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The prevalence of hypertension in non-Hispanic black (BL) individuals is the greatest of any racial/ethnic group. Whereas women generally display lower rates of hypertension than men of the same background, BL women display a similar if not greater burden of hypertension compared with BL men. The risk for cardiovascular disease and related events is also highest in BL individuals. Given the importance of the sympathetic nervous system for the regulation of the cardiovascular system, a growing body of literature has investigated sympathetic function in BL and non-Hispanic white (WH) individuals. Here, we are focused on emerging evidence indicating that sympathetic function may be altered in BL individuals, with particular emphasis on the process by which bursts of muscle sympathetic nerve activity (MSNA) are transduced into vasoconstriction and increases in blood pressure (sympathetic vascular transduction). To synthesize this growing body of literature we discuss sex and race differences in 1 ) sympathetic outflow, 2 ) sympathetic vascular transduction, and 3 ) adrenergic receptor sensitivity. Sex differences are discussed foremost, to set the stage for new data indicating a sex dimorphism in sympathetic regulation in BL individuals. Specifically, we highlight evidence for a potential neurogenic phenotype including greater adiposity-independent sympathetic outflow and enhanced sympathetic vascular transduction in BL men that is not observed in BL women. The implications of these findings for the greater hypertension and cardiovascular disease risk in BL adults are discussed along with areas that require further investigation.

Hypertension affects approximately 100 million U.S. adults and is the leading single contributing risk factor to all-cause mortality. Accurate blood pressure (BP) measurement is essential in the treatment of BP, and a number of devices exist for monitoring. Recently, a new watch-type design was released, the Omron HeartGuide (BP8000), with claims to provide clinically accurate BP measurement while also tracking activity and sleep similar to smart watches. The aim of this research was done in two studies: (1) evaluation of the HeartGuide device for measurement of resting BP and heart rate (HR); and (2) assessment of the HeartGuide for BP, HR, step-counting and sleep monitoring during activities of daily living. Study 1 compared the Omron HeartGuide to the previously validated Welch Allyn ProBP 3400 following a modified version of the Universal Standard for validation of BP measuring devices set by the AAMI/ESH/ISO. While resting HR measured by the HeartGuide was similar to Welch Allyn measures, both systolic and diastolic BP were significantly lower ( P ≤0.001), with differences of 10.4 (11.1) and 3.2 (10.0) mmHg, respectively. Study 2 compared HeartGuide measures to Welch Allyn measures for BP, HR, steps and sleep during various body positions (supine, seated, standing), physiological stressors (cold pressor test, lower body submersion, exercise), and free-living. The HeartGuide significantly underestimated BP though provided accurate HR during most conditions. It also significantly underestimated steps, but reported sleep measures similar to those subjectively reported. Based on the significant differences between the HeartGuide and Welch Allyn, our data indicate the HeartGuide is not a suitable replacement for existing BP monitors., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Inspiratory muscle strength training (IMST) has shown potential to improve both respiratory and cardiovascular function in health and disease. Less is known about acute hemodynamic responses to a single IMST session, therefore we assessed upper and lower limb blood flow via Doppler ultrasound in the brachial and popliteal arteries, respectively. Mean, anterograde, and retrograde blood flow (BF) and shear rate (SR) were assessed relative to baseline during low-intensity (15% maximal inspiratory pressure - PImax) and high-intensity (75% PImax) IMST. During low-intensity IMST, popliteal BF and SR were reduced by ∼10%, and brachial BF and SR were reduced by ∼40%. During high-intensity IMST, popliteal BF and SR were reduced by ∼20%, and brachial BF and SR were reduced by ∼35%. BF and SR responses were not statistically different between low-intensity and high-intensity training for either blood vessel ( P > 0.05). In addition, anterograde BF and SR were significantly decreased in the brachial artery for both low-intensity and high-intensity training ( P < 0.05), but not the popliteal artery ( P > 0.05). Finally, during IMST retrograde BF and SR were significantly increased in both the upper and lower limbs during low-intensity and high-intensity training ( P < 0.05). These data provide novel insight into the acute BF and SR responses to a single bout of IMST and may enhance our understanding of the mechanism(s) by which IMST imparts its beneficial chronic effects on cardiovascular function. NEW & NOTEWORTHY Herein, we demonstrate for the first time that upper and lower limb blood flow and shear rate patterns are altered during a single bout of IMST, at low- and high-intensity training. Specifically, anterograde blood flow and shear rate are significantly reduced in the brachial artery, whereas retrograde blood flow is significantly elevated in both the brachial and popliteal arteries. These findings provide insight into the vascular impact of IMST, which may inform future mechanistic studies.

