Endocrine Abstracts

The ingestion of high-fat diet has been considered a crucial factor in the genesis of subclinical systemic inflammation and insulin resistance. The resistance training (RTr) can be an effective tool for the prevention and treatment of immune-metabolic disorders through physiological and morphological adaptations. The purpose of the present study was to analyze the effects of RTr and cessation of training on muscle inflammation and expression of genes related to glucose metabolism in obese rats. Thirty male Wistar rats aged 2 months were subdivided into three groups: High-Fat Diet (DH), Trained High-fat Diet (DHT) and Detrained High-fat Diet (DHD). RTr was performed for 12 weeks (wk), 3×/wk, three sets of 12 repetitions per session. In the 8th wk, DHD group interrupted training for 4 wk. RT-PCR was performed to analyze genes code TNFα, AMPK, GLUT4 and MEF2A, and Western blotting was assayed to analyze the expression of TNFα in the soleus muscle. Additionally we analyzed the insulin sensitivity by ITT, and muscle fiber area by HE staining. The results showed that RTr (DH vs. DHT) caused increase of muscle fiber area (P<0.05), and insulin sensitivity by 34% (P<0.05), increased AMPK gene levels by 23% (P<0.05), GLUT4 by 24% (P<0.05) and MEF2A by 20% (P<0.05), and reduced protein and gene levels by 51 and 28% of TNFα (P<0.05), respectively. Detraining (DHD vs DHT) increased body weight (P<0.05), and provoked reduction of muscle fiber area (P<0.05). However, TNFα expression remained reduced even after cessation of training. We conclude that RTr exerts positive effects on reduction of the local inflammation, and improves the expression of genes related to glucose metabolism in the oxidative skeletal muscle. These adaptations are maintained even after 4-week detraining.