Muscle Contraction - Science topic
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
Questions related to Muscle Contraction
During skeletal muscle contraction and during the actin–myosin ATPase cycle there is release of Pi and ADP. Can anyone tell me and ideally suggest a reading list of where they actually go?
i want to study muscle contraction mechanism, for that i have to take 100uM concentration . but it is insoluble in water. can i use hot water to disolve it
i need to stimulate a peripheral nerve and record muscle contraction using powerlab and its implanted software. The provided electrodes are gold-plated. Can they stimulate peripheral nerves? I got no increase in pressure at all till now and i do not no the reason. The provided stimulator electrodes are shown in the attached file
It is known that the adaptive response to effort depends on several factors, including duration, intensity, frequency, type of exercise, type of muscle contraction, etc. However, physical intervention programs many times, these variables are not presented, cannot be compared, cannot be reproduced or replicated, by other authors
Usually, passive force is well described by the F-L relationship obtained during isometric contractions. Indeed, it is well known that passive force increase when the muscle is contracted at longer length that its optimum.
However, is it possible to have passive force during concentric dynamic contraction iv-vivo? If yes, how is ti possible to calculate this force?
Thank you very much for your help.
I am planning to investigate the theory that the psoas is the "fight or flight" muscle that tends to become chronically constricted when people have post traumatic stress disorder.
During a muscle contraction by lower to medium motor unit groups, how do high threshold muscle fibers shorten? Passive? Active?
So if I bend my arm in the elbow without weight in my hand, how do high threshold muscle fibers related to high motor unit groups shorten? Do their actin and myosin overlap? Is the tension produced by the other MU groups enough to shorten the connective tissue in the other muscle fibers? Is there active overlap without cross-bridge cycling in the HMU groups and their fibers?
I have a question regarding TMS procedures. I am just wondering if anyone is aware of ways of controlling for varying levels of arousal as a result of using TMS for stimulating different brain sites (e.g. frontal scalp locations vs. vertex) whereat this stimulation brings different levels of face muscle contractions and different levels of possible discomfort / annoyance. Could you please direct me to any studies using such controls?
I'm interested to know muscle state in anxiety or fear state during climbing dangerous or stressed activity. Thanks for helping me.
Swammerdam (17th century) stimulated a muscle in a fluid-filled jar with a small-bore tube attached, measuring a slight decrease in volume, disproving the "balloonist" theory of muscle contraction. This finding is well-replicated in frog sartorius, but there is a recent claim (Clark & Demer 2016) that human eye muscles are different in that they increase as much as 18% in total volume when they contract to rotate the eye. I don't believe it!
Can anyone point me to contraction-volume measurements in vertebrate muscles, or any muscles that might be more like human EOMs, or to an expert who might know about this stuff?
I am testing the effects of inorganic phosphate on the force-pCa relationship in mammalian skinned fibres at room temperature. I have lovely force-pCa relationships, but 20 mM phosphate has no effect on force or the Ca50, which seems ridiculous given the overwhelming evidence that it reduces force and reduces Ca2+ sensitivity. I'm currently using rabbit psoas skinned in glycerol solution.
I have some things to try:
1) Adding phosphocreatine to the solutions in case the PO4 produced by crossbridge cycling is high and the diffusion rate so low that the effects I think I should be seeing are masked.
2) Secondary skinning with triton-x to further dissolve the sarcolemma.
3) I'm using really old samples as practice tissue which could be problematic.
4) The only other thing I can think of is that I have completely bungled the recipes for the solutions. We have a set of standard pCa solutions which work great. To make a 20 mM PO4 solution, I added 20 mM KH2PO4 and reduced the concentration of K-Proprionate to match the ionic strength of the two solution types. pH 7.0.
Has anyone encountered this before or have any other suggestions.
From my point of view, it is possible to find a positive relationships between muscle CSA and muscle stiffness.
However, to my knowledge, there are not paper that explain this mechanism.
Anyone know any good papers about the possible interaction between muscle characteristics (e.g. pennation angle; CSA) and muscle stiffness?
I would like to know if prolongued and accumulated fatigue is related to changes (decrements) in muscle stiffness (loss of muscle tone). If possible, I need some references regarding the physiology behind this phenomena.
I need to know which sEMG descriptors are useful to determine motor unit recruitment or activation of a certain muscle. In our study, we want to see how the pattern of activation / recruitment differs between different inter-electrode distance (IED) and different intensities using an electrostimulator to cause muscle contraction.
In brief, we want to see if different intensities of electrostimulation (50, 75 and 100 mA) with different IED differ in the recruitment of motor units or something similar (i.e., any sEMG useful descriptor for this purpose).
