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Muscle sympathetic nerve activity (MSNA) responsiveness to mental stress is highly variable between individuals. Although stress perception has been posited as a contributor to the MSNA variability during mental stress, prior studies have been inconclusive. Furthermore, the importance of stress appraisal and coping on MSNA reactivity to mental stress has not been investigated. We hypothesize that appraisal of mental stress as a threat (i.e., perceived demands of stress exceed coping resources) versus a challenge (i.e., perceived coping resources sufficient for demands of stress) would be associated with greater MSNA reactivity. Twenty healthy adults (11 males, 9 females, 21 ± 3 yr, 23 ± 3 kg/m 2 ) participated. Beat-by-beat blood pressure (finger plethysmography), heart rate (electrocardiography), and MSNA (microneurography) were recorded during a 10-min quiet rest followed by the Trier Social Stress Test (TSST). After each phase of the TSST (i.e., speech prep, speech, and mental arithmetic), participants reported threat versus challenge appraisal. Endorsement of a threat appraisal was positively associated with changes in MSNA burst frequency ( r = 0.548, P = 0.018), burst incidence ( r = 0.599, P = 0.009), and total MSNA ( r = 0.697, P = 0.037) during the speech stress period. Moreover, increases in threat appraisal across tasks was associated with elevated MSNA burst frequency ( r = 0.531, P = 0.023), incidence ( r = 0.512, P = 0.030), and total MSNA ( r = 0.727, P = 0.027) responsiveness. These findings support an association between stress appraisal processes and postganglionic sympathetic neural reactivity to psychosocial stress and may partially explain interindividual variability in MSNA responses to mental stress. NEW & NOTEWORTHY The present study investigated the association between stress appraisal and muscle sympathetic nerve activity (MSNA) reactivity to the Trier Social Stress Test. Appraisal of the stress task as a threat (i.e., perceived inability to cope with the demands of the task) was associated with exaggerated MSNA reactivity to mental stress in humans. Threat appraisal is associated with exaggerated sympathetic reactivity to stress, potentially underlying the commonly observed interindividual variability in MSNA responsiveness to mental stress.

Core body temperature (CBT) reductions occur before and during the sleep period, with the extent of presleep reductions corresponding to sleep onset and quality. Presleep reductions in CBT coincide with increased cardiac parasympathetic activity measured via heart rate variability (HRV), and while this appears to persist into the sleep period, individual differences in presleep CBT decline and nocturnal HRV remain unexplored. The purpose of the current study was to assess the relationship between individual differences in presleep CBT reductions and nocturnal heart rate (HR) and HRV in a population of 15 objectively poor sleeping adults [10 males, 5 females; age, 33 ± 4 yr; body mass index (BMI) 27 ± 1 kg/m 2 ] with the hypothesis that blunted CBT rate of decline would be associated with elevated HR and reduced nocturnal HRV. Following an adaptation night, all participants underwent an overnight, in-laboratory sleep study with simultaneous recording of polysomnographic sleep including electrocardiography (ECG) and CBT recording. Correlations between CBT rate of change before sleep and nocturnal HRV were assessed. Blunted rate of CBT decline was significantly associated with increased heart rate (HR) in stage 2 ( N2 ; R = 0.754, P = 0.001), stage 3 ( N3 ; R = 0.748, P = 0.001), and rapid-eye movement (REM; R = 0.735, P = 0.002). Similarly, blunted rate of CBT decline before sleep was associated with reduced HRV across sleep stages. These findings indicate a relationship between individual differences in presleep thermoregulatory processes and nocturnal cardiac autonomic function in poor sleeping adults. NEW & NOTEWORTHY Core body temperature (CBT) reductions before sleep onset coincide with increases in heart rate variability (HRV) that persist throughout the sleep period. However, the relationship between individual differences in the efficiency of presleep core temperature regulation and nocturnal heart rate variability remains equivocal. The present study reports an association between the magnitude of presleep core body temperature changes and nocturnal parasympathetic activity, highlighting overlap between thermoregulatory processes before sleep and nocturnal cardiac autonomic function.

