Sympathetic and vascular responses to head-down neck flexion in humans

1997 ◽  
Vol 272 (4) ◽  
pp. H1780-H1784 ◽  
Author(s):  
T. L. Shortt ◽  
C. A. Ray
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Systolic Arterial Pressure ◽  
Neck Flexion ◽  
Thoracic Impedance ◽  
Burst Frequency ◽  
Vascular Responses ◽  
Vestibulosympathetic Reflexes

Animal studies have demonstrated increases in sympathetic nerve outflow with vestibular stimulation. The purpose of the present study was to determine whether vestibulosympathetic reflexes are engaged in humans. Muscle sympathetic nerve activity (MSNA), heart rate, arterial pressure, calf blood flow (CBF), and calculated calf vascular resistance (CVR; mean arterial pressure/CBF) were determined during 10 min of baseline (laying prone with chin supported) and 10 min of head-down neck flexion (HDNF). MSNA responses were measured in nine subjects, and calf vascular responses were determined in seven of these subjects. Heart rate increased during the first minute of HDNF (71 +/- 2 to 76 +/- 3 beats/min; P < 0.05) and remained slightly elevated (71 +/- 2 to 74 +/- 3 beats/min; P < 0.05) for the duration of HDNF. Diastolic and mean arterial pressures also increased slightly with HDNF (80 +/- 3 to 82 +/- 3 and 96 +/- 3 to 98 +/- 3 mmHg, respectively; P < 0.05). Systolic arterial pressure did not change significantly during HDNF. CBF decreased 14% (4.63 +/- 0.78 to 3.97 +/- 0.60 ml x min(-1) x 100 ml(-1); P < 0.05), and CVR increased 12% (24.0 +/- 4.3 to 27.4 +/- 4.7 units; P < 0.05) during HDNF. These changes corresponded with significant increases in MSNA during HDNF. MSNA, expressed as burst frequency, increased from 14 +/- 2 to 20 +/- 2 bursts/min (P < 0.05) and increased 63 +/- 23% (P < 0.05) when expressed as the percent change in total activity. All variables returned to baseline during recovery. Thoracic impedance measured in five subjects did not change during HDNF (19.6 +/- 1.2 to 19.7 +/- 1.5 omega), suggesting no major change in central blood volume. The results indicate that HDNF elicits increases in CVR that are mediated by the augmentation of MSNA. Arterial pressure responses and thoracic impedance data suggest that high and low pressure baroreflexes were not the mechanism for sympathetic activation. The immediate increase in MSNA with HDNF suggests a role for vestibulosympathetic reflexes.

Skin sympathetic outflow during head-down neck flexion in humans

1997 ◽  
Vol 273 (3) ◽  
pp. R1142-R1146 ◽  
Author(s):  
C. A. Ray ◽  
K. M. Hume ◽  
T. L. Shortt
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Neck Flexion ◽  
Nerve Activity ◽  
Calf Blood Flow

We have previously demonstrated increases in muscle sympathetic nerve activity during head-down neck flexion (HDNF). The purpose of the present study was to determine if HDNF also activates skin sympathetic nerve activity (SSNA). SSNA, heart rate, arterial pressure, skin blood flow, calf blood flow, and calculated calf vascular resistance (mean arterial pressure/calf blood flow) were determined in 12 subjects during 3 min of baseline (lying prone with chin supported) and 3 min of HDNF. There were no significant changes in heart rate and arterial pressures during HDNF; however, diastolic and mean arterial pressure tended to increase slightly. Calf blood flow decreased 22% and calf vascular resistance increased 46% during HDNF. SSNA did not significantly change during HDNF. In three subjects we measured both muscle and skin sympathetic nerve activity during HDNF. In these trials, muscle sympathetic nerve activity consistently increased, but SSNA did not. The results indicate that HDNF in humans activates muscle sympathetic nerve activity, but does not activate SSNA. Thus vestibular stimulation may elicit differential activation of sympathetic outflow in humans.

Muscle sympathetic nerve responses to graded leg cycling

1993 ◽  
Vol 75 (2) ◽  
pp. 663-667 ◽  
Author(s):  
M. Saito ◽  
A. Tsukanaka ◽  
D. Yanagihara ◽  
T. Mano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Uptake ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Burst Frequency ◽  
Control Value ◽  
Leg Cycling ◽  
Exercise Muscle ◽  
The Right

The aim of this study was to clarify the relationship between sympathetic outflow to skeletal muscle and oxygen uptake during dynamic exercise. Muscle sympathetic nerve activity (MSNA) was recorded from the right median nerve microneurographically in eight healthy volunteers during leg cycling at four different intensities in a seated position for a 16-min bout. Work loads selected were 20, 40, 60, and 75% of maximal oxygen uptake (VO2max). Heart rate and blood pressure were measured during each exercise test. MSNA burst frequency was suppressed by 28% during cycling at 20% VO2max (23 vs. 33 bursts/min for control). Thereafter, it increased in a linear fashion with increasing work rate, with a significantly higher burst frequency during 60% VO2max than the control value. Both heart rate and mean blood pressure rose significantly during 20% VO2max from the control value and increased linearly with increased exercise intensity. During light exercise, MSNA was suppressed by arterial and cardiopulmonary baroreceptors as a result of the hemodynamic changes associated with leg muscle pumping. The baroreflex inhibition may overcome the muscle metaboreflex excitation to induce MSNA suppression during light exercise. These results suggest that during light exercise MSNA is inhibited, perhaps due to loading of the cardiopulmonary and arterial baroreflexes, and that during heavier exercise the increase in MSNA occurs as muscle metaboreflexes are activated.

