Eccentric contractions impair subsequent contraction-induced
glucose transport in rat skeletal muscle: relation to glut4
content.
Kristiansen, S[stod]oren, Sven Asp, and Erik A. Richter.
Copenhagen Muscle Research Centre, August Krogh Institute,
University of Copenhagen, 13 Universitetsparken, DK-2100 Copenhagen,
Denmark
APStracts 3:0103R, 1996.
Eccentric exercise causes muscle damage and decreased muscle glycogen
and GLUT4 protein content. We investigated whether the contraction
-induced increase in skeletal muscle glucose transport and muscle
performance is affected by prior eccentric contractions. The calf
muscles from rats were stimulated for eccentric (EC) or concentric
(CC) contractions or were passively stretched (ST). Muscles from
unstimulated control (CT) rats were also studied. Two days later all
rats had their isolated hindlimbs perfused either at rest or during
15 min of isometric muscle contractions. EC rats had a significantly
lower total GLUT4 protein content in the white gastrocnemius (GW)
muscle (55%) and red gastrocnemius (GR) muscle (34 %), compared with
muscle from the CT, ST, and CC rats. In contrast, GLUT1 protein
content was approximatively 2 fold higher in the GW muscle in EC rats
than in CT rats. In the GW and GR muscle prior eccentric exercise
decreased contraction-induced stimulation of glucose transport
compared with CT, ST and CC rats in spite of no difference in tension
development and oxygen uptake among the groups. There was no change
in total GLUT4 content and glucose transport in the soleus (S) muscle
among the 4 groups. It is concluded that the GLUT4 and GLUT1 protein
content in fast-twitch muscle are decreased and increased,
respectively, two days after eccentric contractions. The functional
consequence of these changes appears to be decreased contraction
-induced increase in skeletal muscle glucose transport.
Received 16 October 1995; accepted in final form 19 February
1996.
APS Manuscript Number R655-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96