Science topic

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.
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How do advancements in pharmacology improve thesafety and efficacy of these agents ?
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How do vasopressors and inotropes affect cardiacoutput and systemic vascular resistance?
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What is the recommended blood pressure target forpatients receiving vasopressors?
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How does the interprofessional team collaborate tomanage patients on vasopressors?
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What factors influence the choice of a specificvasopressor or inotrope?
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What are the differences between short-term andlong-term use of vasopressors and inotropes?
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What special considerations exist for patients withpreexisting conditions requiring vasopressors?
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How do you manage the side effects of vasopressors,such as extravasation?
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Why is norepinephrine often the first-line agent inseptic shock?
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What is the role of central venous access invasopressor and inotrope therapy?
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How do catecholamines differ in their effects on alphaand beta receptors?
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What are the contraindications for the use ofvasopressors and inotropes?
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What are the adverse effects associated withvasopressors and inotropes?
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What are vasopressors and inotropes, and how dothey work?
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What are the primary indications for usingvasopressors and inotropes?
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How do vasopressors and inotropes differ in theirmechanisms of action?
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What are the common types of vasopressors andinotropes, and when are they used?
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Why is close monitoring essential during vasopressorand inotrope therapy?
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Is there any standardised index to estimate, more or less precisely, muscle mass from body weight (e.g., Bodyweight * index)?
Any reading suggestions are much appreciated.
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A device to measure the percentage of fullness in the body
Where a person weighs himself using an electrical density meter, based on height, weight and gender, and passes an electrical velocity measuring device through the body to measure the area.
It is characterized by having more knowledge than flexibility, and after measuring the scale, the mass value is subtracted from the number 100, in order to obtain a body without fat, part of which develops an intelligent mass, as it gains an intelligent percentage, not an accurate one.
MRI machine
MRI uses calculating the percentage of elasticity in the body, which is considered a gold standard and accurate mass for measurement.
The device uses magnetic rays and removes elastic images. The flow of the person is provided in the magnetic resonance device. The magnetic field rearranges the moisture atoms in the body, giving the device a thin mass in the body.
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Hello,
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?
Thank you
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After release from the binding site during the actin–myosin ATPase cycle, both inorganic phosphate (Pi) and adenosine diphosphate (ADP) remain associated with the myosin head for a brief period. This occurs just after the power stroke, when myosin is bound to actin. Subsequently, Pi and ADP are released from the myosin head as a new molecule of ATP binds to the myosin, initiating the next cycle. This binding and release process is crucial for the cyclic interaction between actin and myosin during muscle contraction.
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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
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The Apocynin solubility in hot water at 60 Celsius degree is 2mg/ml while in phosphate buffer is 5mg/ml, herein you find the solubility study of Apocynin
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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
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Thanks very much for the answer. The stimulator comprises 2 electrodes one may be hidden behind the other.
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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
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Yes of course
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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.
Best regards
Andrea
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There are many conditions, a muscle-tendon-complex can operate on. The force-length relation is only one description, let's say first order. There is the force-velocity relation, too, let's say second order. On top of that, passive tissue like tendon (in serial to fibres) and in parallel to the fibres (titin) can be charged, for example in wallaby hopping (Biewener) or some pre charged motions like catapulting a tongue (de Groot, J. H. & van Leeuwen, J. L. Evidence for an elastic projection mechanism in the chameleon tongue Proceedings. Biological sciences / The Royal Society, 2004, 271, 761-70). In summary, external conditions are of interest and the possible charge (stretch) of passive tissue.
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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.
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This is my area of research as well, we should definitely connect. I'm using biomechanical tests as they are the only thing we have any validity studies on right now and are used clinically, though there is a difference between range of motion and tension. Have you published your research yet?
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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?
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This is a very interesting question and I do not know any study dealing with this problem. Muscle fibres from different MUs (not their filaments) do overlap, so my guess is they shorten passively. However, since the mechanism of the crossbridge action during active muscle lenghtening is still unresolved, it is doubtful that there were any attempts to solve the problem you are asking for, although there may be some old, forgottened studies.
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Hello all,
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?
Many Thanks.
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Hi Eva,
The first thing that comes to my mind is that, beyond the Vertex, you can stimulate the contralateral equivalent of your target region.
