title: Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.
authors: Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
authors: Lichan
authors: L
authors: Tao
authors: Yihua
authors: Y
authors: Bei
authors: Shenghui
authors: S
authors: Lin
authors: Haifeng
authors: H
authors: Zhang
authors: Yanli
authors: Y
authors: Zhou
authors: Jingfa
authors: J
authors: Jiang
authors: Ping
authors: P
authors: Chen
authors: Shutong
authors: S
authors: Shen
authors: Junjie
authors: J
authors: Xiao
authors: Xinli
authors: X
authors: Li
mesh_terms: D000208:Acute Disease; D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D001343:Autophagy / Q000235:genetics / Q000502:physiology; D004261:DNA Replication / Q000235:genetics; D004272:DNA, Mitochondrial / Q000235:genetics; D015536:Down-Regulation / Q000235:genetics / Q000502:physiology; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology*; D006321:Heart / Q000503:physiopathology*; D020287:In Situ Nick-End Labeling / Q000379:methods; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000235:genetics / Q000502:physiology*; D009203:Myocardial Infarction / Q000235:genetics / Q000503:physiopathology*; D001678:Organelle Biogenesis; D010805:Physical Conditioning, Animal / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics; D014158:Transcription, Genetic / Q000235:genetics
chemical_list: D004272:DNA, Mitochondrial