Figure 5. Effect of exercise training on cardiac functions in cardiac Sir2 differential-expression and 5-week-old flies. (A) Heart period. (B) Systolic period. (C) Diastolic period. (D) Diastolic dysfunction index. (E) Fractional shortening. (F) Heart SOD activity level. (G) Heart MDA level. (H) Heart Foxo expression level. (I) Heart TAG level. (J) Heart bmm expression level. (K) Heart Nmnat expression level. (L) Heart SIR2 protein level. “1” indicates hand-Gal4>w1118, “2” indicates hand-Gal4>w1118+Exercise, “3” indicates hand-Gal4>UAS-dSir2-RNAi, “4” indicates hand-Gal4>UAS-dSir2-RNAi+E, “5” indicates hand-Gal4>UAS-dSir2-overexpression, and “6” indicates hand-Gal4>UAS-dSir2-overexpression+E. Independent-sample t tests were used to assess differences between the “Control group” and “Exercise group” in cardiac dSir2 differential-expression flies to explore the effects of exercise training on the heart. Data are represented as means ± SEM. *P<0.05; **P <0.01. Sample size and repetitions were the same as before. (M) Hand-Gal4>w1118 group. (N) hand-Gal4>UAS-dSir2-RNAi, and (O) hand-Gal4>UAS-dSir2-overexpression. In m, n, and o, 1: ultrastructure image of myocardium in the non-exercise group; 2: ultrastructure image of myocardium in the exercise group; 3: microscopic image of cardiac function in the non-exercise group; and 4: microscopic image of cardiac function in the exercise group. It can be observed from m1, n1, and o1 that the cardiac dSir2 knockdown could reduce the number of mitochondria and make the arrangement of myofibrils irregular, but cardiac dSir2 overexpression can increase the number of mitochondria and make the myofibrils more orderly. It can be observed from m3, n3, and o3 that the cardiac dSir2 knockdown can reduce heart period and increase diastolic dysfunction, and cardiac dSir2 overexpression can extend heart period and decrease diastolic dysfunction. Moreover, it can be observed from m, n, and o that exercise training can increase the number of heart mitochondria, make the myofibrils more orderly, extend heart period, and reduce diastolic dysfunction in cardiac dSir2 differential-expression flies.