title: Rehabilitation decreases exercise-induced oxidative stress in chronic obstructive pulmonary disease.
abstract: 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.
authors.affiliation: Department of Respiratory Medicine, University of Maastricht, Maastricht, The Netherlands. e.mercken@pul.unimaas.nl
authors.forename: Evi M
authors.initials: EM
authors.lastname: Mercken
authors.forename: Geja J
authors.initials: GJ
authors.lastname: Hageman
authors.forename: Annemie M W J
authors.initials: AM
authors.lastname: Schols
authors.forename: Marco A
authors.initials: MA
authors.lastname: Akkermans
authors.forename: Aalt
authors.initials: A
authors.lastname: Bast
authors.forename: Emiel F M
authors.initials: EF
authors.lastname: Wouters
mesh_terms: D001944:Breath Tests; D016022:Case-Control Studies; D020552:Comet Assay; D004249:DNA Damage / Q000502:physiology; D005080:Exercise Test; D005081:Exercise Therapy / Q000009:adverse effects* / Q000379:methods; D017079:Exercise Tolerance / Q000502:physiology*; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006861:Hydrogen Peroxide / Q000032:analysis; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000652:urine; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000503:physiopathology / Q000534:rehabilitation*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012146:Rest / Q000502:physiology; D012720:Severity of Illness Index; D013997:Time Factors; D014527:Uric Acid / Q000097:blood; D014797:Vital Capacity
chemical_list: D017382:Reactive Oxygen Species; D014527:Uric Acid; D008315:Malondialdehyde; D006861:Hydrogen Peroxide