Reduction of blood flow to the limb using cuffs before or during exercise has become increasingly popular for training and rehabilitation. Our study tested the effects of cuff brand/width on pressures required to reach limb occlusion pressure (LOP) and developed, cross-validated, and compared accuracy of two LOP prediction equations to previously created methods. Supine LOP was determined in the distal popliteal artery using four different cuff brands/widths in 23 adult participants. Participants then had demographic and resting variables assessed, and two LOP prediction equations were developed from these variables and were compared to five previously developed models and a method using posterior tibial artery palpation for LOP assessment in an independent sample ( n  = 14 adult runners). For cuff comparison, the widest two cuffs had significantly lower LOP (mean ~149 mmHg) than the narrowest cuffs (mean ~176 mmHg), with the narrowest cuff unable to reach LOP. The eight methods used to predict LOP ranged in accuracy (mean absolute percent errors 3.9-23.0%), with highest accuracy in equations using mean arterial pressure (MAP) and BMI. Practitioners using blood flow reduction methods should be consistent with cuff use due to demonstrated differences across brands/widths. Equations using MAP and BMI appear best for prediction of leg LOP.

Heart failure with preserved ejection fraction (HFpEF) is characterized by reduced ability to sustain physical activity that may be due partly to disease-related changes in autonomic function that contribute to dysregulated cardiovascular control during muscular contraction. Thus, we used a combination of static handgrip exercise (HG) and postexercise ischemia (PEI) to examine the pressor response to exercise and isolate the skeletal muscle metaboreflex, respectively. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were assessed during 2-min of static HG at 30 and 40% of maximum voluntary contraction (MVC) and subsequent PEI in 16 patients with HFpEF and 17 healthy, similarly aged controls. Changes in MAP were lower in patients with HFpEF compared with controls during both 30%MVC (Δ11 ± 7 vs. Δ15 ± 8 mmHg) and 40%MVC (Δ19 ± 14 vs. Δ30 ± 8 mmHg), and a similar pattern of response was evident during PEI (30%MVC: Δ8 ± 5 vs. Δ12 ± 8 mmHg; 40%MVC: Δ13 ± 10 vs. Δ18 ± 9 mmHg) (group effect: P = 0.078 and P = 0.017 at 30% and 40% MVC, respectively). Changes in HR, CO, and TPR did not differ between groups during HG or PEI ( P > 0.05). Taken together, these data suggest a reduced pressor response to static muscle contractions in patients with HFpEF compared with similarly aged controls that may be mediated partly by a blunted muscle metaboreflex. These findings support a disease-related dysregulation in neural cardiovascular control that may reduce an ability to sustain physical activity in HFpEF. NEW & NOTEWORTHY The current investigation has identified a diminution in the exercise-induced rise in arterial blood pressure (BP) that persisted during postexercise ischemia (PEI) in an intensity-dependent manner in patients with heart failure with preserved ejection fraction (HFpEF) compared with older, healthy controls. These findings suggest that the pressor response to exercise is reduced in patients with HFpEF, and this deficit may be mediated, in part, by a blunted muscle metaboreflex, highlighting the consequences of impaired neural cardiovascular control during exercise in this patient group.

Above-normal blood pressure (BP) is a primary risk factor for cardiovascular diseases. In a retrospective analysis of five pilot trials, we assessed the BP-lowering effects of high-resistance inspiratory muscle strength training (IMST) in adults aged 18-82 years and the impact of IMST on maximal inspiratory pressure (PI MAX ), a gauge of inspiratory muscle strength and independent disease risk factor. Participants were randomized to high-resistance IMST (75% PI MAX ) or low-resistance sham (15% PI MAX ) training (30 breaths/day, 5-7 days/wk, 6 wk). IMST ( n = 67) reduced systolic BP (SBP) by 9 ± 6 mmHg ( P < 0.01) and diastolic BP (DBP) by 4 ± 4 mmHg ( P < 0.01). IMST-related reductions in SBP and DBP emerged by week 2 of training (-4 ± 8 mmHg and -3 ± 6 mmHg; P ≤ 0.01, respectively) and continued across the 6-wk intervention. SBP and DBP were unchanged with sham training ( n = 61, all P > 0.05). Select subject characteristics slightly modified the impact of IMST on BP. Greater reductions in SBP were associated with older age (β = -0.07 ± 0.03; P = 0.04) and greater reductions in DBP associated with medication-naïve BP (β = -3 ± 1; P = 0.02) and higher initial DBP (β = -0.12 ± 0.05; P = 0.04). PI MAX increased with high-resistance IMST and low-resistance sham training, with a greater increase from high-resistance IMST (+20 ± 17 vs. +6 ± 14 cmH 2 O; P < 0.01). Gains in PI MAX had a modest inverse relation with age (β = -0.20 ± 0.09; P = 0.03) and baseline PI MAX (β = -0.15 ± 0.07; P = 0.04) but not to reductions in SBP or DBP. These compiled findings from multiple independent trials provide the strongest evidence to date that high-resistance IMST evokes clinically significant reductions in SBP and DBP, and increases in PI MAX , in adult men and women. NEW & NOTEWORTHY In young-to-older adult men and women, 6 wk of high-resistance inspiratory muscle strength training lowers casual systolic and diastolic blood pressure by 9 mmHg and 4 mmHg, respectively, with initial reductions observed by week 2 of training. Given blood pressure outcomes with the intervention were only slightly altered by subject baseline characteristics (i.e., age, blood pressure medication, and health status), inspiratory muscle strength training is effective in lowering blood pressure in a broad range of adults.

