scholarly journals Gender-related differences in the sympathetic vasoconstrictor drive of normal subjects

2007 ◽  
Vol 112 (6) ◽  
pp. 353-361 ◽  
Author(s):  
Andrew J. Hogarth ◽  
Alan F. Mackintosh ◽  
David A. S. G. Mary
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor ◽  
Normal Subjects ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Vasoconstrictor Response ◽  
Baroreceptor Reflex Sensitivity

The risk of cardiovascular disease has been linked to sympathetic activation and its incidence is known to be lower in women than in men. However, the effect of gender on the sympathetic vasoconstrictor drive has not yet been established. In the present study, we investigated whether there is a gender difference in MSNA (muscle sympathetic nerve activity) and blood flow, and to determine the mechanisms involved. We examined 68 normal subjects, 34 women and 34 men, matched for age, BMI (body mass index) and waist circumference. MSNA was measured as the mean frequency of single units (s-MSNA) and as multi-unit bursts (m-MSNA) from the peroneal nerve simultaneously with its supplied muscle CBF (calf blood flow). Women had lower (P=0.0007) s-MSNA (24±2.0 impulses/100 cardiac beats) than men (34±2.3 impulses/100 cardiac beats), and a greater baroreceptor reflex sensitivity controlling efferent sympathetic nerve activity than men. The sympathetic activity was inversely and directly correlated respectively, with CBF (P=0.03) and CVR (calf vascular resistance; P=0.01) in men only. The responses of an increase in CVR to cold pressor and isometric handgrip tests were significantly smaller in women (P=0.002) than in men, despite similar increases in efferent sympathetic nerve activity. Women had a lower central sympathetic neural output to the periphery, the mechanism of which involved differences in central and reflex control, as well as a lower vasoconstrictor response to this neural output. It is suggested that this may partly explain the observed lower incidence of cardiovascular events in women compared with men.

scholarly journals Heart rate variability and muscle sympathetic nerve activity response to acute stress: the effect of breathing

2010 ◽  
Vol 299 (1) ◽  
pp. R80-R91 ◽  
Author(s):  
Lindsay D. DeBeck ◽  
Stewart R. Petersen ◽  
Kelvin E. Jones ◽  
Michael K. Stickland
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Nerve ◽  
Spontaneous Breathing ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Controlled Breathing

Previous research has suggested a relationship between low-frequency power of heart rate variability (HRV; LF in normalized units, LFnu) and muscle sympathetic nerve activity (MSNA). However, investigations have not systematically controlled for breathing, which can modulate both HRV and MSNA. Accordingly, the aims of this experiment were to investigate the possibility of parallel responses in MSNA and HRV (LFnu) to selected acute stressors and the effect of controlled breathing. After data were obtained at rest, 12 healthy males (28 ± 5 yr) performed isometric handgrip exercise (30% maximal voluntary contraction) and the cold pressor test in random order, and were then exposed to hypoxia (inspired fraction of O2 = 0.105) for 7 min, during randomly assigned spontaneous and controlled breathing conditions (20 breaths/min, constant tidal volume, isocapnic). MSNA was recorded from the peroneal nerve, whereas HRV was calculated from ECG. At rest, controlled breathing did not alter MSNA but decreased LFnu ( P < 0.05 for all) relative to spontaneous breathing. MSNA increased in response to all stressors regardless of breathing. LFnu increased with exercise during both breathing conditions. During cold pressor, LFnu decreased when breathing was spontaneous, whereas in the controlled breathing condition, LFnu was unchanged from baseline. Hypoxia elicited increases in LFnu when breathing was controlled, but not during spontaneous breathing. The parallel changes observed during exercise and controlled breathing during hypoxia suggest that LFnu may be an indication of sympathetic outflow in select conditions. However, since MSNA and LFnu did not change in parallel with all stressors, a cautious approach to the use of LFnu as a marker of sympathetic activity is warranted.

