Abstract 3545: Exercise Training Prevents Aging-induced Cardiomyocyte Loss via Apoptotic Signaling Activation in the Heart
Aging causes cardiomyocyte loss and impairment of cardiac function and energy metabolic capacity. The cell death via apoptotic signaling activation affects aging-induced cardiomyocyte loss. Exercise training prevents aging-induced elevation of risk of cardiac disoders. However, the mechanisms underlying favorably cardiac adaptation by exercise training remains unclear. To study the contribution of anti-apoptotic system to exercise training-induced cardiac protection against advancing age, we investigated whether Bcl-2 and Bax proteins in the aged heart is affected by exercise training. We used hearts of sedentary young rat (SY: 4-month old), sedentary aged rat (SA: 23-month old), and swim-trained aged rat (TA: 23-month old, swimming training for 8-week, 5 days/wk, 90 min/day). Stroke volume, fractional shortening, and citrate synthase enzyme activity in the heart was higher in the swim-trained aged rats compared with the sedentary aged rats, showing that trained aged rats improved aging-induced reduction of cardiac function and energy metabolic capacity. DNA laddering and fragmentation (using TUNNEL assay), which is an index of apoptotic cardiomyocyte death, was significantly detected in the aged heart, however, exercise training reduced the aging-induced apoptosis. Bcl-2 protein, inhibits apoptotic signaling, in the heart was significantly decreased by aging, whereas exercise training recovered aging-induced reduction of Bcl-2 (SY 3.3±0.3, SA 1.9±0.3*, TA 3.0±0.4 arbitrary unit, both *P<0.05 in SA vs. SY and TA). Additionally, Bax protein, accelerates apoptotic signaling, in the heart was significantly elevated by aging, and exercise training did not changed aging-induced increase in Bax. Bcl-2/Bax ratio was decreased by aging, whereas exercise training recovered Bcl-2/Bax ratio in the aged heart. These findings suggest that exercise training prevents aging-induced cardiomyocyte loss via anti-apoptotic system, i.e., interaction between Bax and Bcl-2, and consequently, this protection effect may contribute to the improvement of cardiac function in the trained-aged hearts.