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The aim of this study was to determine the effect of posture changes on vascular compliance in intracranial (brain) versus extracranial vascular beds (forearm). Eighteen young adults (nine females) performed a supine-to-seated-to-standing protocol involving 5 min of rest in each position. Continuous blood pressure, middle cerebral artery (MCA) blood velocity, and brachial artery blood velocity were recorded at each posture. Three to five consecutive steady-state cardiac cycles at each posture were analyzed by a four-element lumped parameter modified Windkessel model to calculate vascular compliance. Mean arterial pressure (MAP) increased from supine to seated (76(9) vs. 81(12) mmHg; P = 0.006) and from supine to standing (76(9) vs. 82(13) mmHg; P = 0.034). Mean blood flow was greater in the MCA relative to the forearm (forearm: 40(5) mL·min−1, MCA: 224(17) mL·min−1; main effect P < 0.001). Conversely, vascular resistance (forearm: 3.25(0.50) mmHg−1·mL·min−1, brain: 0.36(0.04) mmHg−1·mL·min−1; main effect P < 0.001) and compliance (forearm: 0.010(0.001) mL·min−1·mmHg−1, brain: 0.005(0.001) mL·min−1·mmHg−1; main effect P = 0.001) were greater in the forearm compared to the brain. Significant main effects of posture were observed with decreasing values in upright positions for mean blood flow (P = 0.001) in both vascular beds, but not for resistance (P = 0.163) or compliance (P = 0.385). There were no significant interaction effects between vascular bed and posture for mean flow (P = 0.057), resistance (P = 0.258), or compliance (P = 0.329). This study provides evidence that under steady-state conditions, posture does not affect cerebrovascular compliance. [ABSTRACT FROM AUTHOR]

Body posture and biological sex exhibit independent effects on the sympathetic neural responses to dynamic exercise. However, the neural mechanisms (e.g., baroreflex) by which posture impacts sympathetic outflow during rhythmic muscular contractions, and whether biological sex affects posture-mediated changes in efferent sympathetic nerve traffic during exercise, remain unknown. Thus, we tested the hypotheses that increases in muscle sympathetic nerve activity (MSNA) would be greater during upright compared with supine rhythmic handgrip (RHG) exercise, and that females would demonstrate smaller increases in MSNA during upright RHG exercise than males. Twenty young (30 [6] yr; means [SD]) individuals (9 males, 11 females) underwent 6 min of supine and upright (head-up tilt 45°) RHG exercise at 40% maximal voluntary contraction with continuous measurements of MSNA (microneurography), blood pressure (photoplethysmography), and heart rate (electrocardiogram). In the pooled group, absolute MSNA burst frequency (P < 0.001), amplitude (P = 0.009), and total MSNA (P < 0.001) were higher during upright compared with supine RHG exercise. However, body posture did not impact the peak change in MSNA during RHG exercise (range: P = 0.063–0.495). Spontaneous sympathetic baroreflex gain decreased from rest to RHG exercise (P = 0.006) and was not impacted by posture (P = 0.347). During upright RHG exercise, males demonstrated larger increases in MSNA burst amplitude (P = 0.002) and total MSNA (P = 0.001) compared with females, which coincided with greater reductions in sympathetic baroreflex gain among males (P = 0.004). Collectively, these data indicate that acute attenuation of baroreflex-mediated sympathoinhibition permits increases in MSNA during RHG exercise and that males exhibit a greater reserve for efferent sympathetic neural recruitment during orthostasis than females. NEW & NOTEWORTHY: The impact of posture and sex on cardiovascular control during rhythmic handgrip (RHG) exercise is unknown. We show that increases in muscle sympathetic nerve activity (MSNA) during RHG are partly mediated by a reduction in sympathetic baroreflex gain. In addition, males demonstrate larger increases in total MSNA during upright RHG than females. These data indicate that the baroreflex partly mediates increases in MSNA during RHG and that males have a greater sympathetic vasoconstrictor reserve than females. [ABSTRACT FROM AUTHOR]

