Device-estimated sleep metrics do not mediate the relation between race and blood pressure dipping in young black and white 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.

Melatonin supplementation does not alter vascular function or oxidative stress in healthy normotensive adults on a high sodium diet.

High sodium diets (HSD) can cause vascular dysfunction, in part due to increases in reactive oxygen species (ROS). Melatonin reduces ROS in healthy and clinical populations and may improve vascular function. The purpose was to determine the effect of melatonin supplementation on vascular function and ROS during 10 days of a HSD. We hypothesized that melatonin supplementation during a HSD would improve vascular function and decrease ROS levels compared to HSD alone. Twenty-seven participants (13 M/14 W, 26.7 ± 2.9 years, BMI: 23.6 ± 2.0 kg/m2 , BP: 110 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6900 mg sodium/d) supplemented with either 10 mg of melatonin (HSD + MEL) or a placebo (HSD + PL) daily. Brachial artery flow-mediated dilation, a measure of macrovascular function, (HSD + PL: 7.1 ± 3.8%; HSD + MEL: 6.7 ± 3.4%; p = 0.59) and tissue oxygenation index (TSI) reperfusion rate, a measure of microvascular reactivity, (HSD + PL: 0.21 ± 0.06%/s; HSD + MEL: 0.21 ± 0.08%/s; p = 0.97) and TSI area under the curve (HSD + PL: 199899 ± 10,863 a.u.; HSD + MEL: 20315 ± 11,348 a.u.; p = 0.17) were similar at the end of each condition. Neither nitroxide molarity (HSD + PL: 7.8 × 10-5 ± 4.1 × 10-5 mol/L; HSD + MEL: 8.7 × 10-5 ± 5.1 × 10-5 mol/L; p = 0.55) nor free radical number (HSD + PL: 8.0 × 1015 ± 4.4 × 1015 ; HSD + MEL: 9.0 × 1015 ± 4.9 × 1015 ; p = 0.51) were different between conditions. Melatonin supplementation did not alter vascular function or ROS levels while on a HSD in this sample of young healthy normotensive adults.

Sleep Variability, Eating Timing Variability, and Carotid Intima-Media Thickness in Early Adulthood.

Background Day-to-day variability in sleep patterns and eating timing may disrupt circadian rhythms and has been linked with various adverse cardiometabolic outcomes. However, the extent to which variability in sleep patterns and eating timing relate to atherosclerotic development in subclinical stages remains unclear. Methods and Results Generally healthy adults (N=62, 29.3±7.3 years, 66% female) completed 14 days of sleep and dietary assessments via wrist accelerometry and photo-assisted diet records, respectively. Variability in sleep duration, sleep onset, eating onset (time of first caloric consumption), eating offset (time of last caloric consumption), and caloric midpoint (time at which 50% of total daily calories are consumed) were operationalized as the SD across 14 days for each variable. Separate regression models evaluated the cross-sectional associations between sleep and eating variability metrics with end-diastolic carotid intima-media thickness (CIMT) measured via ultrasonography. Models adjusted for age, sex, systolic blood pressure, sleep duration, and total energy intake. Each 60-minute increase in sleep duration SD and sleep onset SD were associated with a 0.049±0.016 mm (P=0.003) and 0.048±0.017 mm (P=0.007) greater CIMT, respectively. Variability in eating onset and offset were not associated with CIMT; however, each 60-minute increase in caloric midpoint SD was associated with a 0.033±0.015 mm greater CIMT (P=0.029). Exploratory post hoc analyses suggested that sleep duration SD and sleep onset SD were stronger correlates of CIMT than caloric midpoint SD. Conclusions Variability in sleep patterns and eating timing are positively associated with clinically relevant increases in CIMT, a biomarker of subclinical atherosclerosis, in early adulthood.

Melatonin supplementation reduces nighttime blood pressure but does not affect blood pressure reactivity in normotensive adults on a high-sodium diet.

