scholarly journals Sympathetic neural reactivity to mental stress in humans: test-retest reproducibility

2015 ◽  
Vol 309 (11) ◽  
pp. R1380-R1386 ◽  
Author(s):  
Ida T. Fonkoue ◽  
Jason R. Carter

Mental stress consistently increases arterial blood pressure, but this reliable pressor response is often associated with highly variable muscle sympathetic nerve activity (MSNA) responsiveness between individuals. Although MSNA has been shown to be reproducible within individuals at rest and during the cold pressor test (CPT), intraindividual reproducibility of MSNA responsiveness to mental stress has not been adequately explored. The purpose of this study was to examine MSNA reactivity to mental stress across three experimental sessions. Sixteen men and women (age 21 ± 1 yr) performed two experimental sessions within a single laboratory visit and a third experimental session 1 mo later. Each experimental session consisted of a mental stress trial via mental arithmetic and a CPT trial. Blood pressure, heart rate (HR), and MSNA were measured, and the consistencies of these variables were determined using intraclass correlation (Cronbach's α coefficient). MSNA, mean arterial pressure (MAP), and HR were highly reproducible across the baselines preceding mental stress (Cronbach's α ≥ 0.816, P ≤ 0.001) and CPT (Cronbach's α ≥ 0.782, P ≤ 0.001). Across the three mental stress trials, changes in MSNA (Cronbach's α = 0.875; P = 0.001), MAP (Cronbach's α = 0.749; P < 0.001), and HR (Cronbach's α = 0.919; P < 0.001) were reproducible. During CPT, changes in MSNA (Cronbach's α = 0.805; P = 0.008), MAP (Cronbach's α = 0.878; P < 0.001), and HR (Cronbach's α = 0.927; P < 0.001) remained consistent across the three sessions. In conclusion, our findings demonstrate that MSNA reactivity to mental stress is consistent within a single laboratory visit and across laboratory sessions conducted on separate days.

2011 ◽  
Vol 110 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Christopher E. Schwartz ◽  
John J. Durocher ◽  
Jason R. Carter

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.


2020 ◽  
Vol 129 (5) ◽  
pp. 1203-1213
Author(s):  
Gabrielle A. Dillon ◽  
Zachary S. Lichter ◽  
Lacy M. Alexander ◽  
Lauro C. Vianna ◽  
Jing Wang ◽  
...  

The magnitude of the increases in blood pressure and muscle sympathetic nerve activity in response to sympathoexcitatory stimuli such as static handgrip, postexercise ischemia, and the cold pressor test are commonly used to assess neurocardiovascular responsiveness. However, limited studies have comprehensively examined the reproducibility of these responses. We demonstrate that the reproducibility of the pressor response to these perturbations was very good within an individual, whereas the reproducibility of the MSNA response was less consistent.


2018 ◽  
Vol 315 (6) ◽  
pp. R1272-R1280 ◽  
Author(s):  
Ida T. Fonkoue ◽  
Seth D. Norrholm ◽  
Paul J. Marvar ◽  
Yunxiao Li ◽  
Melanie L. Kankam ◽  
...  

Posttraumatic stress disorder (PTSD) is characterized by increased sympathetic nervous system (SNS) activity, blunted parasympathetic nervous system (PNS) activity, and impaired baroreflex sensitivity (BRS), which contribute to accelerated cardiovascular disease. Patients with PTSD also have chronic stress-related elevations in resting blood pressure (BP), often in the prehypertensive range; yet, it is unclear if elevated resting blood pressure (ERBP) augments these autonomic derangements in PTSD. We hypothesized that compared with normotensive PTSD (N-PTSD), those with ERBP (E-PTSD) have further increased SNS, decreased PNS activity, and impaired BRS at rest and exaggerated SNS reactivity, PNS withdrawal, and pressor responses during stress. In 16 E-PTSD and 17 matched N-PTSD, we measured continuous BP, ECG, muscle sympathetic nerve activity (MSNA), and heart rate variability (HRV) markers reflecting cardiac PNS activity [standard deviation of R-R intervals (SDNN), root mean square of differences in successive R-R intervals (RMSSD), and high frequency power (HF)] during 5 min of rest and 3 min of mental arithmetic. Resting MSNA ( P = 0.943), sympathetic BRS ( P = 0.189), and cardiovagal BRS ( P = 0.332) were similar between groups. However, baseline SDNN (56 ± 6 vs. 78 ± 8 ms, P = 0.019), RMSSD (39 ± 6 vs. 63 ± 9 ms, P = 0.018), and HF (378 ± 103 vs. 693 ± 92 ms2, P = 0.015) were lower in E-PTSD versus N-PTSD. During mental stress, the systolic blood pressure response ( P = 0.011) was augmented in E-PTSD. Although MSNA reactivity was not different ( P > 0.05), the E-PTSD group had an exaggerated reduction in HRV during mental stress ( P < 0.05). PTSD with ERBP have attenuated resting cardiac PNS activity, coupled with exaggerated BP reactivity and PNS withdrawal during stress.


