Athlete’s heart is a constellation of structural and functional changes that occur in the heart of people who train for prolonged durations (eg, > 1 hour most days) and/or frequently at high intensities. 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 females are typically less than those in males of the same age, body size, and level of training (1, 2).
The prevalence of coronary artery calcium (CAC) scores greater than or equal to 100 Agatston units appears to be increased in people performing high levels of physical activity (equal to or more than 3000 MET [metabolic equivalent of task]-minutes/week) than those performing lower levels of physical activity. However, this does not translate into a greater risk of all-cause or cardiovascular mortality . The data support that even in the presence of CAC, the risk of all-cause mortality and cardiovascular mortality is less with high levels of physical activity than with lower levels of physical activity (3).
General references
1. Palermi S, Cavarretta E, D’Ascenzi F, et al: Athlete's Heart: A cardiovascular step-by-step multimodality approach. Rev Cardiovasc Med 24(5): 151, 2023. https://doi.org/10.31083/j.rcm2405151
2. Martinez MW, Kim JH, Shah AB, et al: Exercise-induced cardiovascular adaptations and approach to exercise and cardiovascular disease. JACC State-Of-The-Art Review. J Am Coll Cardiol 78 (14): 1454–1470, 2021. doi: 10.1016/j.jacc.2021.08.003
3. DeFina LF, Radford NB, Barlow CE, et al: Association of all-cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiol. 4(2):174–181, 2019. doi:10.1001/jamacardio.2018.4628
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 third heart sound (S3) due to early, rapid diastolic ventricular filling
Hyperdynamic carotid pulses
These signs reflect structural cardiac changes that are adaptive for intense exercise.
The presence of a fourth heart sound (S4) is almost always abnormal in an athlete.
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 [eg, coronary artery disease], arrhythmogenic right ventricular cardiomyopathy—[1]). Cardiac magnetic resonance (CMR) imaging may be helpful when findings from other diagnostic modalities are inconclusive. Sometimes a trial of deconditioning is required to differentiate athlete's heart from cardiomyopathy.
ECG
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/minute. 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 atrial (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, third-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
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 males, 13 to 15 mm
In females, 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.
Exercise echocardiography may help to differentiate athlete's heart from dilated cardiomyopathy. In one study, a change during exercise in left ventricular ejection fraction (LVEF) ≤ 11% and a peak LVEF ≤ 63% during exercise predicted dilated cardiomyopathy with a sensitivity of 85.7% and specificity of 92% (2).
Cardiac magnetic resonance (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 (3), 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 and T2 mapping, extracellular volume quantification, late gadolinium enhancement, deformation imaging and diffusion tensor imaging are all promising techniques to differentiate between athlete's heart and hypertrophic cardiomyopathy. Further studies are required to better determine the ability of these techniques to detect hypertrophic cardiomyopathy in athletes (4, 5).
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
Feature | Athlete’s Heart | Cardiomyopathy |
|---|---|---|
Left ventricular septal thickness* | In males, < 13 mm In females, < 11 mm | In males, > 15 mm In females, > 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 | Symmetric | Asymmetric (in hypertrophic cardiomyopathy) |
Family history | None | May be present |
Blood pressure response to exercise | Normal | Normal or reduced systolic blood pressure response |
Deconditioning | 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 references
1. Palermi S, Cavarretta E, D’Ascenzi F, et al: Athlete's Heart: A cardiovascular step-by-step multimodality approach. Rev Cardiovasc Med 24(5): 151, 2023. https://doi.org/10.31083/j.rcm2405151
2. Millar LM, Fanton Z, Finocchiaro G, et al: Differentiation between athlete's heart and dilated cardiomyopathy in athletic individuals. Heart 106(14):1059–1065, 2020. doi: 10.1136/heartjnl-2019-316147
3. 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.
4. Bakogiannis C, Mouselimis D, Tsarouchas A, et al: Hypertrophic cardiomyopathy or athlete's heart? A systematic review of novel cardiovascular magnetic resonance imaging parameters. Eur J Sports Sci Dec 2;1–12, 2021. doi: 10.1080/17461391.2021.2001576
5. Baggish AL, Battle RW, Beaver TA, et al: Recommendations on the use of multimodality cardiovascular imaging in young adult competitive athletes: A report from the American Society of Echocardiography in collaboration with the Society of Cardiovascular Computed Tomography and the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr 33 (5): 523–549, 2020. doi: 10.1016/j.echo.2020.02.009
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.
Prognosis for Athlete’s Heart
Although gross structural changes resemble those in some cardiac disorders, generally no adverse effects are apparent. However, numerous studies have found an increased risk of developing atrial fibrillation in patients who participate in endurance and mixed sports (1). Athletes younger than 55 years are at higher risk (2). The dose of exercise at which the risk increases has not been documented in high quality studies. 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.
Prognosis references
1. La Gerche A, Wasfy MM, Brosnan MJ, et al: The Athlete's Heart—Challenges and Controversies: JACC Focus Seminar 4/4. J Am Coll Cardiol 80(14):1346–1362, 2022. doi: 10.1016/j.jacc.2022.07.014
2. Newman W, Parry-Williams G, Wiles J, et al: Risk of atrial fibrillation in athletes: a systematic review and meta-analysis. Br J Sports Med 55(21):1233–1238, 2021. doi:10.1136/bjsports-2021-103994
Key Points
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, and a third heart sound (S3); a fourth heart sound (S4) should be considered abnormal.
ECG shows bradycardia and signs of hypertrophy and sometimes other findings such as sinus arrhythmia, atrial or ventricular ectopy, and first or second 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 third-degree AV block should prompt a search for an underlying cardiac disorder.
