Cardiovascular Property of Resistance Training With an Emphasis on PI3K/AKT1 Genes Expression in Type 2 Diabetic Rats

The potential role of exercise in physiological cardiac hypertrophy is rooted in both hormonal and genetic components.

The aim of this study was to determine the impact of resistance exercise on the expression of PI3K and AKT1 in cardiac tissue of type 2 diabetes (T2D) rats and their physiological cardiac hypertrophy.

First, 21 male Wistar rats (220 ± 20 g) were obese with 6-week high-fat diet (HFD) and were randomly assigned into non-diabetes, control T2D, and exercise diabetes groups. After inducing obesity, T2D was induced by intraperitoneal injection of streptozotocin (25 mg/kg) for diabetes groups. Rats in the exercise group completed a 6-week resistance exercise program, 5 sessions per week. PI3K/AKT1 expression and the weight ratio of left ventricular to heart, heart to body, and left ventricular to body were compared by analysis of variance (ANOVA) between groups.

In response to the induction of diabetes, the expression of PI3K/AKT1 in heart tissue decreased significantly compared to that of non-diabetic rats (P = 0.001 and P = 0.001, respectively). Further, resistance training led to a significant increase in PI3K expression (P = 0.028) and AKT1 (P = 0.032) and the weight ratio of left ventricular to heart (P = 0.001), heart to the body (P = 0.001), and left ventricular to the body (P = 0.001) compared to control diabetic rats.

Resistance training is associated with physiological cardiac hypertrophy in diabetic rats, and this improvement may be attributed to the PI3K/AKT1 signaling pathway.