title: Enhanced exercise-induced plasma cytokine response and oxidative stress in COPD patients depend on blood oxygenation.
abstract: In healthy subjects, hypoxemia and exercise represent independent stressors promoting the exercise-induced cytokine response and oxidative stress. We hypothesized that hypoxemia in patients with chronic obstructive pulmonary disease (COPD) may affect the cytokine production and/or the changes in oxidant-antioxidant status in response to maximal exercise. Exercise-induced changes in PaO2 allowed to transiently increase or decrease baseline hypoxemia and to point out its specific action on muscle metabolism. COPD patients with severe to moderate hypoxemia (56 < PaO2 < 72 mmHg) performed an incremental cycling exercise until volitional exhaustion. Two cytokines [interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha] and three blood indices of oxidative stress [plasma thiobarbituric acid reactive substances (TBARS) and two antioxidants, reduced erythrocyte glutathione (GSH), and reduced plasma ascorbic acid, RAA] were measured at rest, then during and after exercise. The changes in the cytokine levels and oxidant-antioxidant status were analysed in relation with the baseline PaO2 and its exercise-induced variations. Data were compared with those obtained in an age- and body mass index-matched group of healthy subjects. Compared with healthy subjects, COPD patients presented a marked accentuation of exercise-induced increase in IL-6 level and earlier changes in their oxidant-antioxidant status. Resting levels of IL-6 and TNF-alpha and exercise-induced peak variations of TBARS, IL-6 and TNF-alpha were negatively correlated with the baseline PaO2. In COPD patients, the peak increases in IL-6 and TBARS were attenuated when exercise hyperventilation reduced the baseline hypoxemia. Our study indicates that the PaO2 level affects both the exercise-induced oxidative stress and cytokine response in hypoxemic COPD patients.
authors.affiliation: Lung Function Laboratory, North Hospital, Assistance Publique-Hôpitaux de Marseille, Marseille, France. yves.jammes@univmed.fr
authors.forename: Yves
authors.initials: Y
authors.lastname: Jammes
authors.forename: Jean Guillaume
authors.initials: JG
authors.lastname: Steinberg
authors.forename: Abdoulaye
authors.initials: A
authors.lastname: Ba
authors.forename: Stéphane
authors.initials: S
authors.lastname: Delliaux
authors.forename: Fabienne
authors.initials: F
authors.lastname: Brégeon
mesh_terms: D000328:Adult; D001205:Ascorbic Acid / Q000097:blood; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015444:Exercise; D005260:Female; D005978:Glutathione / Q000097:blood; D006801:Humans; D000860:Hypoxia / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D010100:Oxygen / Q000097:blood*; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D015850:Interleukin-6; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D005978:Glutathione; D001205:Ascorbic Acid; D010100:Oxygen