Objectively Assessed Habitual Sleep Duration Is Associated with Peripheral and Central Blood Pressure in Non‐Hypertensive Young Adults

Abstract

Habitual short sleep duration (<6 hrs/night) has been reliably shown to predict higher blood pressure (BP) and hypertension in adults. However, most studies evaluating this association in free‐living adults (i.e., non‐experimental settings) have: 1. relied on subjective sleep duration estimates or actigraphy‐derived estimates spanning ≤7 days; 2. failed to consider central BP, which has been reported to provide greater insight into future cardiovascular risk as compared to peripheral BP; and 3. neglected to consider the influence of sleep duration the night prior to BP evaluation despite evidence that episodes of acute sleep loss (e.g., experimentally shortened sleep duration) increases peripheral BP values in young adults. Therefore, the purpose of the present study was to investigate the association between objectively measured habitual sleep duration (HSD) with peripheral and central BP in non‐hypertensive, non‐shift working, apparently healthy, young adults free of sleep disorders. This study also examined whether changes in sleep duration the night before BP measurement (ΔSD) influenced these relationships. We hypothesized that shorter HSD would significantly predict higher peripheral and central BP values, but that the association would be weakened after adjusting for ΔSD the night before assessment. Sleep duration (the total time scored as sleep between sleep onset and offset) was measured via wrist‐worn actigraphy for 14 consecutive nights (days 1‐14) and mean HSD was generated. Additionally, ΔSD was calculated as the difference between sleep duration the night before testing (day 14) and mean sleep duration across days 1‐13. On the morning following the final night of sleep monitoring (day 15), resting supine peripheral BP was measured, and central BP was estimated using pulse wave analysis. BP measures included systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP). The associations between HSD and peripheral and central BP values were evaluated using linear regression models of BP values. Regression models were further adjusted for ΔSD to determine whether this influenced these associations. The analytic sample consisted of 28 participants (11M/17F; 27±7 yrs). Mean HSD for the sample was 6.91±0.74 hours per night. ΔSD sleep was ‐25±53 minutes, indicating that on average, sleep duration was shorter the night before testing. Shorter mean HSD significantly predicted both higher peripheral BP (SPB: β= ‐6.44, SE= 2.11, p< 0.01; DBP: β= ‐5.03, SE= 1.63, p< 0.01; MAP: β= ‐5.42, SE= 1.63, p< 0.01) and higher central BP (cSBP: β= ‐5.79, SE= 2.00, p< 0.01; cDBP: β= ‐5.06, SE= 1.59, p< 0.01; cMAP: β= ‐5.45, SE= 1.74, p< 0.01) values. When models were adjusted for ΔSD, HSD remained a significant predictor of peripheral BP (SPB: β= ‐5.45, SE= 2.06, p= 0.01; DBP: β= ‐4.50, SE= 1.66, p= 0.01; MAP: β= ‐4.71, SE= 1.60, p= 0.01) and central BP (cSBP: β= ‐4.91, SE= 2.00, p= 0.02; cDBP: β= ‐4.57, SE= 1.62, p= 0.01; cMAP: β= ‐4.81, SE= 1.75, p= 0.01). Our findings support prior evidence that HSD plays a key role in peripheral BP regulation and newly demonstrate that HSD is also significantly inversely associated with central BP values. Acute alterations in sleep duration the night prior to BP evaluation has a minimal influence on the association between HSD and BP in young, otherwise healthy free‐living adults.