New Findings: What is the central question of this study? The prevalence of hypertension in black individuals exceeds that in other racial groups. Despite this well-known heightened risk, the underlying contributory factors remain incompletely understood. We hypothesized that young black men would exhibit augmented beat-to-beat blood pressure variability compared with white men and that black men would exhibit augmented total peripheral resistance variability. What is the main finding and its importance? We demonstrate that young, healthy black men exhibit greater resting beat-to-beat blood pressure variability compared with their white counterparts, which is accompanied by greater variability in total peripheral resistance. These swings in blood pressure over time might contribute to the enhanced cardiovascular risk profile in black individuals., Abstract: The prevalence of hypertension in black (BL) individuals exceeds that in other racial groups. Recently, resting beat-to-beat blood pressure (BP) variability has been shown to predict cardiovascular risk and detect target organ damage better than ambulatory BP monitoring. Given the heightened risk in BL individuals, we hypothesized young BL men would exhibit augmented beat-to-beat BP variability compared with white (WH) men. Furthermore, given studies reporting reduced vasodilatation and augmented vasoconstriction in BL individuals, we hypothesized that BL men would exhibit augmented variability in total peripheral resistance (TPR). In 45 normotensive men (24 BL), beat-to-beat BP (Finometer) was measured during 10-20 min of quiet rest. Cardiac output and TPR were estimated (Modelflow method). Despite similar resting BP, BL men exhibited greater BP standard deviation (e.g. systolic BP SD; BL, 7.1 ± 2.2 mmHg; WH, 5.4 ± 1.5 mmHg; P = 0.006) compared with WH men, which was accompanied by a greater TPR SD (P = 0.003), but not cardiac output SD (P = 0.390). Other traditional measures of variability provided similar results. Histogram analysis indicated that BL men exhibited a greater percentage of cardiac cycles with BPs higher (> +10 mmHg higher) and lower (< -8 mmHg lower) than mean systolic BP compared with WH men (interaction, P < 0.001), which was accompanied by a greater percentage of cardiac cycles with high/low TPR (P < 0.001). In a subset of subjects (n = 30), reduced sympathetic baroreflex sensitivity was associated with augmented BP variability (r = -0.638, P < 0.001), whereas cardiac baroreflex sensitivity had no relationship (P = 0.447). Herein, we document an augmented beat-to-beat BP variability in young BL men, which coincided with fluctuations in vascular resistance and reduced sympathetic BRS., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Patients with type 2 diabetes (T2D) exhibit greater daytime blood pressure (BP) variability, increasing their cardiovascular risk. Given the number of daily activities that incorporate short-duration isometric muscle contractions (e.g., carrying groceries), herein we investigated BP and muscle sympathetic nerve activity (MSNA) responses at the onset of isometric handgrip (HG). We tested the hypothesis that, relative to control subjects, patients with T2D would exhibit exaggerated pressor and MSNA responses to the immediate onset of HG. Mean arterial pressure (MAP) and MSNA were quantified during the first 30 s of isometric HG at 30% and 40% of maximal voluntary contraction (MVC) and during a cold pressor test (CPT), a nonexercise sympathoexcitatory stimulus. The onset of 30% MVC HG evoked similar increases in MAP between groups ( P = 0.17); however, the increase in MSNA was significantly greater in patients with T2D versus control subjects with the largest group difference at 20 s ( P < 0.001). At the onset of 40% MVC HG, patients with T2D demonstrated greater increases in MAP (e.g., 10 s, T2D: 9 ± 1 mmHg, controls: 5 ± 2 mmHg; P = 0.04). MSNA was also greater in patients with T2D at 40% MVC onset but differences were only significant at the 20-30 s timepoint (T2D: 15 ± 3 bursts/min, controls: -2 ± 4 bursts/min; P < 0.001). Similarly, MAP and MSNA responses were augmented during the onset of CPT in T2D patients. These findings demonstrate exaggerated pressor and MSNA reactivity in patients with T2D, with rapid and robust responses to both isometric contractions and cold stress. This hyper-responsiveness may contribute to daily surges in BP in patients with T2D, increasing their short-term and long-term cardiovascular risk.

