Published ahead of print on July 22, 2005, doi:10.1164/rccm.200411-1580OC
Am. J. Respir. Crit. Care Med., Volume 172, Number 8, October 2005, 994-1001
A more recent version of this article appeared on October 15, 2005
Submitted on November 24, 2004
Accepted on July 20, 2005
Rehabilitation Decreases Exercise-induced Oxidative Stress in Chronic Obstructive Pulmonary Disease
Evi M Mercken1*, Geja J Hageman2, Annemie M.W.J. Schols1, Marco A Akkermans3, Aalt Bast4, and Emiel F.M. Wouters1
1 Department of Respiratory Medicine, University of Maastricht, Maastricht, The Netherlands,
2 Department of Health Risk Analysis and Toxicology, University of Maastricht, Maastricht, The Netherlands,
3 Asthma Center Hornerheide, Horn, The Netherlands,
4 Department of Pharmacology and Toxicology, University of Maastricht, Maastricht, The Netherlands
* To whom correspondence should be addressed. 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 was studied for chronic obstructive pulmonary disease (COPD). Eleven COPD patients and eleven healthy age-matched controls performed a maximal and submaximal exercise cycle ergometry test at 60% of peak workload. COPD patients performed these tests before and after 8 weeks of pulmonary rehabilitation. Measurements were done before, immediately after and 4 hours after both exercise tests.
At rest, increased oxidative stress was observed in patients compared to controls, as measured by urinary malondialdehyde (MDA) (p<0.05) and hydrogen peroxide (H2O2) in breath condensate (p<0.05). In healthy controls, a significant increase in urinary MDA was observed 4 hours after both exercise tests (p=0.05), whereas H2O2 significantly increased immediately after maximal exercise (p<0.05). In COPD patients, before rehabilitation, reactive oxygen species (ROS)-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 ROS-induced DNA damage was detected after exercise at submaximal intensity despite increased exercise duration of 73%. In summary, COPD patients 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: COPD, oxidative stress, exercise capacity, rehabilitation
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