Introduction: It has been demonstrated that the cerebrovascular response to hypoxia is blunted following 10 d of intermittent hypoxia (IH) in healthy humans. The purpose of this study was to test the hypothesis that IH reduces the cerebrovascular response to CO2.
Methods: Healthy male subjects (N=8; 25±2 yr) were exposed to 10 consecutive days of IH (12% O2 for 5 min followed by 5 min of normoxia for 1 h/d). The cerebrovascular response to CO2 was assessed prior to (PRE-IH) and following (POST-IH) the IH paradigm with transcranial Doppler ultrasound.
Results: There was no change in eupnic measures during or following the IH paradigm; however, the ventilatory response to IH increased by the last exposure (3.0±2.8 L·min(-1)). Cerebral blood flow velocity decreased and increased with hypocapnia and hypercapnia, respectively, but cerebrovascular sensitivity to CO2 remained unchanged with IH (PRE-IH: 2.58±0.50%/mmHg; POST-IH: 2.59±0.74%/mmHg).
Discussion: Our data indicates that 10 d of IH in healthy humans does not alter the cerebrovascular response to CO2. Redundancy of cerebrovascular regulation mechanisms to CO2 may work to counteract IH-induced dysregulation and protect cerebral tissue.