[Effects of heavy-load exercise on skeletal muscle cells apoptosis and mechanisms of mitochondrial apoptosis in rats].

OBJECTIVE

To analyze the molecular mechanisms of skeletal muscle cells apoptosis induced by heavy-load exercise with Omi as the entry point.

METHODS

One hundred and twenty-six adult SD rats were randomly divided into five groups: control group(C), eccentric exercise group (E), simple blocking group (U), DMSO group (D) and exercise block group (EU). In addition to the C group, the other four groups were randomly divided into 0 h after experiment, 12 h after experiment, 24 h after experiment, 48 h after experiment and 72 h after experiment with 6 rats in each group. E and EU group were submitted to a heavy-load exercise on a treadmill down a 16° decline, 16 m/min for 90 minutes. U, D and EU group were one-time intervened with drugs. U and EU groups were intraperitoneally injected with 1.5 μmol/kg ucf-101, D group were intraperitoneally injected with 1.5 μmoL/kg 0.5% DMSO. The rats were sacrificed in batches at different time points after experiment, then the soleus were saved to detect the Caspase-3,-8,-9,-12 activities and protein expressions of Omi and XIAP.

RESULTS

Compared with group C, the mitochondrial distribution and morphology appeared the typical ultrastructure pathological changes, the opening degree of MPTP was increased significantly (＜0.01) or (＜0.05), protein expressions of Omi and XIAP were increased significantly (＜0.01 or ＜0.05), the activities of Caspase-9 and Caspase-3 were increased significantly (＜0.01 or ＜0.05) in group E. Compared with group C, there was no significant difference in XIAP protein and caspase-9, - 3 activities in group U and Group D. The change trend of XIAP protein and Caspase-9, - 3 activities was the same as those between EU group and E group, but the change range of XIAP protein in EU group was significantly higher than that in E group (＜0.01), and the change ranges of caspase-9, - 3 activities in EU group were significantly lower than those in E group (＜0.01).

CONCLUSION

A single heavy-load exercise can induce changes in the mitochondria morphology and structure in rats, open the high permeability of MPTP, and improve the expression of Omi protein, then through its downstream XIAP-Caspase pathway, start the mitochondrial apoptosis pathway mediated by caspase-9, and finally lead to myocyte apoptosis. The inhibition of Omi can reduce the cell apoptosis level of motor induced skeletal muscle cells.