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

¹Department of Physiology, The University of Melbourne, Carlton; ²Department of Physiology, Monash University, Clayton; ³St. Vincent's Institute, Fitzroy; and ⁴CSIRO Molecular and Health Technologies, Parkville, Victoria, Australia

Submitted 18 January 2006 ; accepted in final form 12 April 2006

There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPK2 during exercise in humans. Similarly, increasing glucose levels decreases AMPK2 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% O_{2 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 AMPK2 activity, AMPK2 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.

adenosine monophosphate-activated protein kinase; acetyl-coenzyme A carboxylase; contraction; glucose uptake; metabolism

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