Explore the vast range of titles available.

Hypertension diagnosed via peripheral (brachial) blood pressure (pBP) is a strong independent predictor of overt cardiovascular disease (CVD). However, central (aortic) blood pressure (cBP), which is influenced by arterial stiffness, may be more strongly associated with CVD risk. Young Black women (BLW) demonstrate higher pBP than White women (WHW), but investigations of racial differences in central haemodynamics and arterial stiffness in young women are lacking. We assessed pBP, central haemodynamics and arterial stiffness in young, non‐hypertensive BLW and WHW. We hypothesized that pBP, central haemodynamics (cBP, augmentation pressure (AP), augmentation index normalized to a heart rate of 75 beats per minute (AIx75), arterial wave reflections), and arterial stiffness (carotid–femoral pulse wave velocity (cf‐PWV)) would be higher in BLW. Under standardized resting conditions, supine brachial pBP was measured, and central haemodynamics were estimated via pulse wave analysis using partial cuff inflation. cf‐PWV was assessed via simultaneous carotid artery applanation tonometry and partial cuff inflation over the femoral artery. Participants were young, apparently healthy women who self‐identified their race as Black (BLW: n  = 44) or White (WHW: n  = 40). Systolic pBP ( P  = 0.04) and diastolic pBP ( P  < 0.01) were higher among BLW. Systolic cBP ( P  < 0.01), diastolic cBP ( P  < 0.01), heart rate ( P  < 0.001), AP ( P  = 0.02), AIx75 ( P  < 0.001), arterial wave reflection magnitude ( P  = 0.40) and cf‐PWV ( P  = 0.04) were all higher among BLW. Findings demonstrate elevations in pBP, central haemodynamics and arterial stiffness in young BLW versus WHW. Central haemodynamics and arterial stiffness may be promising targets in the early assessment of CVD risk in young BLW. What is the central question of this study? Are there racial differences in peripheral blood pressure, central haemodynamics and arterial stiffness between young, generally healthy, non‐hypertensive Black and White women? What is the main finding and its importance? Findings demonstrate increased peripheral blood pressure (BP), central BP, augmentation index, and arterial stiffness in young Black women compared with White women.  It is well‐documented that Black women have the highest prevalence of hypertension, a major but modifiable risk factor for cardiovascular disease (CVD). Increased central BP and arterial stiffness are strong independent risk factors for CVD and findings indicate that these may also be important intervention targets for the prevention of CVD in Black women.

Short, disturbed, and irregular sleep may contribute to blunted nocturnal blood pressure (BP) dipping, a predictor of cardiovascular disease. Black women (BLW) demonstrate less BP dipping and poorer sleep health than White women (WHW). However, it remains unclear whether device‐estimated sleep health metrics mediate the relation between race and BP dipping in young women. We hypothesized that the relation between race and BP dipping would be partly mediated by sleep health metrics of sleep duration, sleep efficiency, and sleep regularity. Participants (20 BLW, 17 WHW) were 18–29 years old, normotensive, nonobese, and without evidence of sleep disorders. Systolic and diastolic BP dipping were derived from 24‐h ambulatory BP monitoring. Habitual sleep duration and sleep efficiency were estimated via 14 days of wrist actigraphy. Sleep duration regularity was calculated as the standard deviation (SD) of nightly sleep duration (SDSD). Sleep timing regularity metrics were calculated as the SD of sleep onset and sleep midpoint (SMSD). Mediation analysis tested the mediating effect of each sleep metric on the relation between race and BP dipping. BLW experienced less systolic ( P  = .02) and diastolic ( P  = .01) BP dipping. Sleep duration ( P  = .14) was not different between groups. BLW had lower sleep efficiency ( P  < .01) and higher SDSD ( P  = .02), sleep onset SD ( P  < .01) and SMSD ( P  = .01). No sleep metrics mediated the relation between race and BP dipping (all indirect effects P  > .38). In conclusion, mediation pathways of sleep health metrics do not explain racial differences in nocturnal BP dipping between young BLW and WHW.

Abstract Study Objectives Vascular dysfunction is a hypothesized mechanism linking poor sleep habits to an increased incidence of cardiovascular diseases (CVDs). 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 with 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 CVD.