High-sodium diets (HSDs) can cause exaggerated increases in blood pressure (BP) during physiological perturbations that cause sympathetic activation, which is related to cardiovascular risk. Melatonin supplementation has been shown to play a role in BP regulation. Our aim was to examine the effects of melatonin taken during an HSD on 24-h BP and BP reactivity during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT). Twenty-two participants (11 men/11 women, 26.5 ± 3.1 yr, BMI: 24.1 ± 1.8 kg/m2, BP: 111 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6,900 mg sodium/day) that was supplemented with either 10 mg/day of melatonin (HSD + MEL) or placebo (HSD + PL). Twenty-four-hour ambulatory BP monitoring was assessed starting on day 9. Mean arterial pressure (MAP) was quantified during the last 30 s of IHG at 40% of maximal voluntary contraction and CPT, and during 3 min of PEI. Melatonin did not change 24-h MAP (HSD + PL: 83 ± 6 mmHg; HSD + MEL: 82 ± 5 mmHg; P = 0.23) but decreased nighttime peripheral (HSD + PL: 105 ± 10 mmHg; HSD + MEL: 100 ± 10 mmHg; P = 0.01) and central systolic BP (HSD + PL: 97 ± 9 mmHg; HSD + MEL: 93 ± 8 mmHg; P = 0.04) on the HSD compared with the HSD + PL. The absolute and percent change in MAP during IHG was not different between conditions (all P > 0.05). In conclusion, melatonin supplementation did not alter BP reactivity to the perturbations tested on an HSD but may be beneficial in lowering BP in young healthy normotensive adults.NEW & NOTEWORTHY BP reactivity was assessed during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT) after 10 days of a high-sodium diet with and without melatonin supplementation. Melatonin did not alter BP reactivity in healthy normotensive men and women. However, melatonin did decrease nighttime peripheral and central systolic BP, suggesting it may be beneficial in lowering BP even in those with a normal BP.

We like to move it, move it: A perspective on performing passive leg movement as a non-invasive assessment of vascular function in pediatric populations.

The passive leg movement (PLM) technique is a non-invasive assessment of lower-limb vascular function. PLM is methodologically simple to perform and utilizes Doppler ultrasound to determine leg blood flow (LBF) through the common femoral artery at rest and in response to passive movement of the lower leg. LBF responses to PLM have been reported to be mostly nitric oxide (NO)-mediated when performed in young adults. Moreover, PLM-induced LBF responses, as well as the NO contribution to PLM-induced LBF responses, are reduced with age and in various diseased populations, demonstrating the clinical utility of this non-invasive test. However, no PLM studies to date have included children or adolescents. Since its conception in 2015, our laboratory has performed PLM on hundreds of individuals including a large cohort of children and adolescents. Thus, the purpose of this perspective article is threefold: 1) to uniquely discuss the feasibility of performing PLM in children and adolescents, 2) to report PLM-induced LBF values from our laboratory in 7-17-year-olds, and 3) to discuss considerations for making comparisons among pediatric populations. Based on our experiences performing PLM in children and adolescents (among various other age groups), it is our perspective that PLM can feasibly be performed in this population. Further, data from our laboratory may be used to provide context for typical PLM-induced LBF values that could be observed in children and adolescents, as well as across the lifespan.

Temporal associations between nightly sleep with daytime eating and activity levels in free-living young adults.

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.

Arterial Stiffness and Endothelial Function are Comparable in Young Healthy Vegetarians and Omnivores.

Vegetarians (VEG) are reported to have lower body weight, blood pressure (BP), and cardiovascular disease (CVD) risk compared with omnivores (OMN), yet the mechanisms remain unclear. A vegetarian diet may protect the vascular endothelium, reducing the risk of atherosclerosis and CVD. This cross-sectional study compared vascular function between OMN and VEG. We hypothesized that VEG would have greater vascular function compared with OMN. Fifty-eight normotensive young healthy adults participated (40 women [W]/18 men [M]; 28 OMN [15W/13M] and 30 VEG [25W/5M]; 26 ± 7 years; BP: 112 ± 11/67 ± 8 mm Hg). Arterial stiffness, assessed by carotid-to-femoral pulse wave velocity (OMN: 5.6 ± 0.8 m/s, VEG: 5.3 ± 0.8 m/s; P = .17) and wave reflection assessed by aortic augmentation index (OMN: 6.9 ± 12.3%, VEG: 8.8 ± 13.5%; P = .57) were not different between groups. However, central pulse pressure (OMN: 32 ± 5; VEG: 29 ± 5 mm Hg; P = .048) and forward wave reflection were greater in omnivores (OMN: 26 ± 3; VEG: 24 ± 3 mm Hg; P = .048). Endothelial-dependent dilation measured by brachial artery flow-mediated dilation was not different between groups (OMN: 6.0 ± 2.9%, VEG: 6.9 ± 3.3%; P = .29). Percent change in femoral blood flow from baseline during passive leg movement, another assessment of nitric oxide-mediated endothelial dilation, was similar between groups (OMN: 203 ± 88 mL/min, VEG: 253 ± 192 mL/min; P = .50). These data suggest that in healthy young adults, normotensive VEG do not have significantly improved vascular function compared with OMN; however, they have a lower central pulse pressure and forward wave amplitude which may lower the risk of future CVD.

