Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 81: 1273-1278, 1996;
8750-7587/96 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dorin, R. I.
Right arrow Articles by Icenogle, M. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dorin, R. I.
Right arrow Articles by Icenogle, M. V.

Journal of Applied Physiology, Vol 81, Issue 3 1273-1278, Copyright © 1996 by American Physiological Society


ARTICLES

Insulin resistance limits glucose utilization and exercise tolerance in myophosphorylase deficiency and NIDDM

R. I. Dorin, J. C. Field, P. J. Boyle, R. P. Eaton and M. V. Icenogle
Department of Medicine, Veterans Affairs Medical Center, University of New Mexico School of Medicine, Albuquerque, USA.

Myophosphorylase deficiency [McArdle's disease (MD)] produces a defect in muscle glycogenolysis in which muscular work is limited by delivery of external sources of substrate, primarily glucose and nonesterified fatty acids, to meet energy demands associated with exercise. In the present study, we evaluated an unusual patient with both MD and non-insulin-dependent diabetes mellitus. We hypothesized that insulin resistance would limit transport of extracellular glucose to skeletal muscle during exercise, resulting in impaired exercise performance that was reversible by insulin infusion. The effect of a hyperinsulinemic "euglycemic" clamp on exercise tolerance was evaluated by in vivo 31P-magnetic resonance spectroscopy as well as total work performed. We observed that insulin infusion significantly increased the rate of systemic glucose utilization (P < 0.01) and also significantly decreased the ratio of inorganic phosphate to phosphocreatine (P < 0.001) during forearm exercise compared with the control study. Insulin clamp was also associated with an increase in total work performed (56%) during exercise. Our findings demonstrate that resistance to the biological actions of insulin, as occurs in type II diabetes mellitus, leads to a defect in glucose transport that limits the availability of extracellular glucose to exercising muscle. In our subject with a substrate-limited skeletal muscle metabolism (MD), reversal of this defect in insulin-dependent glucose transport by a hyperinsulinemic euglycemic clamp was associated with significant improvement in magnetic resonance spectroscopy parameters of skeletal muscle metabolism as well as exercise performance.


This article has been cited by other articles:


Home page
Journal of Renin-Angiotensin-Aldosterone SystemHome page
G. J Dietze and E. J Henriksen
Review: Angiotensin-converting enzyme in skeletal muscle: sentinel of blood pressure control and glucose homeostasis
Journal of Renin-Angiotensin-Aldosterone System, June 1, 2008; 9(2): 75 - 88.
[Abstract] [PDF]


Home page
J. Physiol.Home page
P. T Fueger, J. Shearer, T. M Krueger, K. A Posey, D. P Bracy, S. Heikkinen, M. Laakso, J. N Rottman, and D. H Wasserman
Hexokinase II protein content is a determinant of exercise endurance capacity in the mouse
J. Physiol., July 15, 2005; 566(2): 533 - 541.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online