Increased consumption of inorganic phosphate (Pi), an abundant ingredient in processed foods, has been associated with elevated cardiovascular disease risk; however, studies investigating underlying mechanisms are limited. Recently, high dietary Pi was shown to exaggerate the pressor response to static muscle contraction in rodents in part because of overactivation of metabolically sensitive skeletal muscle afferents. Whether acute high Pi consumption affects muscle metaboreflex activation in humans remains unknown. Furthermore, although acute high Pi consumption has been shown to impair vascular function in young healthy men, equivocal results have been reported. Therefore, we hypothesized that acute high Pi consumption augments mean arterial pressure (MAP) responses during muscle metaboreflex activation, impairs endothelial function, and increases arterial stiffness in young healthy men. Subjects performed 35% maximal voluntary contraction static handgrip (HG), followed by postexercise ischemia (PEI) to isolate muscle metaboreflex activation. Resting flow-mediated dilation (FMD) and arterial stiffness were assessed. Measures were made before (pre) and 60 min after (post) subjects consumed either a high-phosphate drink (2,000 mg phosphorus and 1,520 mg sodium) or a sodium drink (1,520 mg sodium; control). MAP responses during HG (preΔ = +23 ± 3 mmHg; postΔ = +21 ± 2 mmHg; P = 0.101) and PEI (preΔ = +21 ± 4 mmHg; postΔ = +18 ± 3 mmHg; P = 0.184) were similar before and after Pi consumption. In contrast, FMD was significantly attenuated following Pi (pre = 5.1 ± 0.5%; post = 3.5 ± 0.5%; P = 0.010), whereas arterial stiffness remained unchanged. There were no changes in any measured variable after control drink consumption. In summary, although the muscle metaboreflex remains unaffected following acute high Pi consumption in young healthy men, endothelial function is impaired. NEW & NOTEWORTHY This study was the first to investigate the influence of acute high-phosphate consumption on the pressor response during isometric handgrip and isolated muscle metaboreflex activation during postexercise ischemia in young healthy humans. We demonstrated that a single high dose of phosphate (2,000 mg) did not augment blood pressure in response to exercise or isolated muscle metaboreflex activation, but endothelial function was blunted in young healthy men.

Approximately 60% of patients with type 2 diabetes mellitus (T2D) develop hypertension. Recent work also indicates greater blood pressure (BP) excursions throughout the day in T2D. Collectively, these findings suggest altered BP control in T2D. Although muscle sympathetic nerve activity (MSNA) recordings in T2D have provided equivocal results, quantification of MSNA alone does not account for ensuing vasoconstriction and BP responses elicited by MSNA. Thus, we tested the hypothesis that patients with T2D exhibit enhanced sympathetic transduction to BP. MSNA (microneurography) and beat-to-beat BP (Finometer) were measured at rest in 21 T2D and 13 age-matched and body mass index-matched control subjects and, signal-averaging was performed to quantify the mean arterial pressure and total vascular conductance responses to spontaneous bursts of MSNA. The peak mean arterial pressure and total vascular conductance responses to spontaneous MSNA were similar between T2D and control (both P>0.05). However, further analysis, separating T2D into those taking statins (n=13, T2D +statin) and not taking statins (n=8, T2D -statin), indicated that T2D -statin patients (4.2±0.6 mm Hg) exhibited greater peak mean arterial pressure responses compared with both T2D +statin patients (2.5±0.3 mm Hg, P=0.01) and control (control: 2.8±0.3 mm Hg, P=0.02). Likewise, nadir total vascular conductance responses to spontaneous MSNA bursts were greater in T2D -statin patients (T2D -statin: -3.3±0.6 mL/(min·mm Hg), T2D +statin: -1.6±0.3 mL/(min·mm Hg), P=0.03; control -2.2±0.3 mL/(min·mm Hg), P=0.08). Notably, T2D +statin patients exhibited similar peak mean arterial pressure and total vascular conductance responses to MSNA compared with control. Collectively, these findings demonstrate, for the first time, that patients with T2D exhibit augmented sympathetic transduction and this effect seems to be offset by statin therapy.

