Quantifying cerebrovascular reactivity in anterior and posterior cerebral circulations during voluntary breath holding

The central respiratory chemoreflex contributes to blood gas homeostasis, particularly in response to accumulation of brainstem CO₂. Cerebrovascular reactivity (CVR) affects chemoreceptor stimulation inversely through CO₂ 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 BHD in 23 healthy human participants. We developed and validated a cerebrovascular stimulus index methodology (SI; P_ETCO₂/P_ETO₂) to quantify CVR by correlating measured and interpolated values of P_ETCO₂ (r = 0.95, P < 0.0001), P_ETO₂ (r = 0.98, P < 0.0001), and SI (r = 0.94, P < 0.0001) during rebreathing. Using transcranial Doppler ultrasound, we then quantified the CVR of the middle (MCAv) and posterior (PCAv) cerebral arteries by plotting cerebral blood velocity against interpolated SI during a maximal end-inspiratory breath-hold. The MCAv CVR magnitude was larger than PCAv (P = 0.001; +70%) during breath-holding. We then correlated MCAv and PCAv CVR with the physiological (involuntary diaphragmatic contractions) and psychological (end-point) break-point, within-individuals. There were significant inverse but modest relationships between both MCAv and PCAv CVR and both physiological and psychological break-points (r0.53, P < 0.03). However, these relationships were absent when MCAv and PCAv cerebrovascular conductance reactivity was correlated with both physiological and psychological break-points (r > –0.42; P > 0.06). Although central chemoreceptor activation is likely contributing to break-point, our data suggests that CVR-mediated CO₂ washout from central chemoreceptors plays no role in determining break-point, likely due to a reduced arterial-tissue CO₂ gradient during breath-holding. (250 words)

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