Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 101, Issue 5, Pages 1368-1376Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00416.2006
Keywords
glucose transport; exertion; insulin sensitivity; Akt; AMP-activated; protein kinase
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Funding
- NIA NIH HHS [AG010026] Funding Source: Medline
- NIDDK NIH HHS [DK20572] Funding Source: Medline
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The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochleanis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [H-3]-2-deoxyglucose without or with insulin (60 mu U/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr(172) phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus(51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr(172) phosphorylation (P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased (P < 0.05) similar to 85 min after exercise in the epitrochlearis (sedentary: 0.266 +/- 0.045 mu mol(.)g(-1.)15 min(-1); exercised: 0.414 +/- 0.051) and soleus (sedentary: 0.102 +/- 0.049; exercised: 0.347 +/- 0.098) but not in the EDL. Akt Set(473) and Akt Thr(308). phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.
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