To maintain heat balance during exercise, humans rely on skin blood flow and sweating to facilitate whole body dry and evaporative heat exchange. These responses are modulated by the rise in body temperature (thermal factors), as well as several nonthermal factors implicated in the cardiovascular response to exercise (i.e., central command, mechanoreceptors, and metaboreceptors). However, the way these nonthermal factors interact with thermal factors to maintain heat balance remains poorly understood. We therefore used direct calorimetry to quantify the effects of dose-dependent increases in the activation of these nonthermal stimuli on whole body dry and evaporative heat exchange during dynamic exercise. In a randomized crossover design, eight participants performed 45-min cycling at a fixed metabolic heat production (200 W/m²) in warm, dry conditions (30°C, 20% relative humidity) on four separate occasions, differing only in the level of lower-limb compression applied via bilateral thigh cuffs pressurized to 0, 30, 60, or 90 mmHg. This model provoked increments in nonthermal activation while ensuring the heat loss required to balance heat production was matched across trials. At end-exercise, dry heat loss was 2 W/m² [1, 3] lower per 30-mmHg pressure increment (P = 0.006), whereas evaporative heat loss was elevated 5 W/m² [3, 7] with each pressure increment (P < 0.001). Body heat storage and esophageal temperature did not differ across conditions (both P ≤ 0.600). Our findings indicate that the nonthermal factors engaged during exercise exert dose-dependent, opposing effects on whole body dry and evaporative heat exchange, which do not significantly alter heat balance. NEW & NOTEWORTHY To maintain heat balance during exercise, humans rely on skin blood flow and sweating to facilitate dry and evaporative heat exchange. These responses are modulated by body temperatures (thermal factors) and several nonthermal factors (e.g., central command, metaboreceptors), although the way thermal and nonthermal factors interact to regulate body temperature is poorly understood. We demonstrate that nonthermal factors exert dose-dependent, opposing effects on dry and evaporative heat loss, without altering heat storage during dynamic exercise. [ABSTRACT FROM AUTHOR]

Posttraumatic stress disorder (PTSD) is associated with an increased risk of developing cardiovascular disease, especially in women. Evidence indicates that men with PTSD exhibit lower maximal oxygen uptake (V̇o2max) relative to controls; however, whether V̇o2max is blunted in women with PTSD remains unknown. Furthermore, it is unclear what determinants (i.e., central and/or peripheral) of V̇o2max are impacted by PTSD. Therefore, we evaluated the central (i.e., cardiac output; Q̇c) and peripheral (i.e., arteriovenous oxygen difference) determinants of V̇o2max in women with PTSD; hypothesizing that V̇o2max would be lower in women with PTSD compared with women without PTSD (controls), primarily due to smaller increases in stroke volume (SV), and therefore Q̇c. Oxygen uptake (V̇oc), heart rate (HR), Q̇c, SV, and arteriovenous oxygen difference were measured in women with PTSD (n = 14; mean [SD]: 43 [11] yr,) and controls (n = 17; 45 [11] yr) at rest, and during an incremental maximal treadmill exercise test, and the Q̇c/V̇oc slope was calculated. V̇o2max was not different between women with and without PTSD (24.3 [5.6] vs. 26.4 [5.0] mL/kg/min; P = 0.265). However, women with PTSD had higher Q̇c [P = 0.002; primarily due to greater SV (P = 0.069), not HR (P = 0.285)], and lower arteriovenous oxygen difference (P = 0.002) throughout exercise compared with controls. Furthermore, the Q̇c/V̇oc slope was steeper in women with PTSD relative to controls (6.6 [1.4] vs. 5.7 [1.0] AU; P = 0.033). Following maximal exercise, women with PTSD exhibited slower HR recovery than controls (P = 0.046). Thus, despite attenuated peripheral oxygen extraction, V̇o2max is not reduced in women with PTSD, likely due to larger increases in Qc. [ABSTRACT FROM AUTHOR]

