Menstrual and oral contraceptive pill cycles minimally influence vascular function and associated cellular regulation in premenopausal females.

Historical exclusion of females in research has been, in part, due to the perceived influence of natural menstrual (NAT) and oral contraceptive pill (OCP) cycles on vascular outcomes. NAT and OCP cycle phases may influence brachial artery (BA) endothelial function, however, findings are mixed. Minimal research has examined arterial stiffness, smooth muscle, and lower limb endothelial function. The purpose of this study was to investigate the influence of NAT and OCP cycles on cardiovascular outcomes and cellular regulation. Forty-nine premenopausal females (n = 17 NAT, n = 17 second generation OCP, n = 15 third generation OCP) participated in two randomized order visits in the low (LH, early follicular/placebo) and high (HH, midluteal/active) hormone cycle phases. BA and superficial femoral artery (SFA) endothelial function [flow-mediated dilation (FMD) test], smooth muscle function (nitroglycerine-mediated dilation test), and carotid and peripheral (pulse wave velocity) arterial stiffness were assessed. Cultured female human endothelial cells were exposed to participant serum for 24 h to examine endothelial nitric oxide synthase (eNOS) and estrogen receptor-α (ERα) protein content. BA FMD was elevated in the HH vs. LH phase, regardless of group (HH, 7.7 ± 3.5%; LH, 7.0 ± 3.3%; P = 0.02); however, allometric scaling for baseline diameter resulted in no phase effect (HH, 7.6 ± 2.6%; LH, 7.1 ± 2.6%; P = 0.052, d = 0.35). SFA FMD, BA, and SFA smooth muscle function, arterial stiffness, and eNOS and ERα protein content were unaffected. NAT and OCP phases examined have minimal influence on vascular outcomes and ERα-eNOS pathway, apart from a small effect on BA endothelial function partially explained by differences in baseline artery diameter. NEW & NOTEWORTHY Comprehensive evaluation of the cardiovascular system in naturally cycling and second and third generation OCP users indicates no major influence of hormonal phases examined on endothelial function and smooth muscle function in the arteries of the upper and lower limbs, arterial stiffness, or underlying cellular mechanisms. Study findings challenge the historical exclusion of female participants due to potentially confounding hormonal cycles; researchers are encouraged to consider the hormonal environment in future study design.

Acute partial sleep restriction does not impact arterial function in young and healthy humans.

Habitual short sleep durations are associated with several cardiovascular diseases. Experimental research generally supports these findings as metrics of arterial function are impaired after complete deprivation of sleep and after longer periods of partial sleep restriction. The acute influence of a single instance of partial sleep restriction (PSR), however, has not been defined. We evaluated arterial structure and function among 32 university-aged participants on two occasions: once after normal habitual sleep (NS), and again the morning after an acute partial sleep restriction (PSR) intervention involving only 3 h of sleep for a single night. Endothelial function was measured using ultrasonography at the brachial artery via flow-mediated dilatation (FMD), and a ramp peak oxygen uptake test was used to evaluate cardiorespiratory fitness. Blood samples were collected from a subset of participants to investigate the influence of circulatory factors on cellular mechanisms implicated in endothelial function. Sleep duration was lower after a night of PSR compared to NS (P < 0.001); however, there were no appreciable differences in any haemodynamic outcome between conditions. FMD was not different between NS and PSR (NS: 6.5 ± 2.9%; PSR: 6.3 ± 2.9%; P = 0.668), and cardiorespiratory fitness did not moderate the haemodynamic response to PSR (all P > 0.05). Ex vivo cell culture results aligned with in vivo data, showing that acute PSR does not alter intracellular processes involved in endothelial function. No differences in arterial structure or function were observed between NS and acute PSR in healthy and young participants, and cardiorespiratory fitness does not modulate the arterial response to acute sleep restriction.

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives.

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health.Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/.

The impact of the 24-h movement spectrum on vascular remodeling in older men and women: a review.