Additionally, I can suggest you take a look at this interactive website for finding TMS-annoyance-matched scalp regions (and other potentially useful features): http://www.tms-smart.info/
Hope it helps!
Good luck,
Tiziano
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I'm interested to know muscle state in anxiety or fear state during climbing dangerous or stressed activity. Thanks for helping me.
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You should have no difficulty in finding literature – where are you looking?
Muscular tension is in the diagnostic criteria for generalized anxiety disorder (GAD), and, in my own research, it is one of the few symptoms that differentiates well between GAD and depression.
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How can I get the maximum muscle contraction value from EMG signal? Is it the hight of the maximum amplitude?
Thanks in advanced.
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EMG signal coresponds to muscle excitation and not directly to muscle tension. The tension (contraction) at the same excitation may vary. One factor to this variation is tirednes.
You can use MC sensor to measure tension directly
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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?
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Re Stephen M Levin: Wouldn't an auxetic muscle decrease in volume when it shortens? In any case, it's actual measurements I'm after. Thanks for your interest.
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Does anyone know whether afferents from muscle spindle contribute to voluntary muscle contractions?
Thanks
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A paper by Meunier, S., and C. Morin (1989) demonstrated that both homonymous and heteronymous Ia facilitations are markedly increased at the beginning of a voluntary isometric contraction.
Another study by Dietz et al. (1979) showed a decreased presynaptic inhibition of Ia afferent during running.
Therefore it seems that the answer to my question: "Do Ia afferents from muscle spindle contribute to voluntary muscle contractions?"
is, yes. regardless the contraction type
Moreover the contribution is also in relation to heteronymous-mediated decrease od presynaptic inhibition on Ia homonymous (contracting) muscle with symultaneous increase of presynaptic inhibition of antagonist
Meunier, S., and C. Morin. "Changes in presynaptic inhibition of Ia fibres to soleus motoneurones during voluntary dorsiflexion of the foot." Exp Brain Res (1989).
Dietz, V., D. Schmidtbleicher, and J. Noth. "Neuronal mechanisms of human locomotion." journal of Neurophysiology 42.5 (1979): 1212-1222.
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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.
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Hello Ian,
As hinted by Sergey above, you are dealing with / thinking about interesting but complex problems, temp, Pi, Ca etc,
Might be worth checking /reading some old papers referred to in Methods and control expts in
Journal of Physiology (2001), 536.3, pp.879–891 (Coupland et al paper).
Hope it helps, regards,
KW,
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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?
Many thanks
Andrea
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We have been measuring human muscle forces during orthopaedic surgery, directly at their tendon and as a function of joint angle after stimulating them. Hence, we obtain muscle force-joint able characteristics, from which muscle stiffness can be determined in active state. We also measure relevant anthropometrics before surgery, including circumference of the limb and tendon cross-sectional area if relevant. One finding which is very striking is that human muscle forces vary a lot from participant to participant despite their similar conditions. One aim we have is to see if such pre-surgery anthropometrics are good metrics to characterise the target muscle. However, there is almost never a correlation between e.g., the peak force and those metrics. In one particular study (which is attached), we looked to see if tendon stress instead of tendon force can remove the variability. In order to achieve that, we calculated tendon cross-sectional areas of the participants and determined the stress as force/cross-sectional area. This did limit some of the variability but did not eliminate it. We have been measuring forces of spastic hamstring muscles of cerebral palsy patients to characterise the pathological knee condition. However, such anthropometrics and the actual muscle force do not seem to correlate. I will attach one recent example of such intraoperative CP work as well.
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Hi everyone,
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.
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Caro Giuseppe,
La perdita di tono è legata alla perdita di massa muscolare, ma non è sempre così. Nella mia esperienza, dopo un esercizio molto eccentrico, la rigidità delle mucose diminuisce molto, il che può essere inteso come una condizione delle proprietà contrattili del muscolo (mancanza di ritorno dell'energia elastica)
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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).
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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.   
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There are several muscle onset detection algorithms (Teager–Kaiser energy operator, fuzzy entropy etc.). You can use one of them to determine the first sample of your fixed window.
In my opinion, if you select your windows manually, your experiment will be less reproducible.
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Some studies pointed the incidence of higher levels of tetranectin in muscle fibres after training.