Naloxone augments muscle sympathetic nerve activity during isometric exercise in humans

1991 ◽  
Vol 260 (3) ◽  
pp. E379-E388 ◽  
Author(s):  
P. A. Farrell ◽  
T. J. Ebert ◽  
J. P. Kampine
Keyword(s):  
Sodium Nitroprusside ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Cardiovascular Variables

The influence of an endogenous opioid peptide (EOP) antagonist (naloxone, 1.2 mg iv bolus) on muscle sympathetic nerve activity (MSNA, microneurography) was studied on 19 young male and female volunteers. Isometric handgrip, cold pressor test, and acute baroreceptor unloading with sodium nitroprusside (autonomic stresses) were carried out under two conditions, one group (n = 11) before (control responses) and after naloxone and another group (n = 8) before and after placebo saline. Monitored cardiovascular variables included heart rate, central venous pressure (jugular vein catheter), arterial blood pressure (radial artery catheter), circulating catecholamines, and forearm blood flow. At rest, cardiovascular variables and MSNA were not affected by either naloxone or saline. MSNA (total activity = burst frequency x burst amplitude/100 cardiac cycles) increased during isometric handgrip to a greater extent (30 +/- 6 vs. 16 +/- 5 arbitrary units) after naloxone compared with control trials (P less than 0.05). After naloxone, arterial systolic and diastolic blood pressures were higher during handgrip exercise. These augmented arterial pressures and MSNA responses were not evident during either the cold pressor test or the sodium nitroprusside stress. These data suggest that isometric muscle contraction elicits a sympathetic neural response that may be modified by EOP. This interaction is not evident during two other stresses, when sympathetic responses are equal to or greater than those provoked by isometric handgrip exercise.

scholarly journals Modulation of muscle sympathetic nerve activity to muscle heating during dynamic exercise

2009 ◽  
Vol 296 (5) ◽  
pp. R1439-R1444 ◽  
Author(s):  
Jonathan S. Cook ◽  
Chester A. Ray
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Interactive Effect ◽  
Total Activity ◽  
Muscle Temperature ◽  
Isometric Handgrip ◽  
Burst Frequency ◽  
Nerve Activity

Previous studies from our laboratory have demonstrated that altering muscle temperature of the exercising forearm can elicit changes in muscle sympathetic nerve activity (MSNA) during ischemic isometric handgrip. The purpose of the current study was to determine the interactive effect of muscle temperature and blood flow on MSNA responses during dynamic handgrip (DHG). Eight subjects performed two bouts of graded DHG to fatigue followed by 2 min of postexercise muscle ischemia (PEMI). Local heating of the forearm increased muscle temperature from 33.6 ± 0.3 to 38.3 ± 0.5°C ( P < 0.05). Mean arterial pressure and heart rate increased in a linear fashion during graded DHG ( P < 0.05) but were not affected by muscle temperature. MSNA (burst frequency and total activity) at fatigue and PEMI were elevated in all conditions ( P < 0.05). However, MSNA responses were not different between temperature conditions. To ascertain the effect of blood flow, eight additional subjects completed two trials of ischemic DHG under control or warm conditions followed by 2 min of PEMI. MSNA, expressed as burst frequency and total activity, was significantly greater in warm compared with the control trial (Δ14 ± 3 and Δ9 ± 2 bursts/30 s, and Δ1,234 ± 260 and Δ751 ± 199 units/30 s, respectively). This finding supports the concept that muscle heating sensitizes skeletal muscle afferents during muscle contractions and augments MSNA in humans. However, on the basis of these findings, we conclude that muscle blood flow modulates the effect of muscle temperature on MSNA during exercise.

Relation between QT interval variability and muscle sympathetic nerve activity in normal subjects

2015 ◽  
Vol 309 (7) ◽  
pp. H1218-H1224 ◽  
Author(s):  
Fatima El-Hamad ◽  
Elisabeth Lambert ◽  
Derek Abbott ◽  
Mathias Baumert
Keyword(s):  
Supine Position ◽  
Sympathetic Nerve ◽  
Qt Interval ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Normal Subjects ◽  
Nerve Activity ◽  
Head Up Tilt ◽  
Low Frequency Power

