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Brachial artery bifurcation has been documented in ∼5%–10% of cadaver models, but our understanding of arterial function in these rare cases is unknown. This case study examined vasodilatory responses between a right bifurcated (right superficial brachial artery, right deep brachial artery) versus a left nonbifurcated brachial artery in a 28-year-old healthy female. Vasodilatory functions were assessed via flow-mediated dilation and nitroglycerin-mediated dilation (0.4 mg sublingual spray) techniques. Bifurcation of the brachial artery promotes lower endothelial-dependent vasodilation and possibly reduced vascular smooth muscle responsiveness to nitric oxide. Our case study indicated that a bifurcated brachial artery exhibited worse vasodilatory responses relative to an intact contralateral artery. [ABSTRACT FROM AUTHOR]

Elevated pulse wave velocity (PWV) determined arterial stiffness is a prominent marker of cardiovascular disease (CVD) risk. Exercise training delays the progression of CVD, but existing reviews on the impact of training on PWV are conflicting. We synthesized the evidence on the effects of exercise training interventions on PWV. We searched Scopus, EMBASE, PubMed, CINAHL, and Academic Search Premier databases for systematic reviews including PWV, and examined the effects of exercise training on PWV. We screened 842 citations that resulted in 44 systematic reviews, including 22 meta-analyses [unique participants, n = 6,719 (3,390 females)]. Studies were conducted in general adults with/without disease(s) (n = 19, 8 meta-analyses), kidney disease (n = 9, 6 meta-analyses), increased CVD risk or CVD (n = 7, 5 meta-analyses), type 2 diabetes mellitus (n = 3, 2 meta-analyses), and other conditions (n = 6, 2 meta-analyses). In general adults, PWV was reduced by aerobic exercise (β, -0.75 to -0.52 m/s) and low-to-moderate intensity resistance exercise training (β, -0.34 m/s). Exercise training was beneficial for patients with kidney disease (β, -1.13 to -0.56 m/s). Aerobic exercise improved PWV in adults with CVD or high CVD risk (β, -0.70 to -0.42 m/s). Combined aerobic and resistance exercise training decreased carotid-femoral (CF) PWV in patients with CVD (β, -1.15 m/s) and decreased brachial-ankle (BA) PWV in postmenopausal females (β, -1.18 m/s). Neither aerobic nor combined training improved PWV in individuals with type 2 diabetes. The potential physiological mechanisms involved are discussed. Overall, the included systematic reviews and meta-analyses documented that exercise training was an effective strategy to improve PWV, but the optimal type of training varied between populations. [ABSTRACT FROM AUTHOR]

These data suggest that augmented transduction may contribute to greater blood pressure fluctuations that could, over time, lead to a pathological cardiovascular phenotype and blood pressure dysregulation. Larger vasoconstrictor responses to MSNA bursts lead to higher pressor responses, which could contribute to greater blood pressure fluctuations (i.e., larger blood pressure variability). Keywords: Sex differences; Muscle sympathetic nerve activity; Pressor responses; Average-real-variability; Blood pressure regulation EN Sex differences Muscle sympathetic nerve activity Pressor responses Average-real-variability Blood pressure regulation 529 532 4 08/22/23 20230801 NES 230801 Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/s10286-023-00949-7. [Extracted from the article]

