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Published ahead of print on July 22, 2005, doi:10.1164/rccm.200411-1580OC
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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 994-1001, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200411-1580OC

Rehabilitation Decreases Exercise-induced Oxidative Stress in Chronic Obstructive Pulmonary Disease

Evi M. Mercken, Geja J. Hageman, Annemie M. W. J. Schols, Marco A. Akkermans, Aalt Bast and Emiel F. M. Wouters

Departments of Respiratory Medicine, Health Risk Analysis and Toxicology, and Pharmacology and Toxicology, University of Maastricht, Maastricht; and Asthma Center Hornerheide, Horn, The Netherlands

Correspondence and requests for reprints should be addressed to Evi M. Mercken, M.Sc., Department of Respiratory Medicine, University of Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands. E-mail: e.mercken{at}pul.unimaas.nl

The effect of exercise at different intensities as well as the effect of intensive supervised pulmonary rehabilitation on oxidative stress were studied for chronic obstructive pulmonary disease (COPD). Eleven patients with COPD and 11 healthy age-matched control subjects performed a maximal and submaximal exercise cycle ergometry test at 60% of peak workload. Patients with COPD performed these tests before and after 8 wk of pulmonary rehabilitation. Measurements were done before, immediately after, and 4 h after both exercise tests. At rest, increased oxidative stress was observed in patients compared with control subjects, as measured by urinary malondialdehyde (MDA; p < 0.05) and hydrogen peroxide (H2O2) in breath condensate (p < 0.05). In healthy control subjects, a significant increase in urinary MDA was observed 4 h after both exercise tests (p = 0.05), whereas H2O2 significantly increased immediately after maximal exercise (p < 0.05). In patients with COPD, before rehabilitation, reactive oxygen species–induced DNA damage in peripheral blood mononuclear cells, urinary MDA, and plasma uric acid were significantly increased after both exercise tests (p < 0.05), whereas no significant increase was observed in plasma MDA. In contrast, exhaled H2O2 was only significantly increased after maximal exercise (p < 0.02). Although after rehabilitation peak workload was increased by 24%, a similar oxidative stress response was found. Remarkably, a decrease in reactive oxygen species–induced DNA damage was detected after exercise at submaximal intensity despite increased exercise duration of 73%. In summary, patients with COPD had increased pulmonary and systemic oxidative stress both at rest and induced by exercise. In addition, pulmonary rehabilitation increased exercise capacity and was associated with reduced exercise-induced oxidative stress.

Key Words: chronic obstructive pulmonary disease • exercise capacity • oxidative stress • rehabilitation




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