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R4051 --> 752.5 --> Background: Posttraumatic stress disorder (PTSD) is more prevalent in women than men and is associated with an increased risk for dementia. Indeed, we previously showed that cognitive function is impaired in women with PTSD, but the underlying mechanisms remain unknown. In patients with mild cognitive impairment, the cardiovascular response during cognitive tasks have been shown to be blunted. Thus, we hypothesized that cardiovascular and sympathetic neural responses to a cognitive task would be smaller in women with PTSD than healthy women. Methods: We measured heart rate (HR), mean arterial pressure (MAP), cardiac output (CO, Modelflow), total peripheral resistance (TPR = MAP/CO), and muscle sympathetic nerve activity (MSNA, microneurography) in 16 women with PTSD (42 ± 11 [SD] yrs) and 9 age‐matched healthy women (controls; 41 ± 9 yrs) during 3 min of the Stroop Color and Word Test (SCWT) in the supine position. Results: In response to SCWT, HR, MAP, and CO increased (all P < 0.001) but TPR remained unchanged (P = 0.753) in both groups. Increases (Δ) in HR (6 ± 4 vs. 11 ± 6 bpm) and CO (0.6 ± 0.6 vs. 0.9 ± 0.4 L/min) during SCWT were smaller in PTSD than controls (both P < 0.05), while ΔMAP was similar between groups (P = 0.169). MSNA burst frequency and incidence were significantly higher in women with PTSD than controls at baseline and throughout SCWT (P = 0.003), but ΔMSNA during SCWT was similar between groups. Conclusions: Cardiovascular, but not sympathetic neural responses to SCWT were blunted in women with PTSD. Our findings suggest that cognitive impairment in women with PTSD may be related to the insufficient cardiac response rather than sympathetic vasoconstriction during cognitive tasks. [ABSTRACT FROM AUTHOR]

R2284 --> 752.6 --> Posttraumatic stress disorder (PTSD) is a debilitating psychiatric disorder that is more prevalent in women than men and has been linked to an elevated risk of developing cardiovascular disease. Although the physiological mechanisms are unclear, it is thought that exaggerated neuro‐cardiovascular reactivity is partially responsible. Indeed, women with PTSD demonstrate exaggerated muscle sympathetic nerve activity (MSNA) responses at the onset of exercise. However, it is unknown whether PTSD modifies the underlying sympathetic action potentials (AP) coding patterns that comprise the integrated MSNA signal during fatiguing exercise in women. We therefore hypothesized that women with PTSD will exhibit exaggerated MSNA and AP recruitment compared to women without PTSD during fatiguing handgrip exercise. MSNA and AP discharge patterns (via microneurography and a continuous wavelet transform) were assessed in eleven women with PTSD (43±11 [SD] years) and thirteen women without PTSD (Controls; 40±8 years) during isometric handgrip exercise (IHG) to fatigue at 40% of maximal voluntary contraction (MVC) force, followed by 2 minutes of post‐exercise circulatory occlusion (PECO), and three minutes of recovery. The IHG time was divided equally into five stages. IHG duration (P=0.867) and MVC (P=0.226) were similar between both groups. PTSD did not modify the increase in MSNA and AP frequency or incidence during IHG and PECO (all group‐by‐stage interactions: P=0.294‐0.380). Conversely, throughout IHG and PECO, AP content per burst was greater in the Controls compared to women with PTSD (main effect of group: P=0.026). Furthermore, relative to Controls, women with PTSD were unable to increase the number of AP clusters per burst during the first (Controls: ∆1.3±1.2 vs. PTSD: ∆‐0.2±0.8 clusters/burst; P=0.016) and last minute (Controls: ∆1.2±1.1 vs. PTSD: ∆‐0.1±0.8 clusters/burst; P=0.022) of PECO, and recruited fewer subpopulations of previously silent axons during the first (Controls: ∆5±4 vs. PTSD: ∆1±2 clusters; P=0.020) and last minute (Controls: ∆4±2 vs. PTSD: ∆1±2 clusters; P=0.021) of PECO. Lastly, although an interaction effect was observed for the AP cluster size‐latency relationship during IHG and PECO (P=0.042), post‐hoc analyses revealed that PTSD did not modify this relationship (all P=0.658‐0.999). These data indicate that the central features of sympathetic outflow are impaired in women with PTSD during skeletal muscle metaboreflex activation. [ABSTRACT FROM AUTHOR]

