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.