Exercise training reduces the insulin-sensitizing effect of acute exercise in human skeletal muscle
Research output: Contribution to journal › Journal article › peer-review
Not only chronic exercise training, but also a single bout of exercise, increase insulin-stimulated glucose uptake in skeletal muscle. However, it is not well described how adaptations to exercise training affect the ability of a single bout of exercise to increase insulin sensitivity. Rodent studies suggest that the insulin-sensitizing effect of a single bout of exercise is AMPK-dependent (presumably via the α2 β2 γ3 AMPK complex). Whether this is also the case in humans is unknown. Previous studies have shown that exercise training decreases expression of the α2 β2 γ3 AMPK complex and diminishes the activation of this complex during exercise. Thus, we hypothesized that exercise training diminishes the ability of a single bout of exercise to enhance muscle insulin sensitivity. We investigated nine, healthy male subjects who performed one-legged knee-extensor exercise at the same relative intensity before and after 12 weeks of exercise training. Training increased VO2peak and expression of mitochondrial proteins in muscle, while expression of AMPKγ3 was decreased. Training also increased whole body as well as muscle insulin sensitivity. Interestingly, insulin-stimulated glucose uptake in the acutely exercised leg was not further enhanced by training. Thus, the increase in insulin-stimulated glucose uptake following a single bout of one-legged exercise was lower in the trained vs. untrained state. This was associated with reduced signalling through confirmed α2 β2 γ3 AMPK downstream targets (ACC and TBC1D4). These results suggest that the insulin-sensitizing effect of a single bout of exercise is also AMPK-dependent in human skeletal muscle.
|Journal||Journal of Physiology|
|Number of pages||15|
|Publication status||Published - 2019|
- Faculty of Science - AMP-activated protein kinase, TBC1D4, Glucose uptake
Final published version