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

May 4, 2006American journal of physiology. Endocrinology and metabolism

Carbohydrate intake does not change muscle energy sensor activity during exercise in humans

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Abstract

CHO ingestion significantly increased plasma glucose levels and tracer-determined glucose disappearance during exercise.

Exercise-induced increases in muscle-free AMP were 17.7-fold with CHO ingestion compared to 11.8-fold with placebo.
Muscle lactate levels increased 3.3-fold with CHO ingestion versus 1.8-fold with placebo.
Despite increased glucose availability, skeletal muscle AMPKalpha2 activity and its phosphorylation were similar in both CHO and placebo trials.
The rise in plasma epinephrine during exercise was suppressed by CHO ingestion without affecting AMPK signaling.
These findings suggest that AMPK activation during exercise may not be influenced by normal variations in plasma glucose levels.

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There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPKalpha2 during exercise in humans. Similarly, increasing glucose levels decreases AMPKalpha2 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% V(O2 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 AMPKalpha2 activity, AMPKalpha2 Thr(172) phosphorylation and acetyl-CoA Ser(222) 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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Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans

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