Dynamic cerebral autoregulation in healthy males during sleep accompanied by intermittent hypoxia

Obstructive sleep apnea (OSA) is an independent risk factor for stroke, potentially due to intermittent hypoxia (IH) induced impairment of cerebral autoregulation. Human cerebral autoregulation during sleep is poorly characterized and whether IH exposure during sleep alters cerebral autoregulation during sleep is unknown. In a secondary, exploratory analysis of previously collected cerebral blood flow (transcranial Doppler ultrasound measurement of peak blood velocity through the middle cerebral artery; V¯P), mean arterial pressure (MAP; finger photoplethysmography) and end-tidal partial pressure of CO 2 (PETCO 2 ) data, dynamic cerebral autoregulation (dCA) was quantified using transfer function analysis gain, phase and coherence in healthy males (n=10; age: 26 ± 6 years; BMI: 24.5 ± 1.7 kg/m 2 ; MAP: 87.5 ± 8.0 mmHg) during wakefulness and during non-rapid eye movement (NREM) sleep in normoxia or accompanied by IH. Compared to wakefulness V¯P variability was lower during both sleep in normoxia and sleep accompanied by IH in the very low frequency (VLF: 0.02 – 0.07 Hz) and low frequency (LF: 0.07 – 0.2 Hz) ranges (both comparisons, p≤0.02) with MAP variability being lower in the LF range (p=0.045); gain, phase, and coherence were similar between wakefulness and sleep (all comparisons, p≥0.062). dCA measures during normoxic and IH-sleep were similar (all comparisons, p≥0.09). Moreover, dCA gain and phase, and multiple and partial coherences during IH-sleep were not different between acute (<1h) and prolonged (~2h) exposure (all comparisons, p≥0.055) even though V¯P was lower following prolonged IH exposure (p=0.002). These findings indicate dCA is effective during stages 2/3 NREM sleep and is not impacted by ~2h of sleep accompanied by IH.