Wearable activity monitors provide objective estimates of time in different physical activity intensities. Each continuous stepping period is described by its length and a corresponding single intensity (in metabolic equivalents of task [METs]), creating square wave–shaped signals. We argue that physiological responses do not resemble square waves, with the purpose of this technical report to challenge this idea and use experimental data as a proof of concept and direct potential solutions to better characterize activity intensity. Healthy adults (n = 43, 19♀; 23 ± 5 years) completed 6-min treadmill stages (five walking and five jogging/running) where oxygen consumption (3.5 ml O2·kg−1·min−1 = 1 MET) was recorded throughout and following the cessation of stepping. The time to steady state was ∼1–1.5 min, and time back to baseline following exercise was ∼1–2 min, with faster stepping stages generally exhibiting longer durations. Instead of square waves, the duration intensity signal reflected a trapezoid shape for each stage. The METs per minute during the rise to steady state (upstroke slopes; average: 1.7–6.3 METs/min for slow walking to running) may be used to better characterize activity intensity for shorter activity bouts where steady state is not achieved (within ∼90 s). While treating each activity bout as a single intensity is a much simpler analytical procedure, characterizing each bout in a continuous manner may better reflect the true physiological responses to movement. The information provided herein may be used to improve the characterization of activity intensity, definition of bout breaks, and act as a starting point for researchers and software developers interested in using wearables to measure activity intensity. [ABSTRACT FROM AUTHOR]

A single bout of prolonged uninterrupted sitting increases oxidative stress, reduces popliteal blood flow-induced shear stress, and diminishes endothelium-dependent, flow-mediated dilation (FMD). The FMD response is also influenced by the sensitivity of vascular smooth muscle cells to nitric oxide (i.e., endothelium-independent dilation), which is also attenuated by elevated oxidative stress. However, it is currently unknown whether prolonged sitting impacts popliteal endothelium-independent dilation responses, which may uncover a novel mechanism associated with sitting-induced vascular dysfunction. This study tested the hypothesis that prolonged sitting attenuates both popliteal FMD and endothelium-independent, nitroglycerin-mediated dilation responses (NMD, 0.4 mg sublingual dose). Popliteal blood flow (mL/min), relative FMD (%), and NMD (%) were assessed via duplex ultrasonography before and after a ~3-h bout of sitting in 14 young, healthy adults (8$; 22 ± 2 yr). Prolonged sitting attenuated resting blood flow (57 ± 23 to 32 ± 16 mL/min, P < 0.001), relative FMD (4.6 ± 2.8% to 2.2 ± 2.5%; P = 0.001), and NMD (7.3 ± 4.0% to 4.6 ± 3.0%; P = 0.002). These novel findings demonstrate that both endothelium-dependent and independent mechanisms contribute to the adverse vascular consequences associated with prolonged bouts of sitting. NEW & NOTEWORTHY We demonstrate that lower-limb vascular smooth muscle function is attenuated in young, healthy adults after an acute bout of prolonged sitting. These data indicate that prolonged sitting-induced vascular dysfunction involves both endothelium-dependent and-independent mechanisms. [ABSTRACT FROM AUTHOR]

Aims: Patients with sympathetic excess are those most likely to benefit from novel interventions targeting the autonomic nervous system. To inform such personalized therapy, we identified determinants of augmented muscle sympathetic nerve activity (MSNA) in heart failure, versus healthy controls. Methods and results: We compared data acquired in 177 conventionally‐treated, stable non‐diabetic patients in sinus rhythm, aged 18–79 years (149 males; 28 females; left ventricular ejection fraction [LVEF] 25 ± 11% [mean ± standard deviation]; range 5–60%), and, concurrently, under similar conditions, in 658 healthy, normotensive volunteers (398 males; aged 18–81 years). In heart failure, MSNA ranged between 7 and 90 bursts·min−1, proportionate to heart rate (p < 0.0001) and body mass index (BMI) (p = 0.03), but was unrelated to age, blood pressure, or drug therapy. Mean MSNA, adjusted for age, sex, BMI, and heart rate, was greater in heart failure (+14.2 bursts·min−1; 95% confidence interval [CI] 12.1–16.3; p < 0.0001), but lower in women (−5.0 bursts·min−1; 95% CI 3.4–6.6; p < 0.0001). With spline modeling, LVEF accounted for 9.8% of MSNA variance; MSNA related inversely to LVEF below an inflection point of ∼21% (p < 0.006), but not above. Burst incidence was greater in ischaemic than dilated cardiomyopathy (p = 0.01), and patients with sleep apnoea (p = 0.03). Burst frequency correlated inversely with stroke volume (p < 0.001), cardiac output (p < 0.001), and peak oxygen consumption (p = 0.002), and directly with norepinephrine (p < 0.0001) and peripheral resistance (p < 0.001). Conclusion: Burst frequency and incidence exceeded normative values in only ∼53% and ∼33% of patients. Such diversity encourages selective deployment of sympatho‐modulatory therapies. Clinical characteristics can highlight individuals who may benefit from future personalized interventions targeting pathological sympathetic activation. [ABSTRACT FROM AUTHOR]