Beat-to-beat variability of the QT interval (QTV) is sought to provide an indirect noninvasive measure of sympathetic nerve activity, but a formal quantification of this relationship has not been provided. In this study we used power contribution analysis to study the relationship between QTV and muscle sympathetic nerve activity (MSNA). ECG and MSNA were recorded in 10 healthy subjects in the supine position and after 40° head-up tilt. Power spectrum analysis was performed using a linear autoregressive model with two external inputs: heart period (RR interval) variability (RRV) and MSNA. Total and low-frequency power of QTV was decomposed into contributions by RRV, MSNA, and sources independent of RRV and MSNA. Results show that the percentage of MSNA power contribution to QT is very small and does not change with tilt. RRV power contribution to QT power is notable and decreases with tilt, while the greatest percentage of QTV is independent of RRV and MSNA in the supine position and after 40° head-up tilt. In conclusion, beat-to-beat QTV in normal subjects does not appear to be significantly affected by the rhythmic modulations in MSNA following low to moderate orthostatic stimulation. Therefore, MSNA oscillations may not represent a useful surrogate for cardiac sympathetic nerve activity at moderate levels of activation, or, alternatively, sympathetic influences on QTV are complex and not quantifiable with linear shift-invariant autoregressive models.

Modulation of sympathetic nerve activity during posthandgrip muscle ischemia in humans

1994 ◽  
Vol 266 (1) ◽  
pp. H79-H83 ◽  
Author(s):  
C. A. Ray ◽  
N. H. Secher ◽  
A. L. Mark
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sensory Nerve ◽  
Vascular Occlusion ◽  
Voluntary Contraction ◽  
Central Command ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

To evaluate modulation of muscle sympathetic nerve activity (MSNA) during posthandgrip muscle ischemia (PHGMI), subjects performed 2 min of isometric handgrip at 33% of maximal voluntary contraction (MVC) followed by 2 min of PHGMI produced by forearm vascular occlusion. The response to PHGMI was studied in the absence and again during the addition of contralateral rhythmic handgrip (RHG; 40 times/min) at 15% (n = 6) and 30% (n = 10) MVC during the second minute of the PHGMI. Additionally, to isolate the effect of central command, response to PHGMI was studied during attempted RHG after sensory nerve blockade (n = 5). RHG for 2 min at 15 and 30% MVC and attempted RHG for 2 min did not increase MSNA. Isometric handgrip elicited an 130 +/- 48% increase in MSNA (P < 0.05), which was maintained during PHGMI. RHG at 15 and 30% MVC elicited an attenuation of MSNA (-10 +/- 7% and -14 +/- 6%, respectively) when performed during the second minute of PHGMI (P < 0.05). In contrast, attempted RHG did not significantly affect MSNA during PHGMI. The findings demonstrate modulation of MSNA during activation of the muscle metaboreflex. The attenuation of metaboreceptor-mediated increases in MSNA appear to be the result of mechanosensitive muscle afferents and not central command.

Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans

2006 ◽  
Vol 290 (4) ◽  
pp. H1419-H1426 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Time Dependent ◽  
Operating Pressure ◽  
Dependent Manner ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Nerve Activity

We investigated the time-dependent modulation of arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) that occurs during isometric handgrip exercise (IHG). Thirteen healthy subjects performed a 3-min IHG at 30% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). The ABR control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between spontaneous variations in diastolic arterial pressure (DAP) and MSNA during supine rest, at each minute of IHG, and during PEMI. We found that 1) the linear relations between DAP and MSNA variables were shifted progressively rightward until the third minute of IHG (IHG3); 2) 2 min into IHG (IHG2), the DAP-MSNA relations were shifted upward and were shifted further upward at IHG3; 3) the sensitivity of the ABR control of total MSNA was increased at IHG2 and increased further at IHG3; and 4) during PEMI, the ABR operating pressure was slightly higher than at IHG2, and the sensitivity of the control of total MSNA was the same as at IHG2. During PEMI, the DAP-burst strength and DAP-total MSNA relations were shifted downward from the IHG3 level to the IHG2 level, whereas the DAP-burst incidence relation remained at the IHG3 level. These results indicate that during IHG, ABR control of MSNA is modulated in a time-dependent manner. We suggest that this modulation of ABR function is one of the mechanisms underlying the progressive increase in blood pressure and MSNA during the course of isometric exercise.

scholarly journals Effects of the cold pressor test on muscle sympathetic nerve activity in humans.

