期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 37, 期 1, 页码 162-175出版社
KARGER
DOI: 10.1159/000430342
关键词
Acute myocardial infarction; Exercise training; Metabolism; Mitochondria; PGC-1 alpha
资金
- National Natural Science Foundation of China [81370332, 81170201, 81200169]
- Priority Academic Program Development of Jiangsu Higher Education Institutions [PAPD20102013]
- Innovation Program of Shanghai Municipal Education Commission [13YZ014]
- Foundation for University Young Teachers by Shanghai Municipal Education Commission
- Shanghai University [sdcx2012038]
- Shanghai Municipal Education Commission
Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury. However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-a and PPAR-gamma. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1 alpha signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis. Copyright (C) 2015 S. Karger AG, Basel
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