Muscle sympathetic nerve responses to dynamic one-legged exercise: effect of body posture

1993 ◽  
Vol 264 (1) ◽  
pp. H1-H7 ◽  
Author(s):  
C. A. Ray ◽  
R. F. Rea ◽  
M. P. Clary ◽  
A. L. Mark
Keyword(s):  
Sympathetic Nerve ◽  
Venous Return ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Arm Exercise ◽  
Exercise Effect ◽  
Leg Exercise ◽  
Cardiac Filling ◽  
Cardiopulmonary Baroreceptors

Previous studies examining muscle sympathetic nerve activity (MSNA) during dynamic exercise have focused on upper extremity exercise. The present study was undertaken to investigate 1) MSNA responses to dynamic one-legged knee extensions (DLE) and 2) the role of the cardiopulmonary baroreflexes in the modulation of MSNA responses to DLE. MSNA was measured during 4 min of DLE at 20 (n = 10) and 30 W (n = 9) and during 3 min of DLE at 40 W (n = 9). DLE was performed in the upright (sitting) position and MSNA was recorded in the contralateral leg (peroneal nerve). DLE elicited significant increases in mean arterial pressure (MAP) and heart rate (HR; P < 0.05). In contrast to previous studies using dynamic arm exercise, MSNA (bursts/min) decreased by 25% (P < 0.05) during the first minute of DLE from resting control and remained suppressed during the remaining 3 min of DLE at 20 and 30 W. During the first minute of DLE at 40 W, MSNA (bursts/min) decreased by 18% (P < 0.05), but returned to control levels during the last minute of exercise. Because dynamic leg exercise in the upright position increases venous return, we postulated that upright DLE might increase cardiac filling pressures and stimulate the cardiopulmonary baroreceptors resulting in suppression of MSNA. To investigate this possibility, we measured MSNA and central venous pressure (CVP) during 4 min of both supine and upright DLE at 30 W. MAP, HR, and CVP increased and MSNA decreased from 30 +/- 3 to 22 +/- 3 bursts/min (mean exercise value; P < 0.05) during upright DLE.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypovolemia and MSNA discharge patterns: assessing and interpreting sympathetic responses

2003 ◽  
Vol 284 (4) ◽  
pp. H1198-H1204 ◽  
Author(s):  
D. S. Kimmerly ◽  
J. K. Shoemaker
Keyword(s):  
Frequency Response ◽  
Sympathetic Nerve ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Distribution Analysis ◽  
Burst Frequency ◽  
Burst Amplitude ◽  
Reflex Control ◽  
Discharge Patterns

We previously demonstrated that diuretic-induced hypovolemia resulted in an enhanced baroreflex-mediated increase in integrated muscle sympathetic nerve activity (MSNA) and vasomotor tone during lower body negative pressure (LBNP) ( Am J Physiol Heart Circ Physiol 282: H645–H655, 2002). The purpose of this study was to perform a retrospective analysis of these data and examine the ability of relative MSNA burst amplitude distributions to highlight differences in baseline sympathetic nerve discharge patterns. An additional purpose was to determine whether differential responses in MSNA burst frequency and burst amplitude affect conclusions regarding sympathetic reflex control. MSNA, stroke volume (SV, Doppler), and estimated central venous pressure (CVP, dependent arm technique) were measured during LBNP within the placebo (Normo) and diuretic (Hypo; 100 mg/day spironolactone for 3 days) conditions ( n = 8). Compared with Normo, MSNA burst frequency at rest was elevated, and there was a rightward shift in the median of the relative burst amplitude distribution ( P < 0.05) in Hypo. During LBNP, the larger rise in total MSNA during Hypo versus Normo was due to greater increases in relative burst amplitude with no difference in the burst frequency response. The MSNA burst frequency response to LBNP was shifted to a higher position on the same MSNA-CVP curve during Hypo compared with Normo. In contrast, the Hypo burst amplitude response was shifted to a new curve with a slope that was similar to the Normo relationship. These data support the use of probability distribution analysis to examine intraindividual differences in baseline and reflex-mediated increases in MSNA burst amplitude. Furthermore, the differential effect of hypovolemia on the responses of burst frequency and amplitude during graded LBNP suggests that burst frequency data alone may not adequately represent reflex control of sympathetic outflow.

