Effect of long-term high intensity aerobic training on left ventricular volume during maximal upright exercise

The purpose of this study was to determine whether high intensity, long-term aerobic training causes the left ventricle to develop different mechanisms for increasing cardiac output during submaximal and maximal upright bicycle exercise. Fifteen competitive collegiate long distance runners and 14 healthy sedentary adults were studied with use of subcostal view four chamber two-dimensional echocardiography at rest and during and at peak maximal upright bicycle exercise. At rest, the athletes had a larger end-diastolic volume index (85 +/- 14 ml/m2) (mean +/- 1 SD) than that of the sedentary adults (62 +/- 14 ml/m2) and a larger end-systolic volume index (37 +/- 11 versus 21 +/- 6 ml/m2). During low and moderate intensity exercise, end-diastolic and stroke volume indexes increased in both groups, but at high intensity exercise and at peak exercise the end-diastolic volume index of both groups decreased significantly below rest value (athletes, 61 +/- 14; sedentary subjects, 46 +/- 10 ml/m2, both p less than 0.001 compared with rest). Reflecting the decreased end-diastolic volume index, at peak exercise, the stroke volume index had decreased from intermediate exercise values in both groups and was not different from rest values. Therefore, although long distance runners have a dilated left ventricle at rest, they utilize the same mechanisms as sedentary adults for increasing cardiac output during upright dynamic exercise. At low and moderate level exercise, the Frank-Starling mechanism is a dominant mechanism for increasing cardiac output, but at peak exercise, probably because of reduced diastolic left ventricular filling, enhanced contractility is the major mechanism for maintaining stroke volume.