Background-We measured cardiovagal baroreflex gain and its vascular mechanical and neural components during dynamic baroreflex engagement in 10 young untrained men, 6 older untrained men, and 12 older, physically active men. Methods and Results-Our newly developed assessment of beat-to-beat carotid diameters during baroreflex engagement estimates the mechanical transduction of pressure into barosensory stretch (⌬diameter/⌬pressure), the neural transduction of stretch into vagal outflow (⌬R-R interval/⌬diameter), and conventional integrated cardiovagal baroreflex gain (⌬R-R interval/⌬pressure). Integrated gain was lower in older untrained men than in young untrained men (6.8Ϯ1.2 versus 15.7Ϯ1.8 ms/mm Hg) due to both lower mechanical (9.1Ϯ1.0 versus 17.1Ϯ2.4 mm Hg/m) and lower neural (0.57Ϯ0.10 versus 0.90Ϯ0.10 ms/m) transduction. Integrated gain in older active men (13.3Ϯ2.7 ms/mm Hg) was comparable to that in young untrained men. This was achieved through mechanical transduction (12.1Ϯ1.4 mm Hg/m) that was modestly higher than that in older untrained men and neural transduction (1.00Ϯ0.20 ms/m) comparable to that in young untrained men. Across groups, both mechanical and neural components were related to integrated gain; however, the neural component carried greater predictive weight (␤ϭ0.789 versus 0.588). Conclusions-Both vascular and neural deficits contribute to age-related declines in cardiovagal baroreflex gain; however, long-term physical activity attenuates this decline by maintaining neural vagal control. Key Words: aging Ⅲ nervous system, autonomic Ⅲ carotid arteries A recent report suggested aerobic exercise attenuates carotid arterial stiffening with age. 1 The importance of this observation is the impact stiffness may have on cardiovascular function. It has been hypothesized that barosensory vessel stiffening would profoundly affect autonomic circulatory control 2 and reduce cardiovagal baroreflex gain with age. 3,4 Indeed, some data indicate a direct relation between arterial compliance and cardiovagal baroreflex control. 5,6 However, basal estimates of vascular stiffness may not represent the mechanical stresses placed on barosensory vessels during the dynamic pressure changes that characterize baroreflex engagement. [7][8][9] Moreover, compromised neural function may play as prominent a role as decreased vascular mechanical function in reducing baroreflex gain with age. 10 We determined the impact of altered carotid stiffness with age and habitual physical activity on baroreflex function using our recently developed, novel approach to quantify vascular and neural components during dynamic baroreflex engagement. 11 Concurrent beat-by-beat arterial pressures, carotid diameters, and R-R intervals during vasoactive drug infusions provide insight into key steps of cardiovagal baroreflex regulation: mechanical transduction of pressure into barosensory vessel stretch and neural transduction of stretch into vagal outflow. On the basis of previous observations, 1 we hypothesized that lower cardiovagal bar...

