scholarly journals Sympathetic activation in chronic anxiety: not just at the “height” of stress. Editorial Focus on “Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety”

2018 ◽  
Vol 120 (1) ◽  
pp. 7-8
Author(s):  
Megan M. Wenner
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Chronic Anxiety

scholarly journals Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety

2018 ◽  
Vol 120 (1) ◽  
pp. 11-22 ◽  
Author(s):  
Seth W. Holwerda ◽  
Rachel E. Luehrs ◽  
Allene L. Gremaud ◽  
Nealy A. Wooldridge ◽  
Amy K. Stroud ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Acute Stress ◽  
Physiological Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Chronic Anxiety

Relative burst amplitude of muscle sympathetic nerve activity (MSNA) is an indicator of augmented sympathetic outflow and contributes to greater vasoconstrictor responses. Evidence suggests anxiety-induced augmentation of relative MSNA burst amplitude in patients with panic disorder; thus we hypothesized that acute stress would result in augmented relative MSNA burst amplitude and vasoconstriction in individuals with chronic anxiety. Eighteen participants with chronic anxiety (ANX; 8 men, 10 women, 32 ± 2 yr) and 18 healthy control subjects with low or no anxiety (CON; 8 men, 10 women, 39 ± 3 yr) were studied. Baseline MSNA and 24-h blood pressure were similar between ANX and CON ( P > 0.05); however, nocturnal systolic blood pressure % dipping was blunted among ANX ( P = 0.02). Relative MSNA burst amplitude was significantly greater among ANX compared with CON immediately preceding (anticipation) and during physiological stress [2-min cold pressor test; ANX: 73 ± 5 vs. CON: 59 ± 3% arbitrary units (AU), P = 0.03] and mental stress (4-min mental arithmetic; ANX: 65 ± 3 vs. CON: 54 ± 3% AU, P = 0.02). Increases in MSNA burst frequency, incidence, and total activity in response to stress were not augmented among ANX compared with CON ( P > 0.05), and reduction in brachial artery conductance during cold stress was similar between ANX and CON ( P = 0.92). Relative MSNA burst amplitude during mental stress was strongly correlated with state ( P < 0.01) and trait ( P = 0.01) anxiety (State-Trait Anxiety Inventory), independent of age, sex, and body mass index. Thus in response to acute stress, both mental and physiological, individuals with chronic anxiety demonstrate selective augmentation in relative MSNA burst amplitude, indicating enhanced sympathetic drive in a population with higher risk for cardiovascular disease. NEW & NOTEWORTHY Relative burst amplitude of muscle sympathetic nerve activity in response to acute mental and physiological stress is selectively augmented in individuals with chronic anxiety, which is a prevalent condition that is associated with the development of cardiovascular disease. Augmented sympathetic burst amplitude occurs with chronic anxiety in the absence of common comorbidities. These findings provide important insight into the relation between anxiety, acute stress and sympathetic activation.

scholarly journals Chronic intermittent hypoxia in humans during 28 nights results in blood pressure elevation and increased muscle sympathetic nerve activity

2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Chronic Intermittent Hypoxia ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Healthy Humans

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

Slow head-up tilt causes lower activation of muscle sympathetic nerve activity: loading speed dependence of orthostatic sympathetic activation in humans

2009 ◽  
Vol 297 (1) ◽  
pp. H53-H58 ◽  
Author(s):  
Atsunori Kamiya ◽  
Toru Kawada ◽  
Shuji Shimizu ◽  
Satoshi Iwase ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Tilt Angle ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Amplitude Dependence ◽  
Sympathetic Activation ◽  
Control Test ◽  
Nerve Activity ◽  
Lower Activation ◽  
Head Up Tilt