R4109 --> 857.2 --> Maternal obesity increases the risk of adverse pregnancy outcomes. The mechanisms that contribute to this elevated risk are unclear but may be related to overactivation of the sympathetic nervous system. Indeed, sympathetic activation during pregnancy is now regarded as a normal adaptation to maintain homeostasis. However, sympathetic overactivation is associated with gestational hypertensive disorders. It is unknown whether the health related problems linked to maternal obesity (i.e., inflammation, insulin resistance, dyslipidemia) results in sympathetic overactivation during pregnancy. We hypothesized that maternal obesity would induce greater increases in resting muscle sympathetic nerve activity (MSNA) during pregnancy when compared with normal‐weight women. Blood pressure (BP), heart rate and MSNA (microneurography) were recorded during 5 min of supine rest in 14 normal‐weight (Age 30±1.6 [SE] yrs; BMI 22.1±0.6 kg/m2) and 14 obese (Age 28±0.8 yrs; BMI 33.9±1.0 kg/m2) women during early pregnancy (5‐12 weeks), late pregnancy (32 to 34 weeks) and 6‐10 weeks postpartum. Gestational weight gain from early to late pregnancy was not significantly different between groups (11.8±0.9 kg vs. 9.2±2.1 kg, P=0.23). Resting MSNA burst frequency was not different between normal‐weight and obese groups during early pregnancy (17±3 bursts/min vs. 22±4 bursts/min, P=0.35) or postpartum (10±2 bursts/min vs. 8±2 bursts/min P=0.74) but was significantly greater in the obese group during late pregnancy (23±4 bursts/min vs. 35±4 bursts/min, Figure A, P=0.031). There were no significant changes in resting MSNA from early to late pregnancy in the normal‐weight group (P=0.67) whereas the obese group had significant increases in MSNA from early to late pregnancy (P=0.002). These findings were also apparent when MSNA was characterized as burst incidence and total activity (Figure B and C). Although still within the normotensive range, women with obesity had greater levels of systolic BP when compared with normal‐weight women across all time points (Figure D, group main effect P=0.002). Diastolic BP was lower during pregnancy when compared with postpartum and this was similar between groups (Figure E, gestation main effect P<0.001). Heart rate was greater during early pregnancy when compared with postpartum and increased similarly in both groups during late pregnancy (Figure F, gestation main effect P<0.001). These findings suggest that maternal obesity is associated with greater increases in sympathetic activation even during normotensive pregnancy and may play a role in the increased risk of adverse maternal and fetal outcomes in women with obesity. [ABSTRACT FROM AUTHOR]

R2816 --> 857.6 --> Post‐menopausal women are at greater risk for cardiovascular disease compared with age‐matched men. An exaggerated morning blood pressure surge (MBPS) in post‐menopausal women is well established as an independent risk factor for cardiovascular events. Dietary nitrate supplements such as nitrate‐rich beetroot juice (BRJ) may reduce blood pressure (BP), but no study has investigated the chronic effects of BRJ on MBPS and sympathetic neural control during orthostasis in post‐menopausal women. We hypothesized that dietary nitrate supplements would decrease MBPS and muscle sympathetic nerve activity (MSNA, microneurography) in post‐menopausal women. We performed a double‐blind, placebo‐controlled, cross‐over trial and randomly assigned healthy women [n=14, 64±3 (SD) yr] to either dietary nitrate supplements (140 ml of BRJ; 800 mg nitrate/day) or placebo (140 ml of nitrate‐depleted BRJ daily) for 2 weeks each with ≥2 weeks of washout. Twenty‐four‐hour ambulatory BP monitoring was performed and MBPS was calculated as the morning systolic BP (SBP; averaged for 2 h after wake‐up) minus