Acute resistance exercise-induced IGF1 expression and subsequent GLUT4 translocation

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Acute aerobic exercise (AE) is a major physiological stimulus for skeletal muscle glucose uptake through activation of 5 AMP-activated protein kinase (AMPK). However, the regulation of glucose uptake by acute resistance exercise (RE) remains unclear. To investigate the intracellular regulation of glucose uptake after acute RE versus acute AE, male Sprague-Dawley rats were divided into three groups: RE, AE, or nonexercise control. After fasting for 12h overnight, the right gastrocnemius muscle in the RE group was exercised at maximum isometric contraction via percutaneous electrical stimulation (3x10sec, 5 sets). The AE group ran on a treadmill (25m/min, 60min). Muscle samples were taken 0, 1, and 3h after completion of the exercises. AMPK, Ca2+/calmodulin-dependent protein kinase II, and TBC1D1 phosphorylation were increased immediately after both forms of exercise and returned to baseline levels by 3h. Muscle IGF1 expression was increased by RE but not AE, and maintained until 3h after RE. Additionally, Akt and AS160 phosphorylation were sustained for 3h after RE, whereas they returned to baseline levels by 3h after AE. Similarly, GLUT4 translocation remained elevated 3h after RE, although it returned to the baseline level by 3h after AE. Overall, this study showed that AMPK/TBC1D1 and IGF1/Akt/AS160 signaling were enhanced by acute RE, and that GLUT4 translocation after acute RE was more prolonged than after acute AE. These results suggest that acute RE-induced increases in intramuscular IGF1 expression might be a distinct regulator of GLUT4 translocation.

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