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????????????????????
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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?
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 Dear Manuela..
Yes i did
But we never use use mesenteric veins, only we use mesenteric artries and the show good contraction
For farther details please let me know
Ahmed
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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?
Thanks.
Best regards,
Hui Min
(PhD student)
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Hello Huimin,
I also had the same problem. I used acetylcholine to stimulate the cell but did not observe any contraction.
Have you found the solution? If yes, would you mind sharing with me?
Thank you very much,
Duy
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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. 
Thanks.
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Hi Marcelo,
There is many reports out there. Here are some recent papers:
Age-Related Changes in Dynamic Postural Control and Attentional Demands are Minimally Affected by Local Muscle Fatigue http://www.ncbi.nlm.nih.gov/pubmed/26834626
Acute effects of muscle fatigue on anticipatory and reactive postural control in older individuals: a systematic review of the evidence http://www.ncbi.nlm.nih.gov/pubmed/24978932
Biomechanical reorganisation of stepping initiation during acute dorsiflexor fatigue http://www.ncbi.nlm.nih.gov/pubmed/21605984
Impact of ankle muscle fatigue and recovery on the anticipatory postural adjustments to externally initiated perturbations in dynamic postural control http://www.ncbi.nlm.nih.gov/pubmed/23111432
Those a few recent studies, and you can go from there to access many more.
Hope this helps. Norbert
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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?
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1. Onset of muscle contraction. Measure the average force (noise) of the baseline and when the line stays 2 Standard deviations above the noise you can be assured that the contraction has started. This is more typically used with EMG signals but should apply to force as well.
2. Peak force is defined by some as the instantaneous peak force and others by a predetermined duration (i.e. 500 ms, 1 s) and the average over that duration. As long as it is well defined I do not think one analysis is better than the other unless you have slack in your system and the instantaneous peak force is significantly higher due to movement artifact (snapping effect of the cable for instance).
Hope that is helpful.
Dave B.
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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?
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The writer's cramp  is the same pathology as musician's focal dystonia (also referred to as musician's dystonia or musician's cramp). A pathology which I developed (as a former professional musician)  and recovered from at the Institut de Fisiologia i Medicina de l’Art-Terrassa (http://www.institutart.com/index.php/en/l-institut/presentacio) with Dr. Jaume Rosset i Llobet team. Treatment is based on a neurological reprogramming program based on movement. You can follow Dr Rosset Lobet's publications here https://www.researchgate.net/profile/Jaume_Rosset.
Hope it helped....!
Regards,
Nuno Correia
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I found several equipments for this task (Biodex, IsoMed2000, ....), but I need more information about the best equipment.
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I  think cybex is good
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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?
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You can inhibit creatine kinase with fdnb (fluro-dinitro-benzene) but you will find the muscle goes into rigor pretty quickly!
I've just read the whole question and realise you are talking about field testing, so probably fdnb wouldn't be the best thing to try!  I don't know of any way you could assess this in a whole animal/person.  NMR studies always show ATP to remain very constant during exercise which suggests that ATP hardly acts as a store at all but is mainly a means of passing high energy P from PCr to myosin, or wherever it is needed.
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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?
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Graphpad Prism is the best program for all things myograph. Worth the investment!
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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.
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During maximal intensity exercise, such as sprinting, ATP is re-synthesized from phosphocreatine and anaerobic glycolysis, while aerobic metabolism plays an important role as duration is increased and/or high intensity exercise bouts are repeated. Interestingly, the concentration of ATP never drops below 60-70% of the resting concentration, i.e. the ATP pool of the muscle is preserved, although in some muscle fibres, ATP may drop to zero (see refs below).This is dependent on fiber type. For furthter reading, please see the papers below
Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK, Nevill AM. Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. J Physiol. 1995 Jan 15;482 ( Pt 2):467-80.
Bogdanis GC, Nevill ME, Lakomy HK, Boobis LH. Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans.Acta Physiol Scand. 1998 Jul;163(3):261-72.
Nevill AM, Jones DA, McIntyre D, Bogdanis GC, Nevill ME.A model for phosphocreatine resynthesis. J Appl Physiol (1985). 1997 Jan;82(1):329-35.
Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK. Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise. J Appl Physiol (1985). 1996 Mar;80(3):876-84.
