Chronic moderate‑intensity exercise can induce physiological hypertrophy in aged cardiomyocytes through autophagy, with minimal Yap/Taz involvement.

Abstract

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.