Associations between noninvasive upper- and lower-limb vascular function assessments: extending the evidence to young women.

Brachial artery (BA) flow-mediated dilation (FMD) is a well-established measure of peripheral vascular function prognostic of future cardiovascular events. The vasodilatory response to FMD (FMD%) reflects upper-limb conduit artery function, whereas reactive hyperemia (RH) following cuff-occlusion release reflects upper-limb resistance artery function. Comparatively, passive leg movement (PLM) is a newer, increasingly utilized assessment of lower-limb resistance artery function. To increase its clinical utility, PLM-induced leg blood flow (LBF) responses have been compared with hemodynamic responses to FMD, but only in men. Therefore, the purpose of this study was to retrospectively compare LBF responses to FMD% and RH responses in women. We hypothesized that LBF responses would be positively associated with both FMD% and RH, but to a greater extent with RH. FMD and PLM were performed on 72 women (23 ± 4 yr). Arterial diameter and blood velocity were assessed using Doppler ultrasound. Pearson correlation coefficients were used to evaluate associations. Measures of resistance artery function were weakly positively associated: change in BA blood flow ΔBABF and ΔLBF (r = 0.33, P < 0.01), BABF area under the curve (BABF AUC) and LBF AUC (r = 0.33, P < 0.01), and BABFpeak and LBFpeak (r = 0.37, P < 0.01). However, FMD% was not associated with any index of PLM (all P > 0.30). In women, indices of resistance artery function in the upper- and lower limbs were positively associated. However, contrary to the previous work in men, upper-limb conduit artery function was not associated with lower-limb resistance artery function suggesting these assessments capture different aspects of vascular function and should not be used interchangeably in women.NEW & NOTEWORTHY Upper- and lower-limb indices of resistance artery function are positively associated in young women when assessed by reactive hyperemia following brachial artery flow-mediated dilation (FMD) cuff-occlusion release and leg blood flow responses to passive leg movement (PLM), respectively. However, despite previous data demonstrating a positive association between upper-limb conduit artery function assessed by FMD and lower-limb resistance artery function assessed by PLM in young men, these measures do not appear to be related in young women.

Impact of angiotensin receptor-neprilysin inhibition on vascular function in heart failure with reduced ejection fraction: A pilot study.

The mechanisms for the benefits of Angiotensin Receptor Neprilysin Inhibition (ARNi) in heart failure patients with reduced ejection fraction (HFrEF) are likely beyond blood pressure reduction. Measures of vascular function such as arterial stiffness and endothelial function are strong prognostic markers of cardiovascular outcomes in HFrEF, yet the impact of ARNi on vascular health remains to be explored. We hypothesized that arterial stiffness and endothelial function would improve after 12 weeks of ARNi in HFrEF. We tested 10 stable HFrEF patients at baseline and following 12 weeks of ARNi [64 ± 9 years, Men/Women: 9/1, left ventricular ejection fraction (EF): 28 ± 6%] as well as 10 stable HFrEF patients that remained on conventional treatment (CON: 60 ± 7 years, Men/Women: 6/4, EF: 31 ± 5%; all p = NS). Arterial stiffness was assessed via carotid-femoral pulse wave velocity (PWV) and endothelial function was assessed via brachial artery flow-mediated dilation (FMD). PWV decreased after 12 weeks of ARNi (9.0 ± 2.1 vs. 7.1 ± 1.2 m/s; p < 0.01) but not in CON (7.0 ± 2.4 vs. 7.5 ± 2.3 m/s; p = 0.35), an effect that remained when controlling for reductions in mean arterial pressure (p < 0.01). FMD increased after 12 weeks of ARNi (2.2 ± 1.9 vs. 5.5 ± 2.1%; p < 0.001) but not in CON (4.8 ± 3.8 vs. 5.4 ± 3.4%; p = 0.34). Baseline PWV (p = 0.06) and FMD (p = 0.07) were not different between groups. These preliminary data suggest that 12 weeks of ARNi therapy may reduce arterial stiffness and improve endothelial function in HFrEF. Thus, the findings from this pilot study suggest that the benefits of ARNi are beyond blood pressure reduction and include improvements in vascular function.

