The activation of cardiac -related pathways mediates physical exercise resistance to heart aging in old .

Cardiac aging is majorly characterized by increased diastolic dysfunction, lipid accumulation, oxidative stress, and contractility debility. The gene overexpression delays cell aging and reduces obesity and oxidative stress. Exercise improves heart function and delays heart aging. However, it remains unclear whether exercise delaying heart aging is related to cardiac -related pathways. In this study, cardiac overexpression or knockdown was regulated using the UAS/hand-Gal4 system in . Flies underwent exercise interventions from 4 weeks to 5 weeks old. Results showed that either cardiac overexpression or exercise remarkably increased the cardiac period, systolic interval, diastolic interval, fractional shortening, SOD activity, dSIR2 protein, , , , and expression levels in the aging flies; they also notably reduced the cardiac triacylglycerol level, malonaldehyde level, and the diastolic dysfunction index. Either cardiac knockdown or aging had almost opposite effects on the heart as those of cardiac overexpression. Therefore, we claim that cardiac overexpression or knockdown delayed or promoted heart aging by reducing or increasing age-related oxidative stress, lipid accumulation, diastolic dysfunction, and contractility debility. The activation of cardiac SOD and pathways may be two important molecular mechanisms through which exercise works against heart aging in .