Impact of acute sleep restriction on cerebrovascular reactivity and neurovascular coupling in young men and women.

Abstract

Chronic exposure to shortened sleep is associated with increased risk of Alzheimer's disease and dementia. Previous studies show insufficient (e.g., poor or fragmented) sleep impairs cerebrovascular reactivity to metabolic stress and may have a detrimental effect on the link between cerebral blood flow (CBF) and neural activity (i.e., neurovascular coupling, NVC). The purpose of this study was to examine the effect of acute sleep restriction on CBF in response to a metabolic (carbon dioxide; CO2) and a cognitive stressor. We hypothesized sleep restriction (4 hours-time in bed) would attenuate CBF and NVC. Sixteen young adults (8M/8F, 28±8 y, 25±3 kg/m2) completed two morning visits following a night of normal (7.38±0.82 hours) or restricted (4.27±0.93 hours, p<0.001) sleep duration. Middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound) was measured at rest and during: 1) five minutes of carbogen air breathing, 2) five trials consisting of a period of eyes closed (30-sec), followed by eyes open (40-sec) while being challenged with a validated visual paradigm (Where's Waldo). Baseline MCAv was unaffected by acute sleep restriction (control: 64±14 cm/s; restricted 61±13 cm/s; p=0.412). MCAv increased with CO2, however, there was no effect of restricted sleep (p=0.488). MCAv increased in response to visual stimulation; the peak NVC response was reduced from control following restricted sleep (control: 16±12 %; restricted: 9±7 %; p=0.008). Despite no effect of acute sleep restriction on resting CBF or the response to CO2 in young men and women, NVC was attenuated following a night of shortened sleep. These data support an important role for sleep in NVC and may have implications for development of neurodegenerative disease states such as Alzheimer's and dementia.