Chronic moderate‑intensity exercise can induce physiological hypertrophy in aged cardiomyocytes through autophagy,...

Aging is known to cause increased comorbidities associated with cardiovascular decline. Physical exercises were known to be an effective intervention for the age-associated decline in cardiac function. Exercise caused physiological hypertrophy influenced by Yap/Taz, autophagy and myosin heavy chain (MHC) dynamics. However, whether exercise-induced changes are associated with aging has yet to be determined. The present study explored the effects of moderate-intensity exercises on autophagy, MHC dynamics, and Yap/Taz activity to understand their complex interactions at the molecular effects on the cardiac function of aging cardiac tissue. The present study used male Wistar (Rattus norvegicus) rats (80 weeks-old) randomly divided into two groups (n=12): control and intervention. The intervention group was given an intervention using an animal treadmill. After 8 weeks, the animal was sacrificed, and data were collected. Statistical analysis was conducted using an independent t-test or Mann-Whitney U test when appropriate. Exercise in aged rats can induce physiological hypertrophy, as shown by gross measurement and histological features. Yap/Taz did not mediate the effects of exercise on hypertrophy. Autophagy function was shown to increase, which may cause the low expression of Yap/Taz. In conclusion, exercise is a viable intervention in increasing heart mass and potentially delaying the decline in function associated with aging.