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Eur Respir J 2004; 23:538-544
Copyright ©ERS Journals Ltd 2004


Does systemic inflammation trigger local exercise-induced oxidative stress in COPD?

C. Koechlin1, A. Couillard1, J.P. Cristol2, P. Chanez3, M. Hayot1, D. Le Gallais4 and C. Préfaut1

1 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, 2 Laboratoire de Biochimie des Lipides et du Stress Oxydant, Hospital Lapeyronie, 3 Service de Pneumologie, Hospital Arnaud de Villeneuve, and 4 Laboratoire Sport Performance Santé, Montpellier, France

CORRESPONDENCE: C. Koechlin, Laboratoire de Physiologie des Interactions, Service Central de Physiologie Clinique, Hôpital Arnaud de Villeneuve, 34295, Montpellier Cedex 5, France. Fax: 33 467335923. E-mail: christelle_koechlin@hotmail.com

Keywords: Cytokine, endurance, muscle, myopathy, superoxide anion

Received: June 18, 2003
Accepted October 31, 2003

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.




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