K-complexes are a key marker of nonrapid eye movement sleep, specifically during stages II sleep. Recent evidence suggests the heart rate responses to a K-complexes may differ between men and women. The purpose of this study was to compare beat-to-beat blood pressure responses to K-complexes in men and women. We hypothesized that the pressor response following a spontaneous K-complex would be augmented in men compared with women. Ten men [age: 23 ± 2 yr, body mass index (BMI): 28 ± 4 kg/m 2 ] and ten women (age: 23 ± 5 yr, BMI: 25 ± 4 kg/m 2 ) were equipped with overnight finger plethysmography and standard 10-lead polysomnography. Hemodynamic responses to a spontaneous K-complex during stable stage II sleep were quantified for 10 consecutive cardiac cycles, and measurements included systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate. K-complex elicited greater pressor responses in men when blood pressures were expressed as SAP (cardiac cycle × sex: P = 0.007) and DAP (cardiac cycle × sex: P = 0.004). Heart rate trended to be different between men and women (cardiac cycle × sex: P = 0.078). These findings suggest a divergent pressor response between men and women following a spontaneous K-complex during normal stage II sleep. These findings could contribute to sex-specific differences in cardiovascular risk that exist between men and women. NEW & NOTEWORTHY K-complexes during stage II sleep have been shown to elicit acute increases in blood pressure and heart rate, but the role of sex (i.e., male vs. female) in this response is unclear. In the present study, we demonstrate that the pressor response following spontaneous K-complexes were augmented in men compared to age-matched women. The augmented blood pressure reactivity to spontaneous K-complexes during stage II sleep in men advance the field of cardiovascular sex differences, with implications for nocturnal blood pressure control.

Black adults have a higher risk of hypertension compared with non-Hispanic white (NHW) adults, but physiological mechanisms underlying this predisposition remain unclear. This study compared muscle sympathetic nerve activity (MSNA) responses to mental stress in a group of young black and NHW participants. We hypothesized that the sympathoexcitation associated with mental stress would be greater in black adults compared with NHW participants. Thirty-five male adults (19 black, 23 ± 1 yr; 16 NHW, 22 ± 1 yr) were examined during 5-min supine baseline and 5 min of mental stress (via mental arithmetic). Baseline mean arterial pressure (80 ± 2 vs. 82 ± 1 mmHg), heart rate (61 ± 4 vs. 61 ± 2 beats/min), MSNA (13 ± 1 vs. 15 ± 2 bursts/min), and sympathetic baroreflex sensitivity (-1.1 ± 0.4 vs. -1.5 ± 0.3 bursts·100 heart beats -1 ·mmHg -1 ) were not significantly different between NHW and black adults ( P > 0.05), respectively. MSNA reactivity to mental stress was significantly higher in NHW compared with black adults (time × race, P = 0.006), with a particularly divergent responsiveness during the first minute of mental stress in NHW (Δ4 ± 1 burst/min) and black (Δ-2 ± 2 burst/min; P = 0.022) men. Blood pressure and heart rate reactivity to mental stress were similar between groups. In summary, black participants demonstrated a lower MSNA responsiveness to mental stress compared with NHW adults. These findings suggest that, despite a higher prevalence of hypertension, black subjects do not appear to have higher neural and cardiovascular responsiveness to mental stress compared with NHW. NEW & NOTEWORTHY Black men have a blunted muscle sympathetic nerve activity response to mental stress compared with non-Hispanic white (NHW) men, especially at the onset of mental stress when muscle sympathetic nerve activity decreased in blacks and increased in NHW men. Thus, despite a high prevalence of hypertension in blacks, normotensive NHW men display a greater peripheral sympathetic neural reactivity to mental stress than black men.

The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women., (Copyright © 2015 the American Physiological Society.)

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA (n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA (n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.