the lowest nocturnal SBP before and after 2‐week BRJ or placebo intervention. BP, heart rate, and MSNA were measured during 3‐min supine rest and 5‐min 60° head‐up tilt (HUT). Cardiac output (Qc; C2H2 rebreathing) and total peripheral resistance (TPR=mean BP/Qc × 80) were also measured. MBPS decreased after BRJ intervention (Figure A; p=0.043). BRJ did not change hemodynamics or MSNA during supine rest (Figure B‐E; all, p>0.05). However, upright TPR was reduced (Figure C; p=0.007), while Qc trended greater (Figure B; p=0.072) after BRJ intervention. During HUT, MSNA burst frequency (53±15 pre vs. 48±10 bursts/min post, p=0.508 for posture × intervention interaction) and burst incidence (70±17 vs. 63±15 bursts/100 heart beats, p=0.199 for interaction) were similar, but mean burst area (Figure D; p=0.010) and total activity (Figure E; p=0.015) were lower after BRJ intervention. Placebo had no significant impact on hemodynamics and MSNA in the supine position or during HUT in post‐menopausal women (all, p<0.05). Collectively, dietary nitrate supplements decrease morning surge in BP and upright MSNA and vasoconstriction in post‐menopausal women. Whether reductions in sympathetic activation and peripheral vasoconstriction during orthostasis contribute to the reduced MBPS in these women remains to be determined. [ABSTRACT FROM AUTHOR]

R2618 --> 857.5 --> Women who reached early menopause (EM, 40‐44 yrs) have a greater risk for cardiovascular disease than women with normal menopause (NM, 50‐54 yrs), which may be attributed to a longer duration of estrogen loss and a greater reduction in nitric oxide bioavailability in both the peripherals and center. Previous studies have shown that dietary nitrate supplementation improves cardiovascular function in older women, but how autonomic neural control changes in daily living, such as during exercise, has been involved is unclear. We examined the hypothesis that 2wks continuous use of dietary nitrate supplements would attenuate the exercise pressor reflex in older women with EM. Six EM (65±4 [SD] yrs) and 8 NM (64±2 yrs) women participated in this randomized, placebo‐controlled, double‐blind, cross‐over pilot study. All subjects underwent 2 wks of beetroot juice (BRJ; 140 ml containing ~800 mg nitrate per day) or placebo (140 ml nitrate‐depleted BRJ, daily) intervention with ≥14 days of wash‐out. Before and after each intervention period, subjects performed SHG using the dominant hand at 40% of maximum voluntary contraction (MVC) until fatigue, followed by 2 min of PECA with an upper arm cuff inflated to 250 mmHg. Heart rate (HR; ECG), blood pressure (BP; finger photoplethysmography), muscle sympathetic nerve activity (MSNA; microneurography), and respiration (capnography) were continuously measured. In addition, 24‐h ambulatory BP standard deviation (SD) was monitored before and after each intervention (an indication of BP variability). There were no differences in baseline HR, BP and MSNA, MVC, and the time to fatigue between the EM and NM groups before and after intervention (all p>0.05). At the first 30 s of SHG, the EM group showed significant decreases in MSNA burst frequency (DBF; ‐4.5±6.5 in EM vs. 2.5±6.2 bursts/min in NM, p=0.065) and burst incidence (DBI; ‐10.6±12.6 vs. 2.6±8.4 bursts/100 heartbeats, p=0.037) after BRJ intervention compared with the NM group (Figure1A and B). However, there were no differences between groups at fatiguing exercise and during PECA after the intervention. The interventional changes in 24‐h diastolic BP SD had a positive correlation with ΔMSNA BF (r=0.55, p=0.053) and BI (r=0.58, p=0.036) at the first 30 s of SHG in all subjects and EM individuals were in the left‐lower area (Figure2 A and B). These results suggest that dietary nitrate supplementation may attenuate and mechanoreflex, but not the metaboreflex, in older women with EM during static hand grip, which has a relation with BP variability during ambulation. Certainly, these preliminary observations need to be verified in more older women in future studies. [ABSTRACT FROM AUTHOR]