Hypertension ◽  
1987 ◽  
Vol 9 (5) ◽  
pp. 429-436 ◽  
Author(s):  
R G Victor ◽  
W N Leimbach ◽  
D R Seals ◽  
B G Wallin ◽  
A L Mark
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Nerve Activity ◽  
Pressor Test

scholarly journals Hypoxia-induced vasodilation and effects of regional phentolamine in awake patients with sleep apnea

2010 ◽  
Vol 108 (5) ◽  
pp. 1234-1240 ◽  
Author(s):  
Raman Moradkhan ◽  
Brett Spitnale ◽  
Patrick McQuillan ◽  
Cynthia Hogeman ◽  
Kristen S. Gray ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sleep Apnea ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Artery Blood Flow ◽  
Nerve Activity ◽  
Premature Cardiovascular Disease ◽  
Obstructive Sleep

Obstructive sleep apnea (OSA) is associated with increased sympathetic nerve activity, endothelial dysfunction, and premature cardiovascular disease. To determine whether hypoxia is associated with impaired skeletal muscle vasodilation, we compared femoral artery blood flow (ultrasound) and muscle sympathetic nerve activity (peroneal microneurography) during exposure to acute systemic hypoxia (fraction of inspired oxygen 0.1) in awake patients with OSA ( n = 10) and controls ( n = 8). To assess the role of elevated sympathetic nerve activity, in a separate group of patients with OSA ( n = 10) and controls ( n = 10) we measured brachial artery blood flow during hypoxia before and after regional α-adrenergic block with phentolamine. Despite elevated sympathetic activity, in OSA the vascular responses to hypoxia in the leg did not differ significantly from those in controls [ P = not significant (NS)]. Following regional phentolamine, in both groups the hypoxia-induced increase in brachial blood flow was markedly enhanced (OSA pre vs. post, 84 ± 13 vs. 201 ± 34 ml/min, P < 0.002; controls pre vs. post 62 ± 8 vs. 140 ± 26 ml/min, P < 0.01). At end hypoxia after phentolamine, the increase of brachial blood flow above baseline was similar (OSA vs. controls +61 ± 16 vs. +48 ± 6%; P = NS). We conclude that despite high sympathetic vasoconstrictor tone and prominent sympathetic responses to acute hypoxia, hypoxia-induced limb vasodilation is preserved in OSA.

scholarly journals Microneurography and sympathetic nerve activity: a decade-by-decade journey across 50 years

2019 ◽  
Vol 121 (4) ◽  
pp. 1183-1194 ◽  
Author(s):  
Jason R. Carter
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
The Past ◽  
Thomson Reuters ◽  
The Impact

The technique of microneurography has advanced the field of neuroscience for the past 50 years. While there have been a number of reviews on microneurography, this paper takes an objective approach to exploring the impact of microneurography studies. Briefly, Web of Science (Thomson Reuters) was used to identify the highest citation articles over the past 50 years, and key findings are presented in a decade-by-decade highlight. This includes the establishment of microneurography in the 1960s, the acceleration of the technique by Gunnar Wallin in the 1970s, the international collaborations of the 1980s and 1990s, and finally the highest impact studies from 2000 to present. This journey through 50 years of microneurographic research related to peripheral sympathetic nerve activity includes a historical context for several of the laboratory interventions commonly used today (e.g., cold pressor test, mental stress, lower body negative pressure, isometric handgrip, etc.) and how these interventions and experimental approaches have advanced our knowledge of cardiovascular, cardiometabolic, and other human diseases and conditions.

Effect of morphine on sympathetic nerve activity in humans

2002 ◽  
Vol 93 (5) ◽  
pp. 1764-1769 ◽  
Author(s):  
Jason R. Carter ◽  
Charity L. Sauder ◽  
Chester A. Ray
Keyword(s):  
Opioid Receptor ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Cardiovascular Responses ◽  
Endogenous Opioids ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Trial Drug

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 × 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.

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