ATP concentrations and muscle tension increase linearly with muscle contraction

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Motor Nerve ◽  
Muscle Tension ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Ventral Roots ◽  
Root Stimulation ◽  
Stimulation Of

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

scholarly journals Optogenetic activation of muscle contraction in vivo

2020 ◽  
Author(s):  
Elahe Ganji ◽  
C. Savio Chan ◽  
Christopher W. Ward ◽  
Megan L. Killian
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Fluorescent Imaging ◽  
Triceps Surae ◽  
Light Activation ◽  
Non Invasive ◽  
Optogenetic Stimulation ◽  
Stimulation Of

AbstractOptogenetics is an emerging alternative to traditional electrical stimulation to initiate action potentials in activatable cells both ex vivo and in vivo. Optogenetics has been commonly used in mammalian neurons and more recently, it has been adapted for activation of cardiomyocytes and skeletal muscle. Therefore, the aim of this study was to evaluate the stimulation feasibility and sustain isometric muscle contraction and limit decay for an extended period of time (1s), using non-invasive transdermal light activation of skeletal muscle (triceps surae) in vivo. We used inducible Cre recombination to target expression of Channelrhodopsin-2 (ChR2(H134R)-EYFP) in skeletal muscle (Acta1-Cre) in mice. Fluorescent imaging confirmed that ChR2 expression is localized in skeletal muscle and does not have specific expression in sciatic nerve branch, therefore, allowing for non-nerve mediated optical stimulation of skeletal muscle. We induced muscle contraction using transdermal exposure to blue light and selected 10Hz stimulation after controlled optimization experiments to sustain prolonged muscle contraction. Increasing the stimulation frequency from 10Hz to 40Hz increased the muscle contraction decay during prolonged 1s stimulation, highlighting frequency dependency and importance of membrane repolarization for effective light activation. Finally, we showed that optimized pulsed optogenetic stimulation of 10 Hz resulted in comparable ankle torque and contractile functionality to that of electrical stimulation. Our results demonstrate the feasibility and repeatability of non-invasive optogenetic stimulation of muscle in vivo and highlight optogenetic stimulation as a powerful tool for non-invasive in vivo direct activation of skeletal muscle.

Effect of barodenervation on c-Fos expression in the medulla induced by static muscle contraction in cats

1998 ◽  
Vol 274 (3) ◽  
pp. H901-H908 ◽  
Author(s):  
Jianhua Li ◽  
Jeffrey T. Potts ◽  
Jere H. Mitchell
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Baroreceptor Reflex ◽  
Reticular Nucleus ◽  
Arterial Blood ◽  
Ventral Roots ◽  
Stimulation Of ◽  
Arterial Baroreceptor Reflex ◽  
Arterial Baroreceptor

A previous study has shown increased Fos-like immunoreactivity (FLI), a marker of neural activation, in the nucleus of the solitary tract (NTS) and the ventrolateral medulla (VLM) after static muscle contraction elicited by electrical stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized, baroreceptor-intact cats. Because the electrically induced static muscle contraction reflexly increased arterial blood pressure, the concomitant activation of the arterial baroreceptor reflex during static muscle contraction may have resulted in some of the FLI labeling that was observed in the medulla. The purpose of this study was to determine regions in the medulla that are activated by muscle contraction in the absence of arterial baroreceptor input. Electrical stimulation of L7 and S1 ventral roots of the spinal cord was used to elicit static muscle contraction, and FLI in the medulla was determined in barointact and barodenervated cats. In barointact contraction cats, FLI was observed in the lateral reticular nucleus (LRN), NTS, lateral tegmental field (FTL), subretrofacial nucleus (SRF), and A1 region of the medulla. In barodenervated contraction cats, FLI increased in the same regions; however, the number of FLI-labeled cells in the NTS, FTL, and A1 region was significantly less than in barointact contraction animals. No significant difference in the number of FLI-labeled cells was found in the LRN and SRF between the two groups. These results clearly demonstrate that cardiovascular regions in the medulla are activated by input from afferent activity originating in skeletal muscle independently of concomitant arterial baroreceptor reflex activation.

scholarly journals KATP channels and NO dilate redundantly intramuscular arterioles during electrical stimulation of the skeletal muscle in mice

2021 ◽  
Author(s):  
Simon Schemke ◽  
Cor de Wit
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Motor Nerve ◽  
Neuromuscular Synapse ◽  
Katp Channels ◽  
Neuromuscular Synapses ◽  
Maximal Diameter ◽  
Motor Nerves ◽  
A Minor ◽  
Stimulation Of