Objective monitors such as the activPAL characterize time when the thigh is horizontal as sedentary time. However, there are physiological differences between lying, bent-legged sitting, and straight-legged sitting. We introduce a three-monitor configuration to assess detailed sedentary postures and demonstrate its use in characterizing such positions in free-living conditions. We explored time spent in each sedentary posture between prolonged (>1 h) versus non-prolonged (<1 h) sedentary bouts. In total, 35 healthy adults (16♀, 24 ± 3 years; 24 h/day for 6.8 ± 1.0 days) wore an activPAL accelerometer on their thigh, torso, and shin. Hip and knee joint flexion angle estimates were determined during sedentary bouts using the dot-product method between the torso–thigh and thigh–shin, respectively. Compared to lying (69 ± 60 min/day) or straight-legged sitting (113 ± 100 min/day), most time was spent in bent-legged sitting (439 ± 101 min/day, p < 0.001). Most of the bent-legged sitting time was accumulated in non-prolonged bouts (328 ± 83 vs. 112 ± 63 min/day, p < 0.001). In contrast, similar time was spent in straight-legged sitting and lying between prolonged/non-prolonged bouts (both, p > 0.26). We document that a considerable amount of waking time is accumulated in lying or straight-legged sitting. This methodological approach equips researchers with a means of characterizing detailed sedentary postures in uncontrolled conditions and may help answer novel research questions on sedentariness. [ABSTRACT FROM AUTHOR]

Purpose: Spontaneous sympathetic transduction reflects the vascular and/or pressor responses to bursts of muscle sympathetic nerve activity (MSNA). Separately, signal-averaging and regression-based approaches have been implemented to quantify resting sympathetic transduction. It is unknown whether the outcomes of these analytical approaches provide (dis)similar information, which is imperative for between-study comparisons and the amalgamation of results for synthesis of multiple studies (i.e., meta-analyses). We explored the diastolic blood pressure (DBP) responses to spontaneous bursts of MSNA between these two methods of analysis. Methods: Resting beat-by-beat DBP (via finger photoplethysmography) and common peroneal nerve MSNA (via microneurography) were recorded in 52 healthy, normotensive adults (age 38 ± 20 years; 19 females). For the signal-averaged method, transduction was quantified as the mean peak increase in DBP (ΔDBP) during the 12 cardiac cycles following each MSNA burst. In addition, DBP was regressed to a moving two-cardiac-cycle window of normalized relative burst height (mmHg/relative %) to provide the regression-based transduction outcome. Results: The signal-averaged (1.2 ± 0.7 mmHg) and regression-based approaches (0.009 ± 0.016 mmHg/%) were unrelated (ρ = 0.03, p = 0.86). Adding to the discrepancy, only the signal-averaging approach demonstrated a lower transduction in middle-aged-older males versus younger males. Conclusions: The decision of which method to use when calculating sympathetic transduction influences study outcomes, with the two most common methods of determining transduction being unrelated. There are challenges of making sweeping conclusions across studies if different analysis strategies are implemented. An understanding of when to use each method is needed to adopt a harmonized approach to quantifying sympathetic transduction. [ABSTRACT FROM AUTHOR]