Hellsten Y, Richter EA, Kiens B, Bangsbo J. AMP deamination and purine exchange in human skeletal muscle during and after intense exercise. J Physiol. 1999 Nov 1;520 Pt 3:909-20.
Söderlund K, Hultman E. ATP and phosphocreatine changes in single human muscle fibers after intense electrical stimulation. Am J Physiol. 1991 Dec;261(6 Pt 1):E737-41.
Gray SR, Söderlund K, Ferguson RA. ATP and phosphocreatine utilization in single human muscle fibres during the development of maximal power output at elevated muscle temperatures. J Sports Sci. 2008 May;26(7):701-7. doi: 10.1080/02640410701744438.
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Hi,
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!
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Your best chance here would be to use traction force microscopy. little fluorescent beads in a gel layer will move in response to the forces applied to it by the smooth muscle cells. as you can vary the elasticity of the gel you can change between measuring mostly the force (small displacements) or focus on displacements alone. alternatively you could bind fluorescent beads to your smooth muscle cells and track their movement. Lastly, if you want to keep it experimentally simple but are willing to to go a bit deeper in image analysis is to use difference imaging in which you subtract the original image from the image in which the cells have contracted. this should easily identify the contracting cells, and in most cases makes it quite easy to see how much they contracted too.
Good Luck!
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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?
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The above assumption is logical. However, the literature is not enough data to draw conclusions. It is possible to partially solve the problem of muscle growth with a lack of methylation Supplementing the necessary amino acids.
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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
Best reagard 
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Not oxygenate, gas with 95%  O2, 5%CO2. The buffering requires the CO2.
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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?
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Previous studies done especially in studying creatine kinase enzymes in muscles have used repetitive eccentric muscle contractions to a particular muscle group until the group becomes exceedingly fatigued. The muscle then fails in its full ability to contract. Beware that this brings about severe delayed muscle soreness.It works well in previously untrained muscles.
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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? 
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Do you want quantitative or qualitative measurement of contraction?  Techniques will differ accordingly.
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relationship between muscle contraction with muscle length and velocity
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Dear Ali,
I think the answer is pretty straightforward if you want a general answer, the classic papers are:
For changes in muscle force with length:  
Gordon AM, Huxley AF, and Julian FJ. The variation in isometric tension with sarcomere length in vertebrate muscle fibres. J. Physiol. (Lond.) 184: 170-192, 1966.
For variations in muscle force with shortening velocity:
Hill AV. The mechanics of active muscle. Proceedings of the Royal Society of London.  Series B: Biological Sciences 141: 104-117, 1953.
For variations in muscle force with lengthening velocity:
Katz B. The relation between force and speed in muscular contraction. J. Physiol. (Lond.) 96: 45-64, 1939.
These have all been implemented in various models, so it really depends on your application.  Good luck!
Rick
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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 )
Best Regard
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For endothelium denudation, I recommend you gently rub the organ with cotton strip. For reference, I attach a file and quote another one for you:
Caricati-Neto, A., Pupo, A.S., Wanderley, A.G., Nuñez-Vergara, M., Koh, I.H., Jurkiewicz, N., Jurkiewicz, A., 1995. Role of the epithelium in the release of contractile agents from the rat vas deferens by clonidine. Annals of the New York Academy of Sciences 763, 463–469.
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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?
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Hi Koushik,
There is an electrostatic interaction between kinesin head and tubulin. This electrostatic interaction keeps the motors (especially single headed motors) from diffusing away. There is a a structural difference in B amd A tubulin. You can refer to the following paper for further details.
"Structure of the alpha beta tubulin dimer by electron crystallography." by Nogales, E
Wolf, S G Downing, K H
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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?
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Dear Dr. Kumar,
I share your opinion on the issue of partial contractions at rest. While recording EMG signal from sternocleidomastoid and temporalis muscles during rest, I also had the same experience as you. The interesting point was that, their resting values differed from each other; consequently, I suppose that not only do resting EMG values differ from one individual to another, but also vary in one individual from one muscle to another. It is natural, since all muscles have different tasks and different positions in relation to spine, head, trunk and upper extremities and different contribution to maintain a desired -supine position in your and my case- position.
Regards,
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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?
