Abstract | 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-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α 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.
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Authors | Lichan Tao, Yihua Bei, Shenghui Lin, Haifeng Zhang, Yanli Zhou, Jingfa Jiang, Ping Chen, Shutong Shen, Junjie Xiao, Xinli Li |
Journal | Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
(Cell Physiol Biochem)
Vol. 37
Issue 1
Pg. 162-75
( 2015)
ISSN: 1421-9778 [Electronic] Germany |
PMID | 26303678
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2015 S. Karger AG, Basel. |
Chemical References |
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Topics |
- Acute Disease
- Animals
- Apoptosis
(genetics, physiology)
- Autophagy
(genetics, physiology)
- DNA Replication
(genetics)
- DNA, Mitochondrial
(genetics)
- Down-Regulation
(genetics, physiology)
- Energy Metabolism
(genetics, physiology)
- Heart
(physiopathology)
- In Situ Nick-End Labeling
(methods)
- Male
- Mice
- Mice, Inbred C57BL
- Mitochondria
(genetics, physiology)
- Myocardial Infarction
(genetics, physiopathology)
- Organelle Biogenesis
- Physical Conditioning, Animal
(physiology)
- Signal Transduction
(genetics)
- Transcription, Genetic
(genetics)
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