Intermittent hypoxia reduces cerebrovascular sensitivity to isocapnic hypoxia in humans

The purpose of this study was to determine the changes in human cerebrovascular function associated with intermittent poikilocapnic hypoxia (IH). Healthy men (n = 8; 24 ± 1 years) were exposed to IH for 10 days (12% O2 for 5 min followed by 5 min of normoxia for 1 h). During the hypoxic exposures, oxyhemoglobin saturation (SaO2) was 85% and the end-tidal partial pressure of CO2 was permitted to fall as a result of hypoxic hyperventilation. Pre- and post-IH intervention subjects underwent a progressive isocapnic hypoxic test where ventilation, blood pressure, heart rate, and cerebral blood flow velocity (middle cerebral artery, transcranial Doppler) were measured to determine the ventilatory, cardiovascular and cerebrovascular sensitivities to isocapnic hypoxia. When compared to the pre-IH trial, cerebrovascular sensitivity to hypoxia significantly decreased (pre-IH = 0.28 ± 0.15; post-IH = 0.16 ± 0.14 cm s−1 %SaO2−1; P < 0.05). No changes in ventilatory, blood pressure or heart rate sensitivity were observed (P > 0.05). We have previously shown that the ability to oxygenate cerebral tissue measured using spatially resolved near infrared spectroscopy is significantly reduced following IH in healthy humans. Our collective findings indicate that intermittent hypoxia can blunt cerebrovascular regulation. Thus, it appears that intermittent hypoxia has direct cerebrovascular effects that can occur in the absence of changes to the ventilatory and neurovascular control systems.