Effects of Hyperoxia on Ventilatory Limitation During Exercise in Advanced Chronic Obstructive Pulmonary Disease

TLDR

The study examined how acute hyperoxia affects exercise endurance, ventilatory demand, lung volumes, and dyspnea in ventilatory‑limited advanced COPD patients. Eleven advanced COPD patients performed two randomized cycle‑exercise tests at 50 % peak capacity breathing room air or 60 % O₂, while endurance time, dyspnea, ventilation, breathing pattern, dynamic inspiratory capacity, and gas exchange were recorded. Hyperoxia increased PaO₂, extended endurance by 4.7 min, lowered dyspnea by 2 Borg units, reduced ventilation and breathing frequency, and improved dynamic inspiratory capacity, thereby enhancing endurance through reduced ventilatory demand, better lung volumes, and less dyspnea.

Abstract

We studied interrelationships between exercise endurance, ventilatory demand, operational lung volumes, and dyspnea during acute hyperoxia in ventilatory-limited patients with advanced chronic obstructive pulmonary disease (COPD). Eleven patients with COPD (FEV1.0 = 31 ± 3% predicted, mean ± SEM) and chronic respiratory failure (PaO2 52 ± 2 mm Hg, PaCO2 48 ± 2 mm Hg) breathed room air (RA) or 60% O2 during two cycle exercise tests at 50% of their maximal exercise capacity, in randomized order. Endurance time (Tlim), dyspnea intensity (Borg Scale), ventilation (V˙ e), breathing pattern, dynamic inspiratory capacity (ICdyn), and gas exchange were compared. PaO2 at end-exercise was 46 ± 3 and 245 ± 10 mm Hg during RA and O2, respectively. During O2, Tlim increased 4.7 ± 1.4 min (p < 0.001); slopes of Borg, V˙ e, V˙ co 2, and lactate over time fell (p < 0.05); slopes of Borg–V˙ e, V˙ e–V˙ co 2, V˙ e–lactate were unchanged. At a standardized time near end-exercise, O2 reduced dyspnea 2.0 ± 0.5 Borg units, V˙ co 2 0.06 ± 0.03 L/min, V˙ e 2.8 ± 1.0 L/min, and breathing frequency 4.4 ± 1.1 breaths/min (p < 0.05 each). ICdyn and inspiratory reserve volume (IRV) increased throughout exercise with O2 (p < 0.05). Increased ICdyn was explained by the combination of increased resting IRV and decreased exercise breathing frequency (r2 = 0.83, p < 0.0005). In conclusion, improved exercise endurance during hyperoxia was explained, in part, by a combination of reduced ventilatory demand, improved operational lung volumes, and dyspnea alleviation.