Document Detail

N-Acetylcysteine infusion does not affect glucose disposal during prolonged moderate-intensity exercise in humans.
MedLine Citation:
PMID:  20308250     Owner:  NLM     Status:  MEDLINE    
There is evidence that reactive oxygen species (ROS) signalling is required for normal increases in glucose uptake during contraction of isolated mouse skeletal muscle, and that AMP-activated protein kinase (AMPK) is involved. The aim of this study was to determine whether ROS signalling is involved in the regulation of glucose disposal and AMPK activation during moderate-intensity exercise in humans. Nine healthy males completed 80 min of cycle ergometry at 62 +/- 1% of peak oxygen consumption ( V(O(2)peak).A 6,6-(2)H-glucose tracer was infused at rest and during exercise, and in a double-blind randomised cross-over design, N-acetylcysteine (NAC) or saline (CON) was co-infused. NAC was infused at 125 mg kg(1) h(1) for 15 min and then at 25 mg kg(1) h(1) for 20 min before and throughout exercise. NAC infusion elevated plasma NAC and cysteine, and muscle NAC and cysteine concentrations during exercise. Although neither NAC infusion nor exercise significantly affected muscle reduced or oxidised glutathione (GSH or GSSG) concentration (P > 0.05), S-glutathionylation (an indicator of oxidative stress) of a protein band of approximately 270 kDa was increased approximately 3-fold with contraction and this increase was prevented by NAC infusion. Despite this, exercised-induced increases in tracer determined glucose disposal, plasma lactate, plasma non-esterified fatty acids (NEFAs), and decreases in plasma insulin were not affected by NAC infusion. In addition, skeletal muscle AMPKalpha and acetyl-CoA carboxylase-beta (ACCbeta) phosphorylation increased during exercise by approximately 3- and approximately 6-fold (P < 0.05), respectively, and this was not affected by NAC infusion. Unlike findings in mouse muscle ex vivo, NAC does not attenuate skeletal muscle glucose disposal or AMPK activation during moderate-intensity exercise in humans.
Troy L Merry; Glenn D Wadley; Christos G Stathis; Andrew P Garnham; Stephen Rattigan; Mark Hargreaves; Glenn K McConell
Publication Detail:
Type:  Journal Article; Randomized Controlled Trial     Date:  2010-03-22
Journal Detail:
Title:  The Journal of physiology     Volume:  588     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-03     Completed Date:  2010-07-29     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1623-34     Citation Subset:  IM    
Department of Physiology, The University of Melbourne, Parkville, Victoria, 3010, Australia.
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MeSH Terms
Acetylcysteine / administration & dosage,  metabolism,  pharmacology*
Anaerobic Threshold / drug effects,  physiology
Cross-Over Studies
Cysteine / blood
Cystine / blood
Double-Blind Method
Exercise / physiology*
Exercise Test
Fatty Acids, Nonesterified / metabolism
Free Radical Scavengers / administration & dosage,  pharmacology*
Glucose / metabolism*
Glutathione / biosynthesis
Heart Rate / physiology
Infusions, Intravenous
Lactic Acid / blood
Muscle, Skeletal / metabolism
Protein Kinases / metabolism
Reactive Oxygen Species / metabolism
Signal Transduction / physiology
Young Adult
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Free Radical Scavengers; 0/Reactive Oxygen Species; 50-21-5/Lactic Acid; 50-99-7/Glucose; 52-90-4/Cysteine; 56-89-3/Cystine; 616-91-1/Acetylcysteine; 70-18-8/Glutathione; EC 2.7.-/Protein Kinases; EC 2.7.1.-/AMP-activated protein kinase kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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