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Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans

Lee-Young, Robert S., Palmer, Matthew J., Linden, Kelly C., LePlastrier, Kieran, Canny, Benedict J., Hargreaves, Mark, Wadley, Glenn D., Kemp, Bruce E. and McConell, Glenn K. 2006, Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans, American journal of physiology : endocrinology and metabolism, vol. 291, pp. E566-E573, doi: 10.1152/ajpendo.00023.2006.

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Title Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans
Author(s) Lee-Young, Robert S.
Palmer, Matthew J.
Linden, Kelly C.
LePlastrier, Kieran
Canny, Benedict J.
Hargreaves, Mark
Wadley, Glenn D.ORCID iD for Wadley, Glenn D.
Kemp, Bruce E.
McConell, Glenn K.
Journal name American journal of physiology : endocrinology and metabolism
Volume number 291
Start page E566
End page E573
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2006-05-02
ISSN 0193-1849
Keyword(s) adenosine monophosphate-activated protein kinase
acetyl-coenzyme A carboxylase
glucose uptake
Summary There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPK{alpha}2 during exercise in humans. Similarly, increasing glucose levels decreases AMPK{alpha}2 activity in rat skeletal muscle in vitro. We examined the effect of CHO ingestion on skeletal muscle AMPK signaling during exercise in nine active male subjects who completed two 120-min bouts of cycling exercise at 65 ± 1% VO2 peak. In a randomized, counterbalanced order, subjects ingested either an 8% CHO solution or a placebo solution during exercise. Compared with the placebo trial, CHO ingestion significantly (P < 0.05) increased plasma glucose levels and tracer-determined glucose disappearance. Exercise-induced increases in muscle-calculated free AMP (17.7- vs. 11.8-fold), muscle lactate (3.3- vs. 1.8-fold), and plasma epinephrine were reduced by CHO ingestion. However, the exercise-induced increases in skeletal muscle AMPK{alpha}2 activity, AMPK{alpha}2 Thr172 phosphorylation and acetyl-CoA Ser222 phosphorylation, were essentially identical in the two trials. These findings indicate that AMPK activation in skeletal muscle during exercise in humans is not sensitive to changes in plasma glucose levels in the normal range. Furthermore, the rise in plasma epinephrine levels in response to exercise was greatly suppressed by CHO ingestion without altering AMPK signaling, raising the possibility that epinephrine does not directly control AMPK activity during muscle contraction under these conditions in vivo.
Language eng
DOI 10.1152/ajpendo.00023.2006
Field of Research 110102 Medical Biochemistry: Carbohydrates
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2006, American Physiological Society
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