Rapid down-regulation of mitochondrial fat metabolism in human muscle after training cessation is dissociated from changes in insulin sensitivity

FEBS Lett. 2009 Sep 3;583(17):2927-33. doi: 10.1016/j.febslet.2009.07.059. Epub 2009 Aug 6.

Abstract

The association between impairment in mitochondrial muscle fat oxidative capacity (OX(FA)) and occurrence of insulin resistance was examined in 14 healthy trained men (age, 24+/-4 yr) submitted to 4 weeks of training cessation. Training stop induced a significant decrease in mRNA levels of proteins involved in muscle fat metabolism, particularly PPARalpha (-58%, P<0.01) and PGC-1alpha (-30%, P<0.05), a 21% reduction in OX(FA) (P<0.01), and reduced fat oxidation during moderately intense exercise (P<0.05). In contrast, there was no significant alteration in insulin sensitivity. In conclusion, decline in OX(FA) is a rapid metabolic event following training cessation. It is involved in the regulation of whole body fat balance but not in the deterioration of insulin sensitivity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Blood Glucose / metabolism
  • Body Composition
  • Down-Regulation*
  • Exercise*
  • Humans
  • Insulin / blood
  • Insulin Resistance*
  • Lipid Metabolism*
  • Male
  • Mitochondria, Muscle / metabolism*
  • Muscle, Skeletal / cytology
  • Muscle, Skeletal / metabolism*
  • Oxidation-Reduction
  • Young Adult

Substances

  • Blood Glucose
  • Insulin