Cerebrovascular conductance reactivity of the anterior and posterior cerebral circulations was not significantly correlated with physiological or psychological breath-hold break-points (r > -0.42; P > 0.06).
Observational (n=23)
Cerebrovascular reactivity-mediated CO2 washout from central chemoreceptors does not appear to play a role in determining breath-hold break-point.
Effect estimate: r > -0.42
p-value: p=>0.06
New Findings What is the central question of this study? We developed and validated a ‘stimulus index’ (SI; ratio of end‐tidal partial pressures of CO 2 and O 2 ) method to quantify cerebrovascular reactivity (CVR) in anterior and posterior cerebral circulations during breath holding. We aimed to determine whether the magnitude of CVR is correlated with breath‐hold duration. What is the main finding and its importance? Using the SI method and transcranial Doppler ultrasound, we found that the magnitude of CVR of the anterior and posterior cerebral circulations is not positively correlated with physiological or psychological break‐point during end‐inspiratory breath holding. Our study expands the ability to quantify CVR during breath holding and elucidates factors that affect break‐point. The central respiratory chemoreflex contributes to blood gas homeostasis, particularly in response to accumulation of brainstem CO 2 . Cerebrovascular reactivity (CVR) affects chemoreceptor stimulation inversely through CO 2 washout from brainstem tissue. Voluntary breath holding imposes alterations in blood gases, eliciting respiratory chemoreflexes, potentially contributing to breath‐hold duration (i.e. break‐point). However, the effects of cerebrovascular reactivity on break‐point have yet to be determined. We tested the hypothesis that the magnitude of CVR contributes directly to breath‐hold duration in 23 healthy human participants. We developed and validated a cerebrovascular stimulus index methodology SI; ratio of end‐tidal partial pressures of CO 2 and O 2 ( ) to quantify CVR by correlating measured and interpolated values of ( r = 0.95, P −0.42; P > 0.06). Although central chemoreceptor activation is likely to be contributing to break‐point, our data suggest that CVR‐mediated CO 2 washout from central chemoreceptors plays no role in determining break‐point, probably because of a reduced arterial‐to‐tissue CO 2 gradient during breath holding.
Bruce et al. (2016) conducted an observational in Healthy (n=23). Voluntary breath holding was evaluated on Correlation between cerebrovascular conductance reactivity and physiological/psychological break-points (r > -0.42, p=>0.06). Cerebrovascular conductance reactivity of the anterior and posterior cerebral circulations was not significantly correlated with physiological or psychological breath-hold break-points (r > -0.42; P > 0.06).
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