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Exercise training, glucose transporters, and glucose transport in rat skeletal musclesIt was previously found that voluntary wheel running induces an increase in the insulin-sensitive glucose transporter, i.e., the GLUT4 isoform, in rat plantaris muscle (K. J. Rodnick, J. O. Holloszy, C. E. Mondon, and D. E. James. Diabetes 39: 1425-1429, 1990). The present study was undertaken to determine whether 1) the increase in muscle GLUT4 protein is associated with an increase in maximally stimulated glucose transport activity, 2) a conversion of type IIb to type IIa or type I muscle fibers plays a role in the increase in GLUT4 protein, and 3) an increase in the GLUT1 isoform is a component of the adaptation of muscle to endurance exercise. Five weeks of voluntary wheel running that resulted in a 33% increase in citrate synthase activity induced a 50% increase in GLUT4 protein in epitrochlearis muscles of female Sprague-Dawley rats. The rate of 2-deoxy-glucose transport maximally stimulated with insulin or insulin plus contractions was increased approximately 40% (P less than 0.05). There was no change in muscle fiber type composition, evaluated by myosin ATPase staining, in the epitrochlearis. There was also no change in GLUT1 protein concentration. We conclude that an increase in GLUT4, but not of GLUT1 protein, is a component of the adaptive response of muscle to endurance exercise and that the increase in GLUT4 protein is associated with an increased capacity for glucose transport.
Document ID
20050000806
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Rodnick, K. J.
(Washington University School of Medicine St. Louis, Missouri 63110)
Henriksen, E. J.
James, D. E.
Holloszy, J. O.
Date Acquired
August 22, 2013
Publication Date
January 1, 1992
Publication Information
Publication: The American journal of physiology
Volume: 262
Issue: 1 Pt 1
ISSN: 0002-9513
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: AG-00425
CONTRACT_GRANT: AG-00078
Distribution Limits
Public
Copyright
Other
Keywords
NASA Discipline Cell Biology
Non-NASA Center

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