Voluntary exercise training enhances glucose transport in muscle
stimulated by insulin-like growth factor i.
Hokama, Jason Y., Ryan S. Streeper, and Erik J. Henriksen.
Muscle Metabolism Laboratory, Department of Physiology, University
of Arizona College of Medicine, Tucson, AZ 85721-0093
APStracts 3:0468H, 1996.
Skeletal muscle glucose transport can be regulated by hormonal factors
such as insulin and insulin-like growth factor I (IGF-I). While it is
well established that exercise training increases insulin action on
muscle glucose transport, it is currently unknown whether exercise
training leads to an enhancement of IGF-I-stimulated glucose
transport in skeletal muscle. Therefore, we measured glucose
transport activity (using 2-deoxyglucose (2-DG) uptake) in the
isolated rat epitrochlearis muscle stimulated by submaximally and
maximally effective concentrations of insulin (0.2 and 13.3 nM) or
IGF-I (5 and 50 nM) following 1, 2, and 3 wk of voluntary wheel
running (WR). After 1 wk of WR, both submaximal and maximal insulin
-stimulated 2-DG uptake rates were significantly (P<0.05)
enhanced (+43% and +31%) compared to sedentary controls, and these
variables were further increased after 2 (+86% and +57%) and 3 wk
(+71% and +70%) of WR. Submaximal and maximal IGF-I-stimulated 2-DG
uptake rates were significantly enhanced following 1 wk of WR (+82%
and +61%), and these increases did not expand substantially after 2
(+71% and +58%) and 3 wk (+96% and +70%) of WR. This enhancement of
hormone-stimulated 2-DG uptake in WR muscles preceded any alteration
in glucose transporter (GLUT-4) protein level, which increased only
after 2 (+24%) and 3 wk (+54%) of WR. Increases in GLUT-4 protein
were significantly correlated (r=0.844) with increases in citrate
synthase. These results indicate that exercise training can enhance
both insulin-stimulated and IGF-I-stimulated muscle glucose transport
activity and that these improvements can develop without an increase
in GLUT-4 protein.
Received 10 June 1996; accepted in final form 25 October 1996.
APS Manuscript Number H536-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996