Glucocorticoid receptor expression on circulating leukocytes in healthy and asthmatic adolescents in response to exercise.

Published

Journal Article

BackgroundPoor aerobic fitness is associated with worsening of asthma symptoms, and fitness training may improve asthma control. The mechanism linking fitness with asthma is not known. We hypothesized that repeated bouts of exercise would lead to a downregulation of glucocorticoid receptor (GR) expression on circulating leukocytes, reflecting a reduced responsiveness to stress.MethodsIn a prospective exercise training intervention of healthy and asthmatic adolescents, GR expression in leukocytes was measured using flow cytometry in response to an acute exercise challenge before and after the exercise training intervention. Peripheral blood mononuclear cell (PBMC) gene expression of GR, GRβ, HSP70, TGFβ1, and TGFβ2 was determined using reverse-transcriptase PCR (RT-PCR).ResultsPeak VO2 increased by 14.6±2.3%, indicating an effective training (P<0.01). There was a significant difference in GR expression among leukocyte subtypes, with highest expression in eosinophils. Following the exercise training intervention, there was a significant decrease in baseline GR expression (P<0.05) in leukocyte and monocyte subtypes in both healthy and asthmatic adolescents.ConclusionsThis is the first study in adolescents to show that exercise training reduces GR expression in circulating leukocytes. We speculate that exercise training downregulates the stress response in general, manifested by decreased GR expression, and may explain why improving fitness improves asthma health.

Full Text

Cited Authors

  • Lu, KD; Cooper, D; Haddad, F; Zaldivar, F; Kraft, M; Radom-Aizik, S

Published Date

  • August 2017

Published In

Volume / Issue

  • 82 / 2

Start / End Page

  • 261 - 271

PubMed ID

  • 28796240

Pubmed Central ID

  • 28796240

Electronic International Standard Serial Number (EISSN)

  • 1530-0447

International Standard Serial Number (ISSN)

  • 0031-3998

Digital Object Identifier (DOI)

  • 10.1038/pr.2017.66

Language

  • eng