Changes in muscle sympathetic nerve activity and calf blood flow during static handgrip exercise

1990 ◽  
Vol 60 (4) ◽  
pp. 277-281 ◽  
Author(s):  
Mitsuru Saito ◽  
Tadaaki Mano ◽  
Satoshi Iwase
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Handgrip Exercise ◽  
Nerve Activity ◽  
Calf Blood Flow

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.

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 Transcranial Doppler estimation of cerebral blood flow and cerebrovascular conductance during modified rebreathing

2007 ◽  
Vol 102 (3) ◽  
pp. 870-877 ◽  
Author(s):  
Jurgen A. H. R. Claassen ◽  
Rong Zhang ◽  
Qi Fu ◽  
Sarah Witkowski ◽  
Benjamin D. Levine
Keyword(s):  
Blood Flow ◽  
Logistic Regression ◽  
Cerebral Blood Flow ◽  
Linear Regression ◽  
Transcranial Doppler ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen ◽  
Nerve Activity

Clinical transcranial Doppler assessment of cerebral vasomotor reactivity (CVMR) uses linear regression of cerebral blood flow velocity (CBFV) vs. end-tidal CO2 (PetCO2) under steady-state conditions. However, the cerebral blood flow (CBF)-PetCO2 relationship is nonlinear, even for moderate changes in CO2. Moreover, CBF is increased by increases in arterial blood pressure (ABP) during hypercapnia. We used a modified rebreathing protocol to estimate CVMR during transient breath-by-breath changes in CBFV and PetCO2. Ten healthy subjects (6 men) performed 15 s of hyperventilation followed by 5 min of rebreathing, with supplemental O2 to maintain arterial oxygen saturation constant. To minimize effects of changes in ABP on CVMR estimation, cerebrovascular conductance index (CVCi) was calculated. CBFV-PetCO2 and CVCi-PetCO2 relationships were quantified by both linear and nonlinear logistic regression. In three subjects, muscle sympathetic nerve activity was recorded. From hyperventilation to rebreathing, robust changes occurred in PetCO2 (20–61 Torr), CBFV (−44 to +104% of baseline), CVCi (−39 to +64%), and ABP (−19 to +23%) (all P < 0.01). Muscle sympathetic nerve activity increased by 446% during hypercapnia. The linear regression slope of CVCi vs. PetCO2 was less steep than that of CBFV (3 vs. 5%/Torr; P = 0.01). Logistic regression of CBF-PetCO2 ( r2 = 0.97) and CVCi-PetCO2 ( r2 = 0.93) was superior to linear regression ( r2 = 0.91, r2 = 0.85; P = 0.01). CVMR was maximal (6–8%/Torr) for PetCO2 of 40–50 Torr. In conclusion, CBFV and CVCi responses to transient changes in PetCO2 can be described by a nonlinear logistic function, indicating that CVMR estimation varies within the range from hypocapnia to hypercapnia. Furthermore, quantification of the CVCi-PetCO2 relationship may minimize the effects of changes in ABP on the estimation of CVMR. The method developed provides insight into CVMR under transient breath-by-breath changes in CO2.

Augmented response of single muscle sympathetic nerve activity to handgrip exercise in heart failure

2004 ◽  
Vol 10 (5) ◽  
pp. S167
Author(s):  
Hisayoshi Murai ◽  
Takata Shigeo ◽  
Furushou Hiroshi ◽  
Maruyama Micchirou ◽  
Takamura Masayuki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Single Muscle ◽  
Handgrip Exercise ◽  
Nerve Activity

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.

Gly16 + Glu27 β2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

2005 ◽  
Vol 98 (3) ◽  
pp. 787-794 ◽  
Author(s):  
Ivani C. Trombetta ◽  
Luciana T. Batalha ◽  
Maria U. P. B. Rondon ◽  
Mateus C. Laterza ◽  
Eliana Frazzatto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Forearm Blood Flow ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Forearm Vascular Conductance

We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

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 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.

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