HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 105/5/1422    most recent 01371.2007v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McConell, G. K. Articles by Wadley, G. D. Search for Related Content PubMed PubMed Citation Articles by McConell, G. K. Articles by Wadley, G. D.

Differential attenuation of AMPK activation during acute exercise following exercise training or AICAR treatment

¹Department of Physiology, The University of Melbourne, Melbourne, Victoria, Australia; ²Department of Physiology, Khon Kaen University, Khon Kaen, Thailand; and ³St. Vincent's Institute, Fitzroy, Victoria, and Commonwealth Scientific and Industrial Research Organisation Molecular Health Technologies, Parkville, Victoria, Australia

Submitted 25 December 2007 ; accepted in final form 11 August 2008

Short-term exercise training in humans attenuates AMP-activated protein kinase (AMPK) activation during subsequent exercise conducted at the same absolute workload. Short-term 5-aminoimidazole-4-carboxyamide- ribonucleoside (AICAR) administration in rats mimics exercise training on skeletal muscle in terms of increasing insulin sensitivity, mitochondrial enzymes, and GLUT4 content, but it is not known whether these adaptations are accompanied by reduced AMPK activation during subsequent exercise. We compared the effect of 10 days of treadmill training (60 min/day) with 10 days of AICAR administration (0.5 mg/g body weight ip) on subsequent AMPK activation during 45 min of treadmill exercise in male Sprague-Dawley rats. Compared with nonexercised control rats, acute exercise significantly (P < 0.05) increased AMPK Thr¹⁷² phosphorylation (p-AMPK; 1.6-fold) and ACCβ Ser²¹⁸ phosphorylation (p-ACCβ; 4.9-fold) in the soleus and p-ACCβ 2.2-fold in the extensor digitorum longus. Ten days of exercise training abolished the increase in soleus p-AMPK and attenuated the increase in p-ACCβ (nonsignificant 2-fold increase). Ten days of AICAR administration also attenuated the exercise-induced increases in AMPK signaling in the soleus although not as effectively as 10 days of exercise training (nonsignificant 1.3-fold increase in p-AMPK; significant 3-fold increase in p-ACCβ). The increase in skeletal muscle 2-deoxyglucose uptake during exercise was greater after either 10 days of exercise training or AICAR administration. In conclusion, 10 days of AICAR administration substantially mimics the effect of 10 days training on attenuating skeletal muscle AMPK activation in response to subsequent exercise.

glucose uptake; glycogen skeletal muscle; acetyl-CoA carboxylase

This article has been cited by other articles:

				V. Ljubicic and D. A. Hood Specific attenuation of protein kinase phosphorylation in muscle with a high mitochondrial content Am J Physiol Endocrinol Metab, September 1, 2009; 297(3): E749 - E758. [Abstract] [Full Text] [PDF]