I am analyzing EMG for squat lifting for 30 squats. The subjects were free to chose the squat speed. The rectus femoris muscle was under investigation. The activation pattern is not constant. And I want to find the Mean power frequency (MPF) for just the time the muscle is fully activated taking a fixed window of 500 ms. I am using Megawin software and it has a setting of manually choosing area of interest for MPF calculation. I wanted to ask is it ok to use this method because if i chose a fixed interval for calculation of MPF for each squat, due to variation in timing it misses the fully activated portion and instead calcualtes the MPF of rest period.
I am trying to mount rat mesenteric veins on a Mulvany's myograph but either I found no contractions or they are too small to work with.
Can anyone help?
I want to determine the drug effect in inhibiting human bronchial smooth muscle contraction induced with histamine. Currently, I tried it with
1. 0.5 X 10^6 cell per well in 24 well plate with 2 mg/ml collagen gel
- histamine concentration : 10 - 100 uM
2. 0.2 X 10^6 cell per well in 24 well plate with 1.5 mg/ml collagen gel
- histamine concentration : 10 - 100 uM
Both conditions did not work. The induced group showed no difference with the normal control group.
And, for the 2 mg/ml collagen gel, the spindle shape of the cell did not look normal as compared to the 1.5 mg/ml collagen gel.
Any recommendations to improve my assay?
I need papers which deal with the topic muscle fatigue and CoM displacements. I would like to know what are the principal effects of muscle fatigue in the CoM displacements. However, I need of the most recent papers about this.
1. What is the best method to set the onset of muscle contraction during isometric strength testing? Is a set value of so many Newtons (e.g. 15 N) preferable?
2. When measuring peak force during an isometric muscle contraction (e.g. if data are obtained at 1000 Hz), what do we define as "peak force"? Is it the highest instantaneous value? If not, what is the best interval for averaging force?
If you know any article which explains ways to cure/ treatment/ betterment/ ... for writer's cramp please introduce me. I am also interested to know if there is any association, institution for writer's cramp. Also, which hospital research center or person is famous in research regarding writer's cramp?
Anaerobic glycolisis energy contribution can be determined through field test for evaluating anaerobic lactic acid contribution during physical effort, but I think there is not yet possible to do the same determination among macroergics compounds? Are there some field test for assessing this in sport / physical training?
Hello, I am measuring smooth muscle contraction by wire myography. Is there any body to give me some information how to analysis data in labchart?
Are there some new reports about ATP contribution for extreme power contractions? I need to develop a model for predicting it and then which variables could be tested.
I have been culturing a mixed culture of enteric neurons and smooth muscle cells for an experiment. After 14 days in vitro, I see parts of the culture contracting. I'd like to measure this contraction but all the available softwares require a clear or contrasting background in order to quantify movement/displacement of the selected object (in this case cells contracting). Since my culture is confluent I don't have a "contrasting" background. Can anyone suggest some ways to quantify this contraction without manual counting?
Thanks in advance!
The amount of 3-methyl histadine per gram of skeletal muscle is a constant. Therefore, if there are issues with methylation, one would expect that this must limit the amount of myofibrillar protein that can anabolically be synthesised. Does anyone know if this concept is, in fact, true?
Krebs Henseleit Solution
For 1 Liter
118mM NaCl 6.90 grams
4.7mM KCL 0.35 grams
1.2mM KH2PO4 0.16 grams
1.2mM MgSO4 0.14 grams
25mM NaHCO3 2.10 grams
11mM Glucose 1.98 grams
2.5mM CaCl2 0.28 grams (I forget to write here now its OK)
0.003mM EDTA.Na2.2H2O 0.0011grams
Please can any one tell me step by step to prepare Krebs Henseleit Solution because sometimes our krebs solution make problem for our experiment
I am looking for ways to partially inhibit the force generating capacity of muscles. Peripherally mediated fatigue if possible. Currently, I am considering inducing local fatigue (i.e. lots of repetitions) and experiential pain (hypertonic saline). Are there any other methods?
In cell what are the parameters that can detect the SMC contraction? I read that some people uses collagen based cell contraction assay? Is it the gold standard? What other options are their to prove relaxation or contraction in cells?
When we isolate rat aorta and soaked in organ bath with Krebs solution, I have two question
1. The best way to remove endothelium
2. The best way to induced endothelial dysfunction (rather than High glucose, H2O2 )
In case of myosin & actin filament pair (muscle Contraction), due asymmetric polarity along the filament, myosin heads feel sawtooth potential but for kinesin movement how does the sawtooth like potential arise? We know kinesin moves from - ve to + ve site of filament but along the filament is there any asymmetry in polarity? Or it just because of the spatial assymetry the potential is sawtooth like?
Lets take a patient in supine position and do needle EMG in Quadriceps muscle.
Standard text book gives At rest there will be no recording after putting the needle.