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If you are using smooth muscle strips or rings the organ bath is fine. If smaller vessels there are myographs that can measure 100u blood vessels. There are pressurized vessel preps too. I'd keep it simple using the bath and generate a length-tension curve using potassium and then test your metals alone-to see if vasoconstrictive as some metals have been reported or force suppression. Then too you could use an agonist like angiotensin or endothelin and determine if metals affect receptor mediated contractions too. 
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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?
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Well the F/G actin makes sense, as does the involvement of ROCK. We have also seen some unexpected changes in protein expression in ASM following treatment with various cytokines. My guess (based on work by Gunst, Chun Seow and others) is that there is a switch from myosin-based to actin-cytoskeleton based contraction. It would be interesting to know if the sensitivity to calcium is changed therefore. You might be able to get some indication of that by constricting with 80 mM KCl with and without ROCK inhibition. You might expect depolarisation induced contraction to go down relative to agonist induced contraction (though there could be other reasons for that of course). Otherwise, might need to use alpha-toxin permeabilized preparations. 
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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
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Hi Mudhir, 
I've had similar things happen with arteries that I have mounted.  Based on what you've said most everything looks alright.  I think the most likely cause is that the endothelium is being damaged in the mounting process.  You can check this by assessing endothlial function with another endothelial dependent dilator like Bradykinin.  If it doesn't dilate to both bradykinin and ACh but does dilate with SNP then it is probably that the endothelium is damaged.  Best of Luck.
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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?
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Hi Mudhir,
in case of shorter resting time period the answers to agents such as KCl, ACh and phenylephrine are generally lower.  For examle as a consequence of lower answers to phenylephrine you cold not apply ACh to evaluate relaxation and the endothelial functions.  Shorter resting time answers are not answers of  well equilibrated adopted to new envoironment (organ chamber).
Best Regards
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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.
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In which case I would use a fresh tissue if you need endothelium-dependent relaxation (ACh) etc. If you are looking at endothelium-independent relaxation it would be fine to use. But why not give it a try, a one-off dose of ACh will tell you quickly if the endothelium is still ok.
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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?
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To smooth muscle cell the mechanism will be very similar. It depends on what vasoactive compounds come out from the neighboring enothelial cellls/epithelial cells. Although endothelial cell and epithelial cell use different NOS to form NO the end product remains the same exceot the amount. Other compunds like H2S, PGs, etc also affect vasomotor tone differently. Another difference will be the smooth mucles cells may be different in the vasculature and epithelial containing organs (say trachea). I have not seen any paper compare these two types of SMC.
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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? 
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Hi,
If you need to stain actin in life cells, my lab has recently published a paper in Nat. Methods where we introduce SiR-actin, a new fluorescent probe for actin that is cell permeable,  fluorogenic and has low cell toxicity.
the paper can be found in the link
And the probes are commercially available here:
Hope it helps!
Luc
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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.
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All vessels are not equal when it comes to their ability to constrict to PE; some arteries are much more responsive to PE than others.  It depends on the amount of adrenergic receptor expressed on the smooth muscle cells, and on the amount of sympathetic innervation of the artery studied (although, I am not 100% sure that the level of sympathetic innervation directly correlates with the expression level of adrenergic receptors...).
In your context (cancer feeding arteries or umbilical cord), I am not so sure that PE is physiologically relevant, I would try other agonists.  I was quickly looking into the literature and found this paper where they show that arterioles within a prostate tumor do not constrict to PE:
I would try other agonists (ET1, AngII, 5-HT, PGI2 etc.) but your choice depends on your hypothesis, what is it that you would like to test on these vessels? Are you studying a pathway in particular or do you "just" want to see the overall contractile ability of these vessels?
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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).
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It is very surprising to hear that single pulse TMS on forearm muscle surface EMG is producing a huge artifact. First you need to assure whether it really is a TMS-induced artifact (I doubt that the TMS pulse disturb such a remote recording source on the forearm?).  Second option is that you got a mechanical (stimulator) artifact, as the forespeakers point out it is important to check cable-crossing, grounding, maybe change the socket. Third point might be that the surface EMG is not only recording FDS but more muscle at the same time that is then generating a artifact-like signal, might be likely because your recording on hand muscles are fine. For filtering I refer to the forespeakers, another option I propose is a linear interpolation filter. Good luck!
