title: Does systemic inflammation trigger local exercise-induced oxidative stress in COPD?
abstract: Inflammatory abnormalities may be involved in the inadequate basal oxidant/antioxidant balance and local exercise-induced oxidative stress in chronic obstructive pulmonary disease (COPD) patients. The time course of oxidative stress and inflammation was investigated in 10 COPD patients and seven healthy subjects before and after local dynamic quadriceps endurance exercise at 40% of maximal strength. Venous samples were collected before, immediately after and up to 48 h after exercise. At rest, levels of an oxidant released by stimulated phagocytes, the superoxide anion, were significantly higher in patients, as were plasma levels of C-reactive protein, tumour necrosis factor-alpha and interleukin-6, inflammatory markers. An inverse relationship was found between baseline C-reactive protein levels and endurance time in patients. Six hours after exercise, superoxide anion release and levels of protein oxidation products, an index of oxidative stress, increased similarly in both groups, whereas thiobarbituric acid reactive substance levels, another index of oxidative stress, increased significantly only in patients. Plasma nonenzymatic antioxidant and inflammatory cytokine levels were unchanged by the exercise protocol. The increased baseline systemic inflammation in chronic obstructive pulmonary disease patients could be related to disturbed oxidant/antioxidant balance, and, together, these may have triggered the exercise-induced oxidative stress. The absence, however, of local exercise-induced systemic inflammation suggests that additional mechanisms explain local exercise-induced oxidative stress.
authors.affiliation: Unité Propre de Recherche et d'Enseignement Supérieur Equipe d'Accueil 701, Laboratoire de Physiologie des Interactions, Service Central de Physiologie Clinique, Hospital Arnaud de Villeneuve, 34295 Montpellier, France. christelle_koechlin@hotmail.com
authors.forename: C
authors.initials: C
authors.lastname: Koechlin
authors.forename: A
authors.initials: A
authors.lastname: Couillard
authors.forename: J P
authors.initials: JP
authors.lastname: Cristol
authors.forename: P
authors.initials: P
authors.lastname: Chanez
authors.forename: M
authors.initials: M
authors.lastname: Hayot
authors.forename: D
authors.initials: D
authors.lastname: Le Gallais
authors.forename: C
authors.initials: C
authors.lastname: Préfaut
mesh_terms: D000975:Antioxidants / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000150:complications; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000502:physiology; D016877:Oxidants / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology*; D010586:Phagocytes / Q000378:metabolism; D010807:Physical Endurance / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology*; D018709:Statistics, Nonparametric; D013481:Superoxides / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000975:Antioxidants; D016207:Cytokines; D015850:Interleukin-6; D016877:Oxidants; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D002097:C-Reactive Protein