Here we tested the hypothesis that the cerebrovascular responses to brief breath hold epochs were coupled not only with increased partial pressure of carbon dioxide (PCO2), but also with decreased partial pressure of oxygen (PO2). fMRI map of cerebrovascular reactivity (CVR) to breath-by-breath O2-CO2 exchange ratio covers similar regions as map of CVR to exogenous CO2 challenge. Substantially fewer regions in fMRI map of CVR to endogenous end-tidal CO2 satisfied statistical significance. Our results support the hypothesis that hypoxia and hypercapnia work synergistically to enhance cerebrovascular responses to breath hold.
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