Acute exercise reverses starvation-mediated insulin resistance in humans.

[Mike Bikov]

Am J Physiol Endocrinol Metab. 2013 Feb 15;304(4):E436-43. doi: 10.1152/ajpendo.00416.2012. Epub 2012 Dec 26.
Acute exercise reverses starvation-mediated insulin resistance in humans.
Frank P, Katz A, Andersson E, Sahlin K.

Source
The Swedish School of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Box 5626, 114 86 Stockholm, Sweden. [email protected]

Abstract
Within 2-3 days of starvation, pronounced insulin resistance develops, possibly mediated by increased lipid load. Here, we show that one exercise bout increases mitochondrial fatty acid (FA) oxidation and reverses starvation-induced insulin resistance. Nine healthy subjects underwent 75-h starvation on two occasions: with no exercise (NE) or with one exercise session at the end of the starvation period (EX). Muscle biopsies were analyzed for mitochondrial function, contents of glycogen, and phosphorylation of regulatory proteins. Glucose tolerance and insulin sensitivity, measured with an intravenous glucose tolerance test (IVGTT), were impaired after starvation, but in EX the response was attenuated or abolished. Glycogen stores were reduced, and plasma FA was increased in both conditions, with a more pronounced effect in EX. After starvation, mitochondrial respiration decreased with complex I substrate (NE and EX), but in EX there was an increased respiration with complex I + II substrate. EX altered regulatory proteins associated with increases in glucose disposal (decreased phosphorylation of glycogen synthase), glucose transport (increased phosphorylation of Akt substrate of 160 kDa), and FA oxidation (increased phosphorylation of acetyl-CoA carboxylase). In conclusion, exercise reversed starvation-induced insulin resistance and was accompanied by reduced glycogen stores, increased lipid oxidation capacity, and activation of signaling proteins involved in glucose transport and FA metabolism.
PMID: 23269410 [PubMed - indexed for MEDLINE]​

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