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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]

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]

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]

While biological sex affects the neurocirculatory adjustments to exercise, the effects of sex hormones on sympathetic action potential (AP) patterns and ensuing vascular transduction remain unknown. We tested the hypothesis that males, and females using oral contraceptive pills (OCPs), would demonstrate larger increases in sympathetic activation and sympathetic vascular transduction compared with naturally menstruating females during static handgrip exercise (SHG) and postexercise circulatory occlusion (PECO). Young males [ n = 14, 25 (5) yr], females using OCPs [ n = 16, 24 (6) yr], and naturally menstruating females [ n = 18, 26 (4) yr] underwent assessments of multiunit muscle sympathetic nerve activity (MSNA)/AP discharge patterns (microneurography) and femoral artery blood flow (ultrasound) during fatiguing SHG at 40% maximum voluntary contraction and 2-min PECO. Sympathetic vascular transduction was determined as the quotient of the change in leg vascular conductance (LVC) and MSNA/AP discharge. Males demonstrated greater increases in APs/burst [males: Δ7 (6) vs. midluteal: Δ2 (3), P = 0.028] and total AP clusters [males: Δ5 (3) vs. midluteal: Δ2 (3), P = 0.008] compared with naturally menstruating females only but not those using OCPs during exercise (APs/burst: P = 0.171, total clusters: P = 0.455). Sympathetic vascular transduction of MSNA burst amplitude, APs/burst, and total AP clusters was greater in males and females using OCPs compared with naturally menstruating females (range: P = 0.004-0.044). In contrast, during PECO no group differences were observed in AP discharge (range: P = 0.510-0.872), and AP discharge was not related to LVC during PECO (range: P = 0.08-0.949). These data indicate that biological sex and OCP use impact the central generation of AP discharge, as well as the transduction of these neuronal messages into peripheral vasoconstriction during static exercise.

The current study evaluated the hypothesis that 6 mo of exercise-based cardiac rehabilitation (CR) would improve sympathetic neural recruitment in patients with ischemic heart disease (IHD). Microneurography was used to evaluate action potential (AP) discharge patterns within bursts of muscle sympathetic nerve activity (MSNA), in 11 patients with IHD (1 female; 61 ± 9 yr) pre (pre-CR) and post (post-CR) 6 mo of aerobic and resistance training-based CR. Measures were made at baseline and during maximal voluntary end-inspiratory (EI-APN) and end-expiratory apneas (EE-APN). Data were analyzed during 1 min of baseline and the second half of apneas. At baseline, overall sympathetic activity was less post-CR (all P < 0.01). During EI-APN, AP recruitment was not observed pre-CR (all P > 0.05), but increases in both within-burst AP firing frequency (Δpre-CR: 2 ± 3 AP spikes/burst vs. Δpost-CR: 4 ± 3 AP spikes/burst; P = 0.02) and AP cluster recruitment (Δpre-CR: -1 ± 2 vs. Δpost-CR: 2 ± 2; P < 0.01) were observed in post-CR tests. In contrast, during EE-APN, AP firing frequency was not different post-CR compared with pre-CR tests (Δpre-CR: 269 ± 202 spikes/min vs. Δpost-CR: 232 ± 225 spikes/min; P = 0.54), and CR did not modify the recruitment of new AP clusters (Δpre-CR: -1 ± 3 vs. Δpost-CR: 0 ± 1; P = 0.39), or within-burst firing frequency (Δpre-CR: 3 ± 3 AP spikes/burst vs. Δpost-CR: 2 ± 2 AP spikes/burst; P = 0.21). These data indicate that CR improves some of the sympathetic nervous system dysregulation associated with cardiovascular disease, primarily via a reduction in resting sympathetic activation. However, the benefits of CR on sympathetic neural recruitment may depend upon the magnitude of initial impairment.