Resistance Training Prevents Muscle Atrophy In Diabetic Rats Via MSTN Pathway

Abstract

Type 1 diabetes mellitus (T1DM) induces serious skeletal muscle atrophy. resistance training is one of the effective ways to improve muscle atrophy. However, the mechanisms underlying exercise preventing muscle atrophy are still not clear. PURPOSE: To explore the influence of resistance training on muscle atrophy of type1 diabetes rats. METHODS: Fifty male Sprague-Dawley rats (8 weeks, 200-240 g) were randomly assigned to either the normal control group (NC = 8) or the T1DM model group (T1DM, n = 42). T1DM was induced by a single intraperitoneal injection of streptozotocin (STZ) at 60 mg/kg. Once T1DM was induced, the diabetic rats were randomly allocated into three groups: sham-treated diabetic control rats (DC + Sham, DC, n = 8), T1DM rats treated with an insulin injection (DC + INS, DI, n = 8), and treated with resistance training (DC + Training, DT, n = 8). The body weight and muscle strength were measured after the resistance training. HE staining of rat gastrocnemius test morphological changes in muscle fiber cross-sectional area. The protein levels and gene expression of MSTN, Akt, and FoxO1 were measured by Western Blot and Quantitative Real-time PCR. RESULTS: The body weights of NC continued to be remarkably higher than those in the other three diabetic groups during the whole experimental period (P < 0.01). After 6 weeks of training, the body weight (295.40 g ± 20.44 vs. 212.79 g ± 13.26, P < 0.01) and average peak force (9.54 N ± 1.57 vs. 7.85 N ± 1.69, P < 0.01) of DT were significantly increased compared with the DC. The muscle fiber cross-sectional area in the DT significantly increased compared with the DC rats (23729.87 μm2 ± 774.69 vs. 11726.46 μm2 ± 755.66, P < 0.01). DT significantly decreased the mRNA expression of MSTN (1.51 ± 0.22 vs. 2.62 ± 0.26, P < 0.01) and FoxO1(1.37 ± 0.12 vs. 2.26 ± 0.19, P < 0.01) compared with the DC group, as were in protein expression of MSTN (1.66 ± 0.02 vs. 2.09 ± 0.08, P < 0.01), and FoxO1(0.76 ± 0.02 vs. 0.92 ± 0.11, P < 0.05). The mRNA expression of Akt (0.47 ± 0.17 vs. 0.03 ± 0.01, P < 0.01) were increased in the DT, as were the protein expression of Akt (2.83 ± 0.22 vs. 1.64 ± 0.08, P < 0.01). CONCLUSION: These results indicate that 6 weeks of resistance training improved muscle atrophy induced by type 1 diabetes, and the MSTN/Akt/FoxO1 signaling pathway may play a role in this improvement.