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1 Physiology, The University of Melbourne, Parkville, Australia
2 Physiology, Monash University, Clayton, Australia
3 Physiology, The University of Melbourne, Parkville, Victoria, Australia
4 St. Vincents Institute, Fitzroy, Australia; CSIRO Health Sciences and Nutrition, Parkville, Australia
* To whom correspondence should be addressed. E-mail: mcconell{at}unimelb.edu.au.
There is evidence that increasing carbohydrate (CHO) availability during exercise by raising pre-exercise muscle glycogen levels attenuates the activation of AMP-activated protein kinase (AMPK) 
2 during exercise in humans. Similarly, increasing glucose levels decreases AMPK 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 64±1% VO2 peak. In a randomized, counter-balanced order, subject’s 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 2 activity, AMPK 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.
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