摘要
为探讨中等强度耐力运动对心脏抗相对缺血性损伤的作用及其机制,采用6周耐力训练后注射大剂量异丙肾上腺素制作相对缺血性损伤模型,结果发现:注射异丙肾上腺素后2个药物组的大鼠心电图J点偏移(P<0.001)。中等强度耐力训练可以显著改善LVSP(P<0.001);缺血损伤后运动组心脏LVEDP显著低于安静对照组(P<0.05),提示运动干预可以促进左心室的功能恢复。运动组大鼠的血清cTnI水平和TNFα水平均非常显著高于安静对照组(P<0.001),运动预处理组的血清TNFα水平非常显著低于安静组(P<0.001)。耐力运动对心肌抗缺血性损伤具有良好的保护作用,可减缓cTnI降解(P<0.05)。Caspase 3蛋白表达与心肌细胞调亡率的变化趋势相似,提示运动干预具有下调Caspase 3蛋白表达的作用。结果说明:耐力运动可以对拮抗异丙肾上腺素引起的心肌细胞损伤,对促进心功能恢复具有良好的作用,其抗相对缺血性损伤的机制可能是中等强度运动训练有助于减缓cTnI降解和下调Caspase 3蛋白表达以减少心肌凋亡率。
In order to probe into the function and mechanism of medium intensity stamina exercising in protecting the heart's resistance to relative ischemic damages, the authors established a relative ischemic damage model by means of a large dose of isoproterenol injection after 6 weeks of stamina training, and revealed the following findings: after isoproterenol injection, points J in the electrocardiograms of the rats in the two drug groups drifted (P〈0.001); medium intensity stamina exercising can significantly improve LVSP (P〈0.001); after an ischemic damage, the LVEDP of the hearts of the rats in the exercise group was significantly lower than that of the rats in the calm control group (P〈0.05), which hints that exercise intervention can promote the recovery of left ventricular functions; the serum cTnⅠ level and TNF α level of the rats in the exercise group were significantly higher than those of the rats in the calm control group (P〈0.001), the serum TNF α level of the rats in the exercise pretreatment group was significantly lower than that of the rats in the calm group (P〈0.001); stamina exercising is provided with a good function in protecting cardiac muscle's resistance to ischemic damages, able to slow down cTnⅠ degradation (P〈0.05); the trend of changing of the protein expression of Caspase 3 is similar to the trend of changing of the apoptosis rate, which hints that exercise intervention is provided with a function to lower the protein expression of Caspase 3. The said findings indicate the followings: stamina exercising can resist cardiac muscle cell damages caused by isoproterenol, have a good function in promoting cardiac function recovery; its mechanism to resist ischemic damages is likely that medium intensity sports training is conducive to slowing down cTnⅠ degradation and lowering the protein expression of Caspase 3 in order to reduce the apoptosis rate.
出处
《体育学刊》
CAS
CSSCI
北大核心
2012年第3期135-139,共5页
Journal of Physical Education
关键词
运动生理学
抗缺血性损伤
中等强度耐力运动
sports physiology
resistance to ischemic damages
medium intensity stamina exercising