The cardiac adaptations associated with athlete’s heart are first: bradycardia or decreased heart rate, which decreases myocardial oxygen demand. Next, a systolic flow murmur at the left lower sternal border can be present as well as extra heart sounds. A third heart sound (S3) can be heard due to early and rapid diastolic filling, and a fourth heart sound (S4) can be heard during resting bradycardia. Furthermore, cardiomegaly, abnormal enlargement of the heart, and cardiac hypertrophy, thickening of the heart wall, are present in athlete’s heart. These will lead to increased volume and pressure loads in the left ventricle and increased stroke volume and cardiac output. This increased stroke volume and cardiac output contribute to a decrease in the resting heart rate; however, the main cause of the decrease in heart rate is due to an increase in vagal nerve tone which is also present in athlete’s heart. Lastly, due to the increase in pressure and stroke volume, athlete’s heart patients present with hyperdynamic carotid pulses, which present as a pulse measured at the neck that has an increase in velocity and amplitude. Female athletes undergo less drastic adaptations than males of the same age, body size and training (McKelvie, 2013). Furthermore, endurance athletes present with eccentric hypertrophy, which is where the cardiac muscle wall thickens along with left ventricular dilatation, whereas weightlifters present with concentric hypertrophy because they exhibit less ventricular dilatation and the heart lumen is decreased (Ellison, 2011).
As mentioned previously, the diagnosis of athlete’s heart is one of exclusion, attempting to rule out similarly presenting conditions like hypertrophic or dilated cardiomyopathies, ischemic heart disease or arrhythmogenic right ventricular dysplasia. The diagnostic clinical evaluation includes an ECG, sometimes an echocardiogram, and on rare occasions stress testing. The findings of the ECG include bradycardia with a heart rate between 40 and 50 beats per minute and less than 40 beats per minute at the lower end, and the bradycardia is usually accompanied with sinus arrhythmia which is a beat-to-beat variation in P-P interval (time period between consecutive atrial depolarizations) resulting in an irregular ventricular rate.
The prognosis for athlete’s heart is quite mild: the physical changes to the heart will usually regress with detraining. However, approximately 20% of athletes will display residual chamber enlargement, which begs the question: is athlete’s heart truly benign? There is no treatment required for this condition, but it is possible that three months of deconditioning will be necessary to monitor the left ventricle regression to make sure there no cardiomyopathies present (McKelvie, 2013).
A major risk of continued, strenuous physical activity is cardiac cell damage following exercise, although this mechanism is poorly understood. Prolonged exercise can cause arrhythmias and even primary cardiac arrest due to cardiac fibrosis and diastolic dysfunction. Despite this risk, prolonged exercise has been shown to cause little or no myocardial apoptosis (programmed cell death) because physical activity increases the expression of HSP70, a protein that inhibits apoptosis (Ellison, 2011). More research needs to be done on the potential risks of strenuous exercise.
Though there are risks associated with athlete’s heart and excessive training, it would seem as though the benefits are far greater. In the future, the medical community must be able to better distinguish between eccentric and concentric cardiac hypertrophy and determine whether concentric is benign or not. Lastly, procedures must be developed to exploit the beneficial molecular and cellular adaptations brought about through exercise in disease states like athlete’s heart such as faster recovery following a heart attack and possibly involving intracoronary injections of helpful biochemical compounds only present in effective concentrations in patients afflicted with athlete’s heart in order to elicit the same accelerated healing in normal patients (Ellison, 2011).
1) Ellison G, Waring C, Vicinanza C, Torella D. Physiological cardiac remodeling in response to endurance exercise training: cellular and molecular mechanisms. Heart 98: 5-10. 2011.
2) McKelvie R. Athlete’s heart. The Merck Manual.http://www.merckmanuals.com/professional/cardiovascular_disorders/sports_and_the_heart/athletes_heart.html?qt=&sc=&alt=. 2013.