Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

Shibata

Ito

et al. 2020

New Findings What is the central question of this study?What are the dynamic characteristics of cerebrovascular carbon dioxide reactivity and the central respiratory chemoreflex? What is the main finding and its importance?The transfer function gain from the end‐tidal partial pressure of carbon dioxide to cerebral blood flow or ventilation decreased in the high frequency range at rest and during exercise. These findings indicate that the dynamic characteristics of both systems were not constant in all frequency ranges, and this trend was not modified by exercise. Abstract The purpose of this study was to examine the dynamic characteristics of cerebrovascular reactivity and ventilatory response to change in arterial CO2 in all frequency ranges at rest using frequency domain analysis, and also to examine whether this is modified by dynamic exercise as with the traditionally determined cerebrovascular CO2 reactivity. In nine healthy young subjects, at rest and during exercise (cycling exercise at constant predetermined work rate corresponding to a V̇normalO2 level of 0.90 l min−1), the dynamic characteristics of cerebrovascular CO2 reactivity and the central respiratory chemoreflex were assessed by transfer function analysis using a binary white‐noise sequence (0–7% inspired CO2 fraction) from the end‐tidal partial pressure of CO2 (PnormalETCO2) to the mean middle cerebral artery mean blood velocity (MCA Vm) or minute ventilation (V̇E), respectively. In the high frequency range, both transfer function gains decreased but, interestingly, the cut‐off frequency in the transfer function gain from PnormalETCO2 to MCA Vm response was higher than that from PnormalETCO2 to V̇E response at rest (0.024 vs. 0.015 Hz) and during exercise (0.030 vs. 0.011 Hz), indicating that cerebrovascular CO2 reactivity or central respiratory chemoreflex was not constant in all frequency ranges, and this trend was not modified by exercise. These findings suggest that dynamic characteristics of the cerebrovascular CO2 reactivity or central chemoreflex need to be assessed to identify the whole system because the traditional method cannot identify the property of time response of these systems.

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Dynamic characteristics of cerebrovascular reactivity or ventilatory response to change in carbon dioxide

Shibata

Ito

et al. 2020

“…Third, we measured CBF after 8 min of hypoxia. This was believed to be sufficient to reach steady‐state levels of

P_{{aO}_{2}}

(MacFarlane & Cunningham, ). Also, when breathing was restrained in hypoxia, a higher level of attention, concentration and cognitive processing was needed to perform the protocol.…”

Section: Discussionmentioning

confidence: 99%

Effects of acute hypoxia on cerebrovascular responses to carbon dioxide

Nakahara

Ueda

et al. 2014

New Findings r What is the central question of this study?In acute hypoxia, the reduction in arterial CO 2 tension due to the hypoxic ventilatory response (respiratory chemoreflex) stimulates cerebral vasoconstriction, which opposes the degree of hypoxic cerebral vasodilatation. The aim was to examine this interaction further. Specifically, we questioned whether arterial CO 2 tension-mediated effects on cerebrovascular regulation are attenuated during acute hypoxia. r What is the main finding and its importance? Cerebrovascular CO 2 reactivity and CO 2 -mediated effects on dynamic cerebral autoregulation were attenuated during acute hypoxia. These findings suggest that blunted cerebrovascular responses to CO 2 may limit the degree of CO 2 -mediated vasoconstriction to help maintain adequate cerebral blood flow for cerebral O 2 homeostasis during acute hypoxia.In normoxic conditions, a reduction in arterial carbon dioxide tension causes cerebral vasoconstriction, thereby reducing cerebral blood flow and modifying dynamic cerebral autoregulation (dCA). It is unclear to what extent these effects are altered by acute hypoxia and the associated hypoxic ventilatory response (respiratory chemoreflex). This study tested the hypothesis that acute hypoxia attenuates arterial CO 2 tension-mediated regulation of cerebral blood flow to help maintain cerebral O 2 homeostasis. Eight subjects performed three randomly assigned respiratory interventions following a resting baseline period, as follows: (1) normoxia (21% O 2 ); (2) hypoxia (12% O 2 ); and (3) hypoxia with wilful restraint of the respiratory chemoreflex. During each intervention, 0, 2.0, 3.5 or 5.0% CO 2 was sequentially added (8 min stages) to inspired gas mixtures to assess changes in steady-state cerebrovascular CO 2 reactivity and dCA. During normoxia, the addition of CO 2 increased internal carotid artery blood flow and middle cerebral artery mean blood velocity (MCA V mean ), while reducing dCA (change in phase = −0.73 ± 0.22 rad, P = 0.005). During acute hypoxia, internal carotid artery blood flow and MCA V mean remained unchanged, but cerebrovascular CO 2 reactivity (internal carotid artery, P = 0.003; MCA V mean , P = 0.031) and CO 2 -mediated effects on dCA (P = 0.008) were attenuated. The effects of hypoxia were not further altered when the respiratory chemoreflex was restrained. These findings support the hypothesis that arterial CO 2 tension-mediated effects on the cerebral vasculature are reduced during acute hypoxia. These effects could limit the degree C

“…Both ICA and VA blood flow were assessed during ventilatory steady‐state conditions (MacFarlane & Cunningham, 1992; Willie et al 2012). Blood flow was measured a minimum of three times during a 2 min period within 10–15 min of exposure to hypoxia.…”

Section: Methodsmentioning

confidence: 99%

Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

Sato

Nakahara

et al. 2012

New Findings r What is the central question of this study? Does hypoxia enhance blood flow to all parts of the brain uniformly? r What is the main finding and its importance?During hypoxia, internal carotid artery flow is maintained despite a reduction in (end-tidal) carbon dioxide tension, while vertebral artery blood flow increases. Only with maintained end-tidal carbon dioxide tension is there an increase in both vertebral and internal carotid blood flow during hypoxia.Hypoxia changes the regional distribution of cerebral blood flow and stimulates the ventilatory chemoreflex, thereby reducing CO 2 tension. We examined the effects of both hypoxia and isocapnic hypoxia on acute changes in internal carotid (ICA) and vertebral artery (VA) blood flow. Ten healthy male subjects underwent the following two randomly assigned respiratory interventions after a resting baseline period with room air: (i) hypoxia; and (ii) isocapnic hypoxia with a controlled gas mixture (12% O 2 ; inspiratory P O 2 = 86 mmHg). In the isocapnic hypoxia intervention, subjects were instructed to maintain the rate and depth of breathing to maintain the level of end-tidal partial pressure of CO 2 (P ET,CO 2 ) during the resting baseline period. The ICA and VA blood flow (velocity × cross-sectional area) were measured using Doppler ultrasonography. The P ET,CO 2 was decreased (−6.3 ± 0.9%, P < 0.001) during hypoxia by hyperventilation (minute ventilation +12.9 ± 2.2%, P < 0.001), while P ET,CO 2 was unchanged during isocapnic hypoxia. The ICA blood flow was unchanged (P = 0.429), while VA blood flow increased (+10.3 ± 3.1%, P = 0.010) during hypoxia. In contrast, isocapnic hypoxia increased both ICA (+14.5 ± 1.4%, P < 0.001) and VA blood flows (+10.9 ± 2.4%, P < 0.001). Thus, hypoxic vasodilatation outweighed hypocapnic vasoconstriction in the VA, but not in the ICA. These findings suggest that acute hypoxia elicits an increase in posterior cerebral blood flow, possibly to maintain essential homeostatic functions of the brainstem.