The middle cerebral artery blood velocity response to acute normobaric hypoxia occurs independently of changes in ventilation in humans

Hypoxia induces ventilatory, cardiovascular and cerebrovascular adjustments to defend against reductions in systemic oxygen delivery. We aimed to determine whether the ventilatory response to moderate acute hypoxia increases cerebral perfusion independently of changes in arterial oxygenation. Eleven young healthy individuals were exposed to four 15 minute experimental conditions; 1) normoxia [partial pressure of end‐tidal oxygen; PETO2 = 100 mmHg], 2) hypoxia [PETO2 = 50 mmHg], 3) normoxia with breathing volitionally matched to levels observed during hypoxia [hyperpnoea; PETO2 = 100 mmHg], and 4) hypoxia [PETO2 = 50 mmHg] respiratory frequency and tidal volume were volitionally matched to levels observed during normoxia (i.e., restricted breathing [RB]). Isocapnia was maintained in all conditions. Middle cerebral artery mean blood flow velocity (MCA Vmean) assessed by transcranial Doppler ultrasound), was increased during hypoxia (58 ± 12 cm s–1, P = 0.04) and hypoxia + RB (61 ± 14 cm s–1, P0.05). These findings suggest that the hypoxic ventilatory response does not increase cerebral perfusion, indexed using MCA Vmean, during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation