Exercise regulation of glucose transport in skeletal muscle. Hayashi, Tatsuya, Jorgen F. P. Wojtaszewski, and Laurie J. Goodyear. Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA 02215, and Copenhagen Muscle Research Centre, August Krogh Institute, University of Copenhagen, DK-2100 Copenhagen, Denmark
APStracts 4:0180E, 1997.
Exercise increases the rate of glucose uptake into the contracting skeletal muscles. This effect of exercise is similar to the action of insulin on glucose uptake, and the mechanism through which both stimuli increase skeletal muscle glucose uptake involves the translocation of GLUT4 glucose transporters to the plasma membrane and transverse tubules. Most studies suggest that exercise and insulin recruit distinct GLUT4-containing vesicles, and/or mobilize different "pools" of GLUT4 proteins originating from unique intracellular locations. There are different intracellular signaling pathways that lead to insulin- and exercise-stimulated GLUT4 translocation. Insulin utilizes a PI 3-kinase-dependent mechanism, whereas the exercise signal may be initiated by calcium release from the sarcoplasmic reticulum leading to the activation of other signaling intermediaries, and there is also evidence for autocrine or paracrine-mediated activation of transport. The period after exercise is characterized by increased sensitivity of muscle glucose uptake to insulin, which can be substantially prolonged in the face of carbohydrate deprivation. The ability of exercise to utilize insulin -independent mechanisms to increase glucose uptake in skeletal muscle has important clinical implications, especially for patients with diseases that are associated with peripheral insulin resistance such as non-insulin-dependent diabetes mellitus. 

Received 2 June 1997; accepted in final form 13 August 1997.
APS Manuscript Number E255-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 27 August 1997