Abstract-Traditionally, arterial baroreflex control of vagal neural outflow is quantified by heart period responses to falling and/or rising arterial pressures (ms/mm Hg). However, it is arterial pressure-dependent stretch of barosensory vessels that determines afferent baroreceptor responses, which, in turn, generate appropriate efferent cardiac vagal outflow. Thus, mechanical transduction of pressure into barosensory vessel stretch and neural transduction of stretch into vagal outflow are key steps in baroreflex regulation that determine the conventional integrated input-output relation. We developed a novel technique for direct estimation of gain in both mechanical and neural components of integrated cardiac vagal baroreflex control. Concurrent, beat-by-beat measures of arterial pressures (Finapres), carotid diameters (B-mode ultrasonography), and R-R intervals (ECG lead II) were made during bolus vasoactive drug infusions (modified Oxford technique) in 16 healthy humans. The systolic carotid diameter/pressure relationship (r 2 ϭ0.79Ϯ0.008, meanϮSEM) provided a gain estimate of dynamic mechanical transduction of pressure into a baroreflex stimulus. The R-R interval/systolic diameter relationship (r 2 ϭ0.77Ϯ0.009) provided a gain estimate of afferent-efferent neural transduction of baroreflex stimulus into a vagal response. Variance between repeated measures for both estimates was no different than that for standard gain (PϾ0.40). Moreover, in these subjects, the simple product of the 2 estimates almost equaled standard baroreflex gain (ms/mm Hgϭ0.98xϩ2.27; r 2 ϭ0.93, Pϭ0.001). This technique provides reliable information on key baroreflex components not distinguished by standard assessments and gives insight to dynamic mechanical and neural events during acute changes in arterial pressure. Key Words: arterial pressure Ⅲ carotid arteries Ⅲ ultrasonography D epressed baroreflex sensitivity is associated with hypertension, 1 heart disease, 2 diabetes, and other pathophysiological states, 3 attesting that appropriate baroreflex regulation of autonomic outflow is crucial to maintenance of cardiovascular health and homeostasis. Traditionally, cardiac-vagal baroreflex sensitivity or gain has been quantified by the magnitude of heart period responses to falling and/or rising arterial pressure (ie, ⌬ R-R interval/⌬ systolic pressure). 4 This estimate represents an integrated input-output relation and provides broad insight to baroreflex function. However, it has long been recognized that baroreceptors respond to deformation not pressure per se. Early in the last century, Sollman and Brown 5 reported that stretch of the carotid artery produces bradycardia and hypotension in dogs. Similar reflex responses in humans derive from proportionalities between changes in carotid diameter and carotid nerve firing 6 and between the R-R interval and the frequency of afferent carotid sinus nerve activation. 7 Thus, mechanical transduction of arterial pressure into carotid stretch and neural transduction of carotid stretch into vaga...

Background-Menopausal estrogen loss has been associated with increased cardiovascular disease in postmenopausal women. However, the link between estrogen and cardiovascular disease remains unclear. Some data suggest estrogen mediates its effect through changes in arterial pressure and its regulation. However, the data available in older women are equivocal regarding estrogen's ability to reduce resting arterial pressure or to improve its regulation. Methods and Results-We studied 11 healthy, postmenopausal women before and after 6 months of estrogen administration. Arterial pressure was measured by brachial auscultation and finger photoplethysmography. Vascular sympathetic nerve activity was measured in the peroneal nerve by microneurography, and the slope of the relations between changes in heart period, sympathetic activity, and arterial pressure caused by bolus infusions of nitroprusside and phenylephrine were used as an index of baroreflex gain. Estrogen therapy did not change systolic pressure (128Ϯ2 versus 123Ϯ2 mm Hg) or cardiac-vagal baroreflex gain (6.6Ϯ0.9 versus 6.7Ϯ0.7 ms/mm Hg

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Given that endothelial dysfunction precedes atherosclerotic cardiovascular disease, exploring the parameters that modify postprandial flow-mediated dilation (FMD) is important for public health. The objectives of the study are to estimate the population effect of meal ingestion on FMD and to determine how the effect varied based on patient characteristics and modifiable methodological features. Articles published before June 2015 were located using MEDLINE, PubMed and Web of Science. One hundred fifty-four effects were derived from 78 articles involving 2,548 subjects were selected. Included articles required measurement of FMD in adults before and after meal ingestion. Effects were analysed using an unstandardized mean gain random effects model, and significant moderators were analysed using meta-regression. Meal consumption significantly reduced FMD by a heterogeneous mean effect size delta (Δ) of -2.03 (95% CI: [-2.28, -1.77]), an ~2% reduction in FMD. FMD reductions were larger among normal weight individuals, males, those with a cardio-metabolic disorder, those with elevated baseline FMD, and individuals with impaired glucose tolerance at baseline. Macronutrient meal ingestion significantly reduced FMD, an effect that was moderated by body mass index, sex and two-way interactions between disease status and both baseline FMD and baseline blood glucose levels.