5'-AMP-activated
protein kinase (AMPK) has been suggested to be a 'metabolic master switch' regulating various aspects of
muscle glucose and
fat metabolism. In isolated
rat skeletal muscle,
glucose suppresses the activity of AMPK and in human
muscle glycogen loading decreases
exercise-induced AMPK activation. We
hypothesized that oral
glucose ingestion during
exercise would
attenuate muscle AMPK activation. Nine male subjects performed two
bouts of one-legged knee-extensor
exercise at 60% of maximal workload. The subjects were randomly assigned to either consume a
glucose containing drink or a placebo drink during the two trials.
Muscle biopsies were taken from the
vastus lateralis before and after 2 h of
exercise.
Plasma glucose was higher (6.0 +/- 0.2 vs. 4.9 +/- 0.1
mmol L-1,
P < 0.001), whereas
glycerol (44.8 +/- 7.8 vs. 165.7 +/- 22.3 micromol L-1), and
free fatty acid (169.3 +/- 9.5 vs. 1161 +/- 144.9 micromol L-1)
concentrations were lower during the
glucose compared to the placebo trial (both
P < 0.001). Calculated
fat oxidation was lower during the
glucose trial (0.17 +/- 0.02 vs. 0.25 +/- 0.03 g min-1,
P < 0.001). Activation of alpha2-AMPK was
attenuated in the
glucose trial compared to the placebo trial (0.24 +/- 0.07 vs. 0.46 +/- 0.14 pmol mg-1 min-1,
P = 0.03), whereas the alpha1-AMPK activity was not different between trials or affected by
exercise. AMPK and the
downstream target of AMPK, acetyl-CoA carboxylase-beta, were phosphorylated as a response to
exercise, but neither was significantly different between the two trials. We conclude that oral
glucose ingestion attenuates the
exercise-induced activation of alpha2-AMPK, bringing further support for a fuel-sensing role of AMPK in
skeletal muscle.