The role of the sympathetic nervous system in cerebral blood flow (CBF) regulation remains unclear. Previous studies have primarily measured middle cerebral artery blood velocity to assess CBF. Recently, there has been a transition toward measuring internal carotid artery (ICA) and vertebral artery (VA) blood flow using duplex Doppler ultrasound. Given that the VA supplies autonomic control centers in the brainstem, we hypothesized that graded sympathetic activation via lower body negative pressure (LBNP) would reduce ICA but not VA blood flow. ICA and VA blood flow were measured during two protocols: protocol 1 , low-to-moderate LBNP (-10, -20, -30, and -40 Torr) and protocol 2 , moderate-to-high LBNP (-30, -50, and -70 Torr). ICA and VA blood flow, diameter, and blood velocity were unaffected up to -40 LBNP. However, -50 and -70 LBNP evoked reductions in ICA and VA blood flow [e.g., -70 LBNP: percent change (%∆)VA-baseline = -27.6 ± 3.0] that were mediated by decreases in both diameter and velocity (e.g., -70 LBNP: %∆VA-baseline diameter = -7.5 ± 1.9 and %∆VA-baseline velocity = -13.6 ± 1.7), which were comparable between vessels. Since hyperventilation during -70 LBNP reduced end-tidal pressure of carbon dioxide ([Formula: see text]), this decrease in [Formula: see text] was matched via voluntary hyperventilation. Reductions in ICA and VA blood flow during hyperventilation alone were significantly smaller than during -70 LBNP and were primarily mediated by decreases in velocity (%∆VA-baseline velocity = -8.6 ± 2.4 and %∆VA-baseline diameter = -0.05 ± 0.56). These data demonstrate that both ICA and VA were unaffected by low-to-moderate sympathetic activation, whereas robust reflex-mediated sympathoexcitation caused similar magnitudes of vasoconstriction in both arteries. Thus, contrary to our hypothesis, the ICA was not preferentially vasoconstricted by sympathetic activation. NEW & NOTEWORTHY Our study demonstrates that moderate-to-high reflex-mediated sympathetic activation with lower body negative pressure (LBNP) decreases internal carotid artery and vertebral artery blood flow via reductions in both vessel diameter and blood velocity. This vasoconstriction was primarily sympathetically mediated as voluntary hyperventilation alone, to isolate the effect of decreases in end-tidal pressure of carbon dioxide that occurred during LBNP, resulted in a significantly smaller vasoconstriction. In contrast to our hypothesis, these data indicate a lack of heterogeneity between the anterior and posterior cerebral circulations in response to sympathoexcitation.

The black population exhibits attenuated vasodilatory function across their lifespan, yet little is known regarding the mechanisms of this impairment. Recent evidence suggests a potential role for oxidative stress. Therefore, we tested the hypothesis that NADPH oxidase (NOX) and/or xanthine oxidase (XO) contribute to blunted nitric oxide (NO)-mediated cutaneous microvascular function in young black adults. In 30 white and black subjects (8 men and 7 women in each group), local heating was performed while NOX and XO were inhibited by apocynin and allopurinol, respectively, via intradermal microdialysis. The plateau in cutaneous vascular conductance (red blood cell flux/mean arterial pressure) during 39°C local heating at each site was compared with a control site perfused with lactated Ringer solution. Subsequent inhibition of NO synthase via N ω -nitro-l-arginine methyl ester allowed for quantification of the NO contribution to vasodilation during heating. Black individuals, relative to white individuals, had a blunted cutaneous vascular conductance plateau at the control site (45 ± 9 vs. 68 ± 13%max, P < 0.001) that was increased by both apocynin (61 ± 15%max, P < 0.001) and allopurinol (58 ± 17%max, P = 0.005). Black men and black women had similar responses to heating at the control site ( P = 0.99), yet apocynin and allopurinol increased this response only in black men (both P < 0.001 vs. control). The NO contribution was also increased via apocynin and allopurinol exclusively in black men. These findings suggest that cutaneous microvascular function is reduced because of NOX and XO activity in black men but not black women, identifying a novel sex difference in the mechanisms that contribute to blunted vascular responses in the black population. NEW & NOTEWORTHY We demonstrate that cutaneous microvascular responses to local heating are consistently reduced in otherwise healthy young black men and women relative to their white counterparts. Inhibition of NADPH oxidase and xanthine oxidase via apocynin and allopurinol, respectively, augments microvascular function in black men but not black women. These data reveal clear sex differences in the mechanisms underlying the racial disparity in cutaneous microvascular function.

New Findings: What is the central question of this study? We aimed to examine leg vascular responses to brief periods of inactivity. What is the main finding and its importance? We demonstrate that a mere 10 min of sitting is sufficient to impair leg microvascular function (reactive hyperaemia). However, conduit artery vasodilatation (flow-mediated dilatation) was unaffected, indicating maintained macrovascular function. Interestingly, immobile supine rest also resulted in a reduction in microvascular function alone that was prevented when calf muscle contractions were performed. Collectively, these data highlight the susceptibility of the microcirculation to short periods of inactivity and the beneficial role of skeletal muscle contraction for vascular health., Abstract: Prolonged sitting for 1-6 h has been shown to impair leg macrovascular [i.e. reduced flow-mediated dilatation (FMD)] and microvascular (i.e. reduced reactive hyperaemia) function. These impairments appear to be mediated through reductions in shear stress. Interestingly, a reduction in shear rate has been observed as early as 10 min into sitting. However, it is unknown whether this acute reduction in shear stress is sufficient to affect vascular function. Accordingly, we studied 18 young men and assessed popliteal artery FMD and reactive hyperaemia before (Baseline) and after (PostSit) a 10 min sitting period. Popliteal artery shear rate was significantly reduced during sitting (Baseline, 62 ± 35 s -1 ; 10 min sitting, 27 ± 13 s -1 ; P < 0.001). Macrovascular function was unaffected by 10 min of sitting (Baseline, 4.4 ± 2.1%; PostSit, 4.3 ± 2.3%; P = 0.97), but microvascular function was reduced (Baseline, 4852 ± 2261 a.u.; PostSit, 3522 ± 1872 a.u.; P = 0.02). In a subset of individuals, we extended the recovery period after sitting and demonstrated that resting shear rate and reactive hyperaemia responses remained low up to 1 h post-sitting (P < 0.001), whereas FMD was unchanged throughout (P = 0.99). Additionally, time control experiments were performed with participants in an immobile supine position, which demonstrated no change in macrovascular function (P = 0.94) but, unexpectedly, a reduction in microvascular function (P = 0.008). Importantly, when calf muscle contractions were performed during supine rest, reactive hyperaemia responses were maintained (P = 0.76), along with FMD (P = 0.88). These findings suggest that the leg microcirculation might be more vulnerable to short periods of inactivity, whereas conduit artery vasodilatation appears well maintained. Moreover, intermittent skeletal muscle contractions are beneficial for microvascular function., (© 2018 The Authors. Experimental Physiology © 2018 The Physiological Society.)

