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Acute exercise and starvation induced insulin resistance
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
Institutionen för Fysiologi och Farmakologi, Karolinska Instititutet.
Swedish School of Sport and Health Sciences, GIH.ORCID iD: 0000-0001-9040-2158
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
2012 (English)In: Medicine & Science In Sports & Exercise, 2012, S498 Vol. 44 No. 5 Supplement. 2661., 2012, 2661- p.Conference paper, (Other academic)
Abstract [en]

It is well known that starvation causes insulin resistance. The mechanism is unclear but may relate disturbances in lipid metabolism i.e. incomplete mitochondrial FA oxidation and/or accumulation of lipid intermediates. Exercise results in increased substrate oxidation and may thus remove interfering lipid metabolites and reverse starvation-induced insulin resistance. However, the effect of acute exercise and starvation on insulin sensitivity is not known.

Purpose: The aim of this study was to investigate the effect of exercise on starvation-induced insulin resistance and to elucidate potential mechanisms.

Methods: Nine healthy lean subjects underwent 84h starvation on two occasions separated by at least 2 weeks. The starvation period was followed by either exercise (EX; 5x10 min intervals with 2-4 min rest, starting at 70 %VO2 max) or an equal period of rest (NE). Before and after the starvation period (3h after exercise/rest) subjects were investigated with muscle biopsies, bloo samples and an intravenous glucose tolerance test. Muscle samples were used for measurement of mitochondrial respiration in permeabilized muscle fibers (Oroboros oxygraph), glycogen content and activation of signaling proteins.

Results: Insulin sensitivity was significantly higher in the EX group compared to the NE group (p<0.05). After starvation mitochondrial respiration was lower in both groups with complex I substrates whereas respiration with complex I+II substrates was higher in EX (p<0.05 vs. basal and NE). Muscle glycogen was decreased to 73% (NE) and 31% (EX) of the basal values. The EX group had a significant increased activation of AS160. Plasma FA increased 3-4 fold to 1.39±0.32(NE) and 1.80±0.49 (EX) (mmol/l) after starvation and plasma beta-hydroxybutyrate increased about 50-fold to 6.43±2.01(NE) and 7.12±1.59 (EX)(mmol/l).

Conclusion: Acute exercise reverses starvation-induced insulin resistance. Plasma FA and BOH were increased to similar extent after NE and EX and cannot explain the changes in insulin sensitivity. However, an increased substrate oxidation together with the observed increased capacity for mitochondrial FA oxidation after EX may be involved in the activation of AS160 and the reversal of starvation-induced insulin resistance.

Place, publisher, year, edition, pages
2012. 2661- p.
National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-2599OAI: oai:DiVA.org:gih-2599DiVA: diva2:581580
Conference
ACSM's 59th Annual Meeting and 3rd World Congress on Exercise is Medicine®, San Francisco, USA, May-Jun, 2012
Note

 

 

Available from: 2013-01-02 Created: 2013-01-02 Last updated: 2016-08-10Bibliographically approved

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Berthelson, PerAndersson, EvaSahlin, Kent
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