Effects of prior high-intensity exercise on glucose metabolism in normal and insulin-resistant men

Extract: The effects of prior high-intensity cycle exercise (85 per cent VO2 max) to muscular exhaustion on basal and insulin-stimulated glucose metabolism were studied in obese, insulin-resistant, and normal subjects. Six obese (30.4 per cent fat) and six lean (14.5 per cent fat) adult males underw...

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Published in:Diabetes (New York, N.Y.) Vol. 34; no. 10; pp. 973 - 979
Main Authors: Devlin, J.T, Horton, E.S
Format: Journal Article
Language:English
Published: Alexandria, VA American Diabetes Association 01-10-1985
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Summary:Extract: The effects of prior high-intensity cycle exercise (85 per cent VO2 max) to muscular exhaustion on basal and insulin-stimulated glucose metabolism were studied in obese, insulin-resistant, and normal subjects. Six obese (30.4 per cent fat) and six lean (14.5 per cent fat) adult males underwent two separate, two-level hyperinsulinemic-euglycemic clamp studies (100-min infusions at 40 and 400 mU/m2/min), with and without exercise 12 h earlier. Carbohydrate oxidation was estimated by indirect calorimetry using a ventilated hood system, and endogenous glucose production by d-(3-3H)-glucose infusion. Glycogen content and glycogen synthase activity (GS per cent I) were measured in vastus lateralis muscle biopsies before and at the end of each insulin clamp procedure. After exercise, the obese and lean subjects had comparably low muscle glycogen concentrations (0.10 versus 0.08 mg/g protein, respectively), and equal activation of muscle GS activity (54.4 versus 45.3 GS per cent I, respectively). In the obese subjects, insulin-stimulated glucose disposal was increased significantly, but not totally corrected to normal. In both groups there was a comparable increase in nonoxidative glucose disposal (NOGD), whereas glucose oxidation was decreased and lipid oxidation was increased. Thus, the major effect of prior exercise was to increase insulin-stimulated glucose disposal in the obese subjects and to alter the pathways of glucose metabolism to favor NOGD and decrease glucose oxidation. No correlation was found between the exercise-induced increase in GS per cent I and NOGD, except in the normal subjects during maximal insulin stimulation. Thus, glycogen synthase activity does not appear to be rate-limiting for NOGD at physiologic insulin concentrations. Our findings suggest that a single bout of glycogen-depleting exercise can increase glucose disposal for at least 12-14 h in obese subjects with insulin resistance.(author)
Bibliography:8726872
S30
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0012-1797
1939-327X
DOI:10.2337/diab.34.10.973