OBJECTIVETo detect the levels of miR-499 and relative proteins in hearts of mice after exercise training, and investigate the mechanism of exercise-regulative apoptosis.

METHODSMale C57BL/6 mice were randomly divided into 3 groups( n = 14): sedentary (SE), exercise training 1 (ET1) and exercise training 2 (ET2) group. SE did not do any exercise. ET1 performed swimming training for 8 weeks. ET2 performed the same work as ET1 until the 5th week. Then, mice trained twice a day until the end of training. TUNEL assay was applied to test myocardial apoptosis, RT-PCR and Western blot were used to detect miR-499 and proteins levels respectively.

RESULTSCompared with SE, stress in ET1 failed to affect apoptotic index (AI) and miR-499-CaN-Drp-1 pathway (P > 0.05). In contrast, exercise load in ET2 increased miR-499 level, decreased Drp-1 level and AI with statistical significance respectively (P < 0.05), but neither CaN expression nor CaN activity was changed significantly (P > 0.05).

CONCLUSIONSwimming training can inhibit myocardial apoptosis, and the decrease in Drp-l may be responsible for the reduced myocardial apoptosis. CaN, the upstream protein, does not participate in exercise-regulative apoptosis.