Subjective sleep score is associated with central and peripheral blood pressure values in children aged 7-12 years.

Shortened and poor-quality sleep have emerged as non-traditional risk factors for the development of hypertension in adults, and it is likely these relations extend to paediatric populations when evaluating sleep subjectively. Therefore, we aimed to evaluate subjective sleep metrics and their associations with central and peripheral blood pressure (BP) values in children. We hypothesized that poor-quality sleep and short sleep duration would be associated with elevated pressures in healthy children. Subjective sleep habits and sleep duration were evaluated using the Children's Sleep Habits Questionnaire (CSHQ) in 29 children aged 7-12 years (13 male/16 female). A total sleep score was generated by summing subscale scores: a higher score indicates poorer sleep habits. Peripheral BP was measured, and central pressures were estimated using pulse wave analysis. Pearson's r correlations were used to assess relations between total sleep score, sleep duration, and sleep score subscales with BP values. Sleep score was positively associated with central and peripheral systolic pressure (r = 0.43, p = 0.02 and r = 0.41, p = 0.03, respectively), diastolic pressure (r = 0.42, p = 0.02 and r = 0.36, p = 0.05, respectively) and mean arterial pressure (r = 0.40, p = 0.03 and r = 0.36, p = 0.03, respectively). Sleep duration was negatively associated with central and peripheral diastolic pressure (r = -0.40, p = 0.03 and r = -0.41, p = 0.03, respectively). Regarding the CSHQ subscales, daytime sleepiness and parasomnias were consistently positively associated with BP values. These findings support sleep as a primordial prevention target for hypertension and the maintenance of cardiovascular health during childhood. Consideration of a variety of sleep habits using tools such as the CSHQ may provide important insights into early-life cardiovascular risk.

Evidence of reduced peripheral microvascular function in young Black women across the menstrual cycle.

Black women (BLW) have a higher prevalence of cardiovascular disease (CVD) morbidity and mortality compared with White women (WHW). A racial disparity in CVD risk has been identified early in life as young adult BLW demonstrate attenuated vascular function compared with WHW. Previous studies comparing vascular function between premenopausal WHW and BLW have been limited to the early follicular (EF) phase of the menstrual cycle, which may not reflect their vascular function during other menstrual phases. Therefore, we evaluated peripheral microvascular function in premenopausal WHW and BLW using passive leg movement (PLM) during three menstrual phases: EF, ovulation (OV), and mid-luteal (ML). We hypothesized that microvascular function would be augmented during the OV and ML phases compared with the EF phase in both groups, but would be attenuated in BLW compared with WHW at all three phases. PLM was performed on 26 apparently healthy premenopausal women not using hormonal contraceptives: 15 WHW (23 ± 3 yr), 11 BLW (24 ± 5 yr). There was a main effect of race on the overall change in leg blood flow (ΔLBF) (P = 0.01) and leg blood flow area under the curve (LBF AUC) (P = 0.02), such that LBF was lower in BLW. However, there was no effect of phase on ΔLBF (P = 0.69) or LBF AUC (P = 0.65), nor an interaction between race and phase on ΔLBF (P = 0.37) or LBF AUC (P = 0.75). Despite peripheral microvascular function being unchanged across the menstrual cycle, a racial disparity was apparent as microvascular function was attenuated in BLW compared with WHW across the menstrual cycle.NEW & NOTEWORTHY This is the first study to compare peripheral microvascular function between young, otherwise healthy Black women and White women at multiple phases of the menstrual cycle. Our novel findings demonstrate a significant effect of race on peripheral microvascular function such that Black women exhibit significant attenuations in microvascular function across the menstrual cycle compared with White women.

Consistency where it counts: Sleep regularity is associated with circulating white blood cell count in young adults.

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 â€‹± â€‹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 â€‹± â€‹0.60 x103 â€‹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 â€‹± â€‹0.60 x103 â€‹cells/µL (p<0.001) increase in WBCs. Sleep duration SD was also associated with lymphocyte count (11.5 â€‹± â€‹3.8 â€‹cells/µL per 1-min increase, p<0.01), while sleep onset SD was associated with neutrophil (34.7 â€‹± â€‹9.8 â€‹cells/µL per 1-min increase, p<0.01) and monocyte counts (3.0 â€‹± â€‹0.9 â€‹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.