Recent evidence suggests that young men and women may have different strategies for regulating arterial blood pressure, and the purpose of the present study was to determine if sex differences exist in diastolic arterial pressure (DAP) and muscle sympathetic nerve activity (MSNA) relations during simulated orthostatic stress. We hypothesized that young men would demonstrate stronger DAP-MSNA coherence and a greater percentage of "consecutive integrated bursts" during orthostatic stress. Fourteen men and 14 women (age 23 ± 1 yr) were examined at rest and during progressive lower body negative pressure (LBNP; -5 to -40 mmHg). Progressive LBNP did not alter mean arterial pressure (MAP) in either sex. Heart rate increased and stroke volume decreased to a greater extent during LBNP in women (interactions, P < 0.05). DAP-MSNA coherence was strong (i.e., r ≥ 0.5) at rest and increased throughout all LBNP stages in men. In contrast, DAP-MSNA coherence was lower in women, and responses to progressive LBNP were attenuated compared with men (time × sex, P = 0.029). Men demonstrated a higher percentage of consecutive bursts during all stages of LBNP (sex, P < 0.05), although the percentage of consecutive bursts increased similarly during progressive LBNP between sexes. In conclusion, men and women demonstrate different firing patterns of integrated MSNA during LBNP that appear to be related to differences in DAP oscillatory patterns. Men tend to have more consecutive bursts, which likely contribute to a stronger DAP-MSNA coherence. These findings may help explain why young women are more prone to orthostatic intolerance.

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120-139 and/or diastolic 80-89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

This study examined the effect of combined heat and mental stress on neurovascular control. We hypothesized that muscle sympathetic nerve activity (MSNA) and forearm vascular responses to mental stress would be augmented during heat stress. Thirteen subjects performed 5 min of mental stress during normothermia (Tcore; 37 ± 0°C) and heat stress (38 ± 0°C). Heart rate, mean arterial pressure (MAP), MSNA, forearm vascular conductance (FVC; venous occlusion plethysmography), and forearm skin vascular conductance (SkVCf; via laser-Doppler) were analyzed. Heat stress increased heart rate, MSNA, SkVCf, and FVC at rest but did not change MAP. Mental stress increased MSNA and MAP during both thermal conditions; however, the increase in MAP during heat stress was blunted, whereas the increase in MSNA was accentuated, compared with normothermia (time × condition; P < 0.05 for both). Mental stress decreased SkVCf during heat stress but not during normothermia (time × condition, P < 0.01). Mental stress elicited similar increases in heart rate and FVC during both conditions. In one subject combined heat and mental stress induced presyncope coupled with atypical blood pressure and cutaneous vascular responses. In conclusion, these findings indicate that mental stress elicits a blunted increase of MAP during heat stress, despite greater increases in total MSNA and cutaneous vasoconstriction. The neurovascular responses to combined heat and mental stress may be clinically relevant to individuals frequently exposed to mentally demanding tasks in hyperthermic environmental conditions (i.e., soldiers, firefighters, and athletes).

Neural and cardiovascular responses to mental stress and acute 6 degrees head-down tilt (HDT) were examined separately and combined. We hypothesized sympathoexcitation during mental stress, sympathoinhibition during HDT, and an additive neural interaction during combined mental stress and HDT. Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate (HR) were recorded in 16 healthy subjects (8 men, 8 women) in the supine position during three randomized trials: 1) mental stress (via mental arithmetic), 2) HDT, and 3) combined mental stress and HDT. Mental stress significantly increased MSNA (7+/-1 to 12+/-2 bursts/min; P<0.01), MAP (91+/-2 to 103+/-2 mmHg; P<0.01), and HR (70+/-3 to 82+/-3 beats/min; P<0.01). HDT did not change MSNA or HR, but MAP was reduced (91+/-2 to 89+/-3 mmHg; P<0.05). Combined mental stress and HDT significantly increased MSNA (7+/-1 to 10+/-1 bursts/min; P<0.01), MAP (88+/-3 to 99+/-3 mmHg; P<0.01), and HR (70+/-3 to 82+/-3 beats/min; P<0.01). Increases in MSNA and HR during the combination trial were not different from the sum of the individual trials. However, the increase in MAP during the combination trial was significantly greater than the sum of the individual trials (change of 11+/-1 vs. 9+/-1 mmHg; P<0.05). We conclude that the interaction for MSNA and HR are additive during combined mental stress and HDT but that MAP responses are slightly augmented during the combined trial. These findings demonstrate that sympathetic neural responses to mental stress are unaltered by simulated microgravity.

