Does hyperoxia stimulate breathing?

Hyperoxia has been shown to stimulate ventilation (V̇E) in a dose-dependent manner. Whether this occurs due to an oxygen (O2)-specific mechanism or secondary to carbon dioxide (CO2) retention at the central chemoreceptors (via the Haldane effect) remains unclear. This study measured the ventilatory response to isoxic-hyperoxic CO2 modified rebreathing (an estimate of central chemoreflex sensitivity) with O2 clamped at increasingly higher hyperoxic pressures. We hypothesized that the slope of the V̇E versus PCO2 relationship is fixed and independent of hyperoxic severity. Fourteen healthy participants (6 females; mean ± SD age: 25 ±7 years) visited the laboratory on four occasions to perform three repetitions of modified rebreathing in four isoxic-hyperoxic conditions: “mild”: PO2=150 mmHg; “moderate”: PO2=200 mmHg; “high”: PO2=300 mmHg; and “extreme”: PO2=700 mmHg. The level of isoxic-hyperoxic PO2 was randomized between visits. Throughout rebreathing, breath-by-breath V̇E, end-tidal PCO2 (PETCO2) and O2 (PETO2) were measured by pneumotach and dual gas analyser. For each trial, the PETCO2 at which V̇E began to rise was identified as the ventilatory recruitment threshold (VRT, mmHg). The V̇E data prior to VRT provided baseline V̇E (V̇Ebsl, L∙min-1) and the slope of the linear response above VRT estimated central respiratory chemoreflex sensitivity (V̇ES, L∙min-1∙mmHg-1). For each hyperoxic condition, VRT, V̇Ebsl, and V̇ES from like-trials were averaged and between condition comparisons were assessed by repeated measures analysis of variance. There was no effect of PETO2 on V̇Ebsl (mild: 6.7±3.4 L∙min-1; moderate: 5.9±3.0 L∙min-1; heavy: 5.5±1.6 L∙min-1; extreme: 6.1±3.2 L∙min-1; p=0.35), VRT (mild: 42.7±3.2 mmHg; moderate: 42.0±2.2 mmHg; heavy: 42.2 ±2.4 mmHg; extreme: 41.5±2.4 mmHg; p=0.17) or V̇ES (mild: 5.04±2.78 L∙min-1∙mmHg-1; moderate: 4.64±1.90 L∙min-1∙mmHg-1; heavy: 4.68±1.92 L∙min-1∙mmHg-1; extreme: 4.49±1.72 L∙min-1∙mmHg-1; p=0.47). The hyperoxic V̇E versus PCO2 relationship was unaltered across a range of PO2 spanning mild to extreme. These data indicate that hyperoxia is not an independent stimulant of breathing. Supported by NSERC This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.