摘要
目的通过建立大鼠过度训练模型,探讨过度运动训练与大鼠心肌组织及线粒体损伤的关系。方法取健康雄性SD大鼠随机分为正常对照组、一般有氧训练组、力竭过度训练组,观察体重变化,检测大鼠血清CK、CK-MB、LDH及cTnⅠ水平,测定心肌组织MDA含量及SOD、GSH-Px、CAT活性,分离心肌线粒体检测其SOD活性及MDA、钙离子含量。结果与正常对照组和一般有氧训练组比较,力竭过度训练组大鼠体重显著减轻,血清CK、CK-MB、LDH及cTnⅠ水平显著增高;心肌MDA含量显著增加,SOD及GSH-Px活性显著降低;心肌线粒体MDA含量显著增高,游离钙、SOD含量显著降低,差异均有统计学意义(P<0.05或P<0.01)。结论经过16周递增负荷训练,力竭过度训练组部分大鼠心肌出现损伤,心肌线粒体自由基生成增多,抗氧化酶活性下降,导致线粒体膜发生脂质过氧化,线粒体内游离钙下降,影响线粒体的氧化磷酸化过程。
Objective To study the effect of overtraining on myocardial and mitochondrial damage by establishing overtrai- ning models of rats. Methods Male Sprague Dawley rats were divided into 3 groups randomly：normal control group,aerobic ex- ercise group and overtraining group. Changes of the body weight were observed. Serum levels of CK,CK-MB,LDH and cTn I were determined. The levels of MDA and the enzyme activities of SOD,GSH-Px and CAT in cardiac muscle tissues were meas- ured. Moreover,the levels of MDA, SOD activity and free calcium in mitochondria of cardiac muscle tissues were also meas- ured. Results Compared with normal control group and aerobic exercise group, the body weight was significantly reduced, the levels of serum CK,CK-MB, LDH and cTn I were significantly increased, the MDA content was substantially enhanced and the activity of SOD,GSH-Px significantly decreased in cardiac muscle tissues and the myocardial mitochondria and the concentration of free calcium in myocardial mitochondria was conspicuously decreased in overtraining group（P^0.05 or P%0.01） Conclusion Myocardial injury may occur in rats after 16 week＇s increasing load training. The mechanism involves generation of a great a- mount of free radical in the mitochondria of cardiac muscle,decreased antioxidant activity leading to lipid peroxidation of the mi- tochondrial membrane and disruption of oxidative phosphorylation process due to decreased free calcium.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2013年第2期148-151,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
安徽高校省级自然科学研究项目(No.KJ2012Z170)
关键词
过度训练
心肌损伤
线粒体
大鼠模型
overtraining
cardiac muscle injury
mitochondria
rat model
