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Published ahead of print on March 2, 2006, doi:10.1164/rccm.200512-1957OC
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American Journal of Respiratory and Critical Care Medicine Vol 173. pp. 1122-1129, (2006)
© 2006 American Thoracic Society
doi: 10.1164/rccm.200512-1957OC


Original Article

Supplemental Oxygen Prevents Exercise-induced Oxidative Stress in Muscle-wasted Patients with Chronic Obstructive Pulmonary Disease

Hanneke A. C. van Helvoort, Yvonne F. Heijdra, Leo M. A. Heunks, Patty L. M. Meijer, Wim Ruitenbeek, Hub M. H. Thijs and P. N. Richard Dekhuijzen

Department of Pulmonary Diseases; Institute for Fundamental and Clinical Human Movement Sciences; and Laboratory of Pediatrics and Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Correspondence and requests for reprints should be addressed to P.N. Richard Dekhuijzen, M.D., Ph.D., Radboud University Nijmegen Medical Centre, Department of Pulmonary Diseases (454), P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. E-mail: R.Dekhuijzen{at}long.umcn.nl

Rationale: Although oxygen therapy is of clear benefit in patients with severe chronic obstructive pulmonary disease (COPD), recent studies have shown that short-term supplementary oxygen may increase oxidative stress and inflammation within the airways.

Objective: We investigated whether systemic inflammation and oxidative stress at rest and during exercise in patients with COPD are influenced by supplemental oxygen.

Methods: Nine normoxemic, muscle-wasted patients with moderate to very severe COPD were studied. Plasma markers of systemic inflammation (leukocyte counts, interleukin 6 [IL-6]) and oxidative stress (lipid peroxidation, protein oxidation, antioxidant capacity) were measured after treatment with either supplemental oxygen (nasal, 4 L · min–1) or compressed air, both at rest (1 h treatment) and after submaximal exercise (40 W, constant work rate). In addition, free-radical production by neutrophils and ATP-degradation products were determined before and after exercise.

Results: Short-term oxygen breathing at rest did not influence systemic low-grade inflammation and oxidative stress. The IL-6 response to exercise was attenuated during cycling with supplemental oxygen. Exercise-induced lipid and protein oxidation were prevented by treatment with supplemental oxygen. This was associated with both decreased free-radical production by neutrophils and reduced formation of (hypo)xanthine and uric acid.

Conclusion: Short-term supplementary oxygen does not affect basal systemic inflammation and oxidative stress but prevents exercise-induced oxidative stress in normoxemic, muscle-wasted patients with COPD, and attenuates plasma IL-6 response. Inhibition of neutrophil activation and ATP degradation appears to be involved in this effect.

Key Words: chronic obstructive pulmonary disease • exercise • oxidative stress • supplemental oxygen • systemic inflammation




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