中等强度耐力训练后心肌损伤标记物及能量代谢通道变化的机制研究

Research on Mechanism of Markers of Myocardial Injury after Moderate-intensity Endurance Training and Changes of Energy Metabolism Pathway

探讨了中等强度耐力训练后大鼠心肌损伤标记物心肌肌钙蛋白、脑钠肽和能量代谢通道哺乳动物雷帕霉素靶蛋白和AMP依赖的蛋白激酶信号通路变化的作用机制.利用健康雄性SD大鼠60只,随机分为耐力运动组和对照组,建立大鼠耐力运动型心肌肥大模型.使用免疫组化结合计算机图像处理技术,对心脏形态结构以及哺乳动物雷帕霉素靶蛋白的分布和表达进行观察和测定;使用real-time PCR技术,对哺乳动物雷帕霉素靶蛋白和AMP依赖的蛋白激酶的mRNA表达进行测定;使用ELISA检测方法,对大鼠血清心肌肌钙蛋白T、心肌肌钙蛋白I、脑钠肽的表达进行测定.8周中等强度耐力训练后:E组大鼠心脏组织未见形态学病理性改变;E组大鼠的哺乳动物雷帕霉素靶蛋白免疫反应阳性面积和光密度显著上调(P<0.05);E组大鼠AMP依赖的蛋白激酶的mRNA表达未见显著改变,而哺乳动物雷帕霉素靶蛋白的mRNA表达显著上调(P<0.05);E组大鼠心脏血浆脑钠素、血浆肌钙蛋白T和肌钙蛋白I表达升高,但未见显著变化.结果表明:8周中等强度耐力训练导致的耐力训练型心肌肥大未发生心功能恶化和慢性心衰;训练后心肌肌钙蛋白和脑钠肽表达升高并不能直接反映心肌细胞坏死和心功能恶化,其变化应是由心脏形态结构功能重塑造成的;8周的中等强度耐力训练未造成大鼠心肌细胞能量环境的改变;中等强度耐力训练中,心肌哺乳动物雷帕霉素靶蛋白和AMP依赖的蛋白激酶信号通路的表达与骨骼肌存在显著差异.

The paper is going to study the working mechanism of the mTOR/AMPK signaling pathway changes and the myocardial injury markers, such as cardiac troponin, BNP and energy metabolism pathway of rats after moderate-intensity training. 60 healthy male SD rats are randomly divided into control group and endurance training group. An athletic endurance myocardial hypertrophy model of those rats is estab- lished, hnmunohistochemistry combined with computer image processing technology is used to observe and detect the morphology of hearts and also the distribution and expression of mTOR. Real-time PCR method is used to test the mRNA expression of mTOR and AMPK. ELISA method is also used to detect the expression of sermn cardiac troponin T, cardiac troponin I and BNP of rats. The results show that after 8 weeks of mod- erate-intensity endurance training, 1）heart tissue of rats in group E shows no pathological changes; 2）The immune-positive area and optical density of mTOR immunoreaction of rats from group E is significantly en- hanced（P 〈 0.05） ;3）AMPK and mRNA expression of rats from group E shows no significant changes ei- ther while the mRNA of roTOR increases dramatically（P 〈 0.05） ;4）The BNP, cardiac troponin T and car- diac troponin I expression of rats in group E increase but demonstrate no significant changes. The conclu- sion drawn is that 1）atheltic endurance cardiac hypertrophy caused by 8 weeks of moderate-intensity train- ing does not deteriorate at all and shows no trend of chronic heart failure;2）the slightly elevation of cardiac troponinT/I and BNP after training does not reflect myocardial cell necrosis and cardiac deterioration. All the changes are caused by the remodeling of cardiac morphology and function; 3）8 weeks of moderate-in- tensity endurance training does not lead to environmental changes of the cardiac cell energy;4）there is a significant difference between the mTOR/AMPK signaling pathway expression and cardiac muscle and skel- etal muscle under moderate intensity endurance training.