scholarly journals Evaluation of the Changes in the Muscle Sympathetic Nerve Activity and Anterior Tibial Muscle Blood Flow Caused by the Valsalva Maneuver in Patients with Lumbago and Healthy Subjects

2005 ◽  
Vol 72 (2) ◽  
pp. 96-104 ◽  
Author(s):  
Akihiko Nambu ◽  
Takafumi Aoki ◽  
Yasumasa Shirai ◽  
Hiromoto Ito
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Valsalva Maneuver ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity ◽  
Anterior Tibial Muscle ◽  
Anterior Tibial

Blunted muscle vasodilatation during chemoreceptor stimulation in patients with heart failure

2007 ◽  
Vol 293 (1) ◽  
pp. H846-H852 ◽  
Author(s):  
Andrea Di Vanna ◽  
Ana Maria F. W. Braga ◽  
Mateus C. Laterza ◽  
Linda M. Ueno ◽  
Maria Urbana P. B. Rondon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Heart Association ◽  
Functional Class ◽  
Nerve Activity ◽  
Normal Controls

Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure (HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptor activation in patients with HF are unknown. We tested the hypothesis that the muscle blood flow responses during peripheral and central chemoreflex stimulation would be blunted in patients with HF. Sixteen patients with HF (49 ± 3 years old, Functional Class II-III, New York Heart Association) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O2 and 90% N2 for 3 min. The central chemoreflex control was evaluated by inhalation of 7% CO2 and 93% O2 for 3 min. Muscle sympathetic nerve activity (MSNA) was directly evaluated by microneurography. Forearm blood flow was evaluated by venous occlusion plethysmography. Baseline MSNA were significantly greater in HF patients (33 ± 3 vs. 20 ± 2 bursts/min, P = 0.001). Forearm vascular conductance (FVC) was not different between the groups. During hypoxia, the increase in MSNA was significantly greater in HF patients than in normal controls (9.0 ± 1.6 vs. 0.8 ± 2.0 bursts/min, P = 0.001). The increase in FVC was significantly lower in HF patients (0.00 ± 0.10 vs. 0.76 ± 0.25 units, P = 0.001). During hypercapnia, MSNA responses were significantly greater in HF patients than in normal controls (13.9 ± 3.2 vs. 2.1 ± 1.9 bursts/min, P = 0.001). FVC responses were significantly lower in HF patients (−0.29 ± 0.10 vs. 0.37 ± 0.18 units, P = 0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptor stimulation is blunted in HF patients. This vascular response seems to be explained, at least in part, by the exaggerated MSNA responses during hypoxia and hypercapnia.

Increased muscle perfusion reduces muscle sympathetic nerve activity during handgripping

1993 ◽  
Vol 75 (6) ◽  
pp. 2450-2455 ◽  
Author(s):  
M. J. Joyner ◽  
W. Wieling
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Perceived Exertion ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Maximum Voluntary Contraction ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
Nerve Activity

This study sought to determine whether increasing blood flow to active muscles can blunt the normal rise in muscle sympathetic nerve activity (MSNA) during heavy rhythmic forearm exercise in humans. Subjects performed 5- to 6-min exercise bouts of handgripping (30/min) at 40–50% of maximum voluntary contraction (MVC). Blood flow was increased by application of suction (50 mmHg) around the forearm. Suction increased deep venous oxygen saturation in blood draining the forearm from 34 +/- 4 to 45 +/- 4%, indicating that muscle blood flow had risen by approximately 20%. Suction had no impact on the heart rate, perceived exertion, or electromyographic responses to the handgripping. During 6 min of exercise at 50% of MVC, MSNA rose from 376 +/- 67 to 970 +/- 125 units during the control trial vs. 396 +/- 69 to 729 +/- 94 units during the suction trial, and the difference was maintained during 2 min of postexercise ischemia (P < 0.05; suction < control). Mean arterial pressure (MAP) rose from 99 +/- 4 to 129 +/- 6 mmHg during control vs. 99 +/- 4 to 126 +/- 6 mmHg during the suction trial, and these responses were only different (P < 0.05; suction < control) during the final minute of the exercise bouts. During postexercise ichemia, MAP was 122 +/- 6 mmHg after the control trial but was only 112 +/- 4 mmHg after the suction trial. These results indicate that forearm suction augmented muscle blood flow, limited the activation of chemosensitive muscle afferents, and blunted the rise in MSNA during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Impact of gender on benefits of exercise training on sympathetic nerve activity and muscle blood flow in heart failure

2009 ◽  
Vol 12 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Ligia M. Antunes-Correa ◽  
Ruth C. Melo ◽  
Thais S. Nobre ◽  
Linda M. Ueno ◽  
Fabio G.M. Franco ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Exercise Training ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity

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.

Skeletal Muscle Vasculature and Systemic Hypoxia

Physiology ◽  
1995 ◽  
Vol 10 (6) ◽  
pp. 274-280
Author(s):  
JM Marshall
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Intravital Microscopy ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity ◽  
Systemic Hypoxia

Studies involving recordings of gross muscle blood flow and intravital microscopy have been used to analyze the behavior of muscle vasculature during systemic hypoxia. The roles of sympathetic nerve activity, circulating hormones (e.g., catecholamines, angiotensin, vasopressin), and locally released adenosine and K+ in determining the behavior of arterial and venous vessels are considered.

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.

Neural control of muscle blood flow during exercise

2004 ◽  
Vol 97 (2) ◽  
pp. 731-738 ◽  
Author(s):  
Gail D. Thomas ◽  
Steven S. Segal
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Neural Control ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity ◽  
Arterial Blood

Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.

Frequency domain characteristics of muscle sympathetic nerve activity in heart failure and healthy humans

1997 ◽  
Vol 273 (1) ◽  
pp. R205-R212 ◽  
Author(s):  
S. Ando ◽  
H. R. Dajani ◽  
J. S. Floras
Keyword(s):  
Heart Failure ◽  
Frequency Domain ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Power ◽  
Breathing Frequency ◽  
Nerve Activity ◽  
Significant Difference

The purpose of this study was to characterize oscillations in muscle sympathetic nerve activity (MSNA) in the frequency domain in healthy subjects and patients with congestive heart failure (CHF) and to relate these to blood pressure (BP), heart rate (HR), and breathing frequency. MSNA burst frequency was significantly greater in CHF [52 +/- 21 (n = 12) vs. 35 +/- 11 (n = 19) bursts/min, P < 0.05], whereas breathing frequency and HR were similar. There was no significant difference between CHF and healthy subjects in total power, harmonic power, and nonharmonic power in the MSNA spectrum from 0 to 0.5 Hz, but low frequency power (LF, 0.05-0.15 Hz, P < 0.05) was reduced in heart failure patients. There was less coherence between BP and MSNA in the LF range, but similar spectral power in both groups in the very LF (VLF, 0-0.05 Hz) and high frequency (0.15-0.5 Hz) ranges. The transfer of MSNA oscillations into BP in the VLF (P < 0.05) and LF (P < 0.02) ranges was significantly lower in CHF, but gains in the transfer function and in the coherence between BP and MSNA and in the coherence between respiration and MSNA were similar in the two groups. These observations indicate that modulation of MSNA by the arterial baroreflex and respiration is preserved in CHF. The loss of LF power in the MSNA signal may be due to impaired neuroeffector transduction. The higher sympathetic nerve firing rate in CHF would therefore appear to be caused by factors other than the loss of regulation by these two inhibitory influences.

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.

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