CAJ | 학술논문

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TNFd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）。Caspase3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Caspase3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Caspase3蛋白表达以减少心肌凋亡率。
위탐토중등강도내력운동대심장항상대결혈성손상적작용급기궤제，채용6주내력훈련후주사대제량이병신상선소제작상대결혈성손상모형，결과발현：주사이병신상선소후2개약물조적대서심전도J점편이（P〈0．001）。중등강도내력훈련가이현저개선LVSP（P〈0．001）；결혈손상후운동조심장LVEDP현저저우안정대조조（P〈0．05），제시운동간예가이촉진좌심실적공능회복。운동조대서적혈청cTnⅠ수평화TNFα수평균비상현저고우안정대조조（P〈0．001），운동예처리조적혈청TNFd수평비상현저저우안정조（P〈0．001）。내력운동대심기항결혈성손상구유량호적보호작용，가감완cTnⅠ강해（P〈0．05）。Caspase3단백표체여심기세포조망솔적변화추세상사，제시운동간예구유하조Caspase3단백표체적작용。결과설명：내력운동가이대길항이병신상선소인기적심기세포손상，대촉진심공능회복구유량호적작용，기항상대결혈성손상적궤제가능시중등강도운동훈련유조우감완cTnⅠ강해화하조Caspase3단백표체이감소심기조망솔。
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.