Abstract 17447: Experimental Sleep Curtailment Increases 24 - Hour Ambulatory Blood Pressure in Healthy Individuals
Introduction: Voluntary sleep curtailment is escalating in the general population. Mounting epidemiological research identifies chronic sleep deficiency as an independent determinant of cardiovascular diseases, with compelling evidence linking short sleep to incident hypertension. Nonetheless, experimental data supporting a causal relationship are scarce.
Hypothesis: We tested the hypothesis that exposure to experimental prolonged sleep restriction would raise 24-hour ambulatory blood pressure (BP) and that this elevation would be driven by baroreflex impairment.
Methods: Fourteen healthy subjects (6 male, age 24±1 years, body mass index 24±1 kg/m2) completed a randomized, controlled, crossover study comprising a 4-day acclimation period, followed by 9 days of experimental sleep restriction (4 hours of sleep/night) or normal sleep, and a 3-day recovery period. Twenty-four hour ambulatory blood pressure monitoring was performed repeatedly throughout the 16-day inpatient protocol. Spontaneous baroreflex sensitivity was estimated by the sequence method.
Results: Both 24-hour systolic (SBP) and diastolic BP (DBP) increased during sleep restriction compared to control sleep (sleep restriction vs normal sleep, SBP/DBP: 118±1/70±1 mmHg vs 115±1/67±1 mmHg, both p<0.001). Analysis of temporal dynamics revealed that BP rose acutely after exposure to short sleep and this increase persisted throughout the entire restricted sleep phase compared to baseline. Neither 24-hour heart rate (p=0.804) nor baroreflex sensitivity varied appreciably (p=0.341).
Conclusions: Prolonged sleep curtailment induces acute and sustained elevations in 24-hour BP in healthy individuals, thus favoring the concept that chronic sleep debt may predispose to development of hypertension. The absence of changes in baroreflex sensitivity suggests that the pressor response is conceivably mediated by different BP-regulatory mechanisms, such as sympathetic activation.
Author Disclosures: N. Covassin: None. J. Bukartyk: None. A.D. Calvin: None. F. Soucek: None. L. Ruzek: None. E.K. St Louis: None. V.K. Somers: Research Grant; Significant; Philips Respironics Foundation. Consultant/Advisory Board; Modest; Respicardia, Sorin Inc, U-Health, Philips, GlaxoSmithKline, Rhonda Grey, Dane Garvin, Biosense Webster. Consultant/Advisory Board; Significant; ResMed.
- © 2016 by American Heart Association, Inc.