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Effect of exercise training intensity on mitochondrial dynamics and mitophagy in post myocardial infarction rats
International Journal of Applied Exercise Physiology Pub Date : 2018-06-10 , DOI: 10.22631/ijaep.v7i2.278
Babak Ebadi , Arsalan Damirchi

Myocardial infarction (MI) is the most common type of heart disease. According to recent studies, mitochondrial dysfunction has been suggested as a central player in cardiac disease and evidences point out the association of mitochondrial morphology with development of heart diseases. Exercise training plays a protective role against cardiovascular disease. However, the role of exercise training on proteins involved in mitochondrial dynamics and mitophagy system are not well understood. Therefore, the aim of the present study was to investigate these on cardiac mitochondrial dynamic and mitophagy proteins in rats with myocardial infarction. The present study was post-test design experiment with the control group. after MI with ligation of the left anterior descending coronary artery (LAD) and ensuring the creation of MI by echocardiography, male rats were subjected to high intensity interval training (HIIT), moderate (MIIT), low (LIIT), sedentary myocardial infarction (SED-MI) and healthy control groups. After six weeks exercise, the levels of MFN2, DRP1, Parkin, P62 and PGC-1I± proteins were measured by ELISA method. Data analysis showed that proteins levels of MFN2, PGC-1I±, Parkin and P62 decreased significantly in SED-MI group compared to healthy control while DRP1 protein levels increased significantly (P≤0.05). Also, MFN2 and PGC-1I± proteins increased in MIIT group compared with SED-MI group and DRP1 protein levels were significantly decreased (P≤0.05). Moderate-intensity interval training (MIIT) resulted to improve mitochondrial fusion and fusion proteins in rats with myocardial infarction. While high and low intensity interval training (HIIT, LIIT), despite increasing MFN2 and PGC-1I± and reducing DRP1, failed to improve fusion and mitochondrial fission

中文翻译:

运动训练强度对心肌梗死后大鼠线粒体动力学和线粒体的影响

心肌梗塞(MI)是最常见的心脏病类型。根据最近的研究,线粒体功能障碍已被认为是心脏病的主要参与者,证据表明线粒体形态与心脏病的发展有关。运动训练对心血管疾病起保护作用。但是,运动训练对涉及线粒体动力学和线粒体系统的蛋白质的作用尚不清楚。因此,本研究的目的是研究心肌梗死大鼠心脏线粒体动态和线粒体蛋白。本研究是与对照组进行的测试后设计实验。结扎左前降支冠状动脉(LAD)并通过超声心动图检查确保产生MI后,对雄性大鼠进行高强度间歇训练(HIIT),中度训练(MIIT),低强度(LIIT),久坐性心肌梗死(SED-MI)和健康对照组。运动六周后,通过ELISA法测定MFN2,DRP1,Parkin,P62和PGC-1I±蛋白的水平。数据分析表明,与健康对照组相比,SED-MI组中MFN2,PGC-1I±,Parkin和P62的蛋白质水平显着降低,而DRP1蛋白质的水平显着升高(P≥0.05)。此外,与SED-MI组相比,MIIT组中的MFN2和PGC-1I±蛋白增加,并且DRP1蛋白水平显着降低(P≥0.05)。中强度间歇训练(MIIT)可以改善心肌梗死大鼠的线粒体融合蛋白和融合蛋白。在进行高强度和低强度间歇训练(HIIT,LIIT)时,
更新日期:2018-06-10
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