The mechanism(s) for the increased occurrence of a grayout or blackout, syncope, immediately after heavy resistance exercise are unclear. It is well-known that orthostatic stress increases the occurrence of postexercise syncope. In addition, previous findings have suggested that hypo-perfusion, especially in the posterior cerebral circulation rather than anterior cerebral circulation, may be associated with the occurrence of syncope. Herein, we hypothesized that the postexercise decrease in posterior, but not anterior, cerebral blood flow (CBF) would be greater during orthostatic stress. Nine healthy subjects performed 3-min isometric handgrip (HG) at 30% maximum voluntary contraction without (CONTROL) and during lower body negative pressure (LBNP; -40 Torr) while vertebral artery (VA) blood flow, as an index of posterior CBF, and middle cerebral artery blood velocity (MCAv), as an index of anterior CBF, were measured. Immediately after HG (0 to 15 sec of recovery phase), mean arterial pressure decreased but there was no difference in this reduction between CONTROL and LBNP conditions (-15.4 ± 4.0% and -17.0 ± 6.2%, P = 0.42). Similarly, MCAv decreased following exercise and was unaffected by the application of LBNP (P = 0.22). In contrast, decreases in VA blood flow immediately following HG during LBNP were significantly greater compared to CONTROL condition (-24.2 ± 9.5% and -13.4 ± 6.6%, P = 0.005). These findings suggest that the decrease in posterior CBF immediately following exercise was augmented by LBNP, whereas anterior CBF appeared unaffected. Thus, the posterior cerebral circulation may be more sensitive to orthostatic stress during the postexercise period., (© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

New Findings: What is the central question of this study? To understand better the effects of acute hyperglycaemia on arterial stiffness in healthy young individuals, we assessed arterial stiffness in physically active men before and after reduced ambulatory physical activity to decrease insulin sensitivity. What is the main finding and its importance? During an oral glucose tolerance test, we identified an increase in leg arterial stiffness (i.e. reduced femoral artery compliance) only when subjects were inactive for 5 days (<5000 steps day -1 ) and not when they were engaging in regular physical activity (>10,000 steps day -1 ). These results demonstrate the deleterious consequence of acute reductions in daily physical activity on the response of the peripheral vasculature to acute hyperglycaemia., Abstract: Acute hyperglycaemia has been shown to augment indices of arterial stiffness in patients with insulin resistance and other co-morbidities; however, conflicting results exist in healthy young individuals. We examined whether acute hyperglycaemia after an oral glucose tolerance test (OGTT) increases arterial stiffness in healthy active men before and after reduced ambulatory physical activity to decrease insulin sensitivity. High-resolution arterial diameter traces acquired from Doppler ultrasound allowed an arterial blood pressure (BP) waveform to be obtained from the diameter trace within a cardiac cycle. In 24 subjects, this method demonstrated sufficient agreement with the traditional approach for assessing arterial compliance using applanation tonometry. In 10 men, continuous recordings of femoral and brachial artery diameter and beat-to-beat BP (Finometer) were acquired at rest, 60 and 120 min of an OGTT before and after 5 days of reduced activity (from >10,000 to <5000 steps day -1 ). Compliance and β-stiffness were quantified. Before the reduction in activity, the OGTT had no effect on arterial compliance or β-stiffness. However, after the reduction in activity, femoral compliance was decreased (rest, 0.10 ± 0.03 mm 2  mmHg -1 versus 120 min OGTT, 0.06 ± 0.02 mm 2  mmHg -1 ; P < 0.001) and femoral β-stiffness increased (rest, 8.7 ± 2.7 a.u. versus 120 min OGTT, 15.3 ± 6.5 a.u.; P < 0.001) during OGTT, whereas no changes occurred in brachial artery compliance (P = 0.182) or stiffness (P = 0.892). Insulin sensitivity (Matsuda index) was decreased after the reduction in activity (P = 0.002). In summary, in young healthy men the femoral artery becomes susceptible to acute hyperglycaemia after 5 days of reduced activity and the resultant decrease in insulin sensitivity, highlighting the strong influence of daily physical activity levels on vascular physiology., (© 2018 The University of Texas at Arlington. Experimental Physiology © 2018 The Physiological Society.)

