Effect Of Exercise-induced Cardiac Hypertrophy In The PI3K / Akt / MTOR Signal

Objective:To exploring the mechanism of signaling pathway IGF-1/PI3K/Akt/mTOR in exercise-induced cardiac hypertrophy, and to provide theory evidences for the prevention against physiologic hypertrophy turn into pathologic hypertrophy. We investigated the expression of mRNA of IGF-1R,PI3K(p110α),PI3K(pl10y), Akt and mTOR of myocardium.Methods:32female SD rats were assigned into2groups:sedentary control (n=16) and swimming Group (n=16). Exercise Protocols:For8weeks, from Monday to Friday, the rats in the SE group completed a1-hour swimming exercise in order to build a cardiac hypertrophy model in rats.24hours after last exercise session, observe morphological of myocardiu,mmeasured heart index, mRNA expression of α-actin,ANP,α-MHC,β-MHC, IGF-1R, and PI3K(p110α),PI3K(p110γ), Aktl, Akt2, Akt3and mTOR.Results:1. exercise group rats compared to control group rats, no significant differences in blood pressure (P>0.05); heart coefficient significantly higher (P<0.05); very significantly higher left ventricular mass coefficient; myocardial cells to grow significantly; a-actin,ANP gene expression without significant difference, α/β-MHC no significant difference (P>0.05), the establishment of animal model of exercise-induced cardiac hypertrophy was successful.2. sports group compared with the control group, rat myocardial PI3K(p110α), Aktl, Akt2and mTOR mRNA expression levels significantly higher (P<0.05).3. sports group compared with the control group, rat cardiac IGF-1R, and PI3K(pllOy),Akt3mRNA expression levels rise, but no significant difference (P>0.05).Conclusion:1. According to previous studies from Femandes et al. and Oliveira et al, the exercise-induced LVH SD rat models were reproduced in this experiment2. After8-week swimming exercise, IGF-1R was not activated in rats’ myocardium3.8-week swimming exercise mediates physiological LVH via PI3K/AKT/mT0R pathway...