The effect of resistance training on PI3K/mTORc1 signaling in left ventricular of diabetes rats

Clinical evidence points to the effective role of genetic factors and intracellular signaling pathways in physiological cardiac hypertrophy. This study aimed to assess the response of PI3K/mTORc1 signaling pathway in cardiac tissue to resistance training in obese diabetic rats.

For this purpose, 21 male wistar rats (220±20 g) were obese by 6 weeks high fat diet (HFD) and randomly assigned to 1) non-diabetes, 2) control T2D, 3) exercise diabetes groups. T2D induced by intraperitoneal injection of streptozotocin (30 mg/kg) for diabetes groups. Rats in the exercise group participated in a resistance training program (6 weeks / 5 times weekly). After exercise training, PI3K and mTORc1 expression in left ventricular and the ratio of left ventricular weight to heart and heart to body were compared between groups. Data compared by One-Way Analysis of Variance (ANOVA) and independent t test (P< 0.05).

Induction of diabetes resulted in significant decrease in all mentioned variables in control diabetes to non-diabetes rats (PI3K; p = 0.021, mTORc1; p = 0.004, left ventricular/heart weight; p = 0.045, heart/body weight; p = 0.035). On the other hand, a significant increase was observed in all of them in response to resistance training compared to the control   group (p = 0.001).

Based on our results, cardiac hypertrophy in studied diabetes rats can be attributed improved PI3K/mTORc1 signaling in response to resistance training. Understanding the exact mechanisms responsible for these changes in response to exercise requires further molecular-cellular studies.