The effects of discontinuous hypoxia on cerebrovascular regulation in humans are unknown. We hypothesized that five nocturnal hypoxic exposures (8 hrs day^-1) at a simulated altitude of 4300m (F_IO₂ =~ 13.8%) would elicit cerebrovascular responses that are similar to those that have been reported during chronic altitude exposures. Twelve male subjects (26.6 ± 4.1 (SD) yrs) volunteered for this study. The technique of end-tidal forcing was used to examine cerebral blood flow (CBF) and regional cerebral oxygen saturation (S_rO₂) responses to acute variations in O₂ and CO₂ twice prior to, immediately after, and 5 days following the overnight hypoxic exposures. Transcranial Doppler ultrasound was used to assess CBF, and near infrared spectroscopy was used to assess S_rO₂. Throughout the nocturnal hypoxic exposures, end-tidal PCO₂ decreased (P < 0.001) while arterial oxygen saturation increased (P < 0.001) compared with overnight normoxic control measurements. Symptoms associated with altitude illness were significantly greater than control values on the 1^st night (P < 0.001) and 2^nd night (P < 0.01) of nocturnal hypoxia. Immediately following the nocturnal hypoxic intervention, the sensitivity of CBF to acute variations in O₂ and CO₂ increased 116% (P < 0.01) and 33% (P < 0.05), respectively, when compared with control values. S_rO₂ was highly correlated with SaO₂ (R² = 0.94 ± 0.04). These results show that discontinuous hypoxia elicits increases in the sensitivity of CBF to acute vartiations in O₂ and CO₂ which are similar to those observed during chronic hypoxia.