Abstract Study Objectives This study aimed to quantify the temporal associations between nightly sleep quantity and timing with daytime eating behavior and activity levels in free-living (i.e. non-experimental) settings. Methods Generally healthy young adults (N = 63; 28.9 ± 7.1 years) completed concurrent sleep (wrist actigraphy), eating (photo-assisted diet records), and activity (waist actigraphy) assessments over 14 days. Multilevel models quantified the associations between nightly sleep (total sleep time, timing of sleep and wake onset) with next-day eating behavior (diet quality, caloric intake, timing of eating onset/offset, eating window duration) and activity levels (total physical activity, sedentary time). Associations in the reverse direction (i.e. eating and activity predicting sleep) were explored. Models adjusted for demographic and behavioral confounders and accounted for multiple testing. Results At within- and between-subject levels, nights with greater-than-average total sleep time predicted a shorter eating window the next day (all p ≤ 0.002). Later-than-average sleep and wake timing predicted within- and between-subject delays in next-day eating onset and offset, and between-subject reductions in diet quality and caloric intake (all p ≤ 0.008). At within- and between-subject levels, total sleep time was bidirectionally, inversely associated with sedentary time (all p < 0.001), while later-than-average sleep and wake timing predicted lower next-day physical activity (all p ≤ 0.008). Conclusions These data underscore the complex interrelatedness between sleep, eating behavior, and activity levels in free-living settings. Findings also suggest that sleep exerts a greater influence on next-day behavior, rather than vice versa. While testing in more diverse samples is needed, these data have potential to enhance health behavior interventions and maximize health outcomes. Graphical Abstract

Abstract Study Objectives We tested associations between serum 25-hydroxyvitamin D concentration ([25(OH)D]) and device-estimated sleep metrics, including sleep duration, sleep efficiency, sleep duration regularity, sleep timing regularity, and sleep regularity index (SRI), in young and early middle-aged adults (18–45 years). We also assessed the mediating effect of nighttime melatonin (urinary 6-sulfatoxymelatonin (aMT6s) excretion) on these associations. Methods Participants (n = 79) completed 14 days of wrist actigraphy. Fasted blood sampling was performed to quantify serum [25(OH)D]. First morning void was used to quantify overnight urinary aMT6s excretion, normalized to creatinine clearance. Associations between [25(OH)D] and sleep metrics were evaluated using linear regression (model 1). Separate models adjusted for age, sex, race, and body fat % (model 2), season of testing, caffeine consumption, and education level (model 3), and device-estimated moderate-to-vigorous physical activity (model 4; n = 68). Results Serum [25(OH)D] was positively associated with sleep duration, sleep efficiency, and SRI, and negatively associated with sleep duration regularity, sleep onset timing regularity, and sleep midpoint timing regularity in model 1 (all p < .03) and model 4 (all p < .02). In model 2, serum [25(OH)D] remained significantly associated with sleep duration only (p = .036). In model 3, serum [25(OH)D] remained significantly associated with all sleep metrics (p < .02) except sleep duration regularity and SRI. Serum [25(OH)D] was not associated with aMT6s:creatinine, indicating no grounds for performing mediation analyses. Conclusions Serum [25(OH)D] is independently associated with several sleep metrics in healthy adults. However, nighttime melatonin concentration did not mediate these associations, thus other mechanistic pathways must be considered. Statement of Significance Here, we utilize 14 days of wrist actigraphy to evaluate cross-sectional associations between serum 25-hydroxyvitamin D ([25(OH)D]) concentration and device-estimated sleep metrics in a sample of healthy adults without evidence of clinical sleep disorders. Our results highlight significant associations between [25(OH)D] and several sleep metrics in this population, extending findings previously observed in only older adults and individuals with sleep disorders. We also newly assess the influence of urinary aMT6s excretion, an indicator of nighttime melatonin production, on the association between [25(OH)D] and sleep, given that melatonin has been proposed as a potential mechanism linking the two. Findings show that nighttime melatonin does not mediate the associations between [25(OH)D] and device-estimated sleep metrics, suggesting other mechanistic pathways should be explored.