Background Expiratory flow limitation and lung hyperinflation promote cardiocirculatory perturbations that might impair O 2 delivery to locomotor muscles in patients with chronic obstructive pulmonary disease (COPD). The hypothesis that decreases in lung hyperinflation after the inhalation of bronchodilators would improve skeletal muscle oxygenation during exercise was tested. Methods Twelve non-or mildly hypoxaemic males (forced expiratory volume in 1 s (FEV 1 )¼38.5612.9% predicted; PaO 2 >60 mm Hg) underwent constant work rate cycle ergometer exercise tests (70e80% peak) to the limit of tolerance (Tlim)
'Qualitative' and 'semi-quantitative' signal-morphology impedance cardiography(™) (PhysioFlow(™)) during incremental exercise provided clinically useful information to estimate disease severity and short-term prognosis in patients with PAH in whom acceptable impedance signals could be obtained.
This study addressed whether hyperoxia (HiOX=50% O2), compared to normoxia, would improve peripheral muscle oxygenation at the onset of supra-gas exchange threshold exercise in patients with chronic obstructive pulmonary disease (COPD) who were not overtly hypoxemic (resting Pa O₂> 60 mmHg ). Despite faster cardiac output and improved blood oxygenation, HiOX did not significantly change pulmonary O2 uptake kinetics ( VO₂p ). Surprisingly, however, HiOX was associated with faster fractional O2 extraction ( approximately Delta[deoxy-Hb+Mb] by near-infrared spectroscopy) (p<0.05). In addition, an "overshoot" in Delta[deoxy-Hb+Mb] was found after the initial fast response only in HiOX (7/11 patients) thereby suggesting impaired intra-muscular O2 delivery ( Q'O ₂mv)-to-utilization. These data indicate that, despite improved "central" O2 delivery, Q'O₂mv adapted at a slower rate than muscle VO₂ under HiOX in non-hypoxaemic patients with COPD. Our results question the rationale of using supplemental O2 to improve muscle oxygenation during the transition to high-intensity exercise in this patient sub-population.
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