The purpose of this study was to determine neurovascular responses to mental stress (MS) in the supine and upright postures. MS was elicited in 23 subjects (26 +/- 1 yr) by 5 min of mental arithmetic. In study 1 (n = 9), Doppler ultrasound was used to measure mean blood flow velocity in the renal (RBFV) and superior mesenteric arteries (SMBFV), and venous occlusion plethysmography was used to measure forearm blood flow (FBF). In study 2 (n = 14), leg blood flow (LBF; n = 9) was measured by Doppler ultrasound, and muscle sympathetic nerve activity (MSNA; n = 5) was measured by microneurography. At rest, upright posture increased heart rate and MSNA and decreased LBF, FBF, RBFV, and SMBFV and their respective conductances. MS elicited similar increases in mean arterial blood pressure ( approximately 12 mmHg) and heart rate ( approximately 17 beats/min), regardless of posture. MS in both postures elicited a decrease in RBFV, SMBFV, and their conductances and an increase in LBF, FBF, and their conductances. Changes in blood flow were blunted in the upright posture in all vascular beds examined, but the pattern of the vascular response was the same as the supine posture. MS did not change MSNA in either posture (change: approximately 1 +/- 3 and approximately 3 +/- 3 bursts/min, respectively). In conclusion, the augmented sympathetic activity of the upright posture does not alter heart rate, mean arterial blood pressure, or MSNA responses to MS. MS elicits divergent vascular responses in the visceral and peripheral vasculature. These results indicate that, although the upright posture attenuates vascular responses to MS, the pattern of neurovascular responses does not differ between postures.

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 +/- 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure (n = 12; automated sphygmomanometer) and MSNA (n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 +/- 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups (P < 0.001), and it significantly decreased systolic (130 +/- 3 to 121 +/- 2 mmHg; P = 0.01), diastolic (69 +/- 3 to 61 +/- 2 mmHg; P = 0.04), and mean (89 +/- 2 to 81 +/- 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 +/- 2 to 67 +/- 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.

There are conflicting reports for the role of endogenous opioids on sympathetic and cardiovascular responses to exercise in humans. A number of studies have utilized naloxone (an opioid-receptor antagonist) to investigate the effect of opioids during exercise. In the present study, we examined the effect of morphine (an opioid-receptor agonist) on sympathetic and cardiovascular responses at rest and during isometric handgrip (IHG). Eleven subjects performed 2 min of IHG (30% maximum) followed by 2 min of postexercise muscle ischemia (PEMI) before and after systemic infusion of morphine (0.075 mg/kg loading dose + 1 mg/h maintenance) or placebo (saline) in double-blinded experiments on separate days. Morphine increased resting muscle sympathetic nerve activity (MSNA; 17 +/- 2 to 22 +/- 2 bursts/min; P < 0.01) and increased mean arterial pressure (MAP; 87 +/- 2 to 91 +/- 2 mmHg; P < 0.02), but it decreased heart rate (HR; 61 +/- 4 to 59 +/- 3; P < 0.01). However, IHG elicited similar increases for MSNA, MAP, and HR between the control and morphine trial (drug x exercise interaction = not significant). Moreover, responses to PEMI were not different. Placebo had no effect on resting, IHG, and PEMI responses. We conclude that morphine modulates cardiovascular and sympathetic responses at rest but not during isometric exercise.

Increases in sympathetic neural activity occur independently with either vestibular or mental stimulation, but it is unknown whether sympathetic activation is additive or inhibitive when both stressors are combined. The purpose of the present study was to investigate the combined effects of vestibular and mental stimulation on sympathetic neural activation and arterial pressure in humans. Muscle sympathetic nerve activity (MSNA), arterial pressure, and heart rate were recorded in 10 healthy volunteers in the prone position during 1) head-down rotation (HDR), 2) mental stress (MS; using arithmetic), and 3) combined HDR and MS. HDR significantly (P < 0.05) increased MSNA (9 +/- 2 to 13 +/- 2 bursts/min). MS significantly increased MSNA (8 +/- 2 to 13 +/- 2 bursts/min) and mean arterial pressure (87 +/- 2 to 101 +/- 2 mmHg). Combined HDR and MS significantly increased MSNA (9 +/- 1 to 16 +/- 2 bursts/min) and mean arterial pressure (89 +/- 2 to 100 +/- 3 mmHg). Increases in MSNA (7 +/- 1 bursts/min) during the combination trial were not different from the algebraic sum of each trial performed alone (8 +/- 2 bursts/min). We conclude that the interaction for MSNA and arterial pressure is additive during combined vestibular and mental stimulation. Therefore, vestibular- and stress-mediated increases of MSNA appear to occur independently in humans.