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See above.
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Hi Lorenzo,
For animal cardiomyocyte studies, neonatal rat ventricular myocytes (NRVMs) are often used as a primary cell model.  If you'd like to model human cardiomyocyte contractions specifically, you will want to use hESC- and iPSC- derived cardiomyocytes, such as those provided by Cellular Dynamics International.  Hope that helps!
-Max
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What is their importance in vascular physiology? We know that the pEC50 is defined as the negative logarithm of the EC50.
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Before doing experiments requiring pre constriction it helps to know the the concentration of PE that will cause half the maximal possible constriction with this agent; it doesn't really matter if you express this as a EC50 or as as a pEC50 it is just the pEC50 is a visually easier way to express this valuer particularly as as concentration response curves are normally done on a semi log scale. This most quickly done by conducting a cumulative concentration response curve to PE start adding at a low concentration that does not cause constriction increase the final bath concentration by approximately 3 fold each time ("half log units" of final bath concentration is a good idea i.e. 1nM then 3nM then10nM,30nM etc) continue doing this until you cannot elicit any more contraction. Draw a concentration response curve on a semi log scale i.e log concentration of PE (x axis) vs response (y axis) the concentration that causes 50% of the maximal response is the EC50. Read as log EC50 from the graph, the pEC50 is just the postive number of this value (often referred to as giving a measure of agonist potency)
Why is this important? you can study the effect of treatments that affect PE induced contraction (changes in the pEC50 inducate either an increase or decrease in contractile ablity). The other important consideration is that if you want to study agents that relax PE preconstriction you need to avoid over constricting the vessel (physiological antagonism) by choosing a concentration of PE that is is somewhere between the EC50 and EC80 (i.e. causes between 50 and 80% of maximal constriction to PE). If you constrict more than this you may underestimate the ability of a dilator to cause relaxation. Think of a scale or see saw  the more weight (constriction) you put on one side the more effort you have to make to reverse this pre-constriction. Thus if you over constrict it can look like vasodilator agents only work at higher concentrations (greater levels of stimulus known as physiological antagonism as there is no effect at the level of the dilators receptor rather the receptor needs to generate a greater stimulus to overcome the constriction).
Almost any good pharmacology text book will help explain these concepts in the opening chapters.I hope that helps and was the answer you were looking for.
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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?
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Dear Mudhir,
The guinea pig is in general a better predictor for the airway pharmacology of different drugs/mediators. First of all the mastcells in the guinea pig (of importance to asthma) release  the same mediators (histamine, leukotrienes, prostaglandins) as in humans, whereas mastcells in mice and rats primarily relase serotonin. Secondly the potencies and effects of these endogeneous mediators in the guinea pig are more comparable than rats/mice to the human responses (nicely reviewed in Pulm Pharmacol Ther. 2008 Oct;21(5):702-20). Your observation is a good example that guinea pigs are in general a better predictor than mice and rats as these two species don't respond to histamine in airway smooth muscle with a contraction.
Guinea pigs on the other hand have the disadvantage that very few molecular tools (antibodies, etc) are available.
If you want to work in the guinea pig trachea, please read in on papers from our group for the method.
Am J Physiol Lung Cell Mol Physiol. 2012 Dec 1;303(11):L956-66
Br J Pharmacol. 2013 Feb;168(4):794-806)
Because with these protocols the GP trachea is an easy to model to eather study relaxations or contractions.
 
Good luck with your studies!
 
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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?
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Co-contraction is activity of agonist and antagonist muscle around the targeted joint. For this purpose it should estimate all forces of muscles that act around the specific joint. Eke this method is difficult in practice and the result is often have many limitation and assumptions. Muscle co-activation has been examined by comparing the EMGs of the involved muscles expressed as percentages of reference EMG values (MVC). In other word, muscle co activation is an index for demonstrating the actual co-contraction with mathematical approaches that is performed on the EMG data of agonist and antagonists which demonstrate the existence and percentage of co-contraction at any given joint and phase With this assumption that the force and the EMG activity is Correlated with each other. Beside in the literature and articles it is pronounced as Co-activation index or briefly CI.
Wish that, it helps you.
Yours truly
Alighanbari.
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All methods to remove aortic endothelial cell and which one are the best?
