Cycle Training Increased GLUT4 and Activation of Mammalian Target of Rapamycin in Fast Twitch Muscle Fibers

STUART, C. A., M. E. HOWELL, J. D. BAKER, R. J. DYKES, M. M. DUFFOURC, M. W. RAMSEY, and M. H. STONE. Cycle Training Increased GLUT4 and Activation of Mammalian Target of Rapamycin in Fast Twitch Muscle Fibers. Med. Sci. Sports Exerc., Vol. 42, No. 1, pp. 96-106, 2010. Purpose: To determine whether cycle training of sedentary subjects would increase the expression of the principle muscle glucose transporters, six volunteers completed 6 wk of progressively increasing intensity stationary cycle cycling. Methods: In vastus lateral is muscle biopsies, changes in expression of GLUT 1, GLUT4, GLUT5, and 3GLUTI2 were compared using quantitative immunoblots with specific protein standards. Regulatory pathway components were evaluated by immunoblots of muscle homogenates and immunohistochemistry of microscopic sections. Results: GLUT I was unchanged, GLUT4 increased 66%. GLUTI2 increased 104%, and GLUT5 decreased 72%. A mitochondrial marker (cytochrome c) and regulators of mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator 1 alpha and phospho-5'-adenosine monophosphate-activated protein kinase) were unchanged, but the muscle hypertrophy pathway component, phospho-inarrimalian target of rapamycin (mTOR), increased 83% after the exercise program. In baseline biopsies, GLUT4 by immunohistochemical techniques was 37% greater in Type I (slow twitch, red) muscle fibers, but the exercise training increased GLUT4 expression in Type II (fast twitch. white) fibers by 50%, achieving parity with the Type I fibers. Baseline phosplio-mTOR expression was 50% higher in Type II fibers and increased more in Type II fibers (62%) with training but also increased in Type I fibers (34%). Conclusion: Progressive intensity stationary cycle training of previously sedentary subjects increased muscle insulin-responsive glucose transporters (GLUT4 and GLUTI2) and decreased the fructose transporter (GLUT5). The increase in GLUT4 occurred primarily in Type II muscle fibers, and this coincided with activation of the mTOR muscle hypertrophy pathway. There,vas little impact on Type I fiber GLUT4 expression and no evidence of change in mitochondrial biogenesis.