Cardiac enlargement mechanisms with exercise training and pressure overload

Abstract

The effects of exercise training were examined in the adult male rat heart using biochemical and fiber size measurements. These effects have been compared with those observed following simulated pathological cardiac enlargement associated with both moderate and severe pressure overloads. The combination of desoxycorticosterone acetate (DOCA) injections and salt loading for 21 to 25 days produced a moderate pressure overload (146 ± 5 mm Hg systolic pressure) when compared to control animals (132 ± 3 mm Hg). A 10% increase in left ventricular mass and increased fiber size accompanied the moderate pressure overload. There was no evidence for cellular proliferation in the left ventricle of DOCA injected animals. Abdominal aortic constriction for 21 to 25 days produced a severe pressure overload (210 ± 5 mm Hg) and increased left ventricular mass by 35%. There was evidence that fiber growth and cell proliferation had been stimulated. In contrast to pressure overload stimuli, 80 to 90 days of treadmill exercise did not increase left ventricular mass above control levels. There was no evidence for either increased fiber size or cellular proliferation; however, exercise established a relative left ventricular enlargement by allowing left ventricular mass to increase at approximately normal rate while simultaneously reducing the overall growth rate of the animal. The data indicate that the mechanism for achieving relative cardiac enlargement during exercise training is in direct contrast with the cardiac enlargement mechanism employed during either DOCA injection or aortic constriction.