But we have been taught all muscles are in a state of partial contraction even at rest and no muscle is completely relaxed. If it is true my doubt is that whether the EMG will be able to record that partial contraction.
Does it have anything to do with the ground electrode?
I am using an organ bath instrument to understand smooth muscle contraction by metal pollutants, are there any new techniques to understand the same mechanism?
Dear esteemed scientists. I am currently doing ex vivo contraction experiments with isolated bovine smooth muscle strips. We have found an increased maximum contraction for the agonist that I am interested in. However, these changes go hand in hand with a dramatic reduction in smooth muscle myosin (heavy chain) expression, as measured with a Western blot. I am really puzzled by these findings, since they seem contradictory at first hand. Could anyone explain these events?
The endothelium was considered to be present when the Ach-induced relaxation was at least 80% after pre-contracted with Phe (10−6 M – EC80).
Why didn't it work like this sample :
please see attached image
After that, rings were placed under a resting tension of 2 g and equilibrated for 90 min before starting the experimental protocols.
If less or more than 90 min what occurs?
We want to use thoracic aorta isolated from rats yesterday then we preserved in a refrigerator then we used in tissue bath after that we pre-contracted aorta by PE then relaxing by ACh.
Smooth muscle contraction is tightly regulated by endothelium or epithelium depending upon the presence of either of the two layers in particular tissues. Endothelium/epithelium modulates various signaling pathways via generation of molecules like NO, COX, ROS or by calcium signaling. I want to know if there is a difference between regulation of contraction by endothelium and epithelium, if so, what signaling cascade do each regulate?
In my previous lab they extract actin from muscle and then label it with rhodamine phalloidin, but I see polymerized- and labelled-actin is available commercially as well.
I wonder if somebody has experience in it and could suggest me one?
We are using arteries from humans for myographical studies, but we have problems during contraction when we use phenylphrine (PE)? But, the arteries contract normally when we use KCl.
I have a dataset with MEPs elicited in a forearm muscle (the FDS). In around 50% of participants the TMS artifact is very large and still present for some of the 10-40ms window in which I look for MEPs. In these cases there are visible MEPs, but I'm not sure to what extent they are distorted by the artifact. My question is: are these data salvageable? Is there a way (using ICA perhaps) to filter out the artifact? Or is it a problem as the latency and magnitude of the artifact varies between participants?
In case it is important: I was eliciting MEPs in the hand simultaneously and those data are fine (i.e. the TMS artifact is of the 'usual' small amplitude and short latency).
When we use rat trachea and histamine to induce contraction, there was no response in rats but isolated guinea-pig trachea produced high response with histamine. Why was this?
I know the co-contraction means simultaneous contraction of agonist and antagonist muscles around a joint to hold a position. I don't know what differences are there between muscle co-contraction and muscle co-activation?
Can someone explain the origin of the post-EFS peak observed in EFS tracings after stimulation of enteric neurons? In all of my organ bath studies there is a strong post-EFS contraction that changes as the frequency is altered. I was once told that it is glial in origin, but I haven't found any literature to back that up.
Creatine monohydrate is a supplement taken to increase muscular activity. It does so by increasing the production of ATP through creatine kinase activity. However, creatine monohydrate draws water into muscles. This influx of water may cause electrolyte imbalances which could also cause cramping. There have been multiple accounts of both decreased cramping frequency and increased cramping frequency in subjects who take creatine monohydrate.
The case applies to the load sustained by neck muscles and all the cervical anatomy (provided by an acceleration and deceleration head), in an occupant's neck, during a car collision.
So, it makes sense to say that a neck with some key muscles in a prestressed state (or should I say full activated or in isometric contraction?), is better prepared to sustain flexion/extension loads and will be subjected to a fewer number of (or less severe) injuries than a neck with muscles in a relaxed state, independent of the amount of load?
I am looking for any article that describes experiences with Electrical Muscle Stimulation in isometric contraction of skeletal muscle until the tetanic contraction. I need to know the values for frequency (Mhz) and power (W) used to produce that kind of contraction.
Depending on location, shape and presence of channels and pumps, especially related to the mechanisms of contraction and relaxation.
I am working over different muscle models to compute muscle forces and most of them include the so-called "width" parameter, but it is not referenced how to compute it, nor its meaning, just a simple value on a table. I would appreciate any help on this.
I have tested participants at 30 deg/sec and 200 deg/sec pre and post an intervention, and recognize that at 200 deg/sec the observed adaptation are FT orientated.
How do I calculate just the ST fibre contribution at 30 deg/sec? Is it just a case of removing FT values from ST? Does anyone have a reference for this?
Ten sets of ten repetitions were performed at an angular velocity of 90 deg/s using isokinetic dynamometer.