scholarly journals Simultaneous measurements of cardiac noradrenaline spillover and sympathetic outflow to skeletal muscle in humans.

1992 ◽  
Vol 453 (1) ◽  
pp. 45-58 ◽  
Author(s):  
B G Wallin ◽  
M Esler ◽  
P Dorward ◽  
G Eisenhofer ◽  
C Ferrier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sympathetic Outflow ◽  
Simultaneous Measurements

Muscle reflex stimulates sympathetic postganglionic efferents innervating triceps surae muscles of cats

1996 ◽  
Vol 271 (1) ◽  
pp. H38-H43 ◽  
Author(s):  
J. M. Hill ◽  
C. M. Adreani ◽  
M. P. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Cardiovascular Function ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Central Command ◽  
Muscle Reflex ◽  
Triceps Surae Muscles ◽  
Nerve Recordings ◽  
Stimulation Of

Two neural mechanisms contribute to the cardiovascular responses to exercise. The first, central command, proposes a parallel activation of central locomotor and brain stem circuits controlling cardiovascular function. The second, the muscle reflex, proposes that contraction-activated group III and IV afferents increase cardiovascular function. In humans, whole nerve recordings of sympathetic discharge suggest that central command increases sympathetic outflow to skin but not to skeletal muscle and that the muscle reflex increases sympathetic outflow to skeletal muscle but not to skin. We therefore tested the hypothesis that the muscle reflex, but not central command, increases the discharge of single sympathetic postganglionic efferents innervating the triceps surae muscles of decerebrate unanesthetized cats. Central command was evoked by electrical stimulation of the mesencephalic locomotor region. The reflex was evoked by electrical stimulation of the tibial nerve, which in turn contracted the triceps surae muscles. Hexamethonium abolished spontaneous and evoked activity, verifying that the recordings were from sympathetic postganglionic fibers. The discharge of 13 efferents was increased by static contraction (from 0.6 +/- 0.2 to 1.0 +/- 0.3 imp/s; P < 0.05) but was not increased by central command (from 0.6 +/- 0.2 to 0.8 +/- 0.2 imp/s; P > 0.05). Nevertheless, the discharge of nine efferents, not increased by central command before alpha-adrenergic blockade (from 0.5 +/- 0.2 to 0.9 +/- 0.4 imp/s; P > 0.05), was increased after blockade (from 1.3 +/- 0.2 to 3.2 +/- 0.8 imp/s; P < 0.05). We conclude that the muscle reflex stimulates sympathetic postganglionic efferents innervating the vasculature of skeletal muscle. Furthermore, baroreceptors appear to buffer the central command-induced increases in the discharge of these efferents.

Respiratory modulation of the activity in postganglionic neurons supplying skeletal muscle and skin of the rat hindlimb

1993 ◽  
Vol 70 (3) ◽  
pp. 920-930 ◽  
Author(s):  
H. J. Habler ◽  
W. Janig ◽  
M. Krummel ◽  
O. A. Peters
Keyword(s):  
Skeletal Muscle ◽  
Tidal Volume ◽  
Phrenic Nerve ◽  
Sympathetic Activity ◽  
Artificial Ventilation ◽  
Sympathetic Outflow ◽  
Experimental Conditions ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Respiratory Modulation

1. The respiratory modulation of activity in postganglionic neurons of the lumbar sympathetic outflow to skeletal muscle and hairy skin of the hindlimb was studied in anesthetized rats, either breathing spontaneously or paralyzed and artificially ventilated, using single- and multifiber recordings. The activity of the neurons was analyzed with respect to the phrenic nerve discharges or with respect to the cycle of artificial ventilation under various experimental conditions. 2. In total, 19 single and 62 multiunit preparations supplying skeletal muscle and 42 single and 95 multiunit preparations supplying skin were analyzed. Qualitatively, both populations and single- and multiunit preparations exhibited similar patterns. The majority (187/218 preparations) exhibited a depression of activity during inspiration and a peak of activity during expiration that was mostly accentuated during early expiration. The remainder exhibited a peak of activity at the transition between expiration and inspiration (n = 15) or showed no respiratory modulation (n = 16). 3. Respiratory modulation in the postganglionic neurons was similar in animals breathing spontaneously and in those that were paralyzed and artificially ventilated. 4. Systemic hypercapnia and asphyxia in most cases enhanced both the peak of activity during early expiration and the depression of activity during inspiration. 5. No peripheral (reflex) component mediated by arterial baroreceptors was found in vagotomized animals that was related to the cycle of artificial ventilation using a tidal volume of 1-2 ml and a ventilation frequency of 70 +/- 7 (SD) strokes, min-1. However, a small ventilation-related rhythm of arterial baroreceptor activity recorded from the aortic nerve was found under these conditions. 6. Respiratory modulation of postganglionic activity was similar before and after bilateral vagotomy. 7. It is concluded that respiratory modulation of sympathetic activity in rats is less differentiated than in cats. The observed differences between neurons supplying different targets are only quantitative. Possible mechanisms involved in the generation of respiratory modulation are discussed.

Differential sympathetic outflow elicited by active muscle in rats

2007 ◽  
Vol 293 (4) ◽  
pp. H2335-H2343 ◽  
Author(s):  
Satoshi Koba ◽  
Jihong Xing ◽  
Lawrence I. Sinoway ◽  
Jianhua Li
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Sympathetic Activation ◽  
Active Muscle ◽  
Internal Organs ◽  
Contracting Muscle ◽  
Distribution Of Cardiac Output

The present study was undertaken to test the hypothesis that activation of the muscle reflex elicits less sympathetic activation in skeletal muscle than in internal organs. In decerebrate rats, we examined renal and lumbar (mainly innervating hindlimb blood vessels) sympathetic nerve activities (RSNA and LSNA, respectively) during 1 min of 1) repetitive (1- to 4-s stimulation-to-relaxation) contraction of the triceps surae muscle, 2) repetitive tendon stretch, and 3) repetitive contraction with hindlimb circulatory occlusion. During these interventions, RSNA and LSNA responded synchronously as tension developed. The increase was greater in RSNA than in LSNA [+51 ± 14 vs. +24 ± 5% ( P < 0.05) with contraction, +46 ± 8 vs. +17 ± 4% ( P < 0.05) with stretch, +76 ± 20 vs. 39 ± 7% ( P < 0.05) with contraction during occlusion] during all three interventions: repetitive contraction ( n = 10, +508 ± 48 g tension from baseline), tendon stretch ( n = 12, +454 ± 34 g), and contraction during occlusion ( n = 9, +473 ± 33 g). Additionally, hindlimb circulatory occlusion significantly enhanced RSNA and LSNA responses to contraction. These data demonstrate that RSNA responses to muscle contraction and stretch are greater than LSNA responses. We suggest that activation of the muscle afferents induces the differential sympathetic outflow that is directed toward the kidney as opposed to the limbs. This differential outflow contributes to the distribution of cardiac output observed during exercise. We further suggest that as exercise proceeds, muscle metabolites produced in contracting muscle sensitize muscle afferents and enhance sympathetic drive to limbs and renal beds.

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