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Acute exercise reverses starvation-mediated insulin resistance in humans.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Forskningsgruppen Mitokondriell funktion och metabolisk kontroll.
Karolinska Institutet. (Inst f Fysiologi och Farmakologi)
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Forskningsgruppen Mitokondriell funktion och metabolisk kontroll.ORCID-id: 0000-0001-9040-2158
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Forskningsgruppen Mitokondriell funktion och metabolisk kontroll.
2013 (engelsk)Inngår i: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 304, nr 4, s. E436-43Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
2013. Vol. 304, nr 4, s. E436-43
HSV kategori
Forskningsprogram
Medicin/Teknik
Identifikatorer
URN: urn:nbn:se:gih:diva-2852DOI: 10.1152/ajpendo.00416.2012PubMedID: 23269410OAI: oai:DiVA.org:gih-2852DiVA, id: diva2:639010
Tilgjengelig fra: 2013-08-05 Laget: 2013-08-05 Sist oppdatert: 2018-01-11bibliografisk kontrollert
Inngår i avhandling
1. Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis
Åpne denne publikasjonen i ny fane eller vindu >>Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis
2014 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Regular exercise plays a key role in the maintenance of health and physical capabilities. Extensive research shows that exercise is an efficient method to prevent diabetes. Both resistance and aerobic exercise training are well known countermeasures for insulin resistance. However, depending on factors like purpose, capability and accessibility, different exercise modes need to be evaluated on both applied and molecular levels. In addition, exercise is the means to improve performance. New training strategies have emerged, like training with low glycogen stores or combining strength with endurance training, and guidelines based on empirical data are needed. Although knowledge of exercise physiology has advanced, much more needs to be learned before we can exploit the full potential of exercise with regard to health and performance. Therefore, the overall aim of this thesis is to provide knowledge of how different exercise strategies improve performance and insulin sensitivity. The mitochondria represent a central part of this thesis considering their key role in both health and performance. Study I was an acute crossover investigation of the effect of exercise with low glycogen levels on markers of mitochondrial biogenesis. Study II investigated the effect of concurrent resistance and endurance training on mitochondrial density and endurance performance. Study III investigated the acute effect of exercise on starvation-induced insulin resistance. In Study IV, the effect of resistance exercise training on health and performance in the elderly was investigated. The main findings were:

  • Training with low glycogen levels enhanced the response in markers of mitochondrial biogenesis.
  • Adding resistance training to endurance training did not improve mitochondrial density or endurance performance in trained individuals. 
  • Resistance training for only eight weeks is an efficient strategy to improve strength, heart rate (HR) during submaximal cycling and glucose tolerance in elderly. It also improves muscular quality by increasing mitochondrial and hypertrophy signaling proteins. 
  • Starvation-induced insulin resistance is attenuated by exercise. Mitochondrial respiration and reactive oxygen species (ROS) production is reduced during starvation. Exercise during starvation reduced glycogen stores and resulted in the activation of enzymes involved in glucose metabolism.
  • When exercise was performed during starvation there was an increase in markers for mitochondrial lipid oxidation.


In conclusion, training with low glycogen stores seems to be a promising strategy to increase mitochondrial density. In contrast to our previous acute findings, concurrent training had no effect on mitochondrial biogenesis or endurance performance. Exercise can reverse yet another mode of insulin resistance (starvation) which strengthens its role in the treatment for other states of insulin resistance, e.g. Type 2 diabetes (T2D). Resistance exercise training is an efficient and safe strategy for the elderly to improve health and performance.

sted, utgiver, år, opplag, sider
Karolinska institutet, 2014
HSV kategori
Forskningsprogram
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-3502 (URN)978-91-7549-712-9 (ISBN)
Disputas
2014-11-07, Aulan, GIH, Lidingövägen 1, Stockholm, 09:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2014-10-16 Laget: 2014-10-16 Sist oppdatert: 2018-03-19bibliografisk kontrollert

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