title: Skeletal muscle effects of electrostimulation after COPD exacerbation: a pilot study.
abstract: Muscle dysfunction is a major problem in chronic obstructive pulmonary disease (COPD), particularly after exacerbations. We thus asked whether neuromuscular electrostimulation (NMES) might be directly useful following an acute exacerbation and if such a therapy decreases muscular oxidative stress and/or alters muscle fibre distribution. A pilot randomised controlled study of NMES lasting 6 weeks was carried out in 15 in-patients (n=9 NMES; n=6 sham) following a COPD exacerbation. Stimulation was delivered to the quadriceps and hamstring muscles (35 Hz). Primary outcomes were quadriceps force and muscle oxidative stress. At the end of the study, quadriceps force improvement was statistically different between groups (p=0.02), with a significant increase only in the NMES group (median (interquartile range) 10 (4.7-11.5) kg; p=0.01). Changes in the 6-min walking distance were statistically different between groups (p=0.008), with a significant increase in the NMES group (165 (125-203) m; p=0.003). NMES did not lead to higher muscle oxidative stress, as indicated by the decrease in total protein carbonylation (p=0.02) and myosin heavy chain carbonylation (p=0.01) levels. Finally, we observed a significant increase in type I fibre proportion in the NMES group. Our study shows that following COPD exacerbation, NMES is effective in counteracting muscle dysfunction and decreases muscle oxidative stress.
authors.affiliation: INSERM U1046, Clinique du Souffle La Vallonie - Fontalvie, 800 avenue Joseph Vallot, 34700 Lodève, France. aldjia.abdellaoui@inserm.fr
authors.forename: A
authors.initials: A
authors.lastname: Abdellaoui
authors.forename: C
authors.initials: C
authors.lastname: Préfaut
authors.forename: F
authors.initials: F
authors.lastname: Gouzi
authors.forename: A
authors.initials: A
authors.lastname: Couillard
authors.forename: M
authors.initials: M
authors.lastname: Coisy-Quivy
authors.forename: G
authors.initials: G
authors.lastname: Hugon
authors.forename: N
authors.initials: N
authors.lastname: Molinari
authors.forename: T
authors.initials: T
authors.lastname: Lafontaine
authors.forename: O
authors.initials: O
authors.lastname: Jonquet
authors.forename: D
authors.initials: D
authors.lastname: Laoudj-Chenivesse
authors.forename: M
authors.initials: M
authors.lastname: Hayot
mesh_terms: D000208:Acute Disease; D000368:Aged; D000447:Aldehydes / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004599:Electric Stimulation Therapy / Q000379:methods*; D005260:Female; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction / Q000502:physiology; D018657:Muscle Fibers, Slow-Twitch / Q000378:metabolism; D009135:Muscular Diseases / Q000209:etiology* / Q000378:metabolism / Q000628:therapy*; D018384:Oxidative Stress / Q000502:physiology*; D010865:Pilot Projects; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000378:metabolism; D052097:Quadriceps Muscle / Q000166:cytology / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000447:Aldehydes; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; C027576:4-hydroxy-2-nonenal