Athlete's Heart Syndrome

Can an Athlete Have Heart Failure?

Although non-pathological and often asymptomatic, high-intensity exercise and training can lead to structural, functional, and electrical transformations of the athlete’s heart. This exercise-adaptative physiological remodeling is known as athlete’s heart syndrome, characterized by an enlarged heart and a lower heart rate due to cardiac loading [1].

However, no evidence exists linking athlete’s heart syndrome and heart failure in athletes that have no underlying cardiac conditions [2].

What Is Athlete’s Heart Syndrome?

Athlete’s Heart Syndrome is a physiological state of the heart characterized by an enlarged left ventricular cavity (dilatation), an increased wall thickness (hypertrophy), and a lower heart rate (Bradycardia). It is associated with athletes who exercise or follow a training program for most days and for more than one hour.

  • What Causes Cardiac Enlargement?

They are two types of hypertrophies that are associated with the type of training whether it is resistance or isometric. For instance, isometric exercises, such as the ones performed in one position and without movement (e.g., weightlifting), promote hypertrophy with normal cavity dimensions, while resistance exercises (e.g., running) stimulate hypertrophy and cavity dilatation [3].

  • What Causes Bradycardia?

During physical activities and resting, the heart rate is controlled by the sympathetic and parasympathetic nervous systems. In athletes, there is an increase in the parasympathetic input and a decrease in the sympathetic input during the resting state [4].

What Causes Heart Problems in Athletes?

There are no heart problems in healthy athletes who are diagnosed with athlete’s heart syndrome. Potential heart problems in athletes may be associated with pre-existing cardiac conditions such as hypertrophic cardiomyopathy, a genetic disorder characterized by thickening of the heart [5].

Additionally, although athlete’s heart syndrome may resemble a heart pathological state, markers of heart contraction (systolic) and relaxation (diastolic), are consistently normal in athletes and there is no evidence involving athlete’s heart syndrome as a cause for cardia fibrosis nor fiber disarray [6].

How Is Athlete Heart Syndrome Diagnosed?

Athlete Heart Syndrome is usually detected during routine examinations or following athletes complaining of palpitations, or chest pain [7].

1- Electrocardiogram (ECG)

An electrocardiogram is a test that measures the heart’s rhythms and electrical activity. In athletes, this test can detect the following changes that are not considered pathologic:

  • Sinus bradycardia: Regular heart rhythm with a lower heartbeat of less than 60 (Normal range is between 60 and 100.
  • Atrial or ventricular ectopy: Extra heartbeat associated with a signal to the upper chambers of the heart. 
  • Wandering supraventricular pacemaker: Shifting of the natural cardiac pacemaker site between the sinoatrial node, the atria, and/or the atrioventricular node.
  • Deep anterolateral T-wave inversion: Changes in T-wave associated with the repolarization of the ventricles
  • Incomplete right bundle branch block: Denotes a slowdown in the electrical conduction as it passes through the right side of the heart.
  • First-degree atrioventricular block: Slowdown of electrical conduction through the atrioventricular node
  • Second-degree atrioventricular block: Slowdown of electrical conduction between the atria and the ventricles
  • High-voltage QRS with inferolateral T-wave changes: Increased depolarization of the right and left ventricles of the heart and changes in the depolarization of the ventricular inferolateral walls

2- Echocardiography

Echocardiography is a type of ultrasound scan that uses sound waves to create moving pictures of your heart. Although echocardiography can be used to differentiate between an athlete’s heart and hypertrophic cardiomyopathy, the changes that are detected by echocardiographic poorly correlate with the level of training and cardiovascular performance. 

3- Cardiovascular magnetic resonance imaging (CMR) imaging

This MRI (magnetic resonance imaging)-based technology is adapted for the imaging of the cardiovascular system. Unlike the limitation of echocardiography in differentiating between athlete’s heart and hypertrophic cardiomyopathy, CMR can identify focal hypertrophy, particularly in the apex, anterior free wall, and posterior septum. 

4- Stress testing

This test assesses athletes’ systolic, diastolic, and mean blood pressures following exercise-induced stress levels. At a low-stress level, the heart rate remains low, and it increases with the increase in stress level before recovering after exercise. The gradual stress levels also increase the athletes’ systolic, diastolic, and mean blood pressures. Results that indicate a different pattern may suggest a pathological condition.

How Is Athlete Heart Syndrome Treated?

Several studies have shown that athlete heart syndrome is not the cause of sudden death during or after exercise, and therefore, treatment is not required. However, if requested by the athlete an exercise deconditioning of three months could revert the cardiac hypertrophy [8][9].


Athlete Heart Syndrome is observed in athletes following training programs for most days and for more than one hour. Although it results in the enlargement of the heart and bradycardia, no evidence exists that links athlete’s heart syndrome with heart failure in athletes.

However, if symptoms of chest pain or palpitations manifest, it is extremely important to perform different tests to ensure that these symptoms are not associated with cardiomyopathies that can lead to sudden death during or after exercise.

Additionally, similarities between athlete heart syndrome and cardiomyopathies such as hypertrophic cardiomyopathy can result in diagnostic errors that can lead to the ruining of the athlete’s career or worse to death.


[1] Prior, D.L. and La Gerche, A., 2012. The athlete’s heart. Heart98(12), pp.947-955.

[2] Maron, B.J. and Pelliccia, A., 2006. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation114(15), pp.1633-1644.

[3] MORGANROTH, J., MARON, B.J., HENRY, W.L. and EPSTEIN, S.E., 1975. Comparative left ventricular dimensions in trained athletes. Annals of internal medicine82(4), pp.521-524.

[4] Hammond, H.K. and Froelicher, V.F., 1985. Normal and abnormal heart rate responses to exercise. Progress in cardiovascular diseases27(4), pp.271-296.

[5] Kimura, A., 2016. Molecular genetics and pathogenesis of cardiomyopathy. Journal of human genetics61(1), pp.41-50.

[6] Shapiro, L.M., 1984. Physiological left ventricular hypertrophy. Heart52(2), pp.130-135.


[8] Pelliccia, A., Maron, B.J., De Luca, R., Di Paolo, F.M., Spataro, A. and Culasso, F., 2002. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation105(8), pp.944-949.

[9] Martin, W.H., Coyle, E.F., Bloomfield, S.A. and Ehsani, A.A., 1986. Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume. Journal of the American College of Cardiology7(5), pp.982-989.

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