不同运动方式对心肌梗死大鼠心肌线粒体稳态的影响

Effect of different type of exercise on mitochondrial homeostasis in rats with myocardial infarction

目的探讨中等强度持续运动（MCT）和高强度间歇运动（HIT）对急性心肌梗死（AMI）后心室重构及线粒体稳态的干预差异。方法雄性SD大鼠制备AMI模型，随机（随机数字法）分为假手术组（Sham，n=10）、AMI对照组（AMI，n=9）、AMI＋MCT运动组（AMI＋M，n=9）和AMI＋HIT运动组（AMI＋H，n=10）。AMI＋M组和AMI＋H组分别进行4周MCT或HIT运动训练。左心室导管法检测心功能，荧光探针法检测线粒体膜电位、ROS生成速率及ATP合成活力，Western blot法检测PINK1、Beclin1、Mfn2、Drp1、Tfam、COXⅣ和PGC-1α蛋白表达量。结果与AMI组比较，AMI＋M和AMI＋H组Beclin1、PINK1、Mfn2和PGC-1α表达显著升高（P〈0．05或P〈0．01），ROS生成速率和Drpl表达显著降低（P〈0．05或P〈0．01）；AMI＋H组±dp／dt max绝对值、膜电位、ATP合成活力、Tram和COXⅣ表达显著升高（P〈0．05）。与AMI＋M组比较，AMI＋H组±dp/dtmax绝对值、Tfam、COXⅣ和PGC-1α表达显著升高（P〈0．05）。结论HIT在干预AMI后心室重塑及线粒体稳态方面较MCT更具时效性。

Objective To investigated the different effect of moderate-intensity continuous training （MCT） and high-intensity interval exercise training （HIT） on ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction （AMI）. Methods The AMI rat model was achieved by ligating coronary artery. The AMI and sham operation rats were randomly （ random number） divided into four groups ： sham operation group （ Sham）, AMI control group （ AMI）, AMI MCT group （ AMI ＋ M）, and AMI HIT group （AMI ＋ H） . Animals in the AMI ＋ M and AMI ＋ H groups underwent 4 weeks MCT and HIT respectively. Five weeks after AMI, hemodynamic changes, mitochondrial bioenergetics, and PINK1, Beclinl, Mfn2, Drpl, Tfam, COX1V, PGC-1α were detected. Results Comparing with AMI group, in AMI ＋ M and AMI ＋ H groups, Beclinl, PINK1, Mfn2 and PGC-hx expression elevated significantly （P 〈 0. 05 or P 〈 0. 01 ） , whereas ROS generation and Drpl expression showed dramatic decrease （ P 〈 0. 05 or P〈0.01）. In addition, in AMI ＋ H group, ＋- dp/dt max, mitochondrial membrane potential, ATP synthesis activity, Tfam and COX1Vexpression improved significantly （P 〈 0. 05 ）. Comparing with AMI ＋ M group, in AMI ＋ H group, ＋ dp/dt max, PGC-1α, Tram and COX 1V expression improved significantly （P 〈 0. 05 ）. Conclusions HIT is superior to MCT for ameliorating ventricular remodeling and mitochondrial homeostasis after AMI.