Exercise protects against age-induced cardiac myocardial contractile dysfunction via correction of cardiac autophagy

AIM:To evaluate the effect of exercise training on cardiac myocardial contractile dysfunction and the underlying mechanism involved with a special focus on autophagy. METHODS: Young (4 months) and aged (20 months) mice maintained 9-week free-loading exercise training (swimming 1 h/day, 5 days/week). In vitro study was performed on cardiomyocytes from each group and cardiac contractile functions were evaluated using edge-detection system. Protein expression was measured by Western blot. RESULTS: Exercise training significantly improved the cardiomyocyte contractile function in aged hearts, which was evidenced by increased peak shortening (PS) and maximal velocity of shortening/relengthening (±dL/dt) along with reduced time-to-90% relengthening (TR90) (P<0.05). Exercise training ameliorated the AMPK activity and inhibited mTOR in aged hearts. Myocardial autophagy level markedly decreased in aged hearts compared with that in their younger counterparts. However, exercise training significantly improved the aging myocardium autophagy. Exercise-induced upregulation of cardiac autophagy was blunted in AMPK KD mice. Autophagy inducer rapamycin significantly reduced aged cardiomycyte contractile dysfunction (P<0.05). CONCLUSION: Our data suggest that exercise may suppress aging-induced cardiac contractile defects through AMPK regulated autophagy in aged hearts.