Evi M Mercken1, Harry R Gosker2, Erica P Rutten3, Emiel F Wouters4, Aalt Bast5, Geja J Hageman6, Annemie M Schols2. 1. Department of Respiratory Medicine, Maastricht University, Maastricht, the Netherlands. Electronic address: e.mercken@pul.unimaas.nl. 2. Department of Respiratory Medicine, Maastricht University, Maastricht, the Netherlands. 3. Centre for Integrated Rehabilitation Organ Failure, Horn, the Netherlands. 4. Centre for Integrated Rehabilitation Organ Failure, Horn, the Netherlands; Department of Respiratory Medicine, Maastricht University, Maastricht, the Netherlands. 5. Department of Pharmacology and Toxicology, Maastricht University, Maastricht, the Netherlands. 6. Department of Health Risk Analysis and Toxicology, Maastricht University, Maastricht, the Netherlands.
Abstract
BACKGROUND: Our aim for this study was to disentangle the contribution of muscular vs pulmonary oxidative stress during endurance exercise in patients with COPD. METHODS: Fifteen COPD patients and 10 healthy age-matched control subjects performed a continuously submaximal single-leg ergometer test (40% of peak workload) for 20 min or until they stopped (muscle endurance [Tlim]). Venous blood, urine samples, and exhaled breath condensate were sampled before, immediately after, and 2 h after exercise. RESULTS: Tlim was lower in COPD patients than in control subjects (p < 0.01). No exercise-induced systemic inflammation (ie, no raised levels of interleukin-6 or tumor necrosis factor-alpha) was found in the groups. Urinary malondialdehyde and uric acid levels (p < 0.05) were increased in COPD patients, whereas erythrocyte oxidized glutathione/reduced glutathione levels tended to be increased in COPD patients compared with control subjects after exercise (p = 0.08). Despite the relatively low cardioventilatory response to this localized muscle exercise, hydrogen peroxide levels in breath condensate significantly increased in COPD patients (p < 0.01). Nuclear factor kappaB DNA-binding activity of p50 in peripheral blood monocytes was elevated after exercise in both COPD patients (p < 0.01) and control subjects (p < 0.05), whereas p65 protein levels were not altered. CONCLUSION: COPD patients showed increased pulmonary and systemic oxidative stress after localized leg muscle exercise compared with healthy control subjects, without evidence of increased levels of systemic inflammation.
BACKGROUND: Our aim for this study was to disentangle the contribution of muscular vs pulmonary oxidative stress during endurance exercise in patients with COPD. METHODS: Fifteen COPDpatients and 10 healthy age-matched control subjects performed a continuously submaximal single-leg ergometer test (40% of peak workload) for 20 min or until they stopped (muscle endurance [Tlim]). Venous blood, urine samples, and exhaled breath condensate were sampled before, immediately after, and 2 h after exercise. RESULTS: Tlim was lower in COPDpatients than in control subjects (p < 0.01). No exercise-induced systemic inflammation (ie, no raised levels of interleukin-6 or tumor necrosis factor-alpha) was found in the groups. Urinary malondialdehyde and uric acid levels (p < 0.05) were increased in COPDpatients, whereas erythrocyte oxidized glutathione/reduced glutathione levels tended to be increased in COPDpatients compared with control subjects after exercise (p = 0.08). Despite the relatively low cardioventilatory response to this localized muscle exercise, hydrogen peroxide levels in breath condensate significantly increased in COPDpatients (p < 0.01). Nuclear factor kappaB DNA-binding activity of p50 in peripheral blood monocytes was elevated after exercise in both COPDpatients (p < 0.01) and control subjects (p < 0.05), whereas p65 protein levels were not altered. CONCLUSION:COPDpatients showed increased pulmonary and systemic oxidative stress after localized leg muscle exercise compared with healthy control subjects, without evidence of increased levels of systemic inflammation.
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