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Original Research: COPD |

Decreased Exercise-Induced Expression of Nuclear Factor-κB-Regulated Genes in Muscle of Patients With COPD

Evi M. Mercken, MSc; Geja J. Hageman, PhD; Ramon C. Langen, PhD; Emiel F. Wouters, MD, FCCP; Annemie M. Schols, PhD
Author and Funding Information

From the NUTRIM School for Nutrition, Toxicology and Metabolism, Department of Respiratory Medicine (Ms Mercken, and Drs Langen, Wouters, and Schols) and Health Risk Analysis and Toxicology (Dr Hageman), Maastricht University Medical Centre+ (MUMC+), Maastricht; and the Centre for Integrated Rehabilitation Organ Failure (Dr Wouters), Horn, The Netherlands.

Correspondence to: Evi M. Mercken, MSc, Department of Respiratory Medicine, Maastricht University, PO Box 5800, 6202 AZ Maastricht, The Netherlands; e-mail: e.mercken@pul.unimaas.nl


Funding/Support: This work was supported by Numico Research (Dr Mercken) and by a VENI grant [916.56.112] from the Netherlands Organization for Scientific Research (NWO) (Dr Langen).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(2):337-346. doi:10.1378/chest.10-0275
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Background:  Nuclear factor (NF)-κB activation and oxidative stress are physiologic responses of skeletal muscle to exercise but may be impaired in patients with COPD. Therefore, we investigated NF-κB activity and expression of NF-κB-regulated genes in muscle of patients with COPD and control subjects before and after exercise.

Methods:  Quadriceps specimens were obtained before, immediately after, and 2 h after a submaximal cycle ergometry test from seven patients with COPD (50.6 ± 5.7 SEM FEV1 of patients with COPD) and seven age-matched control subjects. NF-κB DNA-binding activity in muscle and peripheral blood mononuclear cells (PBMCs) was determined using electrophoretic mobility shift assay and enzyme-linked immunosorbent assay, respectively. mRNA expression and protein carbonylation were measured by real-time polymerase chain reaction and Western blot, respectively.

Results:  In control subjects, IL-6, IκBα, tumor necrosis factor-α, IL-1β, superoxide dismutase, thioredoxin, heme oxygenase 1, and heat shock protein-70 were upregulated in muscle after exercise, whereas in patients with COPD only IL-6 mRNA was increased. Exercise-induced antiapoptotic Bcl2 mRNA levels were attenuated in patients with COPD compared with control subjects. Basal muscle protein oxidation was higher in patients with COPD than in control subjects, but attenuated in response to exercise. No exercise-induced changes in NF-κB DNA-binding activity in muscle and PBMCs of either group were detected.

Conclusions:  Skeletal muscle of patients with COPD is characterized by an impaired response to exercise of NF-κB-regulated genes encoding inflammatory cytokines, antioxidants, stress proteins, and survival factors.

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