Sleep deprivation and sleep intensity exert distinct effects on cerebral vasomotion and brain pulsations driven by the respiratory and cardiac cycles.

The flow of cerebrospinal fluid (CSF) through the brain is driven by cerebral vasomotion, along with respiratory and cardiac forces. Growing evidence suggests that sleep facilitates this flow, yet the role of homeostatic sleep mechanisms remains largely unknown. In a circadian-controlled sleep and sleep deprivation study in humans, we used accelerated neuroimaging to investigate how sleep pressure and slow-wave-rich sleep affect low-frequency brain pulsations (LFPs; 0.012-0.034 Hz) as well as brain pulsations originating from the respiratory and cardiac cycles. These pulsations cause movement of CSF and brain tissue which may facilitate waste clearance. We also examined the origin of LFPs through pharmacological vasodilation of the cerebral vasculature with the adrenergic antagonist carvedilol in a randomized, cross-over, double-blinded, placebo-controlled design (NCT03576664). We find that sleep deprivation increases LFPs more than nonrapid eye movement (NREM) sleep does, with LFPs during sleep correlating with cognitive measures of sleep pressure. Conversely, NREM sleep (combined stages N2 and N3) enhances brain pulsations driven by the respiration and cardiac cycles, with more pronounced effects in gray and white matter than in the ventricles. The strength of these brain pulsations escalates with sleep depth (N3 > N2) and correlates with EEG delta power, a measure of slow wave activity. Moreover, carvedilol dampens LFPs, supporting that these reflect cerebral vasomotion. In summary, our findings indicate that heightened sleep pressure promotes vasomotion, whereas slow-wave-rich sleep amplifies respiration- and cardiac-driven brain pulsations, possibly indicating increased CSF flow to the brain. Together, this suggests that homeostatic sleep mechanisms are integral to human brain fluid dynamics and potentially also waste clearance.