2000 ◽  
Vol 279 (2) ◽  
pp. R440-R447 ◽  
Author(s):  
Atsunori Kamiya ◽  
Satoshi Iwase ◽  
Daisaku Michikami ◽  
Qi Fu ◽  
Tadaaki Mano

Astronauts usually work under much mental stress. However, it is unclear how and whether or not an exposure to microgravity affects physiological response to mental stress in humans. To examine effects of microgravity on vasomotor sympathetic and peripheral vasodilator responses to mental stress, we performed 10 min of mental arithmetic (MA) before and after 14 days of 6° head-down bed rest (HDBR), a ground-based simulation of spaceflight. Total muscle sympathetic nerve activity (MSNA, measured by microneurography) slightly increased during MA before HDBR, and this increase was augmented after HDBR. Calf blood flow (measured by venous occlusion plethysmography) increased and calf vascular resistance (calculated by dividing mean blood pressure by calf blood flow) decreased during MA before HDBR, but these responses were abolished after HDBR. Increases in heart rate and mean blood pressure during MA were not different between before and after HDBR. These findings suggest that HDBR augmented vasomotor sympathoexcitation but attenuated vasodilatation in the calf muscle in response to mental stress.


2007 ◽  
Vol 103 (1) ◽  
pp. 228-233 ◽  
Author(s):  
J. K. Shoemaker ◽  
L. Mattar ◽  
P. Kerbeci ◽  
S. Trotter ◽  
P. Arbeille ◽  
...  

The mechanism of the pressor response to small muscle mass (e.g., forearm) exercise and during metaboreflex activation may include elevations in cardiac output (Q̇) or total peripheral resistance (TPR). Increases in Q̇ must be supported by reductions in visceral venous volume to sustain venous return as heart rate (HR) increases. Therefore, this study tested the hypothesis that increases in Q̇, supported by reductions in splanchnic volume (portal vein constriction), explain the pressor response during handgrip exercise and metaboreflex activation. Seventeen healthy women performed 2 min of static ischemic handgrip exercise and 2 min of postexercise circulatory occlusion (PECO) while HR, stroke volume and superficial femoral artery flow (Doppler), blood pressure (Finometer), portal vein diameter (ultrasound imaging), and muscle sympathetic nerve activity (MSNA; microneurography) were measured followed by the calculation of Q̇, TPR, and leg vascular resistance (LVR). Compared with baseline, mean arterial blood pressure (MAP) ( P < 0.001) and Q̇ ( P < 0.001) both increased in each minute of exercise accompanied by a ∼5% reduction in portal vein diameter ( P < 0.05). MAP remained elevated during PECO, whereas Q̇ decreased below exercise levels. MSNA was elevated above baseline during the second minute of exercise and through the PECO period ( P < 0.05). Neither TPR nor LVR was changed from baseline during exercise and PECO. The data indicate that the majority of the blood pressure response to isometric handgrip exercise in women was due to mobilization of central blood volume and elevated stroke volume and Q̇ rather than elevations in TVR or LVR resistance.


2013 ◽  
Vol 304 (5) ◽  
pp. H759-H766 ◽  
Author(s):  
Seth T. Fairfax ◽  
Jaume Padilla ◽  
Lauro C. Vianna ◽  
Michael J. Davis ◽  
Paul J. Fadel

Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, −2.9 ± 1.1%; and multiple bursts, −11.0 ± 1.4%; both, P < 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (+3.1 ± 0.5%; P < 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.


1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.


1993 ◽  
Vol 3 (5) ◽  
pp. 303-310 ◽  
Author(s):  
Frank Weise ◽  
Dominique Laude ◽  
Arlette Girard ◽  
Philippe Zitoun ◽  
Jean-Philippe Siché ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Maciej Sinski ◽  
Jacek Lewandowski ◽  
Joanna Bidiuk ◽  
Piotr Abramczyk ◽  
Anna Dobosiewicz ◽  
...  

Rationale : Peripheral chemoreflex contributes to regulation of arterial blood pressure and chemoreceptors respond not only to hypoxia but they are also continuously activated by normal ambient oxygen concentration. Stimulation of chemoreceptors activates sympathetic traffic and this response may be altered in subjects with essential hypertension.. Objective: The aim of our study was to investigate the effect of deactivation of carotid body chemoreceptors on sympathetic activity directly measured as MSNA (muscle sympathetic nerve activity) in young subjects with mild to moderate untreated hypertension. Methods: Twelve patients with essential hypertension (36±9 years, all men, BMI 29±4 kg/m 2 ,) and 8 controls (37±7, men BMI 27±5kg/m 2 ) participated in the study. None of the patients or controls received any medications. MSNA (burst/minute and mean burst amplitude - au), systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate (HR), ECG, hemoglobin saturation with oxygen (Sat%), end tidal CO 2 and respiratory movements were monitored and measured after 10 minute of respiration by non-rebreathing mask with 100% 0 2 or 21% O 2 applied in blinded fashion. Results: Hypertensives had higher resting MSNA (38.6 ±8.6 burst/min vs. 30.3±.7 burst/min, p<0.05), SBP (149.1± 9.9 vs. 124.1 ±11.6, p < 0.05) and DBP (92.1 ±8.6 vs. 78.1 ± 8.9, p< 0.05) than controls. Breathing with 100% oxygen caused significant decrease in MSNA in hypertensives (from 38.6 ± 8.6 burst/min to 26.3 burst/min ± 6.8 and from 100 ± 0 au to 86 ± 18 au, p< 0.05) and no change in MSNA in controls (30.3 ± 5.7 burst/min initially and 27.3 burst/min ± 6.2 after 100% 0 2 , 100 ± 0 au vs. 98 ± 11 au). Blood pressure, end tidal CO 2 , respiration frequency did not change significantly after hyperoxia while HR decreased (from 69.6 ± 9 to 64.1 ± 7 in hypertensives p<0.05 and from 67± 8 to 62.5 ± 7 in controls, p< 0.05). Sat% increased significantly in both groups to 99%. Conclusions: Increased sympathetic activity in young, untreated hypertensives may be caused by the elevated tonic chemoreflex activation.


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