Blacks have the highest prevalence of hypertension, putting them at greater risk of cardiovascular disease and death. Previous studies have reported that, relative to whites, healthy black men have augmented pressor responses to sympathoexcitatory stressors. Although important, these studies do not inform about the resting state and the influence of spontaneous changes in resting muscle sympathetic nerve activity (MSNA). Likewise, little is known about the transduction of MSNA into a vascular response at rest on a beat-to-beat basis. Accordingly, we tested the hypothesis that relative to whites, blacks would exhibit greater vasoconstriction and pressor responses following spontaneous bursts of MSNA. Mean arterial pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 minutes of supine rest in 35 young healthy men (17 blacks and 18 whites). Signal averaging was used to characterize changes in leg vascular conductance, total vascular conductance, and mean arterial pressure following spontaneous MSNA bursts. Blacks demonstrated significantly greater decreases in leg vascular conductance (blacks: -15.0±1.0%; whites: -11.5±1.2%; P =0.042) and total vascular conductance (blacks: -8.6±0.9%; whites: -5.1±0.4%; P =0.001) following MSNA bursts, which resulted in greater mean arterial pressure increases (blacks: +5.2±0.6 mm Hg; whites: +3.9±0.3 mm Hg; P =0.04). These exaggerated responses in blacks compared with whites were present whether MSNA bursts occurred in isolation (singles) or in combination (multiples) and were graded with increases in burst height. Collectively, these findings suggest that healthy young black men exhibit augmented sympathetic vascular transduction at rest and provide novel insight into potential mechanism(s) by which this population may develop hypertension later in life., (© 2017 American Heart Association, Inc.)

Increased daily sitting time is associated with greater cardiovascular risk, and, on average, women are more sedentary than men. Recent reports have demonstrated that prolonged sitting reduces lower leg microvascular (reactive hyperemia) and macrovascular [flow-mediated dilation (FMD)] vasodilator function. However, these studies have predominately included men, and the effects of sitting in young women are largely unexplored. This becomes important given known sex differences in vascular function. Thus, herein, we assessed popliteal artery reactive hyperemia and FMD before and after a 3-h sitting period in healthy young women ( n = 12) and men ( n = 8). In addition, resting popliteal artery hemodynamics (duplex Doppler ultrasound) and calf circumference were measured before, during, and after sitting. Resting popliteal artery shear rate was reduced to a similar extent in both groups during the sitting period (women: -48.5 ± 8.4 s -1 and men: -52.9 ± 12.3 s -1 , P = 0.45). This was accompanied by comparable increases in calf circumference in men and women ( P = 0.37). After the sitting period, popliteal artery FMD was significantly reduced in men (PreSit: 5.5 ± 0.9% and PostSit: 1.6 ± 0.4%, P < 0.001) but not women (PreSit: 4.4 ± 0.6% and PostSit: 3.6 ± 0.6%, P = 0.29). In contrast, both groups demonstrated similar reductions in hyperemic blood flow area under the curve (women: -28,860 ± 5,742 arbitrary units and men: -28,691 ± 9,685 arbitrary units, P = 0.99), indicating impaired microvascular reactivity after sitting. These findings indicate that despite comparable reductions in shear rate during 3 h of uninterrupted sitting, macrovascular function appears protected in some young women but the response was variable, whereas men exhibited more consistent reductions in FMD. In contrast, the leg microvasculature is susceptible to similar sitting-induced impairments in men and women. NEW & NOTEWORTHY We demonstrate that leg macrovascular function was consistently reduced in young men but not young women after prolonged sitting. In contrast, both men and women exhibited similar reductions in leg microvascular reactivity after sitting. These data demonstrate, for the first time, sex differences in vascular responses to prolonged sitting., (Copyright © 2017 the American Physiological Society.)

Study Objectives: New and effective strategies are needed to manage the autonomic and cardiovascular sequelae of obstructive sleep apnea (OSA). We assessed the effect of daily inspiratory muscle strength training (IMT) on sleep and cardiovascular function in adults unable to use continuous positive airway pressure (CPAP) therapy., Methods: This is a placebo-controlled, single-blind study conducted in twenty four adults with mild, moderate, and severe OSA. Subjects were randomly assigned to placebo or inspiratory muscle strength training. Subjects in each group performed 5 min of training each day for 6 w. All subjects underwent overnight polysomnography at intake and again at study close., Results: We evaluated the effects of placebo training or IMT on sleep, blood pressure, and plasma catecholamines. Relative to placebo-trained subjects with OSA, subjects with OSA who performed IMT manifested reductions in systolic and diastolic blood pressures (-12.3 ± 1.6 SBP and -5.0 ± 1.3 DBP mmHg; P < 0.01); plasma norepinephrine levels (536.3 ± 56.6 versus 380.6 ± 41.2 pg/mL; P = 0.01); and registered fewer nighttime arousals and reported improved sleep (Pittsburgh Sleep Quality Index scores: 9.1 ± 0.9 versus 5.1 ± 0.7; P = 0.001). These favorable outcomes were achieved without affecting apneahypopnea index., Conclusions: The results are consistent with our previously published findings in normotensive adults but further indicate that IMT can modulate blood pressure and plasma catecholamines in subjects with ongoing nighttime apnea and hypoxemia. Accordingly, we suggest IMT offers a low cost, nonpharmacologic means of improving sleep and blood pressure in patients who are intolerant of CPAP., (© 2016 Associated Professional Sleep Societies, LLC.)

