通过研究不同运动强度对心肌细胞凋亡基因Bcl-2、Bax和Caspase-3的影响，探讨了运动对心肌细胞凋亡的作用机制。将大鼠分为3组（正常对照组、一般游泳有氧训练组和力竭性过度训练组）并建立运动模型；采用实时荧光定量PCR技术观察心肌细胞中凋亡基因Bcl-2、Bax和Caspase-3 mRNA的表达；采用Western blot方法观察Bcl-2、Bax、Caspase-3蛋白表达情况。结果显示，与对照组相比，一般游泳有氧训练组大鼠调控基因Bcl-2表达显著增加，对细胞的凋亡起到一定的抑制作用；而力竭过度训练组中心肌细胞相关调控基因Bcl-2表达下降，Bax、Caspase-3的表达升高促进凋亡。因此推定超负荷的运动会加重大鼠心肌细胞的凋亡，凋亡的发生可能与调控基因Bcl-2、Bax和Caspase-3有关。
In order to investigate the mechanism of myocardial apoptosis by exercise, we studied the effects of different exercise intensities on apoptotic gene Bcl-2, Bax and Caspase-3 in rat myocardium cells. The rats were randomly divided into three groups (control group, aerobic exercise group and overtraining group), the mRNA and protein expressions of apoptotic gene Bax, Bcl-2 and Caspase-3 were observed in myocardium cells by quantitative fluorescent polymerase chain reaction (qPCR) and westernblot. As results, compared with the control group, the mRNA and protein expressions of Bcl-2 both increased in aerobic exercise group which inhibited myocardial apoptosis. However, the decreased Bcl-2 expression and the increased expressions of Bax and Caspase-3 in the overtraining group indicated the promoted apoptosis. In conclusion, overtraining exercise can increase apoptosis in rat cardiac myocytes, and the occurrence of apoptosis may be related to the regulation of gene Bcl-2, Bax and Caspase-3.