Abstract 3535: Beneficial Effects of Regular Physical Exercise on LV Remodeling and Hypertrophy Depend Critically on the Underlying Cause of Hypertrophy and Remodeling
Although initiated as a compensatory mechanism, left ventricular (LV) hypertrophic remodeling resulting from hypertension or myocardial infarction (MI) increases the risk for heart failure. The effect of regular exercise (EX) on pathological LV hypertrophic remodeling and function remains incompletely understood. Here, we compared the effect of 8 weeks of voluntary wheel running on LV remodeling and dysfunction after MI and transverse aortic constriction (TAC) in mice. MI and TAC both increased LV weight, reduced fractional shortening (FS) and maximum rate of rise of LV pressure (LVdP/dtmax). Lung wet weight was increased, indicating pulmonary congestion. Furthermore, SERCA2a levels were reduced in both MI and TAC. LV systolic dysfunction and dilation (LV diameter) was more pronounced in MI, whereas LV end diastolic pressure (LVEDP) and pulmonary congestion increased particularly in TAC. In MI mice, EX had no effect on LV dimensions, but improved FS and LV dP/dtmax, attenuated pulmonary congestion and increased SERCA2a levels. In contrast, in TAC mice, cardiac dysfunction tended to further decrease following exercise, while SERCA2a levels were not affected. In conclusion, the beneficial effects of regular physical exercise on LV remodeling and hypertrophy depend critically on the underlying cause of hypertrophy and remodeling.