Bursts of muscle sympathetic nerve activity (MSNA) and the ensuing vasoconstriction are pivotal determinants of beat-by-beat blood pressure regulation. Although age and sex impact blood pressure regulation, how these factors affect the central and peripheral arcs of the baroreflex remains unclear. In 27 young [25 (SD 3) yr] males (YM; n = 14) and females (YF; n = 13) and 23 older [71 (SD 5) yr] males (OM; n = 11) and females (OF; n = 12), femoral artery blood flow, blood pressure, and MSNA were recorded for 10 min of supine rest. Sympathetic baroreflex sensitivity (i.e., central arc) was quantified as the relationship between diastolic blood pressure and MSNA burst incidence. Signal averaging was used to determine sympathetic vascular transduction into leg vascular conductance (LVC) for 12 cardiac cycles following MSNA bursts (i.e., peripheral arc). Older adults demonstrated attenuated sympathetic transduction into LVC (both P < 0.001) following MSNA bursts, and smaller increases in sympathetic transduction as a function of MSNA burst size and firing pattern compared with young adults (range, P = 0.004-0.032). YM (r² = 0.36; P = 0.032) and OM (r² = 0.51; P = 0.014) exhibited an inverse relationship between the central and peripheral arcs of the baroreflex, whereas females did not (YF, r² = 0.03, P = 0.621; OF, r² = 0.06, P = 0.445). MSNA burst incidence was inversely related to sympathetic transduction in YM and OF (range, P = 0.03-0.046) but not in YF or OM (range, P = 0.360-0.603). These data indicate that age is associated with attenuated sympathetic vascular transduction, whereas age- and sex-specific changes are present in the relationship between the central and peripheral arcs of the baroreflex regulation of blood pressure. [ABSTRACT FROM AUTHOR]

The article discusses the role of the peripheral chemoreflex in constraining skeletal muscle blood flow in individuals with treated hypertension. The peripheral chemoreflex is responsible for regulating oxygen levels in the body and is hypersensitive in conditions such as heart failure and hypertension. The study found that inhibiting the peripheral chemoreflex increased skeletal muscle blood flow during exercise in individuals with hypertension. The findings suggest that the peripheral chemoreflex negatively impacts blood flow distribution in people with hypertension, highlighting the need for further research on the impact of anti-hypertensive medications on cardiovascular function during exercise. [Extracted from the article]

Sympathetic activation is a hallmark of pregnancy. However, longitudinal assessments of muscle sympathetic nerve activity (MSNA) in pregnancy are scarce and have primarily focused on burst occurrence (frequency) at rest, despite burst strength (amplitude) representing distinct characteristics of sympathetic outflow. Thus, we assessed MSNA burst amplitude distributions in healthy women to determine the impact of normal pregnancy on neural discharge patterns in response to orthostatic stress. Twenty-six women were studied longitudinally during pre-, early- (4-8 wk of gestation), and late (32-36 wk) pregnancy, as well as postpartum (6-10 wk after delivery). MSNA, blood pressure (BP), and heart rate (HR) were measured in the supine posture and during graded head-up tilt (30° and 60° HUT). Mean and median MSNA burst amplitudes were used to characterize burst amplitude distribution. In late pregnancy, women demonstrated smaller increases in HR (P < 0.001) during 60° HUT and larger increases in systolic BP (P = 0.043) throughout orthostasis, compared with prepregnancy. The increase in MSNA burst frequency during late-relative to prepregnancy (Late: D14[10] vs. Pre: D21[9] bursts/min; P = 0.001) was smaller during 60° HUT, whereas increases in burst incidence were smaller in late-relative to prepregnancy throughout orthostasis (P = 0.009). Nonetheless, median burst amplitude was smaller throughout orthostasis in late compared with prepregnancy (P = 0.038). Thus, while supine MSNA burst frequency was greater in late pregnancy, increases in burst frequency and strength during orthostasis were attenuated. These smaller, orthostatically induced MSNA increases may reflect natural adaptions of pregnancy serving to prevent sympathetic hyper-reactivity that is common in pathological states. [ABSTRACT FROM AUTHOR]