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

1999 ◽  
Vol 277 (6) ◽  
pp. H2348-H2352 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
D. B. Farr
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Whole Body ◽  
Nerve Activity ◽  
Arterial Blood

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

Differential sympathetic nerve and heart rate spectral effects of nonhypotensive lower body negative pressure

2001 ◽  
Vol 281 (2) ◽  
pp. R468-R475 ◽  
Author(s):  
John S. Floras ◽  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
Steven C. Brooks ◽  
Michael J. Pollard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Harmonic Component ◽  
Lower Body

Lower body negative pressure (LBNP; −5 and −15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (PL/PH), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at −5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas PL/PH and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (−15 mmHg) increased MSNA and PL/PH, but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.

Does infusion of ANG II increase muscle sympathetic nerve activity in patients with primary aldosteronism?

2008 ◽  
Vol 294 (6) ◽  
pp. R1873-R1879 ◽  
Author(s):  
Toshiyoshi Matsukawa ◽  
Takenori Miyamoto
Keyword(s):  
Primary Aldosteronism ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Ang Ii ◽  
Nerve Activity ◽  
Unilateral Adrenalectomy

Patients with primary aldosteronism (PA) were shown to have suppressed muscle sympathetic nerve activity (MSNA) in our previous study. Although baroreflex inhibition probably accounts in part for this reduced MSNA in PA, we hypothesized that the lowered activity of the renin-angiotensin system in PA may also contribute to the suppressed SNA. We recorded MSNA in 9 PA and 16 age-matched normotensive controls (NC). In PA, the resting mean blood pressure (MBP) and serum sodium concentrations were increased, and MSNA was reduced. We examined the effects of infusion of a high physiological dose of ANG II (5.0 ng·kg−1·min−1) on MSNA in 6 of 9 PA and 9 of 16 NC. Infusion of ANG II caused a greater pressor response in PA than NC, but, in spite of the greater increase in pressure, MSNA increased in PA, whereas it decreased in NC. Simultaneous infusion of nitroprusside and ANG II, to maintain central venous pressure at the baseline level and reduce the elevation in MBP induced by ANG II, caused significantly greater increases in MSNA in PA than in NC. Baroreflex sensitivity of heart rate, estimated during phenylephrine infusions, was reduced in PA, but baroreflex sensitivity of MSNA was unchanged in PA compared with NC. All the abnormalities in PA were eliminated following unilateral adrenalectomy. In conclusion, the suppressed SNA in PA depends in part on the low level of ANG II in these patients.

Muscle sympathetic nerve responses to static leg exercise

1992 ◽  
Vol 73 (4) ◽  
pp. 1523-1529 ◽  
Author(s):  
C. A. Ray ◽  
R. F. Rea ◽  
M. P. Clary ◽  
A. L. Mark
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Knee Extension ◽  
Voluntary Contraction ◽  
Leg Exercise

Previous studies of muscle sympathetic nerve activity (MSNA) during static exercise have employed predominantly the arms. These studies have revealed striking increases in arm and leg MSNA during static handgrip (SHG) and postexercise circulatory arrest (PECA). The purpose of this study was to examine MSNA during static leg exercise (SLE) at intensities and duration commonly used during SHG followed by PECA. During 2 min of SLE (static knee extension) at 10% of maximal voluntary contraction (MVC; n = 18) in the sitting position, mean arterial pressure and heart rate increased significantly. Surprisingly, MSNA in the contralateral leg did not increase above control levels during SLE but rather decreased (23 +/- 5%; P < 0.05) during the 1st min of SLE at 10% MVC. We compared MSNA responses to SHG and SLE (n = 8) at 30% MVC. SHG and SLE elicited comparable increases (P < 0.05) in arterial pressure and heart rate, but SHG elicited significant increases in MSNA, whereas SLE did not. During PECA after SHG and SLE, mean arterial pressure remained significantly above control. However, MSNA was unchanged during PECA after SLE but was significantly greater than control during PECA after SHG. Because previous studies have indicated differences in MSNA responses to the arm and leg, we measured arm and leg MSNA simultaneously in six subjects during SLE at 20% MVC and PECA. During SLE and PECA, MSNA in the contralateral arm and leg did not differ significantly from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Suppression of sympathetic nervous system is involved in hypotension and bradycardia during hemofiltration in anesthetized dogs

