Postinfarction exercise training alleviates cardiac dysfunction and adverse remodeling via mitochondrial biogenesis and SIRT1/PGC‐1α/PI3K/Akt signaling. Issue 12 (11th June 2019)

• Record Type: Journal Article
• Authors: Jia, Dandan; Hou, Lu; Lv, Yongzhi; Xi, Lei; Tian, Zhenjun
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 12(2019:Dec.)
• Page Start: 23705
• Page End: 23718
• Publication Date: 2019-06-11
• Subjects: cardiac remodeling -- cardioprotection -- exercise -- mitochondrial biogenesis -- myocardial infarction; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.28939
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Exercise training mitigates cardiac pathological remodeling and dysfunction caused by myocardial infarction (MI), but its underlying cellular and molecular mechanisms remain elusive. Our present study in an in vivo rat model of MI determined the impact of post‐MI exercise training on myocardial fibrosis, mitochondrial biogenesis, antioxidant capacity, and ventricular function. Adult male rats were randomized into: (a) Sedentary control group; (b) 4‐week treadmill exercise training group; (c) Sham surgery group; (d) MI group with permanent ligation of left anterior descending coronary artery and kept sedentary during post‐MI period; and (e) post‐MI 4‐week exercise training group. Results indicated that exercise training significantly improved post‐MI left ventricular function and reduced markers of cardiac fibrosis. Exercise training also significantly attenuated MI‐induced mitochondrial damage and oxidative stress, which were associated with enhanced antioxidant enzyme expression and/or activity and total antioxidant capacity in the heart. Interestingly, the adaptive activation of the SIRT1/PGC‐1α/PI3K/Akt signaling following MI was further enhanced by post‐MI exercise training, which is likely responsible for exercise‐induced cardioprotection and mitochondrial biogenesis. In conclusion, this study has provided novel evidence on the activation of SIRT1/PGC‐1α/PI3K/Akt pathway, which may mediate exercise‐induced cardioprotection through reduction of cardiac fibrosis and oxidative stress, as well as improvement of mitochondrial integrity and biogenesis in post‐MI myocardium. Abstract : The present study has provided novel evidence on activation of SIRT1/PGC‐1α/PI3K/Akt pathway in postinfarction myocardium by moderate exercise training, which reduced cardiac fibrosis and oxidative stress, and improved mitochondrial integrity and biogenesis following heart attack.