Exercise-induced increase in muscle insulin sensitivity

J Appl Physiol (1985). 2005 Jul;99(1):338-43. doi: 10.1152/japplphysiol.00123.2005.

Abstract

Exercise/muscle contraction activates glucose transport. The increase in muscle glucose transport induced by exercise is independent of insulin. As the acute effect of exercise on glucose transport wears off, it is replaced by an increase in insulin sensitivity. An increase in insulin sensitivity results in a shift in the insulin dose-response curve to the left, with a decrease in the concentration of insulin needed to induce 50% of the maximal response. This phenomenon, which plays a major role in rapid muscle glycogen accumulation after exercise, is not mediated by amplification of the insulin signal. Development of the increase in insulin sensitivity after contractions does not require protein synthesis or activation of p38 MAPK. It does require the presence of a serum protein during the period of contractile activity. The effect of exercise on muscle insulin sensitivity is mimicked by hypoxia and by treatment of muscles with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside to activate AMP-activated protein kinase. The postexercise increase in sensitivity of muscle glucose transport to activation is not specific for insulin but also involves an increased susceptibility to activation by a submaximal contraction/hypoxia stimulus. The increase in insulin sensitivity is mediated by translocation of more GLUT4 glucose transporters to the cell surface in response to a submaximal insulin stimulus. Although the postexercise increase in muscle insulin sensitivity has been characterized in considerable detail, the basic mechanisms underlying this phenomenon remain a mystery.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • AMP-Activated Protein Kinases
  • Animals
  • Biological Transport, Active / physiology
  • Exercise / physiology*
  • Glucose / metabolism*
  • Glucose Transporter Type 4
  • Humans
  • Insulin / metabolism*
  • Monosaccharide Transport Proteins / metabolism
  • Multienzyme Complexes / metabolism*
  • Muscle Contraction / physiology*
  • Muscle Proteins / metabolism
  • Muscle, Skeletal / physiology*
  • Protein-Serine-Threonine Kinases / metabolism*
  • Signal Transduction / physiology*

Substances

  • Glucose Transporter Type 4
  • Insulin
  • Monosaccharide Transport Proteins
  • Multienzyme Complexes
  • Muscle Proteins
  • SLC2A4 protein, human
  • Protein-Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • Glucose