Morning attenuation in cerebrovascular CO2 reactivity in healthy humans is associated with a lowered cerebral oxygenation and an augmented ventilatory response to CO2

Abstract

We hypothesized that, in healthy subjects without pharmacological intervention, an overnight reduction in cerebrovascular CO2 reactivity would be associated with an elevated hypercapnic ventilatory [ventilation (V̇e)] responsiveness and a reduction in cerebral oxygenation. In 20 healthy male individuals with no sleep-related disorders, continuous recordings of blood velocity in the middle cerebral artery, arterial blood pressure, V̇e, end-tidal gases, and frontal cortical oxygenation using near infrared spectroscopy were monitored during hypercapnia (inspired CO2, 5%), hypoxia [arterial O2 saturation (SaO2) ∼84%], and during a 20-s breath hold to investigate the related responses to hypercapnia, hypoxia, and apnea, respectively. Measurements were conducted in the evening (6–8 PM) and in the early morning (6–8 AM). From evening to morning, the cerebrovascular reactivity to hypercapnia was reduced (5.3 ± 0.6 vs. 4.6 ± 1.1%/Torr; P < 0.05) and was associated with a reduced increase in cerebral oxygenation ( r = 0.39; P < 0.05) and an elevated morning hypercapnic V̇e response ( r = 0.54; P < 0.05). While there were no overnight changes in cerebrovascular reactivity or V̇e response to hypoxia, there was greater cerebral desaturation for a given SaO2 in the morning (AM, −0.45 ± 0.14 vs. PM, −0.35 ± 0.14%/SaO2; P < 0.05). Following the 20-s breath hold, in the morning, there was a smaller surge middle cerebral artery velocity and cerebral oxygenation ( P < 0.05 vs. PM). These data indicate that normal diurnal changes in the cerebrovascular response to CO2 influence the hypercapnic ventilatory response as well as the level of cerebral oxygenation during changes in arterial Pco2; this may be a contributing factor for diurnal changes in breathing stability and the high incidence of stroke in the morning.