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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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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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I wanted to gather detailed evidence and mechanisms on their effects on hypertrophy and how we would apply this in practice.
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I mean when someone consumes food with antioxidants, how does it affect muscle hypertrophy?
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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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To the best of my knowledge the only study done on this topic was conducted by Gallagher et al. (2000) comparing 3 and 6 grams per day of HMB and finding no differences between the two on outcomes measured (strength and body composition). However no HMB "threshold" has been determined in the way that it has been for leucine. Any information on this would be greatly appreciated.
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Not, it was not the only paper about that cuestion. You need to search for the papers from Steve Nissen. He starts to study HMB suplementation from models in animals and in 1996 he published a interesting paper with his use in sports. On other study he shows that 3 g is better than 1.5 g by day, then most of the studies start to use 3 g. 
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We know that muscle fibers are composed of myofibrils, and each one of those is a series of small contractile units called sarcomeres. Within each sarcomere, there are contractile proteins (actin and myosin) which interact to shorten the sarcomere and therefore contract the muscle. My questions are:
+ Is there a certain number of myofibrils in each muscle fiber ? Could their number increase or decrease in response to training or detraining?
+ Is there a certain number of contractile proteins in each sarcomere ? Could their number increase or decrease in response to training or detraining?
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The general rule of thought is that muscles hypertrophy/atrophy by increasing/decreasing fiber diameter and not by changing fiber number. However, there is some evidence for fiber number changing, mainly under extreme loading/unloading conditions. Fiber diameter increases/decreases by adding/degrading myofibrils in parallel to the existing ones. Regarding your last question, I would think that the amount of contractile protein per sarcomere would stay constant and not change with training/detraining. I am somewhat guessing on this because I have never heard of sarcomeres or myofibrils changing in size.
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When humans are allowed to choose their work rate, they tend to lower it under greater heat stress.
Nice study, very practical.
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Some studies pointed the incidence of higher levels of tetranectin in muscle fibres after training.
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There are many studies in the literature regarding the muscle myosin dynamics/mechanics. However I could not find any for non-muscle myosin II (NMM II) . I was wondering if there is any reported values of cross bridge stiffness for NMM II. Also are there any reported quantitative data of NMM II bond stabilization under force?
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I don't know
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Hi! I'm doing mouse muscle snap freezing and HE staining. Liquid nitrogen and isopentane were used to snap freeze the muscle tissue. The frozen tissue was then cut with cryostat to get 12um sections. However, my HE staining always have these artificial effects look like ridge (see the picture attached). I'm wondering if anyone has some idea of what causes these. Is it because I didn't freeze the muscle very well, or is it artifacts caused during cutting sections? Any information will be very appreciated! 
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Hi Lu,
we normaly freshly embedd muscle into OCT and snap freeze in liquid nitrogen for 10-13 seconds in relation to the muscle size. You must play attention to well dry muscle tissue before embedding.
Good luck
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Third head of Biceps Brachii muscle.
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This is a very rare variant of m.biceps brachii. It should not be called "triceps" because it will cause some confusion. M. triceps brachii is an extensor of the elbow. 
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What is the consequences of oxygen dept on muscles how it causes fatigue?
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Muscular fatigue is a multifaceted phenomenon that comprises failure at one or more of the sites along the chain of actions that leads to muscular contraction. It can be classified as central or peripheral on the basis of the location of the site of fatigue.
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I have been collecting soleus H reflex data in 4 subjects with RRMS and have only been able to get one subject's M wave to plateau. It appears that most everyone tested so far has an increased threshold for depolarization as I start seeing the reflex only at "higher" intensities. Since the system I use tops out at 10V I have limited stimulation abilities. I am hoping I can get some advice sooner than later in case I need to modify my design. Thanks in advance to all!!
Greg
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Dear Gregory S Cantrell
perhaps the (partly older) literature can help - at least to avoid to reinvent the wheel:
1: Squintani G, Donato F, Turri M, Deotto L, Teatini F, Moretto G, Erro R.
Cortical and spinal excitability in patients with multiple sclerosis and
spasticity after oromucosal cannabinoid spray. J Neurol Sci. 2016 Nov
15;370:263-268. doi: 10.1016/j.jns.2016.09.054. PubMed PMID: 27772772.
2: Ayromlou H, Mohammad-Khanli H, Yazdchi-Marandi M, Rikhtegar R, Zarrintan S, Golzari SE, Ghabili K. Electrodiagnostic evaluation of peripheral nervous system changes in patients with multiple sclerosis. Malays J Med Sci. 2013
Jul;20(4):32-8. PubMed PMID: 24043994; PubMed Central PMCID: PMC3773350.
3: Stein RB, Everaert DG, Roy FD, Chong S, Soleimani M. Facilitation of
corticospinal connections in able-bodied people and people with central nervous
system disorders using eight interventions. J Clin Neurophysiol. 2013
Feb;30(1):66-78. doi: 10.1097/WNP.0b013e31827ed6bd. PubMed PMID: 23377445.
