Identification of fast and slow ventilatory responses to carbon dioxide under hypoxic and hyperoxic conditions in humans

Abstract

1. Under conditions of both euoxia and hypoxia, it is generally accepted that the ventilatory response to COµ has both rapid (peripheral chemoreflex) and slow (central chemoreflex) components. However, under conditions of hyperoxia, it is unclear in humans whether the fast component is completely abolished or merely attenuated in magnitude. 2. The present study develops a technique to determine whether or not a two-compartment model fits the ventilatory response to COµ significantly better than a one-compartment model. Data were collected under both hypoxic (end-tidal POµ = 50 Torr) conditions, when two components would be expected, and under hyperoxic (end-tidal POµ = 200 Torr) conditions, when the presence of the fast compartment is under question. 3. Ten subjects were recruited, of whom nine completed the study. The end-tidal PCOµ of each subject was varied according to a multi-frequency binary sequence that involved 13 steps into and 13 steps out of hypercapnia lasting altogether 1408 s. 4. In four out of nine subjects in hypoxia, and six out of nine subjects in hyperoxia, the twocompartment model fitted the data significantly better than the one-compartment model (F ratio test on residuals). This improvement in fit was significant for the pooled data in both hypoxia (P < 0·05) and hyperoxia (P < 0·005). Mean ventilatory sensitivities for the central chemoreflex were (mean ± s.e.m.) 1·69 ± 0·39 l min¢ Torr¢ in hypoxia and 2·00 ± 0·32 l min¢ Torr¢ in hyperoxia. Mean ventilatory sensitivities for the peripheral chemoreflex were 2·42 ± 0·36 l min¢ Torr¢ in hypoxia and 0·75 ± 0·16 l min¢ Torr¢ in hyperoxia. 5. It is concluded that the rapid and slow components of the ventilatory response to COµ can be separately identified, and that a rapid component persists under conditions of hyperoxia.9773

The Contribution of Chemoreflex Drives to Resting Breathing in Man

“…However, some investigators have suggested that the hyperoxia of the Dejours test does not completely silence the peripheral chemoreflex (Dahan et al 1990;Pedersen et al 1999). Our finding, that a 20 % peripheral chemoreflex contribution is insufficient to result in an exact intersection with the average resting point, could also be interpreted to suggest that a peripheral chemoreflex contribution persists.…”

Human Physiology in an Aquatic Environment

“…It has been hypothesized that the depth-dependent hyperoxic hyperventilation is due to the effects of high P O2 at depth on the reduced peripheral chemoreceptor sensitivity (293). Reactive oxygen species, secondary to the high P O2 at depth are proposed to accumulate in the tissues of the brain and result in stimulation of the central chemoreceptors in the caudal solitary complex (84), resulting in the observed hyperventilation, by dampening the feedback in the respiratory control.…”

Comparing and characterizing transient and steady‐state tests of the peripheral chemoreflex in humans

“…hypoxia) of the peripheral chemoreceptors (e.g. Pedersen et al 1999;Smith et al 2006). Not only does this isolate the peripheral chemoreceptors more accurately, but it may also avoid potential confounders of complex interactions between the central and peripheral chemoreceptors (e.g.…”

“…It is difficult to separate the contribution of either of these chemoreceptors to ventilation in humans, but temporal domains (e.g. slow versus fast; Pedersen et al 1999;Smith et al 2006) and stimulus specificity (e.g. hypoxia; Steinback & Poulin, 2007) have been exploited in the past.…”