scholarly journals Adrenomedullin increases cardiac sympathetic nerve activity in normal conscious sheep

2005 ◽  
Vol 187 (2) ◽  
pp. 275-281 ◽  
Author(s):  
C J Charles ◽  
D L Jardine ◽  
M G Nicholls ◽  
A M Richards
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vehicle Control ◽  
Cardiac Sympathetic Nerve ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.

Naloxone does not affect the cardiovascular and sympathetic adjustments to static exercise in humans

1994 ◽  
Vol 77 (1) ◽  
pp. 231-235 ◽  
Author(s):  
C. A. Ray ◽  
J. A. Pawelczyk
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Static Exercise ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Double Blind ◽  
Endogenous Opiates ◽  
Muscle Ischemia

Previous studies suggested that endogenous opiates may attenuate the cardiovascular and sympathetic adjustments to static exercise. We tested whether this effect originates from exercising skeletal muscle. Eight men performed 2 min of static handgrip (30% maximum) followed by 2 min of posthandgrip muscle ischemia after three interventions: 1) control, 2) intra-arterial injection of naloxone HCl (60 micrograms) or vehicle (saline) in the exercising arm, and 3) systemic infusion of naloxone (4 mg) or vehicle. Naloxone and vehicle trials were performed double blind on separate days. Preexercise baseline muscle sympathetic nerve activity (burst frequency), heart rate, and blood pressure were similar across interventions on either day. During static handgrip, control, intra-arterial, and systemic administration of vehicle and naloxone elicited similar increases in total muscle sympathetic nerve activity (58 +/- 24 vs. 68 +/- 26, 146 +/- 49 vs. 132 +/- 42, 137 +/- 54 vs. 164 +/- 44%, respectively), heart rate (9 +/- 2 vs. 8 +/- 3, 16 +/- 3 vs. 16 +/- 2, 20 +/- 4 vs. 19 +/- 3 beats/min, respectively), and mean arterial pressure (22 +/- 4 vs. 21 +/- 4, 29 +/- 5 vs. 26 +/- 3, 28 +/- 4 vs. 27 +/- 4 mmHg, respectively). Additionally, there were no differences between vehicle and naloxone trials during posthandgrip muscle ischemia. Thus, contrary to previous reports, we conclude that the endogenous opiate peptide system does not modulate cardiovascular and sympathetic responses to brief periods of static exercise or muscle ischemia in humans.

Spectral analysis of heart rate, arterial pressure, and muscle sympathetic nerve activity in normal humans

1998 ◽  
Vol 274 (4) ◽  
pp. H1211-H1217 ◽  
Author(s):  
Akio Nakata ◽  
Shigeo Takata ◽  
Toyoshi Yuasa ◽  
Atsuhiro Shimakura ◽  
Michiro Maruyama ◽  
...  
Keyword(s):  
Heart Rate ◽  
Spectral Analysis ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Autoregressive Model ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Model Fitting ◽  
Power Spectral Analysis ◽  
Nerve Activity

We investigated the frequency components of fluctuations in heart rate, arterial pressure, respiration, and muscle sympathetic nerve activity (MSNA) in 11 healthy women using an autoregressive model and examined the relation among variables using Akaike’s relative power contribution analysis with multivariate autoregressive model fitting. Power spectral analysis of MSNA revealed two peaks, with low-frequency (LF) and high-frequency (HF) components. The LF component of MSNA was a major determinant of the LF component of arterial pressure and R-R interval variability (0.70 ± 0.07 and 0.18 ± 0.05, respectively). The effect of the LF component of MSNA on arterial pressure showed no change in response to propranolol but was diminished (0.35 ± 0.08) by phentolamine ( P < 0.02). The effect of the LF component of MSNA on R-R interval was not altered by pharmacological sympathetic nerve blockade. The HF component of MSNA did not influence other variables but was influenced by R-R interval, arterial pressure, and respiration. These findings indicate that the LF component of MSNA reflects autonomic oscillations, whereas the HF component is passive and influenced by other cardiovascular variables.

