Study Objectives Vascular dysfunction is a hypothesized mechanism linking poor sleep habits to an increased incidence of cardiovascular diseases. However, the vascular profile associated with free-living sleep duration and sleep regularity has not been well elucidated, particularly in young adults. Thus, this study aimed to evaluate the associations between mean sleep duration, regularity in sleep duration, and peripheral vascular function in young adult college students. Methods Fifty-one healthy undergraduate students (20±1 years) completed 14 days of 24-hour wrist actigraphy and subsequent vascular assessments. Macrovascular function was measured using brachial artery flow-mediated dilation (FMD) while microvascular function was measured via passive leg movement (PLM). Results Mean sleep duration was unrelated to FMD and PLM. Conversely, more irregular sleep duration (14-day sleep duration standard deviation [SD]) was unfavorably associated with all three measures of PLM-induced hyperemia (peak leg blood flow [LBF], p=0.01; change in LBF from baseline to peak, p<0.01; LBF area under the curve, p<0.01), and remained significant in regression models which adjusted for sex, body mass index, blood pressure, physical activity, alcohol and caffeine consumption, and sleep duration (all p<0.05). When using a median split to dichotomize “low” and “high” sleep duration SD groups, those demonstrating high variability in sleep duration exhibited ~45% lower PLM responses compared to those demonstrating low variability. Conclusions Irregular sleep duration is associated with poorer microvascular function as early as young adulthood. These findings support the growing body of evidence that irregular sleep patterns may be an independent and modifiable risk factor for cardiovascular disease.

New Findings What is the central question of this study?Is there a racial disparity in macrovascular and/or microvascular function between young black and white women? What is the main finding and its importance?Black women (BLW) demonstrated impaired microvascular function but similar macrovascular function compared to white women (WHW). These findings suggest an identifiable racial disparity in microvascular function between BLW and WHW as early as young adulthood. Microvascular dysfunction is predictive of future cardiovascular disease (CVD) and generally precedes the development of macrovascular dysfunction. Therefore, these findings also suggest that evaluating microvascular function and CVD risk in young, otherwise healthy BLW are important, as there are known racial disparities in CVD morbidity and mortality in black adults. Abstract Black women (BLW) have a higher incidence of cardiovascular disease (CVD) morbidity and mortality compared to white women (WHW). Vascular dysfunction is a non‐traditional risk factor for CVD and BLW demonstrate impaired vascular function when compared to WHW throughout the lifespan. Several previous studies assessed macrovascular and microvascular function in young BLW compared to WHW, but there has been no recent work exploring this disparity in young women using current, up‐to‐date methodologies. Therefore, the purpose of this study was to evaluate both macrovascular and microvascular function as assessed by haemodynamic responses to flow‐mediated dilatation (FMD), following current FMD guidelines, in young adult BLW and WHW. We hypothesized that BLW would demonstrate attenuated macrovascular and microvascular responses to FMD compared to WHW. Macrovascular function was assessed as the percentage dilatation of the brachial artery following FMD occlusion‐cuff release (FMD%). Microvascular function was assessed by total reactive hyperaemia area under the curve (RH‐AUC), calculated as the cumulative increase in brachial artery blood flow above baseline following FMD occlusion‐cuff release. Participants were tested in the morning hours during the early follicular phase of their menstrual cycle. Twenty‐eight young, apparently healthy women completed the study: 17 WHW (23 ± 4 years) and 11 BLW (24 ± 5 years). FMD% was lower in BLW (WHW: 8.0 ± 1.6, BLW: 6.2 ± 2.4%; P = 0.02), but significance was abolished when FMD% was normalized for shear (WHW: 0.1230 ± 0.0388, BLW: 0.1132 ± 0.0405; P = 0.53). RH‐AUC was lower in BLW (WHW: 438 ± 133, BLW: 268 ± 66 ml/min; P < 0.001). Young, otherwise healthy BLW demonstrated impaired microvascular function compared to WHW.

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Background Sleep irregularity is predictive of poor health outcomes, and particularly those of cardiometabolic origins. The immune system is implicated in the pathogenesis of cardiometabolic diseases, however the relation between sleep regularity and immune cell profile is unclear. Methods and results Forty-two healthy young adults (20 ​± ​2 years) completed 14 days of 24-h wrist actigraphy followed by a morning blood sample to evaluate circulating white blood cells (WBC) and subtypes (neutrophils, lymphocytes, monocytes). Sleep regularity was operationalized as the standard deviation (SD) of nightly sleep duration and SD of sleep onset time. Every 60-min increase in sleep duration SD was associated with an estimated 2.7 ​± ​0.60 x10 3 ​cells/μL (p<0.001) increase in total WBC count, while every 60-min increase in sleep onset SD was associated with an estimated 2.4 ​± ​0.60 x10 3 ​cells/μL (p<0.001) increase in WBCs. Sleep duration SD was also associated with lymphocyte count (11.5 ​± ​3.8 ​cells/μL per 1-min increase, p<0.01), while sleep onset SD was associated with neutrophil (34.7 ​± ​9.8 ​cells/μL per 1-min increase, p<0.01) and monocyte counts (3.0 ​± ​0.9 ​cells/μL per 1-min increase, p<0.01). Sleep regularity metrics remained significantly associated with WBCs in a series of regressions which adjusted for sex, body mass index, resting blood pressure, mean sleep duration, physical activity, dietary sodium, and alcohol consumption. Conclusions Unfavorable associations between irregular sleep patterns and circulating immune cells are apparent in young adulthood. These findings contribute to the growing body of evidence suggesting that consistent sleep schedules are an important dimension of sleep and circadian health and may reduce excess chronic disease risk.

Introduction: Misalignment between lifestyle behaviors and endogenous circadian rhythms is associated with elevated nocturnal blood pressure (BP) in experimental studies; however, less is known about free-living (i.e. nonlaboratory) circadian disruption and nocturnal BP. Additionally, sex-specific cardiovascular implications of circadian disruption are unclear.Objective: To examine the associations between restactivity rhythms (RAR), a field-based estimate of circadian disruption, and nocturnal BP characteristics in young men and women.Methods: Fifty participants (20 AE 1 years; 20 men/30 women) underwent 24-h ambulatory BP monitoring following 14 days of wrist actigraphy. RAR variables of interdaily stability (day-to-day consistency in RAR), intradaily variability (within-day fragmentation of RAR), and relative amplitude (difference between peak vs. trough activity) were derived from actigraphy. Multivariable regression models of mean nocturnal SBP, DBP, and SBP dipping were generated to test main associations with RAR variables, and sex  RAR interactions. Daytime BP, race, BMI, physical activity, sleep duration, alcohol, caffeine, and sodium intake were considered as covariates.Results: In the full sample, no main associations between RAR and nocturnal BP characteristics were found. Sex interacted with RAR such that in women, higher interdaily stability (b ¼ À5.39, 95% CI ¼ À10.04 to À0.73, P ¼ 0.024) and relative amplitude (b ¼ À4.78, 95% CI ¼ À9.22 to À0.34, P ¼ 0.036) were both associated with lower nocturnal SBP. Sex-stratified multivariable models of nocturnal BP also revealed associations between interdaily stability and relative amplitude with SBP dipping in women (all P 0.01). No associations were apparent in men. Conclusion:Consistent and high-amplitude RAR are favorably associated with nocturnal BP characteristics in young women.