Published ahead of print on March 2, 2006, doi:10.1164/rccm.200512-1957OC Am. J. Respir. Crit. Care Med., Volume 173, Number 10, May 2006, 1122-1129 A more recent version of this article appeared on May 15, 2006
Submitted on December 23, 2005 Supplemental Oxygen Prevents Exercise-Induced Oxidative Stress in Muscle-wasted Patients with COPDHanneke A.C. van Helvoort1*,1 Department of Pulmonary Diseases, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; Radboud University Nijmegen Medical Centre, Institute for Fundamental and Clinical Human Movement Sciences, Nijmegen, The Netherlands, 2 Department of Pulmonary Diseases, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands, 3 Laboratory of Pediatrics and Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands * To whom correspondence should be addressed. E-mail: H.vanHelvoort{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) or compressed air, both at rest (1h treatment) and after submaximal exercise (40W, constant work rate). Additionally, 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 COPD patients, and attenuates plasma IL-6 response. Inhibition of neutrophil activation and ATP degradation appear to be involved in this effect. Key words: COPD, systemic inflammation, oxidative stress, supplemental oxygen, exercise
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