Postexercise glucose uptake and glycogen synthesis in skeletal muscle from GLUT4‐deficient mice

ABSTRACT To determine the role of GLUT4 on postexercise glucose transport and glycogen resynthesis in skeletal muscle, GLUT4‐deficient and wild‐type mice were studied aftera3h swim exercise. In wild‐type mice, insulin and swimming each increased 2‐deoxyglucose uptake by twofold in extensor digitorum longus muscle. In contrast, insulin did not increase 2‐deoxyglucose glucose uptake in muscle from GLUT4‐null mice. Swimming increased glucose transport twofold in muscle from fed GLUT4‐null mice, with no effect noted in fasted GLUT4‐null mice. This exercise‐associated 2‐deoxyglucose glucose uptake was not accompanied by increased cell surface GLUT1 content. Glucose transport in GLUT4‐null muscle was increased 1.6‐fold over basal levels after electrical stimulation. Contraction‐induced glucose transport activity was fourfold greater in wild‐type vs. GLUT4‐null muscle. Glycogen content in gastrocnemius muscle was similar between wild‐type and GLUT4‐null mice and was reduced ~50% after exercise. After 5 h carbohydrate refeeding, muscle glycogen content was fully restored in wild‐type, with no change in GLUT4‐null mice. After 24 h carbohydrate refeeding, muscle glycogen in GLUT4‐null mice was restored to fed levels. In conclusion, GLUT4 is the major transporter responsible for exercise‐induced glucose transport. Also, postexercise glycogen resynthesis in muscle was greatly delayed; unlike wild‐type mice, glycogen supercompensation was not found. GLUT4 it is not essential for glycogen repletion since muscle glycogen levels in previously exercised GLUT4‐null mice were totally restored after 24 h carbohydrate refeeding.—Ryder, J. W., Kawano, Y., Galuska, D., Fahlman, R., Wallberg‐Henriksson, H., Charron, M. J., Zierath, J. R. Postexercise glucose uptake and glycogen synthesis in skeletal muscle from GLUT4‐deficient mice. FASEB J. 13, 2246–2256 (1999)