Many earlier human studies have reported that increasing the tilt angle of head-up tilt (HUT) results in greater muscle sympathetic nerve activity (MSNA) response, indicating the amplitude dependence of sympathetic activation in response to orthostatic stress. However, little is known about whether and how the inclining speed of HUT influences the MSNA response to HUT, independent of the magnitude of HUT. Twelve healthy subjects participated in passive 30° HUT tests at inclining speeds of 1° (control), 0.1° (slow), and 0.0167° (very slow) per second. We recorded MSNA (tibial nerve) by microneurography and assessed nonstationary time-dependent changes of R-R interval variability using a complex demodulation technique. MSNA averaged over every 10° tilt angle increased during inclination from 0° to 30°, with smaller increases in the slow and very slow tests than in the control test. Although a 3-min MSNA overshoot after reaching 30° HUT was observed in the control test, no overshoot was detected in the slow and very slow tests. In contrast with MSNA, increases in heart rate during the inclination and after reaching 30° were similar in these tests, probably because when compared with the control test, greater increases in plasma epinephrine counteracted smaller autonomic responses in the very slow test. These results indicate that slower HUT results in lower activation of MSNA, suggesting that HUT-induced sympathetic activation depends partially on the speed of inclination during HUT in humans.

Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

1991 ◽  
Vol 261 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
T. Matsukawa ◽  
E. Gotoh ◽  
K. Minamisawa ◽  
M. Kihara ◽  
S. Ueda ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Nerve Activity ◽  
Intravenous Infusions

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.

scholarly journals Effects of dynamic arm and leg exercise on muscle sympathetic nerve activity and vascular conductance in the inactive leg

2019 ◽  
Vol 127 (2) ◽  
pp. 464-472
Author(s):  
Connor J. Doherty ◽  
Trevor J. King ◽  
Anthony V. Incognito ◽  
Jordan B. Lee ◽  
Andrew D. Shepherd ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Burst Frequency ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Leg Cycling ◽  
Concurrent Exercise

The influence of muscle sympathetic nerve activity (MSNA) responses on local vascular conductance during exercise are not well established. Variations in exercise mode and active muscle mass can produce divergent MSNA responses. Therefore, we sought to examine the effects of small- versus large-muscle mass dynamic exercise on vascular conductance and MSNA responses in the inactive limb. Thirty-five participants completed two study visits in a randomized order. During visit 1, superficial femoral artery (SFA) blood flow (Doppler ultrasound) was assessed at rest and during steady-state rhythmic handgrip (RHG; 1:1 duty cycle, 40% maximal voluntary contraction), one-leg cycling (17 ± 3% peak power output), and concurrent exercise at the same intensities. During visit 2, MSNA (contralateral fibular nerve microneurography) was acquired successfully in 12/35 participants during the same exercise modes. SFA blood flow increased during RHG ( P < 0.0001) and concurrent exercise ( P = 0.03) but not cycling ( P = 0.91). SFA vascular conductance was unchanged during RHG ( P = 0.88) but reduced similarly during concurrent and cycling exercise (both P < 0.003). RHG increased MSNA burst frequency ( P = 0.04) without altering burst amplitude ( P = 0.69) or total MSNA ( P = 0.26). In contrast, cycling and concurrent exercise had no effects on MSNA burst frequency (both P ≥ 0.10) but increased burst amplitude (both P ≤ 0.001) and total MSNA (both P ≤ 0.007). Across all exercise modes, the changes in MSNA burst amplitude and SFA vascular conductance were correlated negatively ( r = −0.43, P = 0.02). In summary, the functional vascular consequences of alterations in sympathetic outflow to skeletal muscle are most closely associated with changes in MSNA burst amplitude, but not frequency, during low-intensity dynamic exercise. NEW & NOTEWORTHY Low-intensity small- versus large-muscle mass exercise can elicit divergent effects on muscle sympathetic nerve activity (MSNA). We examined the relationships between changes in MSNA (burst frequency and amplitude) and superficial femoral artery (SFA) vascular conductance during rhythmic handgrip, one-leg cycling, and concurrent exercise in the inactive leg. Only changes in MSNA burst amplitude were inversely associated with SFA vascular conductance responses. This result highlights the functional importance of measuring MSNA burst amplitude during exercise.