We tested the hypotheses that spontaneous baroreflex control of integrated muscle sympathetic nerve activity (MSNA) burst occurrence and action potential (AP) subpopulations would be blunted in older compared with young adults and that sympathetic transduction will be blunted in older adults relative to young adults. Integrated muscle sympathetic nerve activity (MSNA) and the underlying sympathetic APs were obtained using microneurography and a continuous wavelet analysis approach, respectively, during 5 min of supine rest in 13 older (45-75 yr, 6 females) and 14 young (21-30 yr, 7 females) adults. Baroreflex threshold relationships were quantified as the slope of the linear regression between MSNA burst occurrence (%) and diastolic blood pressure (mmHg), or AP cluster firing probability (%) and diastolic blood pressure (mmHg). Integrated MSNA baroreflex threshold gain was greater in older compared with young adults (older: -5.7 ± 2.6%/mmHg vs. young: -2.7 ± 1.4%/mmHg, P < 0.001). Similarly, the baroreflex threshold gain of AP clusters was modified by aging (group-by-cluster effect: P < 0.001) such that older adults demonstrated greater baroreflex threshold gains of medium-sized AP clusters (e.g., Cluster 4, older: -8.2 ± 3.2%/mmHg vs. young: -3.6 ± 1.9%/mmHg, P = 0.003) but not for the smallest-sized (Cluster 1, older: -1.6 ± 1.9%/mmHg vs. young: -1.0 ± 1.7%/mmHg, P > 0.999) and largest-sized (Cluster 10, older: -0.5 ± 0.5%/mmHg vs. young: -0.2 ± 0.1%/mmHg, P = 0.819) AP clusters compared with young adults. In contrast, the peak change in mean arterial pressure (MAP) following a spontaneous MSNA burst (i.e., sympathetic transduction) was impaired with aging (older: -0.7 ± 0.3 mmHg vs. young: 1.8 ± 1.2 mmHg, P < 0.001). We conclude that aging is associated with elevated baroreflex control over high-probability AP content of sympathetic bursts that may compensate for impaired sympathetic neurovascular transduction. [ABSTRACT FROM AUTHOR]

Muscle sympathetic nerve activity (MSNA) increases during isometric exercise via increased firing of low-threshold action potentials (AP), recruitment of larger, higher-threshold APs, and synaptic delay modifications. Recent work found that women with post-traumatic stress disorder (PTSD) demonstrate exaggerated early-onset MSNA responses to exercise; however, it is unclear how PTSD affects AP recruitment patterns during fatiguing exercise. We hypothesized that women with PTSD (n = 11, 43 [11] [SD] years) would exhibit exaggerated sympathetic neural recruitment compared to women without PTSD (controls; n = 13, 40 [8] years). MSNA and AP discharge patterns (via microneurography and a continuous wavelet transform) were measured during 1 min of baseline, isometric handgrip exercise (IHG) to fatigue, 2 min of post-exercise circulatory occlusion (PECO), and 3 min of recovery. Women with PTSD were unable to increase AP content per burst compared to controls throughout IHG and PECO (main effect of group: P = 0.026). Furthermore, relative to controls, women with PTSD recruited fewer AP clusters per burst during the first (controls: ∆1.3 [1.2] vs. PTSD: ∆−0.2 [0.8]; P = 0.016) and second minute (controls: ∆1.2 [1.1] vs. PTSD: ∆−0.1 [0.8]; P = 0.022) of PECO, and fewer subpopulations of larger, previously silent axons during the first (controls: ∆5 [4] vs. PTSD: ∆1 [2]; P = 0.020) and second minute (controls: ∆4 [2] vs. PTSD: ∆1 [2]; P = 0.021) of PECO. Conversely, PTSD did not modify the AP cluster size–latency relationship during baseline, the end of IHG, or PECO (all P = 0.658–0.745). Collectively, these data indicate that women with PTSD demonstrate inherent impairments in the fundamental neural coding patterns elicited by the sympathetic nervous system during IHG and exercise pressor reflex activation. [ABSTRACT FROM AUTHOR]

Group mean slopes and r2 are given in E and F. AP indicates action potential; PTSD, posttraumatic stress disorder; and TPR, total peripheral resistance. Keywords: action potentials; stress disorders, post-traumatic; sympathetic nervous system EN action potentials stress disorders, post-traumatic sympathetic nervous system 1483 1485 3 11/08/22 20221108 NES 221108 Posttraumatic stress disorder (PTSD) is highly prevalent in women and is associated with an increased risk of developing cardiovascular disease.[1] Sympathetic nervous system dysregulation (eg, exaggerated sympathetic outflow) is thought to contribute to this increased risk[2]; however, previous studies of sympathetic activity in individuals with PTSD were conducted in the supine position, despite humans spending majority of their day upright. Our hypothesis was that women with PTSD would display greater vasoconstrictor responses associated with exaggerated increases in sympathetic action potential (AP) recruitment patterns during orthostasis. [Extracted from the article]

