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Aerobic interval training protects against myocardial infarction-induced oxidative injury by enhancing antioxidase system and mitochondrial biosynthesis.

Authors: Jiang, HK  Miao, Y  Wang, YH  Zhao, M  Feng, ZH  Yu, XJ  Liu, JK  Zang, WJ 
Citation: Jiang HK, etal., Clin Exp Pharmacol Physiol. 2014 Mar;41(3):192-201. doi: 10.1111/1440-1681.12211.
Pubmed: (View Article at PubMed) PMID:24471974
DOI: Full-text: DOI:10.1111/1440-1681.12211

1. Aerobic interval training (AIT) exerts beneficial effects on cardiovascular disease. However, its cardioprotective mechanisms are not fully understood. The aim of the present study was to evaluate AIT-mediated anti-oxidation by focusing on anti-oxidase and mitochondrial biogenesis in rats after myocardial infarction (MI). 2. Sprague-Dawley rats were divided into three groups: (i) a sham-operated control (CON); (ii) an MI group; and (iii) an MI + AIT group. Myocardial microstructure and function, markers of oxidative stress, mitochondrial anti-oxidase, Phase II enzymes and mitochondrial biogenesis were assessed. In addition, levels of nuclear factor-erythroid 2-related factor (Nrf2) and phosphorylated (p-) AMP-activated protein kinase (AMPK) were determined. The anti-oxidative gene sirtuin 3 (SIRT3) and the prosurvival phosphatidylinositol-3 kinase (PI3-K)-protein kinase B (Akt) signalling cascade were also evaluated. 3. Compared with CON, there was noticeable microstructure injury, cardiac dysfunction and oxidative damage in rats after MI. In addition, decreased mitochondrial anti-oxidase content, Phase II enzyme (except heme oxygenase-1) expression and mitochondrial biogenesis were observed in the post-MI rats as well as reduced protein levels of the regulators Nrf2 and p-AMPK and suppression of SIRT3 levels and PI3-K/Akt signalling. These detrimental modifications were considerably ameliorated by AIT, as evidenced by increases in anti-oxidase, mitochondrial biogenesis, Nrf2 and AMPK phosphorylation, as well as SIRT3 upregulation and PI3-K/Akt signalling activation. Moreover, PI3-K inhibitor-LY294002 (20 mg/kg) treatment partly attenuated AIT-elicited increases in Nrf2 levels and AMPK phosphorylation. 4. Based on these results, we conclude that AIT effectively alleviates MI-induced oxidative injury, which may be closely correlated with activation of the anti-oxidase system and mitochondrial biosynthesis. Increased SIRT3 expression and activation of PI3-K/Akt signalling may play key roles in AIT-mediated anti-oxidation. These results open up new avenues for exercise intervention therapies for MI patients.


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CRRD Object Information
CRRD ID: 9586050
Created: 2014-09-25
Species: All species
Last Modified: 2014-09-25
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.