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A clinically relevant decrease in contractile force differentially regulates control of glucocorticoid receptor

Kirsten R Dunlap1, Jennifer L Steiner1,2, Michael L Rossetti1

  • 1Department of Nutrition, Food and Exercise Science, Florida State University, Tallahassee, Florida.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 18, 2021
PubMed
Summary
This summary is machine-generated.

High-force muscle contractions can prevent glucocorticoid-induced muscle atrophy by blocking the glucocorticoid receptor

Keywords:
autophagydexamethasonemuscle atrophyprotein synthesis

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Area of Science:

  • Muscle physiology and endocrinology
  • Skeletal muscle biology
  • Exercise science

Background:

  • Glucocorticoids (GCs) induce muscle atrophy by activating the glucocorticoid receptor (GR), promoting protein degradation.
  • Mechanical overload can counteract GC-induced atrophy, but the role of contractile force in mitigating GR activation is unclear.
  • GCs impair muscle force generation, potentially limiting the effectiveness of exercise interventions.

Purpose of the Study:

  • To investigate if muscle contractile force influences the ability of resistance exercise to mitigate GR translocation and promote anabolic signaling during elevated GCs.
  • To determine the effects of high versus moderate force contractions on GR signaling and protein balance in mice treated with dexamethasone.

Main Methods:

  • Mice underwent unilateral, electrically induced tibialis anterior muscle contractions at 100 Hz (high force) or 50 Hz (moderate force).
  • Dexamethasone was administered to activate the glucocorticoid receptor.
  • GR nuclear translocation, muscle protein synthesis, and autophagy markers (LC3 II:I) were assessed.

Main Results:

  • Dexamethasone increased GR signaling, but high force contractions mitigated GR nuclear translocation.
  • High force contractions promoted muscle protein synthesis, an effect not observed with moderate force contractions.
  • Both high and moderate force contractions reduced the GC-mediated increase in autophagy markers.

Conclusions:

  • Muscle contractile force is critical for resistance exercise to counteract GC-induced GR translocation and promote muscle anabolism.
  • High force generation is necessary to blunt GR nuclear translocation and stimulate muscle protein synthesis during GC elevation.
  • These findings define therapeutic parameters for using muscle contractions to manage GC-induced muscle atrophy.