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Athlete’s Heart


Robert S. McKelvie

, MD, PhD, Western University

Last full review/revision Oct 2020| Content last modified Oct 2020
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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, a systolic murmur, and extra heart sounds. Electrocardiographic (ECG) abnormalities are common. Diagnosis is clinical or by echocardiography. No treatment is necessary. Athlete’s heart is significant because it must be distinguished from serious cardiac disorders.

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.

General reference

  • Brosnan MJ, Rakit D: Differentiating athlete's heart from cardiomyopathies − The left side. Heart Lung Circ 27(9):1052-1062, 2018. doi: 10.1016/j.hlc.2018.04.297

Diagnosis of Athlete’s Heart

  • Clinical evaluation

  • Usually ECG

  • Sometimes echocardiography

  • 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, dilated cardiomyopathy, 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

  • Sinus bradycardia

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 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), 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. 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.

CMR imaging

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), 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.

Stress testing

During exercise stress testing, 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.


Features Distinguishing Athlete's Heart From Cardiomyopathy


Athlete’s Heart


Left ventricular septal thickness*

In men, < 13 mm

In women, < 11 mm

In men, > 15 mm

In women, > 13 mm

Left ventricular end-diastolic diameter†

< 60 mm

> 70 mm

Diastolic function

Normal (E:A ratio > 1)

Abnormal (E:A ratio < 1)

Septal hypertrophy


Asymmetric (in hypertrophic cardiomyopathy)

Family history


May be present

Blood pressure response to exercise


Normal or reduced systolic blood pressure response


Left ventricular hypertrophy regression

No left ventricular hypertrophy regression

* A value of 13 to 15 mm in men and 11 to 13 mm in women is indeterminate.

† A value of 60 to 70 mm is indeterminate.

E:A ratio = ratio of early to late atrial transmitral flow velocity.

Diagnosis reference

  • 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 of 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.

Key Points about Athlete’s Heart

  • 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.

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