1995 ◽  
Vol 73 (10) ◽  
pp. 1495-1501 ◽  
Author(s):  
Tetsuya Hayashi ◽  
Toshishige Shibamoto ◽  
Yoshihiro Yamaguchi ◽  
Hong-Gang Wang ◽  
Satoshi Tanaka
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Induced Hypotension ◽  
Anesthetized Dogs ◽  
Sympathetic Nervous

Hypotension occurring during hemodialysis is often accompanied by paradoxical bradycardia. However, the mechanism is poorly understood. This study was designed to determine the role of the sympathetic nervous system in hemodialysis-induced hypotension and bradycardia. We measured efferent sympathetic nerve activities to the heart (CNA), kidney (RNA), liver (HNA), spleen (SpNA), and adrenal gland (AdNA), along with heart rate (HR), blood pressure (BP), central venous pressure (CVP), and left atrial pressure (LAP) during hemofiltration performed at a rate of 0.3 mL∙kg−1∙min−1 for 30 min in anesthetized dogs. The response to hemorrhage was also studied at the same bleeding speed. Hemorrhage caused a decrease in BP (−18 ± 1 mmHg; 1 mmHg = 133.3 Pa) with reflex increases in HR (7 ± 2 beats/min) and sympathetic nerve activities. In contrast, hemofiltration caused a decrease in CNA (85 ± 18%), HNA (86 ± 11%), and SpNA (88 ± 11%) with greater decreases in BP (−43 ± 10 mmHg) and HR (−27 ± 14 beats/min) than hemorrhage. During hemofiltration, the decreases in BP, HR, CNA, HNA, and SpNA were attenuated after vagotomy. Hematocrit increased by 6.5% at 30 min after hemofiltration, whereas it decreased by 4.3% after hemorrhage. These results suggest that hemofiltration suppresses the sympathetic nervous system, resulting in decreases in HR and BP. Furthermore, this sympathetic suppression during hemofiltration is mediated by vagal afferents.Key words: hemodialysis, baroreceptor reflex, sympathetic nerve activity, hemorrhage, vagus nerve.

A comparative study of the hemodynamic actions of histamine and endotoxin

1962 ◽  
Vol 203 (4) ◽  
pp. 600-606 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Thomas E. Emerson ◽  
P. F. Iampietro ◽  
Charles M. Brake
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Underlying Mechanism ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Relative Role ◽  
Small Vein ◽  
Early Increase ◽  
Logical Extension

The present study is a logical extension of earlier work with the aim of evaluating the relative role of histamine in endotoxin shock. A variety of experiments on 91 dogs were carried out in which the hemodynamic actions of histamine, a histamine releaser (48/80), and endotoxin were compared. Results indicate definite similarities of action in a number of vascular parameters: a) an early increase in portal venous pressure coincident with a decrease in venous return, pooling, and a rapid decrease in systemic arterial pressure and b) eventual increases in foreleg resistance, foreleg small vein pressure, leg weight, and circulating hematocrit. The early responses to endotoxin are greatly altered when 48/80 is administered prior to endotoxin which suggests a common underlying mechanism for the action of each agent. Histamine appears to serve as a triggering device for the sustained release of adrenergic-like agents which superimpose their effects on those of histamine. These findings offer additional evidence for the early release of histamine in endotoxin shock.

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