The amplitude of low-frequency (LF) oscillations of heart rate (HR) usually reflects the magnitude of sympathetic activity, but during some conditions, e.g., physical exercise, high sympathetic activity results in a paradoxical decrease of LF oscillations of HR. We tested the hypothesis that this phenomenon may result from a feedback inhibition of sympathetic outflow caused by circulating norepinephrine (NE). A physiological dose of NE (100 ng x [kg.sup.-1] x [min.sup.-1]) was infused into eight healthy subjects, and infusion was continued alter [alpha]-adrenergic blockade [with phentolamine (Phe)]. Muscle sympathetic nervous activity (MSNA) from the peroneal nerve, LF (0.04-0.15 Hz) and high frequency (HF; 0.15-0.40 Hz) spectral components of HR variability, and systolic blood pressure variability were analyzed at baseline, during NE infusion, and during NE infusion after Phe administration. The NE infusion increased the mean blood pressure and decreased the average HR (P < 0.01 for both). MSNA (10 [+ or -] 2 vs. 2 [+ or -] 1 bursts/min, P < 0.01), LF oscillations of HR (43 [+ or -] 13 vs. 35 [+ or -] 13 normalized units, P < 0.05), and systolic blood pressure (3.1 [+ or -] 2.3 vs. 2.0 [+ or -] 1.1 mm[Hg.sup.2], P < 0.05) decreased significantly during the NE infusion. During the NE infusion after PHE, average HR and mean blood pressure returned to baseline levels. However, MSNA (4 [+ or -] 2 bursts/ min), LF power of HR (33 [+ or -] 9 normalized units), and systolic blood pressure variability (1.7 [+ or -] 1.1 mm[Hg.sup.2]) remained significantly (P < 0.05 for all) below baseline values. Baroreflex gain did not change significantly during the interventions. Elevated levels of circulating NE cause a feedback inhibition on sympathetic outflow in healthy subjects. These inhibitory effects do not seem to be mediated by pressor effects on the baroreflex loop but perhaps by a presynaptic autoregulatory feedback mechanism or some other mechanism that is not prevented by a nonselective [alpha]-adrenergic blockade. heart rate dynamics; catecholamines; blood pressure oscillation

Hypovolemia and neurovascular control during orthostatic stress. Am J Physiol Heart Circ Physiol 282: H645-H655, 2002. First published September 27, 2001; 10.1152/ajpheart.00535.2001.--Humans exposed to real or simulated microgravity experience decrements in blood pressure regulation during orthostatic stress that may be related to autonomic dysregulation and/or hypovolemia. We examined the hypothesis that hypovolemia, without the deconditioning effects of bed rest or spaceflight, would augment the sympathoneural and vasomotor response to graded orthostatic stress. Radial artery blood pressure (tonometry), stroke volume (SV), brachial blood flow (Doppler ultrasound), heart rate (electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA; microneurography), and estimated central venous pressure (CVP) were recorded during five levels (-5, -10, -15, -20 and -40 mmHg) of randomly assigned lower body negative pressure (LBNP) (n = 8). Forearm (FVR) and total peripheral vascular resistance (TPR) were calculated. The test was repeated under randomly assigned placebo (normovolemia) or diuretic (spironolactone: 100 mg/day, 3 days) (hypovolemia) conditions. The diuretic produced an ~16% reduction in plasma volume. Compared with normovolemia, SV and cardiac output were reduced by ~12% and ~10% at baseline and during LBNP after the diuretic. During hypovolemia, there was an upward shift in the %[DELTA]MSNA/[DELTA]CVP, [DELTA]FVR/[DELTA]CVP, and [DELTA]TPR/[DELTA]CVP relationships during 0 to -20 mmHg LBNP. In contrast to normovolemia, blood pressure increased at -40 mmHg LBNP during hypovolemia due to larger gains in the %[DELTA]MSNA/[DELTA]CVP and [DELTA]TPR/[DELTA]CVP relationships. It was concluded that acute hypovolemia augmented the neurovascular component of blood pressure control during moderate orthostasis, effectively compensating for decrements in SV and cardiac output. baroreflex; muscle sympathetic nerve activity; Doppler ultrasound; lower body negative pressure; vascular resistance; spironolactone