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Intense, sustained physical activity results, over time, in physiological conditioning. In aiming to optimise cardiovascular performance, the heart undergoes quite dramatic changes. Some of these physiological changes, in particular those relating to myocardial hypertrophy, may mimic pathological states, which are well known to pose cardiovascular risk.
The description of “athlete’s heart” first appears in the literature in 1899, with Henschen1 reporting the changes associated with cross-country skiing. Using only physical examination, and careful percussion, he was able to describe enlargement of both the left and right heart. He concluded that these changes were favourable in improving performance.
With the advent of modern echocardiography and other imaging techniques, these changes have been further observed and documented. Over the years, opinion has ranged from the one extreme of considering these changes favourable in order to optimise cardiovascular performance, to the other extreme of considering these physiological changes potentially dangerous. More important clinically is whether the athlete has any pre-existing pathological conditions, being masked by, or being wrongly attributed to, physiological conditioning.
PHYSIOLOGICAL ADAPTATION OF THE CARDIOVASCULAR SYSTEM TO EXERCISE
The physiological responses to physical activity vary according to the type of conditioning. Endurance training (also known as aerobic), such as cross-country running, produces different changes compared with strength training (also known as power, or anaerobic), such as weight-lifting.2
Endurance training results in an increase in oxygen consumption and delivery. Stroke volume and cardiac output increase. Peripheral vascular resistance decreases. But, in strength training, the heart rate, systolic and diastolic blood pressures increase with little increase in cardiac output or oxygen consumption.3
The long duration of sustained high cardiac output in endurance athletes results in a volume-loaded heart with an increase in left ventricular (LV) cavity size, and a mild increase in ventricular wall thickness.4 5 At the other end of the spectrum, high afterloads induced …