期刊名称：International Journal of Applied Exercise Physiology
电子版ISSN：2322-3537
出版年度：2018
卷号：7
期号：2
页码：46-55
DOI：10.22631/ijaep.v7i2.278
语种：English
出版社：Asian Exercise and Sport Science Association
摘要：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-1α proteins were measured by ELISA method. Data analysis showed that proteins levels of MFN2, PGC-1α, 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-1α 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-1α and reducing DRP1, failed to improve fusion and mitochondrial fissio.
关键词：Myocardial infarction; interval exercise training; mitochondrial dynamic; mitophagy and PGC-1α