Aging is associated with increased risk of cardiovascular and cerebrovascular events, which are preceded by early, negative remodeling of the vasculature. Low physical activity is a well-established risk factor associated with the incidence and development of disease. However, recent physical activity literature indicates the importance of considering the 24-h movement spectrum. Therefore, the purpose of this review was to examine the impact of the 24-h movement spectrum, specifically physical activity (aerobic and resistance training), sedentary behavior, and sleep, on cardiovascular and cerebrovascular outcomes in older adults, with a focus on recent evidence (<10 yr) and sex-based considerations. The review identifies that both aerobic training and being physically active (compared with sedentary) are associated with improvements in endothelial function, arterial stiffness, and cerebrovascular function. Additionally, there is evidence of sex-based differences in endothelial function: a blunted improvement in aerobic training in postmenopausal women compared with men. While minimal research has been conducted in older adults, resistance training does not appear to influence arterial stiffness. Poor sleep quantity or quality are associated with both impaired endothelial function and increased arterial stiffness. Finally, the review highlights mechanistic pathways involved in the regulation of vascular and cerebrovascular function, specifically the balance between pro- and antiatherogenic factors, which mediate the relationship between the 24-h movement spectrum and vascular outcomes. Finally, this review proposes future research directions: examining the role of duration and intensity of training, combining aerobic and resistance training, and exploration of sex-based differences in cardiovascular and cerebrovascular outcomes.

Differences in cardiovascular risk factors associated with sex and gender identity, but not gender expression, in young, healthy cisgender adults.

Background: Sex differences exist in cardiovascular disease risk factors including elevated blood pressure and arterial stiffness, and decreased endothelial function in males compared to females. Feminine gender expression may be associated with elevated risk of acute coronary syndrome. However, no study has investigated the associations between sex, gender identity, and gender expression and cardiovascular disease risk factors in young adults. Methods: One hundred and thirty participants (22 ± 3 years) underwent assessments of hemodynamics, arterial stiffness [pulse wave velocity (PWV)], and brachial artery endothelial function (flow-mediated dilation; %FMD). Participants completed a questionnaire capturing sex category (50 male/80 female), gender identity category (49 men/79 women/2 non-binary), and aspects of gender expression assessed by the Bem Sex Role Inventory-30 (39 androgynous/33 feminine/29 masculine/29 undifferentiated). Sex/gender identity category groups were compared using unpaired t-tests and gender expression groups compared using one-way ANOVAs. Results: Resting systolic and mean arterial pressure (p < 0.01) were elevated in males vs. females. Central PWV was elevated in males [median (interquartile range): 6.4 (1.8) vs. 5.8 (2.2) m/s, p = 0.02]; however, leg and arm PWV were not different between sexes. %FMD was elevated in males vs. females, after accounting for a larger baseline artery diameter in males (8.8 ± 3.3% vs. 7.2 ± 3.1%, p = 0.02); since the majority of participants were cisgender, the same results were found examining gender identity (men vs. women). There were no differences across gender expression groups (p > 0.05). Conclusions: Sex/gender identity category, but not gender expression, influence cardiovascular risk factors (blood pressure, arterial stiffness, endothelial function) in cisgender adults; further research is needed in gender-diverse populations.

Statistical Inferences Using Effect Sizes in Human Endothelial Function Research.

INTRODUCTION: Magnitudes of change in endothelial function research can be articulated using effect size statistics. Effect sizes are commonly used in reference to Cohen's seminal guidelines of small (d = 0.2), medium (d = 0.5), and large (d = 0.8). Quantitative analyses of effect size distributions across various research disciplines have revealed values differing from Cohen's original recommendations. Here we examine effect size distributions in human endothelial function research, and the magnitude of small, medium, and large effects for macro and microvascular endothelial function. METHODS: Effect sizes reported as standardized mean differences were extracted from meta research available for endothelial function. A frequency distribution was constructed to sort effect sizes. The 25th, 50th, and 75th percentiles were used to derive small, medium, and large effects. Group sample sizes and publication year from primary studies were also extracted to observe any potential trends, related to these factors, in effect size reporting in endothelial function research. RESULTS: Seven hundred fifty-two effect sizes were extracted from eligible meta-analyses. We determined small (d = 0.28), medium (d = 0.69), and large (d = 1.21) effects for endothelial function that corresponded to the 25th, 50th, and 75th percentile of the data distribution. CONCLUSION: Our data indicate that direct application of Cohen's guidelines would underestimate the magnitude of effects in human endothelial function research. This investigation facilitates future a priori power analyses, provides a practical guiding benchmark for the contextualization of an effect when no other information is available, and further encourages the reporting of effect sizes in endothelial function research.