Sex differences in dynamic blood pressure regulation: beat-by-beat responses to muscle sympathetic nerve activity

2020 ◽  
Vol 319 (3) ◽  
pp. H531-H538 ◽  
Author(s):  
Yasmine Coovadia ◽  
Tessa E. Adler ◽  
Craig D. Steinback ◽  
Graham M. Fraser ◽  
Charlotte W. Usselman
Keyword(s):  
Blood Pressure ◽  
Sex Differences ◽  
Young Women ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Blood Pressure Regulation ◽  
Sympathetic Outflow ◽  
Pressure Regulation ◽  
Nerve Activity

We demonstrate that during acute sympathoinhibition, women demonstrate more sustained increases in blood pressure following sympathetic bursts of activity than men. Likewise, during prolonged sympathetic quiescence, blood pressure is less labile in women than men. This suggests that lower overall blood pressure in young women may not be mediated by smaller beat-by-beat changes in blood pressure in response to sympathetic outflow but may instead be mediated by a lower frequency of sympathetic bursts.

Basis for the cardiac-related rhythm in muscle sympathetic nerve activity of humans

2003 ◽  
Vol 284 (2) ◽  
pp. H584-H597 ◽  
Author(s):  
Susan M. Barman ◽  
Paul J. Fadel ◽  
Wanpen Vongpatanasin ◽  
Ronald G. Victor ◽  
Gerard L. Gebber
Keyword(s):  
Sympathetic Nerve ◽  
Nonlinear Oscillator ◽  
Inverse Relationship ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cyclic Change ◽  
Nerve Activity ◽  
Random Activity ◽  
Burst Amplitude ◽  
Central Oscillator

We tested the hypothesis that the cardiac-related rhythm in muscle sympathetic nerve activity (MSNA) of humans reflects entrainment of a central oscillator by pulse-synchronous baroreceptor nerve activity. Partial autospectral analysis was used to mathematically remove the portion of cardiac-related power in MSNA autospectra that was attributable to its linear relationship to the ECG. In 54 of 98 cases, ≥15% of cardiac-related power remained after partialization with the ECG; peak residual cardiac-related power was often at a frequency different than heart rate. When assessed on a cardiac-related burst-by-burst basis, there was a progressive and cyclic change in the ECG-MSNA interval (delay from R wave to peak of cardiac-related burst) on the time scale of respiration in four subjects. In these subjects, as well as in some in which the interval appeared to change randomly, there was an inverse relationship between the ECG-MSNA interval and cardiac-related burst amplitude. However, in 45% of the cases, these parameters were not related. These results support the view that the cardiac-related rhythm in MSNA reflects forcing of a nonlinear oscillator rather than periodic inhibition of unstructured, random activity.

Changes in muscle sympathetic nerve activity and renal function during positive-pressure breathing in humans

1994 ◽  
Vol 266 (4) ◽  
pp. R1220-R1228 ◽  
Author(s):  
S. Tanaka ◽  
S. Sagawa ◽  
K. Miki ◽  
J. R. Claybaugh ◽  
K. Shiraki
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Recovery Period ◽  
Cardiovascular Responses ◽  
Positive Pressure ◽  
Urinary Flow ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Continuous Positive Pressure

The possibility that the decreased urinary flow during continuous positive-pressure breathing (CPPB) may be a consequence of a reflex mediated via the cardiopulmonary baroreceptors to increase neurohumoral secretion or to change the sympathetic outflow was assessed. Muscle sympathetic nerve activity (MSNA) on the right peroneal nerve, vasoactive hormones, and renal and cardiovascular responses were measured during CPPB (+12 mmHg) in 10 male subjects (22.0 +/- 0.6 yr, 66.8 +/- 1.5 kg body wt). The experiments consisted of a 1-h control, 1 h with CPPB (experimental) or without CPPB (a time control), and a 1-h recovery period. Two blood samples were taken during each period for measurements of arginine vasopressin (AVP), plasma aldosterone (PAldo), plasma renin activity (PRA), norepinephrine, and atrial natriuretic peptide (ANP), and urine was collected hourly for the measurement of urine volume and electrolytes and clearances. MSNA rapidly increased (P < 0.05) at the onset of CPPB, continued to increase during exposure, and rapidly returned to the normal level at recovery. The MSNA changes coincided with increased plasma NE and were concurrent with a reduced (P < 0.05) urine output associated with a reduction of both free water and osmolal clearances, Na+ and osmolal excretions, and creatinine clearance (glomerular filtration rate). AVP and PRA increased (P < 0.05), whereas PAldo and ANP were unchanged. The results are consistent with the concept that increased sympathetic outflow may play a role in the reduction of urinary output and Na+ excretion during unloading of the cardiopulmonary receptors.

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