The mechanism by which exercise training increases glucose transport capacity in skeletal muscle

Muscle contraction stimulates glucose transport by an insulin-independent mechanism. The purpose of this study was to investigate the effects of chronic increased muscle contractile activity (exercise training) on GLUT4 protein content and contraction or insulin stimulated glucose transport capacity in skeletal muscle. In first experiment, male rats were trained by swimming exercise, Insulin stimulated maximal glucose transport activity in epitrochlearis muscle was increased by training roughly in proportional to increase of GLUT4 protein content. But, increase of contraction stimulated maximal glucose transport activity in epitrochlearis muscle was not proportional to increase of GLUT4 content. In second experiment, streptozotocin induced insulin deficient diabetic rats were trained by running exercise. Decreased GLUT4 content in diabetic rats' soleus muscle was increased by training. And, when sciatic nerve was denervated in insulin- deficient diabetic rats, decreased GLUT4 content in diabetic rats' soleus muscle was further decreased. Decrease of GLUT4 content by insulin deficiency and denervation were additive. These results suggest that insulin and contraction stimulated glucose transport pathways in skeletal muscle are differently regulated by exercise training (chronic muscle contractile activity) and muscle contractile activity influences GLUT4 protein content independently of insulin action.