During intensive, prolonged endurance- and strength-training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time. After time, these pressures cause the muscle mass, wall thickness, and chamber size of the left ventricle of the heart to increase.
Cardiac output, the amount of blood that leaves the heart, is proportional to both the chamber sizes of the heart and the rate at which the heart beats. With a larger left ventricle, the heart rate can decrease and still maintain a level of cardiac output necessary for the body. Therefore, it is very common for athletes to have lower resting heart rates than nonathletes.
There are no symptoms for people with athletic heart syndrome, although an indicator would be a consistently low resting heart rate. AHS is usually diagnosed during a routine screening or during tests for other medical issues. An enlarged heart can be seen on an echocardiogram or sometimes a chest X-ray. Due to the similarities between AHS and more serious cardiac problems, an electrocardiogram (EKG) and exercise stress tests are sometimes performed.
The EKG can detect sinus bradycardia, a resting heart rate of fewer than 60 beats per minute. This is often accompanied by sinus arrhythmia. The heartbeat of a person with AHS can sometimes be irregular while at rest, but usually returns to normal after exercise begins.
One common cardiovascular disease that has similar EKG reads is hypertrophic cardiomyopathy, which is characterized by the thickening of the heart's walls. This genetic disorder is found in 1 out of 500 Americans and is responsible for thousands of sudden death cases every year. Of all sudden death cases, only about 8% are exercise related. The following table shows distinguishing characteristics of the two conditions.
|Feature||Athletic Heart Syndrome||Cardiomyopathy|
|Left ventricular hypertrophy||< 13 mm||> 15 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|
|BP response to exercise||Normal||Normal or reduced systolic BP response|
|Deconditioning||Left ventricular hypertrophy regression||No left ventricular hypertrophy regression|
Although the heart experiences structural changes (i.e. wall thickening) that are common with some cardiac disease, no unfavorable effects are evident. 80% of people affected by this syndrome show a decrease in such structural changes and in bradycardia with detraining. Unfortunately, the lack of long-term data limits our ability to determine whether or not the remaining 20% of people who do indeed have residual chamber enlargement have experienced any negative side effects.
No treatment is required for people with athletic heart syndrome. In some cases, 3 months of deconditioning are required in order to distinguish AHS from cardiomyopathy, though this may be met with resistance since training is an integral part of an athlete's life.