Introduction: Increasing age is associated with decrements in sweat rate that compromise whole-body total heat loss (evaporative + dry heat exchange) in both men and women during moderate-to-vigorous exercise in dry heat. Similarly, young women also display reductions in sweating (that lower evaporative heat loss) relative to young men in such conditions. Nevertheless, it remained unclear whether these effects act synergistically to exacerbate the age-related decline in whole-body total heat loss in women relative to men. We therefore assessed the interrelation between age and sex on whole-body total heat loss during light, moderate, and vigorous exercise in dry heat. Methods: To achieve this, we used direct and indirect calorimetry to assess whole-body total heat loss and metabolic heat production (respectively) in 46 men and 34 women age between 18 and 70 yr. Participants performed three, 30-min bouts of cycling at metabolic heat productions of 150 (light), 200 (moderate), and 250 (vigorous) W·m−2, each separated by 15-min recovery in dry heat (40°C, ~15% relative humidity). Results: Whole-body total heat loss was ~5% lower in women relative to men during moderate and vigorous exercise (both, P < 0.01), irrespective of age. Total heat loss declined with age during moderate and vigorous exercise in both men and women (all, P < 0.050), although the rate of that decline (~4% per decade) was similar between men and women across all exercise bouts (all, P > 0.050). Conclusions: We show that, when assessed in dry heat, whole-body total heat loss is lower in women relative to men, irrespective of age. Furthermore, total heat loss declines with increasing age in both men and women during moderate-to-vigorous exercise, albeit the rate of that decline is not appreciably modified by sex. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Black‐African descendants are thought, by some, to possess genotypic adaptations conducive to survival in hot climates. We therefore assessed whether Canadian residents of black‐African descent display enhanced whole‐body total heat loss (evaporative plus dry heat exchange) in comparison to Caucasian Canadians during exercise eliciting matched heat‐loss requirements in dry heat.What is the main finding and its importance?Neither whole‐body total heat loss nor body heat storage differed significantly between groups, irrespective of the exercise intensity. Our findings indicate that genotypic adaptations associated with ethnicity do not appreciably modify whole‐body heat exchange during exercise–heat stress. Ethnicity has long been thought to modulate thermoregulatory function; however, an evaluation of whole‐body heat exchange in men of black‐African descent and Caucasian men (white‐European descendants), born and raised in the same climate, during exercise eliciting matched heat‐loss requirements remained unavailable. We therefore used direct calorimetry to assess whole‐body total heat loss (evaporative plus dry heat exchange) in young (18–30 years of age), second‐generation (or higher) black‐African (n = 11) and Caucasian (n = 11) men. Participants performed three 30 min bouts of semi‐recumbent cycling at fixed metabolic heat productions (and therefore matched heat‐loss requirements between groups) of 200 (light), 250 (moderate) and 300 W m−2 (vigorous), each followed by 15 min recovery, in dry heat (40°C, ∼13% relative humidity). Across all exercise bouts, dry (P = 0.435) and evaporative (P = 0.600) heat exchange did not differ significantly between groups. As such, total heat loss during light, moderate and vigorous exercise was similar between groups (P = 0.777), averaging [mean (SD)] 177 (10), 217 (13) and 244 (20) W m−2 in black‐African men and 172 (13), 212 (17) and 244 (17) W m−2 in Caucasian men. Accordingly, body heat storage across all exercise bouts (summation of metabolic heat production and total heat loss) was also similar between the black‐African [568 (142) kJ] and Caucasian groups [623 (124) kJ; P = 0.356]. We demonstrated that, when assessed in young, second‐generation (or higher) black‐African and Caucasian men during exercise eliciting matched heat‐loss requirements in dry heat, ethnicity did not significantly modulate whole‐body dry and evaporative heat exchange or the resulting changes in total heat loss and body heat storage. [ABSTRACT FROM AUTHOR]

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss. [ABSTRACT FROM AUTHOR]