Normobaric Intermittent Hypoxia Increases Middle Cerebral Arterial Blood Flow Velocity With No Systemic Hypertension

PURPOSE: To study vascular responses to intermittent hypoxia (IH) exposures. METHODS: Six healthy men (26 ± 1 yr) were exposed to 5 IH bouts, each comprising 6-min breathing 10% O2 interspersed with 4 min breathing room air. During IH, middle cerebral arterial blood flow velocity (VMCA, Ez-Dop), blood pressure (BP, NIBP100D), O2 saturation (SaO2, Radiometer), breathing frequency (Fbr), tidal volume (VT, Universal Ventilation Meter), inspired and expired O2 and CO2 fractions (1100 Medical Gas Analyzer; Perkin-Elmer) were continuously monitored. RESULTS: The SaO2 was decreased during 6-min IH (P < 0.001), which was more significant in the 5th than the 1st bout of IH exposures (P < 0.001). The VMCA was significantly increased by IH and its magnitude was greater in the 5th than the 1st bout of IH exposures (P = 0.002). IH did not change mean BP (MBP) from the baseline (min 0) during either the 1st or 5th bout (see Table). Minute ventilation (VE) was stimulated by IH (P = 0.023) with no difference between the bouts. The increased VE was driven by increases in VT because Fbr remained constant throughout IH exposures. There was a decrease (P < 0.001) in partial pressure of end-tidal CO2 (PETCO2) during IH, which was not different between the 1st and the 5th bouts of IH exposures.Table: No title available.CONCLUSION: Normobaric IH exposures enhance cerebral perfusion, which is mediated by a moderate hypoxemia. There is no hypertensive response during the IH exposures.