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Updated: Aug 11, 2026

Home-Based Prescribed Pulmonary Exercise in Patients with Stable Chronic Obstructive Pulmonary Disease
Published on: August 24, 2019
Supplemental oxygen prevents exercise-induced oxidative stress in muscle-wasted patients with chronic obstructive
Hanneke A C van Helvoort1, Yvonne F Heijdra, Leo M A Heunks
1Radboud University Nijmegen Medical Centre, Department of Pulmonary Diseases (454), P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.
Rationale:
Although oxygen therapy is of clear benefit in patients with severe chronic obstructive pulmonary disease (COPD), recent studies have shown that short-term supplementary oxygen may increase oxidative stress and inflammation within the airways.
Objective:
We investigated whether systemic inflammation and oxidative stress at rest and during exercise in patients with COPD are influenced by supplemental oxygen.
Methods:
Nine normoxemic, muscle-wasted patients with moderate to very severe COPD were studied. Plasma markers of systemic inflammation (leukocyte counts, interleukin 6 [IL-6]) and oxidative stress (lipid peroxidation, protein oxidation, antioxidant capacity) were measured after treatment with either supplemental oxygen (nasal, 4 L . min(-1)) or compressed air, both at rest (1 h treatment) and after submaximal exercise (40 W, constant work rate). In addition, free-radical production by neutrophils and ATP-degradation products were determined before and after exercise.
Results:
Short-term oxygen breathing at rest did not influence systemic low-grade inflammation and oxidative stress. The IL-6 response to exercise was attenuated during cycling with supplemental oxygen. Exercise-induced lipid and protein oxidation were prevented by treatment with supplemental oxygen. This was associated with both decreased free-radical production by neutrophils and reduced formation of (hypo)xanthine and uric acid.
Conclusion:
Short-term supplementary oxygen does not affect basal systemic inflammation and oxidative stress but prevents exercise-induced oxidative stress in normoxemic, muscle-wasted patients with COPD, and attenuates plasma IL-6 response. Inhibition of neutrophil activation and ATP degradation appears to be involved in this effect.
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