Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis.

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.

• 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)
• Copyright: © 2015 S. Karger AG, Basel.

Chemical References

• DNA, Mitochondrial

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)