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1 Division of Diabetes and Endocrine Research, Department of Medicine, Mount Zion Medical Center, University of California San Francisco, San Francisco, California 94143; and 2 Human Performance Laboratory, Department of Exercise and Sport Science, East Carolina University, Greenville, North Carolina 27858
Exercise training improves insulin
action in skeletal muscle, but the mechanisms of this effect are not
completely understood. In particular, the role of the insulin receptor
(IR) is unclear. We examined the IR and an enzyme indicative of
oxidative capacity in muscle in relation to improved insulin action in
20 previously sedentary individuals before and after a 7-day program of
moderate-intensity cycle ergometry. After training, insulin sensitivity
increased 33% (6.20 ± 0.91 vs. 8.22 ± 1.12 min · µU
1 · ml1 mean ± SE, pre- vs. posttraining, respectively, P < 0.05).
The mitochondrial marker enzyme cytochrome c oxidase (COX)
increased in vastus lateralis biopsies by 21% (P < 0.05). After training, IR autophosphorylation, determined by ELISA, was
significantly increased by ~40% at insulin concentrations from 1 to
100 nM (P < 0.05). The training-induced improvements in IR
autophosphorylation were significantly correlated with changes in
muscle COX content (r = 0.65, P < 0.05).
These studies indicate that, in this model of increased physical
activity, improvements in IR function are an early adaptation to
exercise in humans, are correlated with increases in muscle oxidative
capacity, and likely contribute to the beneficial effects of exercise
training on insulin action.
insulin resistance; physical activity; membrane glycoprotein PC-1
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