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I use one of my own hairs!... I do it while the artery is mounted between wires with some tension on and gently rub in a circular motion with very gentle pressue against the artery wall/endothelium in one direction....this decreases Ach responses to less then 10%.
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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.
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I understand that by EFS you meant Electrical Field Stimulation. When you stimulate a large population of enteric neurons and nerve fibers, there is a massive release of neurotransmitters that are excitatory or inhibitory to the intestinal muscles. The overall effect on the muscle is a summation of these actions, depending on the species and region of the GI tract. When the EFS is turned off, the balance between contraction and relaxation is altered, which may result in a large contraction -- rebound excitation. Check the literature under "rebound excitation", "after-contraction", "rebound contractile response", etc.
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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.
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Ok james, as son as possible we contact to investigate this
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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?
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First things first. Thank you all for your kind and suggestive reply. Fortunately I had already in my base of knowledge a paper which have the contribution from Doc. Sylvia Schick «In-vivo Kinematics of the Cervical Spine in Frontal Sled Tests» and from where I was able to get some interesting information. I spend the last few weeks trying to read more and more about the mechanisms of injury and the kinematic of the cervical spine. It is a truly complex and vulnerable sub-system of the body. Nevertheless, I am still trying to find if there is room to improve the protection of the most critical and life threatening of that sub-system, namely the spinal cord, extracting the full available power of the complex musculoskeletal anatomy, plus the full capability of the central and peripheral nervous systems. I believe and I'm betting everything on a theory that there is room, to a certain point, to increase the ability to prevent fatal cervical lesions exploring in the first instance, the biological characteristics of this sub-system, never ignoring the evidences supporting the benefits of existing active safety systems in the vehicle and the biomechanic limits. I am working to find where is that point.
From what I've read and discussed, I'm trying to figure out if there is indeed a positive balance between the pros and cons on the maximum exploitation of the protective capacity of muscles and ligaments. I am working upon a "supposed" solid starting point: by the time when an impact event occurs, the central nervous system cannot compute all the information available in time to react, send the right orders, to the right pack of muscles, inside the ideal window time. So, there must be a way to short-cut that delay. Plus, there must be a way to explore the maximum available contraction performance from a musculoskeletal system of an individual, something that he can not do consciously. I fully understand and support the point of Doc. Sylvia Schick when she says "muscle contraction might lead to some fixed unfavourable relative positions of the vertebra and increased compressive forces which lead to higher vulnerability to the shear forces and non-physiolgic intervertebral angles occurring in phase one of the kinematics during rear impact." and "Muscle forces are not high enough in high velocity impacts to sustain the external forces leading to relative motion of vertebra.", however I still think that from a given point forward, we have to realize what kind of lesion is acceptable and what kind is not. As Nikolay says, "... then preactivation makes it very hard to stretch the muscle rapidly and forcefully, and elastic compliance thus provides a power attenuating and shock absorbing mechanism for lengthening muscle". We are dealing with two tough ladies, namely acceleration and deceleration. We have to somehow reduce them and to do that, I am giving a look to our musculoskeletal and nervous systems. So, I will raise some questions:
1 -Can we consider, theoretically, that our muscles can offer a high lengthening short-time resistance (through Isometric contraction until tetanic contraction), higher and quicker than they usually do? I mean, there is room to extract more and quicker contraction power from a muscle, when compared to the power delivered from central nervous system order (no matter if it its conscious or a reflex) ?
2 -In a presence of an high amount of load, such a contraction power ( even if exists will probably be overwhelmed by the load) will for sure bring pain to our brain, from the central nervous system (pain and other consequences reinforced by Doc Sylvia Schick). Would pain be a contraction limitation factor when the moment to ask a muscle to give it all come?
3 -Is the idea that inside of a certain load amount, make sense to explore the biomechanical capabilities and maximize them to reduce the severity of neck injury, acceptable?
4-It is acceptable from an ethic point of view that I could be exchanging a complete spinal cord injury by a few subluxations, acute and disrupt soft tissue injuries and non life threatening vertebral lesions?
Waiting for your next reviews.
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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.
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Actually I am from Dr. Collin's lab. We published a couple of papers about the triceps surae, tibialis anterior and quadriceps muscles. Check out the 2 reviews that we published lately: Bergquist 2011EJAP and Collins 2007ESS. Good luck!
