventricular dilation and systolic dysfunction predominate. Symptoms include dyspnea, fatigue, and peripheral edema... read more , ischemic heart disease, arrhythmogenic right ventricular dysplasia). Cardiac magnetic resonance (CMR) imaging may be helpful when findings from other diagnostic modalities are inconclusive.
Numerous changes in rhythm and ECG morphology can occur; they correlate poorly with level of training and cardiovascular performance. The most common ECG finding is
Rarely, heart rate is < 40 beats/min. Sinus arrhythmia often accompanies the slow heart rate. Resting bradycardia may also predispose to
Atrial or ventricular ectopy (including couplets and bursts of nonsustained ventricular tachycardia); pauses after ectopic beats do not exceed 4 seconds
Wandering supraventricular pacemaker
Other ECG findings that may occur include
First-degree atrioventricular (AV) block (in up to one third of athletes)
Second-degree AV block (mainly type I); this finding occurs during rest and disappears with exercise
High-voltage QRS with inferolateral T-wave changes (reflecting LV hypertrophy)
Deep anterolateral T-wave inversion
Incomplete right bundle branch block
However, 3rd-degree AV block Third-degree AV block Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction... read more is abnormal and should be investigated thoroughly.
These ECG and rhythm changes have not been associated with adverse clinical events, suggesting that various arrhythmias are not abnormal in athletes. The arrhythmias are usually abolished or substantially reduced after a relatively brief period of deconditioning.
Echocardiography can usually distinguish athlete’s heart from cardiomyopathies (see table Features Distinguishing Athlete's Heart From Cardiomyopathy Features Distinguishing Athlete's Heart From Cardiomyopathy ), but the distinction is not always clear because there is a continuum from physiologic to pathologic cardiac enlargement. The zone of overlap between athlete’s heart and cardiomyopathy is left ventricular septal thickness:
In men, 13 to 15 mm
In women, 11 to 13 mm
In this overlap area, the presence of mitral valve systolic anterior motion strongly suggests hypertrophic cardiomyopathy Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy is a congenital or acquired disorder characterized by marked ventricular hypertrophy with diastolic dysfunction but without increased afterload (eg, due to valvular... read more . Also, diastolic indexes may be abnormal in cardiomyopathy but are usually normal in athlete's heart. In general, echocardiographic changes correlate poorly with level of training and cardiovascular performance. Trace mitral regurgitation and tricuspid regurgitation are commonly detected. Of note, reduction of physical training will result in regression of cardiac enlargement in patients with athlete's heart but not in those with cardiomyopathy.
Although confirmation in large studies is pending, data so far suggest that CMR may also help differentiate athlete's heart from cardiomyopathy. In hypertrophic cardiomyopathy ( 1 Diagnosis reference Athlete’s heart is a constellation of structural and functional changes that occur in the heart of people who train for > 1 hour most days. The changes are asymptomatic; signs include bradycardia... read more ), CMR may identify focal hypertrophy not identified on the echocardiogram, particularly in the apex, anterior free wall, and posterior septum. Delayed imaging after injection of contrast may show a typical pattern of mid-wall fibrosis in some patients with hypertrophic cardiomyopathy, particularly in left ventricular wall segments that exhibit maximal hypertrophy. However, this finding is absent in up to 60% of patients with hypertrophic cardiomyopathy.
Delayed enhancement on CMR is also evident in nonischemic dilated cardiomyopathy and may help differentiate dilated cardiomyopathy from athlete's heart. However, the finding is absent in 68% of patients with genetically proven dilated cardiomyopathy. T1 mapping techniques have shown some potential to differentiate between athlete's heart and DCM, but further studies are required. Although exercise capacity as measured by stress testing does not differentiate between athlete's heart and dilated cardiomyopathy, reduced cardiac contractile reserve with exercise observed on CMR imaging may be useful in establishing a diagnosis of dilated cardiomyopathy in an athlete.
During exercise stress testing Stress Testing In stress testing, the heart is monitored by electrocardiography (ECG) and often imaging studies during an induced episode of increased cardiac demand so that ischemic areas potentially at risk... read more , heart rate remains lower than normal at submaximal stress and increases appropriately and comparably to heart rate in nonathletes at maximal stress; it rapidly recovers after exercise. Blood pressure response is normal if:
Systolic blood pressure increases
Diastolic blood pressure falls
Mean blood pressure stays relatively constant
Many resting ECG changes decrease or disappear during exercise; this finding is unique to athlete's heart, distinguishing it from pathologic conditions. However, pseudonormalization of T-wave inversions could reflect myocardial ischemia and thus warrants further investigation in older athletes. Also, a normal exercise stress test result does not rule out a cardiomyopathy.
1. Czimbalmos C, Csecs I, Toth A, et al: The demanding grey zone: Sport indices by cardiac magnetic resonance imaging differentiate hypertrophic cardiomyopathy from athlete's heart. PLoS ONE 14(2): e0211624. 2019.
Prognosis for Athlete’s Heart
Although gross structural changes resemble those in some cardiac disorders, no adverse effects are apparent. In most cases, structural changes and bradycardia regress with detraining, although up to 20% of elite athletes have residual chamber enlargement, raising questions, in the absence of long-term data, about whether athlete’s heart is truly benign.
Treatment of Athlete’s Heart
Possibly a period of deconditioning to monitor LV regression
No treatment is required, although 3 months of deconditioning may be needed to monitor LV regression as a way of distinguishing this syndrome from cardiomyopathy. Such deconditioning can greatly interfere with an athlete’s life and may meet with resistance.
Intensive physical exercise increases left ventricular muscle mass, wall thickness, and chamber size but systolic function and diastolic function remain normal.
Resting heart rate is slow and there may be a systolic ejection murmur at the left lower sternal border, a 3rd heart sound (S3), and/or a 4th heart sound (S4).
ECG shows bradycardia and signs of hypertrophy and sometimes other findings such as sinus arrhythmia, atrial or ventricular ectopy, and 1st or 2nd degree atrioventricular (AV) block.
Structural and ECG changes due to athlete's heart are asymptomatic; the presence of cardiovascular symptoms (eg, chest pain, dyspnea, palpitations) or 3rd degree AV block should prompt a search for an underlying cardiac disorder.