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.

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.

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/.