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Depending on location, shape and presence of channels and pumps, especially related to the mechanisms of contraction and relaxation.
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Dear Mudhir,
I have no information w.r.t. trachea, but I think there is not considerable amount of smooth muscle within aorta. That is, aorta would not dilate as smaller arteries. I am not an expert in this area by the way.
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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.
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Certainly, one could use geometric principles to estimate an index of architecture from those parameters -- ultimately, the index of architecture takes advantage of those same geometric principles anyhow. RD Woittiez actually described the determination and use of the index of architecture in a pair of papers from 1983 and 1984. The 1984 paper (in the Journal of Morphology) has some illustrations that might help you conceptualize it all.
Depending on the muscle(s) that you are modelling, you could also look up architecture papers in the literature that report things like fascicle and muscle belly lengths, and compute your own ia -- some papers even report values of ia for the various muscles studied.
Of course, there are also other normalized mathematical representations of the force-length relationship for which you could implement your "length at maximum isometric force" parameter to specify the relationship for a specific muscle(s).
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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?
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Matthew, let me make some points.
First, proper isokinetic testing assumes that the subject performing the exercise would always (i.e. for the whole range of motion) apply the maximal voluntary force. In turn, this value changes as the muscle lenght changes. Thus, your dynamometer will read a more or less long plateau where force is maximized. The lenght of this plateaux will shorten as the angular velocity will increase as well as, in accordance with the force-velocity relationship, the absolute maxim value of the force will decrease. In the case you have a number of experimental points, then you may build a force-velocity exponential curve. I suggest to take into account only force values only at plateaux (avoid the transient phases).
Seconds, if you are recording surface EMG data, at the highest angular velocities, your EMG will last a few milliseconds (the duration of the stationary force phase). This makes in most instances a frequency domain analysis of the sEMG almost meaningless. For certain, based on median/mean frequency of the sEMG power spectrum, you can not say anything about MU recruitment, especially in this particular experimental protocol. Based upon that , I have suggested to you (if applicable) to rather determine the muscle fibers CV.
My best
Francesco
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Sliding filament theory does not seem to apply here.
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The muscles of the tongue actually do still shorten, and so the sliding filament theory still applies. The Genioglossus muscle is responsible for sticking out the tongue. If you look at its position relative to the tongue you can visualize how it performs its action. Rather than thinking of the tongue elongating, think of the back of the tongue being pulled and stretched forward.
The wikipedia page has a figure from Gray's anatomy that highlights the muscle pretty well.
I hope this helps.
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Ten sets of ten repetitions were performed at an angular velocity of 90 deg/s using isokinetic dynamometer.
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I agree with Cristiano Marchis: spanning through the range of motion of your movement the electrodes receive influence from different portions of the muscle (that is sliding under the skin), thus it would make sense to perform an angle-based appropriate windowing (assuming a reasonable amount of sliding velocity of the muscle) and perform spectral or amplitude analyses taking into account that you can only compare windows from the same angular position. The joint angle information, or any other geometrical reference, is however needed.
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What are the differences between them?
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Dear Mr. Esmaelie.
According to the literatures there are three models of contractions that include isometric, isotonic (which consist of concentric and eccentric contraction), and isokinetic contractions that this three type of contraction use as models of training (isometric, isotonic, and isokinetic training). However there are other types of training which consist of concentric and eccentric model of contraction which can not apply to those three types like isoinertia training. Conforming to publications the difference between isokinetic and isoinertia test is:
Isokinetic tests allows for the examination of the muscle output at a various velocity throughout the movement range and therefore are often considered more specific to human physical performance than isometric assessment. However, isokinetic tests have not always provided data which accurately differentiate performance between athletes of varying skill levels (Fry et al. 1991; Hurley et al. 1988). Perhaps it is a consequence of the very nature of isokinetic tests, which require that movement velocity be constant. Typical human movement, however, particularly in athletic performance, is characterized by acceleration and deceleration of a constant mass of the body. Similarly, throwers exerted maximal forces to accelerate the constant mass of the implement. Thus in assessment of the dynamic qualities of muscles, perhaps it may be more specific to measure the forces or torques that can be produced against a constant mass, rather than at constant velocity. Such testing modal