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Copenhagen Muscle Research Center, Rigshospitalet, and Department of Medical Physiology, The Panum Institute, University of Copenhagen, 2200 Copenhagen N, Denmark
We questioned the
general view that contraction-induced muscle glucose transport only
depends on stimulation frequency and not on workload. Incubated soleus
muscles were electrically stimulated at a given pattern for 5 min.
Resting length was adjusted to achieve either no force (0% P), maximum
force (100% P), or 50% of maximum force (50% P). Glucose transport
(2-deoxy-D-glucose uptake)
increased directly with force development
(P < 0.05) [27 ± 2 (basal), 45 ± 2 (0% P), 68 ± 3 (50% P), and 94 ± 3 (100%
P)
nmol · g
1 · 5 min
1]. Glycogen
decreased at 0% P but did not change further with force development
(P > 0.05). Lactate, AMP, and IMP
concentrations were higher (P < 0.05) and ATP concentrations lower
(P < 0.05) when force was
produced than when it was not. 5'-AMP-activated protein kinase
(AMPK) activity increased directly with force [20 ± 2 (basal), 60 ± 11 (0% P), 91 ± 12 (50% P), and 109 ± 12 (100% P)
pmol · mg
1 · min
1].
Passive stretch (~86% P) doubled glucose transport without altering
metabolism. In conclusion, contraction-induced muscle glucose transport
varies directly with force development and is not solely determined by
stimulation frequency. AMPK activity is probably an essential
determinant of contraction-induced glucose transport. In contrast,
glycogen concentrations per se do not play a major role. Finally,
passive stretch per se increases glucose transport in muscle.
2-deoxy-D-glucose; metabolism; exercise; GLUT-4; signal transduction
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