Open Collections

The effect of acute intermittent hypercapnic hypoxia on ventilatory plasticity and cerebral neurovascular coupling in humans

University of British Columbia

Healthy humans exposed to acute intermittent hypoxia (IH) demonstrate comparable physiological responses to those with obstructive sleep apnea (OSA) and chronic exposure to IH. Responses include elevated sympathetic vasomotor outflow, arterial blood pressure, and changes in ventilatory and cerebrovascular sensitivity. Additionally, prolonged elevations in resting ventilation (V̇I) or ventilatory long-term facilitation (vLTF) manifest following IH, although to date only shown when hypercapnia is sustained throughout exposure and recovery. We aimed to determine (1) if acute intermittent hypercapnic hypoxia (IHH) elicits vLTF during isocapnic-normoxic recovery, (2) whether peripheral chemoreceptor drive contributes to vLTF, and (3) if IHH alters cerebral neurovascular coupling (NVC) in healthy men and women. Twenty individuals (age: 22±1; 9 females, tested 0-5 days early follicular phase) were exposed to 40-minutes of IHH comprised of 40-seconds hypercapnic hypoxia (nadir SPO₂ = 83.31.0%, peak PETCO₂ = 3.20.3 mmHg above baseline), and 20-seconds of normoxic recovery. Nine males returned for a time-matched room-air control. Beat-by-beat mean arterial blood pressure (MAP; finger-photoplethysmography) was recorded throughout the trial. The peak relative posterior cerebral blood velocity (PCAV; transcranial Doppler ultrasound) and conductance (PCACVC; quotient of PCAV and MAP) response to 5 repeated cycles of 30-seconds eyes-open with standardized visual stimulation determined cerebral NVC before and after IHH. Resting ventilation (V̇₁) was recorded for 50-minutes of recovery following IHH and 1-minute bouts of hyperoxia were administered to attenuate peripheral chemoreceptor drive at 5-minute intervals. Resting MAP was elevated from baseline at all time points throughout recovery (main effect; P<0.01). Following IHH, peak relative PCAV response to visual stimulus was not different, however PCACVC response was increased by 4.51.5% (P<0.01) and did not changed during time-matched control. Throughout 50-minutes of recovery V̇₁ was increased by 4.6±0.1 l/min compared to baseline (P<0.01). Hyperoxia depressed V̇₁ at baseline and V̇₁ depression was augmented throughout recovery (ΔV̇₁ = -0.8±0.2 vs. -1.7±0.3 l/min respectively, P<0.01). V̇₁ depression was not different during time-matched control. In summary, following IHH (1) vLTF is evident during isocapnic-normoxic recovery, (2) peripheral chemoreceptor inhibition led to greater depression of V̇₁ and (3) coupling of cerebral oxygen delivery to metabolic demands was augmented in healthy individuals.

Text

2019-10-24

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/72052

Health and Exercise Sciences

University of British Columbia

UBCO

http://creativecommons.org/licenses/by-nc-nd/4.0/