High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance.

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Abstract

Fat accumulation in skeletal muscle combined with low mitochondrial oxidative capacity is associated with insulin resistance (IR). Endurance-trained athletes, characterized by a high oxidative capacity, have elevated intramyocellular lipids, yet are highly insulin sensitive. We tested the hypothesis that a high oxidative capacity could attenuate lipid-induced IR. Nine endurance-trained (age = 23.4 +/- 0.9 years; BMI = 21.2 +/- 0.6 kg/m(2)) and 10 untrained subjects (age = 21.9 +/- 0.9 years; BMI = 22.8 +/- 0.6 kg/m(2)) were included and underwent a clamp with either infusion of glycerol or intralipid. Muscle biopsies were taken to perform high-resolution respirometry and protein phosphorylation/expression. Trained subjects had similar to 32% higher mitochondrial capacity and similar to 22% higher insulin sensitivity (P <0.05 for both). Lipid infusion reduced insulin-stimulated glucose uptake by 63% in untrained subjects (P <0.05), whereas this effect was blunted in trained subjects (29%, P <0.05). In untrained subjects, lipid infusion reduced oxidative and nonoxidative glucose disposal (NOGD), whereas trained subjects were completely protected against lipid-induced reduction in NOGD, supported by dephosphorylation of glycogen synthase. We conclude that chronic exercise training attenuates lipid-induced IR and specifically attenuates the lipid-induced reduction in NOGD. Signaling data support the notion that high glucose uptake in trained subjects is maintained by shuttling glucose toward storage as glycogen. Diabetes 61:2472-2478, 2012

Original languageEnglish
Pages (from-to)2472-2478
Number of pages7
JournalDiabetes
Volume61
Issue number10
DOIs
Publication statusPublished - Oct 2012

Keywords

  • FREE FATTY-ACIDS
  • PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY
  • TYPE-2 DIABETIC PARENTS
  • HUMAN SKELETAL-MUSCLE
  • MITOCHONDRIAL-FUNCTION
  • TRIGLYCERIDE
  • DYSFUNCTION
  • HUMANS
  • SENSITIVITY
  • OBESITY

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