We and others have recently reported that prolonged sitting impairs endothelial function in the leg vasculature; however, the mechanism(s) remain unknown. Herein, we tested the hypothesis that a sustained reduction in flow-induced shear stress is the underlying mechanism by which sitting induces leg endothelial dysfunction. Specifically, we examined whether preventing the reduction in shear stress during sitting would abolish the detrimental effects of sitting on popliteal artery endothelial function. In 10 young healthy men, bilateral measurements of popliteal artery flow-mediated dilation were performed before and after a 3-h sitting period during which one foot was submerged in 42°C water (i.e., heated) to increase blood flow and thus shear stress, whereas the contralateral leg remained dry and served as internal control (i.e., nonheated). During sitting, popliteal artery mean shear rate was reduced in the nonheated leg (pre-sit, 42.9 ± 4.5 s(-1); and 3-h sit, 23.6 ± 3.3 s(-1); P < 0.05) but not in the heated leg (pre-sit, 38.9 ± 3.4 s(-1); and 3-h sit, 63.9 ± 16.9 s(-1); P > 0.05). Popliteal artery flow-mediated dilation was impaired after 3 h of sitting in the nonheated leg (pre-sit, 7.1 ± 1.4% vs. post-sit, 2.8 ± 0.9%; P < 0.05) but not in the heated leg (pre-sit: 7.3 ± 1.5% vs. post-sit, 10.9 ± 1.8%; P > 0.05). Collectively, these data suggest that preventing the reduction of flow-induced shear stress during prolonged sitting with local heating abolishes the impairment in popliteal artery endothelial function. Thus these findings are consistent with the hypothesis that sitting-induced leg endothelial dysfunction is mediated by a reduction in shear stress., (Copyright © 2016 the American Physiological Society.)

Inspiratory muscle training holds promise as a non-pharmacologic treatment that can improve respiratory muscle strength, reduce blood pressure, and improve autonomic balance in hypertensive patients. There is a gap in knowledge regarding the specific respiratory stimulus that gives rise to these favorable outcomes. We implemented five respiratory training protocols that differed in the magnitude and direction of the lung volumes and/or intrathoracic pressures generated by subjects in training. Normotensive adults were randomly assigned to each group and trained daily for 6 weeks. Pre-post and weekly measures of blood pressure showed significant declines in systolic [-8.96 mmHg (95% CI, 7.39-10.53)] and diastolic [-5.25 mmHg (95% CI, 3.67-6.83)] blood pressures for subjects who trained with large positive or negative intrathoracic pressures. Subjects who trained with modest intrathoracic pressures or large lung volumes saw no improvement in blood pressure (P > 0.3). Large intra-thoracic pressures are the specific respiratory stimulus underpinning breathing training related improvements in blood pressure., (Copyright © 2015 Elsevier B.V. All rights reserved.)

The genioglossus (GG) is an extrinsic muscle of the human tongue that plays a critical role in preserving airway patency. In the last quarter century, >50 studies have reported on respiratory-related GG electromyographic (EMG) activity in human subjects. Remarkably, of the studies performed, none have duplicated subject body position, electrode recording locations, and/or breathing task(s), making interpretation and integration of the results across studies extremely challenging. In addition, more recent research assessing lingual anatomy and muscle contractile properties has identified regional differences in muscle fiber type and myosin heavy chain expression, giving rise to the possibility that the anterior and posterior regions of the muscle fulfill distinct functions. Here, we assessed EMG activity in anterior and posterior regions of the GG, across upright and supine, in rest breathing and in volitionally modulated breathing tasks. We tested the hypotheses that GG EMG is greater in the posterior region and in supine, except when breathing is subject to volitional modulation. Our results show differences in the magnitude of EMG (%regional maximum) between anterior and posterior muscle regions (7.95 ± 0.57 vs. 11.10 ± 0.99, respectively; P < 0.001), and between upright and supine (8.63 ± 0.73 vs. 10.42 ± 0.90, respectively; P = 0.008). Although the nature of a task affects the magnitude of EMG (P < 0.001), the effect is similar for anterior and posterior muscle regions and across upright and supine (P > 0.2)., (Copyright © 2015 the American Physiological Society.)