Actigraphy-derived rest--activity rhythms are associated with nocturnal blood pressure in young women.

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 rest--activity rhythms (RAR), a field-based estimate of circadian disruption, and nocturnal BP characteristics in young men and women. METHODS: Fifty participants (20 ±â€Š1 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 (ß = -5.39, 95% CI = -10.04 to -0.73, P = 0.024) and relative amplitude (ß = -4.78, 95% CI = -9.22 to -0.34, P = 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.

Young black women demonstrate impaired microvascular but preserved macrovascular function compared to white women.

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.

Rest-activity rhythms in emerging adults: implications for cardiometabolic health.

Emerging adulthood (18-25 years) represents a window of opportunity to modify the trajectory of cardiometabolic disease risk into older adulthood. Not known is the extent to which rest-activity rhythms (RAR) may be related to biomarkers of cardiometabolic health in this population. In this cross-sectional, observational study, 52 healthy emerging adults wore wrist accelerometers (14 consecutive days; 24 h/day) for assessment of nonparametric RAR metrics, including interdaily stability (IS; day-to-day RAR consistency), intradaily variability (IV; within-day RAR fragmentation), and relative amplitude (RA; robustness of RAR), as well as autocorrelation (correlation of rest/activity levels at 24-h lag-times). Cardiometabolic biomarkers, including body mass index (BMI), body fat percentage, blood pressure (BP), fasting lipids, glucose, and C-reactive protein (CRP) were assessed. Additional measures including physical activity, sleep duration, and habitual caffeine and alcohol consumption were also evaluated. A series of multivariable regression models of cardiometabolic biomarkers were used to quantify associations with RAR metrics. On average, participants were 20 ± 1 years of age (21 males, 31 females), non-obese, and non-hypertensive. All were nonsmokers and free of major diseases or conditions. In separate models, which adjusted for sex, BMI, moderate-vigorous physical activity, sleep duration, caffeine, and alcohol consumption, IS was inversely associated with total cholesterol (p ≤ 0.01) and non-HDL cholesterol (p < .05), IV was positively associated with CRP (p < .05), and autocorrelation was inversely associated with total cholesterol (p < .05) and CRP (p < .05). Conversely, associations between RA and cardiometabolic biomarkers were nonsignificant after adjustment for BMI, alcohol, and caffeine consumption. In conclusion, RAR metrics, namely, a higher IS, lower IV, and higher autocorrelation, emerged as novel biomarkers associated with more favorable indices of cardiometabolic health in this sample of apparently healthy emerging adults.

Sleep duration regularity, but not sleep duration, is associated with microvascular function in college students.

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.

Short-term water deprivation attenuates the exercise pressor reflex in older female adults.

Older adults have reduced fluid intake and impaired body fluid and electrolyte regulation. Older female adults exhibit exaggerated exercise blood pressure (BP) responses, which is associated with an increased risk of adverse cardiovascular events. However, it is unclear if dysregulated body fluid homeostasis contributes to altered exercise BP responses in older female adults. We tested the hypothesis that short-term water deprivation (WD) increases exercise BP responses in older female adults. Fifteen female adults (eight young [25 ± 6 years] and seven older [65 ± 6 years]) completed two experimental conditions in random crossover fashion; a euhydration control condition and a stepwise reduction in water intake over three days concluding with a 16-hr WD period. During both trials, beat-to-beat BP (photoplethysmography) and heart rate (electrocardiogram) were continuously assessed during rest, handgrip exercise (30% MVC), and post-exercise ischemia (metaboreflex isolation). At screening, older compared to young female adults had greater systolic and diastolic BP (p ≤ .02). Accelerometer-assessed habitual physical activity was not different between groups (p = .65). Following WD, 24-hr urine flow rate decreased, whereas thirst, urine specific gravity, and plasma osmolality increased (condition: p < .05 for all), but these WD-induced changes were not different between age groups (interaction: p ≥ .31 for all). Resting systolic and diastolic BP values were higher in older compared to young adults (p < .01 for both), but were not different between experimental conditions (p ≥ .20). In contrast to our hypothesis, WD was associated with attenuated systolic BP responses during handgrip exercise (post hoc: p < .01) and post-exercise ischemia (post hoc: p = .03) in older, but not young, female adults. These data suggest that reduced water intake-induced challenges to body fluid homeostasis do not contribute to exaggerated exercise BP responses in post-menopausal female adults.

