Mild sleep restriction increases 24-hour ambulatory blood pressure in premenopausal women with no indication of mediation by psychological effects

Abstract

Background: Studies assessing the impact of sleep restriction (SR) on blood pressure (BP) are limited by short study length, extreme SR (<4 hours a night), and lack of attention to psychological distress as a possible mediator.

Methods: A community-based cohort was assembled with 237 women (age 34.1 ± 13.5 years; body mass index 25.4 ± 5.4 kg/m2), and a randomized, crossover, intervention study was conducted in 41 women (24 completed: age 30.2 ± 6.5 years; body mass index 24.3 ± 2.8 kg/m2) to determine the causal effect of SR on BP. Sleep was maintained as usual (HS) or reduced by 1.5 hours a night (SR) for 6 weeks. In the cohort, associations between sleep and psychosocial factors were evaluated using multivariable models adjusted for demographic and clinical confounders. In the intervention study, in-office BP was measured weekly; ambulatory BP was measured at end point. Psychological factors were assessed at baseline and end point. Mixed-model analyses with total sleep time (TST, main predictor), week and fraction of time spent in physical activity (covariates), and subject (random effect) were performed.

Results: Among the community cohort, higher perceived stress, stressful events and distress, and lower resilience were associated with shorter sleep, worse sleep quality, and greater insomnia symptoms (P < .05). In the intervention, systolic BP increased as TST decreased (TST × week interaction, [coefficient ± standard error] -0.0097 ± 0.0046, P = .036). Wake ambulatory diastolic blood pressure (-0.059 ± 0.022, P = .021) and mean arterial pressure (-0.067 ± 0.023, P = .018) were higher after SR versus HS. Psychological distress variables were not affected by TST and did not mediate the effects of SR on BP.

Conclusions: These results suggest that SR influences CVD risk in women via mechanisms independent of psychological stressors.

Conflict of interest statement

Declaration of competing interest None of the authors have any conflicts of interest to declare. All authors have made substantial contributions to the conception or design of the work, or the acquisition, analysis, or interpretation of the data; drafted or revised the manuscript for important intellectual content; approved the final version; and agree to be accountable for all aspects of the work reported herein. M. P. S. O. and B. A. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Copyright © 2020 Elsevier Inc. All rights reserved.

Figures

Figure 1.

Weekly sleep duration measured by actigraphy during the 6-wk intervention periods (HS, solid line, and SR, hatched line). Panel A represents data from all women who completed the clinical trial (n=24); panel B represents data from women who have provided ambulatory blood pressure measurements (n=17). Week 0 sleep duration represents average sleep duration during the screening period. Data are weekly averages and SD.

Figure 2.

Weekly SBP (panel A) and DBP (panel B) during the 6-wk intervention periods (HS, solid line, and SR, hatched line). Data are unadjusted raw means±SD; n=24. There is a significant sleep x week interaction on SBP (P=0.0048) and trend for main effect of sleep (P=0.061). Twenty-four-hour wake SBP, DBP, and mean arterial pressure after 6 wk of HS (white bars) and SR (black bars) is shown in panel C. Data are unadjusted raw means±SD; n=17 for HS and 14 for SR. * Significantly higher than HS, P<0.05.