AbstractFunctional hyperemia is fundamental to provide enhanced oxygen delivery during exercise in skeletal muscle. Different mechanisms are suggested to contribute, mediators from skeletal muscle, transmitter spillover from the neuromuscular synapse as well as endothelium-related dilators. We hypothesized that redundant mechanisms that invoke adenosine, endothelial autacoids, and KATP channels mediate the dilation of intramuscular arterioles in mice. Arterioles (maximal diameter: 20–42 µm, n = 65) were studied in the cremaster by intravital microscopy during electrical stimulation of the motor nerve to induce twitch or tetanic skeletal muscle contractions (10 or 100 Hz). Stimulation for 1–60 s dilated arterioles rapidly up to 65% of dilator capacity. Blockade of nicotinergic receptors blocked muscle contraction and arteriolar dilation. Exclusive blockade of adenosine receptors (1,3-dipropyl-8-(p-sulfophenyl)xanthine) or of NO and prostaglandins (nitro-L-arginine and indomethacin, LN + Indo) exerted only a minor attenuation. Combination of these blockers, however, reduced the dilation by roughly one-third during longer stimulation periods (> 1 s at 100 Hz). Blockade of KATP channels (glibenclamide) which strongly reduced adenosine-induced dilation reduced responses upon electrical stimulation only moderately. The attenuation was strongly enhanced if glibenclamide was combined with LN + Indo and even observed during brief stimulation. LN was more efficient than indomethacin to abrogate dilations if combined with glibenclamide. Arteriolar dilations induced by electrical stimulation of motor nerves require muscular contractions and are not elicited by acetylcholine spillover from neuromuscular synapses. The dilations are mediated by redundant mechanisms, mainly activation of KATP channels and release of NO. The contribution of K+ channels and hyperpolarization sets the stage for ascending dilations that are crucial for a coordinated response in the network.

scholarly journals Interstitial K+ concentration in active muscle after myocardial infarction

2007 ◽  
Vol 292 (2) ◽  
pp. H808-H813 ◽  
Author(s):  
Jianhua Li ◽  
Zhaohui Gao ◽  
Valerie Kehoe ◽  
Lawrence I. Sinoway
Keyword(s):  
Myocardial Infarction ◽  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Active Muscle ◽  
Pump Activity ◽  
Healthy Control ◽  
Sciatic Nerves ◽  
K Concentration ◽  
Stimulation Of

Previous work demonstrated that Na+-K+ pump activity within skeletal muscle is attenuated in myocardial infarction (MI). This may lead to enhanced interstitial K+ concentration ([K+]o) in the muscle. We tested the hypothesis that [K+]o rises with muscle contraction and that, in rats with MI, the rate of rise in [K+]o is greater than it is in control animals. Microdialysis probes were inserted in the skeletal muscle of six healthy control and six MI rats. The ends of the probes were then attached to the K+ electrodes, and [K+]o was continuously measured. Muscle contraction was induced by electrical stimulation of the sciatic nerves for 1 min. Stimulation at 1 and 3 Hz increased muscle [K+]o by 14.2% and 44.7% in controls and by 22.9% and 62.8% in MI rats ( P < 0.05 vs. controls), respectively. When ouabain, an inhibitor of Na+-K+ pump, was added to the perfusate, muscle [K+]o rose significantly. This effect of ouabain was significantly attenuated in MI animals. In conclusion, when compared with that in control animals, an increase of [K+]o in exercising muscle is augmented in MI rats, likely due to an attenuation of Na+-K+ pump activity.

Reflex responses evoked from cats' coccygeal ventral roots by electrical stimulation of the tail nerves

1987 ◽  
Vol 96 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Margarita Martinez-Gomez ◽  
Pablo Pacheco ◽  
Bernardo Dubrovsky
Keyword(s):  
Electrical Stimulation ◽  
Reflex Responses ◽  
Ventral Roots ◽  
Stimulation Of

Assessment of specific muscle tension in dogs through functional electrical stimulation of the gastrocnemius muscle

2017 ◽  
Vol 113 ◽  
pp. 33-39
Author(s):  
B. Dries ◽  
B. Vanwanseele ◽  
I. Jonkers ◽  
J. Vander Sloten ◽  
E. Van der Vekens ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Functional Electrical Stimulation ◽  
Gastrocnemius Muscle ◽  
Muscle Tension ◽  
Specific Muscle ◽  
Stimulation Of

CONDUCTION BLOCK OF TERMINAL SOMATIC MOTOR FIBERS IN TICK PARALYSIS

1960 ◽  
Vol 38 (3) ◽  
pp. 287-295 ◽  
Author(s):  
Maurice F. Murnaghan
Keyword(s):  
Motor Nerve ◽  
Conduction Block ◽  
Nerve Impulse ◽  
Nerve Fibers ◽  
Treated Animal ◽  
Direct Stimulation ◽  
High Potassium ◽  
Control Value ◽  
Choline Acetylase ◽  
Stimulation Of

In the perfused anterior tibial muscle of the tick-paralyzed dog acetylcholine in excess of the control value is not liberated on stimulation of the peroneal nerve; in the normal muscle 7 μμg of acetylcholine is liberated per nerve volley. The paralysis is evidently not due to defective synthesis of acetylcholine because acetylcholine is liberated in control and high-potassium perfusates, the choline acetylase activity and the acetylcholine content of lumbar ventral roots and peroneal nerves do not differ from that in normal dogs, and the tick-paralyzed muscle differs from that in the hemicholinium-treated animal in its response to a train of nerve pulses after previous tetanization. As somatic motor nerve fibers in the paralyzed dog have previously been shown to conduct a nerve impulse and the factors required for acetylcholine release at the nerve terminal apparently are not absent in the paralyzed animal, the mechanism of the paralysis is probably due to an inability of the nerve impulse to traverse the terminal presynaptic fibers. The 'lesion' evidently extends to the end of the presynaptic fiber, i.e. more distally than in botulism, because direct stimulation of the tick-paralyzed muscle fails to liberate acetylcholine.

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