Passive leg movement in chronic obstructive pulmonary disease: evidence of locomotor muscle vascular dysfunction.

Chronic obstructive pulmonary disease (COPD), characterized by pulmonary dysfunction, is now also recognized to be associated with free radical-mediated vascular dysfunction. However, as previous investigations have utilized the brachial artery flow-mediated dilation technique, whether such vascular dysfunction exists in the locomotor muscle of patients with COPD remains unclear. Therefore, in patients with COPD (n = 13, 66 ± 6 yr) and healthy age- and sex-matched control subjects (n = 12, 68 ± 6 yr), second-by-second measurements of leg blood flow (LBF) (ultrasound Doppler), mean arterial pressure (MAP) (Finapres), and leg vascular conductance (LVC) were recorded before and during both 2 min of continuous upright seated continuous-movement passive leg movement (PLM) and a single-movement PLM (sPLM). In response to PLM, both peak change in LBF (COPD 321 ± 54, Control 470 ± 55 ∆mL/min) and LVC (COPD 3.0 ± 0.5, Control 5.4 ± 0.5 ∆mL·min-1·mmHg-1) were significantly attenuated in patients with COPD compared with control subjects (P < 0.05). This attenuation in the patients with COPD was also evident in response to sPLM, with peak change in LBF tending to be lower (COPD 142 ± 26, Control 169 ± 14 ∆mL/min) and LVC being significantly lower (P < 0.05) in the patients than the control subjects (COPD 1.6 ± 0.4, Control 2.5 ± 0.3 ∆mL·min-1·mmHg-1). Therefore, utilizing both PLM and sPLM, this study provides evidence of locomotor muscle vascular dysfunction in patients with COPD, perhaps due to redox imbalance and reduced nitric oxide bioavailability, which is in agreement with an increased cardiovascular disease risk in this population. This locomotor muscle vascular dysfunction, in combination with the clearly dysfunctional lungs, may contribute to the exercise intolerance associated with COPD.NEW & NOTEWORTHY Utilizing both the single and continuous passive leg movement (PLM) models, which induce nitric oxide (NO)-dependent hyperemia, this study provides evidence of vascular dysfunction in the locomotor muscle of patients with chronic obstructive pulmonary disease (COPD), independent of central hemodynamics. This impaired hyperemia may be the result of an oxidant-mediated attenuation in NO bioavailability. In addition to clearly dysfunctional lungs, vascular dysfunction in locomotor muscle may contribute to the exercise intolerance associated with COPD and increased cardiovascular disease risk.

Strong Relationship Between Vascular Function in the Coronary and Brachial Arteries.

Early detection of coronary artery dysfunction is of paramount cardiovascular clinical importance, but a noninvasive assessment is lacking. Indeed, the brachial artery flow-mediated dilation test only weakly correlated with acetylcholine-induced coronary artery function ( r=0.36). However, brachial artery flow-mediated dilation methodologies have, over time, substantially improved. This study sought to determine if updates to this technique have improved the relationship with coronary artery function and the noninvasive indication of coronary artery dysfunction. Coronary artery and brachial artery function were assessed in 28 patients referred for cardiac catheterization (61±11 years). Coronary artery function was determined by the change in artery diameter with a 1.82 µg/min intracoronary acetylcholine infusion. Based on the change in vessel diameter, patients were characterized as having dysfunctional coronary arteries (>5% vasoconstriction) or relatively functional coronary arteries (<5% vasoconstriction). Brachial artery function was determined by flow-mediated dilation, adhering to current guidelines. The acetylcholine-induced change in vessel diameter was smaller in patients with dysfunctional compared with relatively functional coronary arteries (-11.8±4.6% versus 5.8±9.8%, P<0.001). Consistent with this, brachial artery flow-mediated dilation was attenuated in patients with dysfunctional compared with relatively functional coronaries (2.9±1.9% versus 6.2±4.2%, P=0.007). Brachial artery flow-mediated dilation was strongly correlated with the acetylcholine-induced change in coronary artery diameter ( r=0.77, P<0.0001) and was a strong indicator of coronary artery dysfunction (receiver operator characteristic=78%). The current data support that updates to the brachial artery flow-mediated dilation technique have strengthened the relationship with coronary artery function, which may now provide a clinically meaningful indication of coronary artery dysfunction.