Force response to electrical stimulation of canine skeletal muscles

1981 ◽  
Vol 14 (9) ◽  
pp. 595-599 ◽  
Author(s):  
J. Moreno-Aranda ◽  
A. Seireg
2005 ◽  
Vol 22 (2) ◽  
pp. 227-243 ◽  
Author(s):  
Tatiana Y. Kostrominova ◽  
Douglas E. Dow ◽  
Robert G. Dennis ◽  
Richard A. Miller ◽  
John A. Faulkner

Loss of innervation in skeletal muscles leads to degeneration, atrophy, and loss of force. These dramatic changes are reflected in modifications of the mRNA expression of a large number of genes. Our goal was to clarify the broad spectrum of molecular events associated with long-term denervation of skeletal muscles. A microarray study compared gene expression profiles of 2-mo denervated and control extensor digitorum longus (EDL) muscles from 6-mo-old rats. The study identified 121 genes with increased and 7 genes with decreased mRNA expression. The expression of 107 of these genes had not been identified previously as changed after denervation. Many of the genes identified were genes that are highly expressed in skeletal muscles during embryonic development, downregulated in adults, and upregulated after denervation of muscle fibers. Electrical stimulation of denervated muscles preserved muscle mass and maximal force at levels similar to those in the control muscles. To understand the processes underlying the effect of electrical stimulation on denervated skeletal muscles, mRNA and protein expression of a number of genes, identified by the microarray study, was compared. The hypothesis was that loss of nerve action potentials and muscle contractions after denervation play the major roles in upregulation of gene expression in skeletal muscles. With electrical stimulation of denervated muscles, the expression levels for these genes were significantly downregulated, consistent with the hypothesis that loss of action potentials and/or contractions contribute to the alterations in gene expression in denervated skeletal muscles.


2006 ◽  
Vol 47 (3) ◽  
pp. 441-453 ◽  
Author(s):  
Petr Dobsák ◽  
Marie Nováková ◽  
Bohumil Fiser ◽  
Jarmila Siegelová ◽  
Pavla Balcárková ◽  
...  

2004 ◽  
Vol 04 (01) ◽  
pp. 77-92 ◽  
Author(s):  
MARGIT GFÖHLER ◽  
THOMAS ANGELI ◽  
PETER LUGNER

Functional Electrical Stimulation (FES) enables paraplegics to move their paralyzed limbs; the skeletal muscles are artificially activated. The purpose of this study is to establish a mechanical muscle model for an artificially activated muscle, based on a Hill-type muscle model. In comparison to modeling a physiologically activated muscle, for the artificially activated muscle, a number of additional parameters and their influence on the force generation has to be considered. The model was implemented into a forward dynamic simulation of paraplegic cycling. The stimulation patterns were optimized for surface stimulation of gluteus maximus, quadriceps, hamstrings, and peronaeus reflex. A simulation of a startup with 50% of maximum activation in the optimized stimulation intervals analyses drive torques and mean power per cycle and the resulting riding performance of the rider-cycle system. For validation of the simulation, the results were compared to measurements of the forces applied to the crank during steady-state cycling of a paraplegic test person.


1991 ◽  
Vol 261 (3) ◽  
pp. E298-E303 ◽  
Author(s):  
M. Sudo ◽  
Y. Minokoshi ◽  
T. Shimazu

Effects of electrical and chemical stimulation of the ventromedial (VMH) and lateral hypothalamic (LH) nuclei on glucose uptake in peripheral tissues were studied by the 2-deoxy-D-[3H]glucose (2-[3H]DG) method in anesthetized rats. Electrical stimulation of the VMH increased the rate constant of glucose uptake in brown adipose tissue (BAT; 8 times), heart (3 times), and skeletal muscles (1.5 times) but not in white adipose tissue, diaphragm, and brain, without detectable changes in plasma insulin levels. Chemical stimulation of the VMH by microinjection of L-glutamate also enhanced the rate constant of glucose uptake in BAT, heart, and skeletal muscles preferentially, which indicates that the enhancement of glucose uptake in these tissues is derived from activation of VMH neurons. The increased rate of glucose uptake in BAT in response to VMH stimulation was effectively suppressed by surgical sympathetic denervation, suggesting a mediation of the sympathetic nerve in this effect. On the other hand, electrical stimulation of the LH had no appreciable effect on 2-[3H]DG uptake in any tissues. It is concluded that glucose uptake in certain peripheral tissues is accelerated selectively by activation of VMH neurons, the action of which is independent of plasma insulin but which is probably via the sympathetic nervous system.


2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Harumi Hotta ◽  
Kaori Iimura ◽  
Nobuhiro Watanabe ◽  
Kazuhiro Shigemoto

AbstractThis study aimed to clarify whether the reflex excitation of muscle sympathetic nerves induced by contractions of the skeletal muscles modulates their contractility. In anesthetized rats, isometric tetanic contractions of the triceps surae muscles were induced by electrical stimulation of the intact tibial nerve before and after transection of the lumbar sympathetic trunk (LST), spinal cord, or dorsal roots. The amplitude of the tetanic force (TF) was reduced by approximately 10% at 20 min after transection of the LST, spinal cord, or dorsal roots. The recorded postganglionic sympathetic nerve activity from the lumbar gray ramus revealed that both spinal and supraspinal reflexes were induced in response to the contractions. Repetitive electrical stimulation of the cut peripheral end of the LST increased the TF amplitude. Our results indicated that the spinal and supraspinal somato-sympathetic nerve reflexes induced by contractions of the skeletal muscles contribute to the maintenance of their own contractile force.


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