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)

Isometric handgrip training reduces arterial pressure at rest without changes in sympathetic nerve activity

2000 ◽  
Vol 279 (1) ◽  
pp. H245-H249 ◽  
Author(s):  
Chester A. Ray ◽  
Dario I. Carrasco
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

The purpose of this study was to determine whether isometric handgrip (IHG) training reduces arterial pressure and whether reductions in muscle sympathetic nerve activity (MSNA) mediate this drop in arterial pressure. Normotensive subjects were assigned to training ( n = 9), sham training ( n = 7), or control ( n = 8) groups. The training protocol consisted of four 3-min bouts of IHG exercise at 30% of maximal voluntary contraction (MVC) separated by 5-min rest periods. Training was performed four times per week for 5 wk. Subjects' resting arterial pressure and heart rate were measured three times on 3 consecutive days before and after training, with resting MSNA (peroneal nerve) recorded on the third day. Additionally, subjects performed IHG exercise at 30% of MVC to fatigue followed by muscle ischemia. In the trained group, resting diastolic (67 ± 1 to 62 ± 1 mmHg) and mean arterial pressure (86 ± 1 to 82 ± 1 mmHg) significantly decreased, whereas systolic arterial pressure (116 ± 3 to 113 ± 2 mmHg), heart rate (67 ± 4 to 66 ± 4 beats/min), and MSNA (14 ± 2 to 15 ± 2 bursts/min) did not significantly change following training. MSNA and cardiovascular responses to exercise and postexercise muscle ischemia were unchanged by training. There were no significant changes in any variables for the sham training and control groups. The results indicate that IHG training is an effective nonpharmacological intervention in lowering arterial pressure.

Endotoxemia causes central downregulation of sympathetic vasomotor tone in healthy humans

2008 ◽  
Vol 295 (3) ◽  
pp. R891-R898 ◽  
Author(s):  
Friedhelm Sayk ◽  
Alexander Vietheer ◽  
Bernhard Schaaf ◽  
Peter Wellhoener ◽  
Gunther Weitz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Blood Levels ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Healthy Humans ◽  
Vascular Bed

Experimental endotoxemia as a model of the initial septic response affects the autonomic nervous system with profound cardiovascular sequelae. Whether the postsynaptic sympathoneural activity to the muscle vascular bed is altered in the early septic phase remains to be determined. The present study aimed to elucidate the early effects of LPS on muscle sympathetic nerve activity (MSNA) and cardiovascular regulation in healthy humans. Young, healthy volunteers randomly received either an LPS bolus (4 ng/kg body wt, n = 11) or placebo (saline; n = 7). Experimental baroreflex assessment (baseline measurements followed by infusion of vasoactive drugs nitroprusside/phenylephrine) was done prior to and 90 min following LPS or placebo challenge. MSNA, heart rate, blood pressure, and blood levels of catecholamines, TNF-α and IL-6 were measured sequentially. Endotoxin but not placebo-induced flu-like symptoms and elevated cytokine levels. In contrast to placebo, LPS significantly suppressed MSNA burst frequency 90 min after injection [mean ± SE: 12.1 ± 2.9 vs. 27.5 ± 3.3 burst/min (post- vs. pre-LPS); P < 0.005] but increased heart rate [78.4 ± 3.1 vs. 60.6 ± 2.0 beats/min (post- vs. pre-LPS); P < 0.001]. Baseline blood pressure was not altered, but baroreflex testing demonstrated a blunted MSNA response and uncoupling of heart rate modulation to blood pressure changes in the endotoxin group. We conclude that endotoxin challenge in healthy humans has rapid suppressive effects on postsynaptic sympathetic nerve activity to the muscle vascular bed and alters baroreflex function which may contribute to the untoward cardiovascular effects of sepsis.

Sympathetic neural discharge and vascular resistance during exercise in humans

1989 ◽  
Vol 66 (5) ◽  
pp. 2472-2478 ◽  
Author(s):  
D. R. Seals
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Lower Leg ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Exercise In Humans

The purpose of this study was to determine the relationship between changes in efferent muscle sympathetic nerve activity (MSNA) to the lower leg and calf vascular resistance (CVR) during isometric exercise in humans. We made intraneural (microneurographic) determinations of MSNA in the right leg (peroneal nerve) while simultaneously measuring calf blood flow to the left leg, arterial pressure, and heart rate in 10 subjects before (control), during, and after (recovery) isometric handgrip exercise performed for 2.5 min at 15, 25, and 35% of maximal voluntary contraction (MVC). Heart rate and arterial pressure increased above control within the initial 30 s of handgrip at all levels, and the magnitudes of the increases at end contraction were proportional to the intensity of the exercise. In general, neither MSNA nor CVR increased significantly above control levels during handgrip at 15% MVC. Similarly, neither variable increased above control during the initial 30 s of handgrip at 25 and 35% MVC; however, during the remainder of the contraction period, progressive, parallel increases were observed in MSNA and CVR (P less than 0.05). The correlation coefficients relating changes in MSNA to changes in CVR for the individual subjects averaged 0.63 +/- 0.07 (SE) (range 0.30–0.91) and 0.94 +/- 0.06 (range 0.80–0.99) for the 25 and 35% MVC levels, respectively. During recovery, both MSNA and CVR returned rapidly toward control levels. These findings demonstrate that muscle sympathetic nerve discharge and vascular resistance in the lower leg are tightly coupled during and after isometric arm exercise in humans. Furthermore, the exercise-induced adjustments in the two variables are both contraction intensity and time dependent.

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