Effect Of Acute Sleep Restriction On Neurovascular Coupling In Healthy Men And Women

PURPOSE: Insufficient sleep is associated with increased risk of Alzheimer’s disease and dementia. Cerebral blood flow is temporally linked to neuronal activity, a phenomenon known as neurovascular coupling. Although the role of sleep is not fully understood, data suggest insufficient sleep may have a detrimental effect on the link between cerebral blood flow and neural activity. Herein we examined the effect of acute sleep restriction on indices of cerebral blood flow and neurovascular coupling in healthy men and women. We hypothesized sleep restriction (4 hours time in bed) would attenuate indices of cerebral blood flow and neurovascular coupling in healthy young adults. METHODS: 7 healthy adults (4 M/3F, 28 ± 9 y, 26 ± 3 kg/m2) completed two morning visits following a night of normal (sleep duration: 446 ± 53 min) or restricted (sleep duration: 296 ± 58 min, p < 0.001) sleep. Middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound) was measured at rest and during five cyclical trials consisting of a period of eyes-closed (30-sec), followed by eyes open (40-sec) while being challenged with a validated visual search paradigm (Where’s Waldo). Neurovascular coupling was assessed as the relative (%) increase in MCAv from baseline during the first 30-sec of visual stimulation as well as area under the curve (AUC). RESULTS: Baseline MCAv was unaffected by acute sleep restriction (control: 67 ± 14 cm/s; restricted 63 ± 15 cm/s; p = 0.49). MCAv increased in response to visual stimulation, and this response was lower following restricted sleep (control: 12 ± 8%; restricted: 4 ± 8%; p = 0.01). Results were consistent when analyzed as AUC from baseline (control: 3125 ± 186 AU; restricted: 2903 ± 250 AU, p = 0.02). CONCLUSION: Despite no effect of acute sleep restriction on resting cerebral blood in healthy men and women, neurovascular coupling was attenuated following a night of shortened sleep. These data support an important role for sleep in neurovascular coupling and have implications for the development of cerebrovascular dysfunction in conditions of short sleep. Future studies should examine the mechanisms by which sleep disrupts neurovascular coupling.