Exercise Training ameliorates Left Ventricular Dysfunction after Myocardial Infarction but not Left Ventricular Dysfunction in Pressure Overload induced Cardiac Hypertrophy

Abstract

Hypertension and myocardial infarction (MI) both result in left ventricular (LV) hypertrophic remodeling. Despite the apparent appropriateness of the process, this increases the risk of heart failure. In contrast, physiological LV hypertrophic remodeling after exercise training decreases the risk for heart failure. However, information on the effect of exercise on pathological LV hypertrophic remodeling and function is scarce. Consequently, we study the effect of exercise on LV geometry and function after MI and after transverse aortic constriction (TAC) in mice. LV weight was increased and fractional shortening (FS) was decreased compared to controls 8 weeks after induction of MI or TAC. Right ventricular (RV) weight and lung weight were also increased, indicating LV backward failure. Only MI increased LV end-diastolic diameter and decreased the rate of LV pressure increase at 30 mmHg (LV dP/dtP30). Exercise had no effect on LV remodeling in either group, but while exercise after MI improved FS and LV dP/dtP30, FS was not improved and LV dP/dtP30 even worsened following exercise in TAC mice. Furthermore, exercise normalized RV weight and lung weight in MI mice but tended to aggravate pulmonary congestion in TAC mice. In conclusion, exercise training ameliorates LV dysfunction after myocardial infarction but aggravates LV dysfunction in pressure overload induced cardiac hypertrophy.