Ventilatory long‐term facilitation following acute intermittent or continuous hypoxaemia in awake humans: the role of carotid chemoreceptors and ventilatory drift to sustained hypercapnia

Abstract

In awake humans, acute intermittent hypoxaemia (IH) causes a sustained increase in ventilation upon reoxygenation, known as ventilatory long‐term facilitation (vLTF), but only if combined with mild hypercapnia. It is not known if mild hypercapnia also unmasks vLTF following continuous hypoxia (CH). Carotid chemoreceptor (CC) sensitisation has been proposed as a mechanism for vLTF. We hypothesised that silencing the CC with 100% O2 would transiently abolish vLTF.12 males undertook 3 trials. Mild hypercapnia was maintained in all trials and one minute exposures to 100% O2 occurred at baseline and recovery. Trials differed only in their hypoxic exposure; Trial 1‐Acute IH, Trial 2‐Acute CH, Trial 3‐Euoxia. Ventilation in Trial 1 and 2 increased from baseline to recovery (T1: 20.1 ± 1.1 vs. 25.1 ± 1.6, T2: 20.0 ± 1.2 vs. 25.1 ± 1.4 L/min).Ventilation also increased in Trial 3 but to a lesser extent (19.8 ± 1.17 vs. 22.4 ± 1.84 L/min). Ventilation during 100% O2 increased from baseline to recovery in all trials (T1: 17.1 ± 1.2 vs. 21.8 ± 1.6, T2: 18.0 ± 1.5 vs. 22.5 ± 1.5, T3: 17.6 ± 1.4 vs. 20.2 ± 2.1).In awake humans, during mild hypercapnia, CH induces a similar magnitude of vLTF as IH. However, a gradual positive drift in ventilation to mild hypercapnia accounts for ~50% of the vLTF. Silencing of the CC with 100% O2 exposure does not transiently abolish vLTF following acute IH or CH, suggesting CC sensitisation may not mediate vLTF.