Resistance Training Activates the Signaling Pathway of FSTL1-Akt-mTOR and Induces Cardiomyocyte Proliferation in Rats with Myocardial Infarction

Objectives: This study aimed at discussing the effect of resistance training on expression of Follistatin-like protein 1 (FSTL1) and its receptor Disco-interacting protein 2 homolog A ( DIP2 A) , downstream signaling pathway of Akt-mTOR and cardiomyocyte proliferation in rats with Myocardial Infarction (MI) . Methods: 30 male Sprague-Dawley rats, weight about 180-220 g were randomly divided into three groups: Sham-operated group (S) , sedentary MI group (MI) and MI with resistance training group (MR) after the MI model was established by ligation of left anterior descending coronary artery. After surgery 1 week, rats in MR took adaptability climbing up ladder unload training for 1 week. Then subjected progressive loading training for 4 weeks. The 24 hours after training, rats were anesthetized, the LVSP, LVEDP, ± dp/dt max were tested in order to evaluate cardiac function. The protein expression of FSTL1, DIP2A, p Akt, Akt, p-mTOR, mTOR, Cyclin D1 and CDK4 in Myocardium were measured by Western blot, cardiomyocyte proliferation was observed and analyzed by immunofluorescence. Collagen volume fraction (%) of Myocardium were calculated by Masson Staining. Results: Compared with S, the protein expression of FSTL1, DIP2A, p Akt/Akt, p-mTOR/mTOR, Cyclin D1 and CDK4, cardiomyocyte proliferation, the CVF% and LVEDP of MI increased, the LVSP and ± dp/dt max significantly decreased; Compared with MI, the protein expression of FSTL1, DIP2A, p Akt/Akt, pmTOR/mTOR, Cyclin D1 and CDK4, cardiomyocyte proliferation, the CVF% and LVEDP of MR significantly upregulated, the LVSP, ± dp/dt max significantly downregulated. Conclusions: Resistance training may via upregulate the expression of FSTL1 and its receptor DIP2A in Myocardium, activates the signaling pathway of Akt-mTOR, induces cardiomyocyte proliferation, and improves cardiac function.