4: Sosnoff JJ, Motl RW. Effect of acute unloaded arm versus leg cycling exercise
on the soleus H-reflex in adults with multiple sclerosis. Neurosci Lett. 2010 Aug
2;479(3):307-11. doi: 10.1016/j.neulet.2010.05.086. PubMed PMID: 20570604.
5: Motl RW, Snook EM, Hinkle ML, McAuley E. Effect of acute leg cycling on the
soleus H-reflex and modified Ashworth scale scores in individuals with multiple
sclerosis. Neurosci Lett. 2006 Oct 9;406(3):289-92. PubMed PMID: 16916583.
6: Magistris MR, Rösler KM, Truffert A, Landis T, Hess CW. A clinical study of
motor evoked potentials using a triple stimulation technique. Brain. 1999 Feb;122
( Pt 2):265-79. PubMed PMID: 10071055.
7: Nielsen J, Petersen N, Crone C. Changes in transmission across synapses of Ia afferents in spastic patients. Brain. 1995 Aug;118 ( Pt 4):995-1004. PubMed PMID: 7655894.
8: Sinkjaer T, Toft E, Hansen HJ. H-reflex modulation during gait in multiple
sclerosis patients with spasticity. Acta Neurol Scand. 1995 Apr;91(4):239-46.
PubMed PMID: 7625147.
9: Toft E, Sinkjaer T. H-reflex changes during contractions of the ankle
extensors in spastic patients. Acta Neurol Scand. 1993 Nov;88(5):327-33. PubMed PMID: 8296530.
10: Feeney DM, Gold GN. Chronic dorsal column stimulation: effects on H reflex
and symptoms in a patient with multiple sclerosis. Neurosurgery. 1980
May;6(5):564-6. PubMed PMID: 6968046.
11: Illis LS, Oygar AE, Sedgwick EM, Awadalla MA. Dorsal-column stimulation in
the rehabilitation of patients with multiple sclerosis. Lancet. 1976 Jun
26;1(7974):1383-6. PubMed PMID: 59019.
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I am working on developing an assay to assess muscle contractility using an ATPase assay, but I have not been able to establish a working, consistent protocol.
To begin, I isolate individual myofibrils from fresh (not frozen) tissue which is homogenized using a handheld polytron and B-Pestles. Using a series of buffers with added protease inhibitors and chelating reagents, I reduce the tissue to only myofibrils. Special steps are taken to rid the end product of mitochondria to ensure measured ATPase activity is strictly from the myofibril.
After isolation, the ATPase assay is carried out. I add 5 ug myofibril to the reaction and conduct the experiment using different quantities of available calcium (pCa). Because contractility is a function of pCa, when activity is observed, we expect the lowest pCa (most available Calcium) to show greatest phosphate release and thus higher contractility. However, every execution of this assay so far has resulted in very high readings of free phosphate in calcium-free reactions, and the lowest amount of free phosphate coming from reactions with the lowest pCa.
I have remade my calcium and calcium EGTA solutions with no improvements. I identified the source of phosphate contamination to be the ATP and cleaned it with phosphate-binding resin before proceeding with the next trial. The fresh tissue seems so show a little more activity than frozen tissue, so I no longer use frozen tissue for this assay. I run the assay at around 25 C, but this has been the least controlled parameter. I have been advised to control for temperature, but I'm wondering if there are other parameters that I am overlooking, either in the isolation step or the plate assembly for the ATPase assay.
Does anyone have experience with measuring muscle activity by phosphate release, or with ATPase assays in general?? I am at a loss and need help! I have attached a general protocol to this question, but if you need more information, let me know!
Thanks!!
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Robert Stehle gave an excellent explanation for your findings.
It is possible to prevent myofibrils from over-contracting by slight cross-linking of the actin to myosin (Biochemistry. 1993 Jul 20;32(28):7255-63. A structural and kinetic study on myofibrils prevented from shortening by chemical cross-linking. Herrmann C1, Sleep J, Chaussepied P, Travers F, Barman T.) which will allow you to measure something like the 'true' MgATPase rate under quasi isometric conditions.
The phosphate assay is OK, but it may be easier to use a linked assay in a spectrophotometer cuvette using pyruvate kinase and Phosphoenol pyruvate to replenish the ATP using the ADP produced by the myofibrils. Lactate dehydrogenase in the solution turns pyruvate, the product of the previous reaction, into lactate. The lactate dehydrogenase causes oxidation of NADH to NAD+ which can be detected continuously at 340 nm in a spectrophotometer or by fluorescence. The rate of absorption change is proportional to the ATPase. The assay works well at room temperature. This assay is insensitive to Pi contamination, so this is a real advantage. Look up 'linked-assay, ATP and NAD'. There are plenty of publications giving the required conditions etc.
As Richard Lieber says, contractility is not the same as the ATPase rate.
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There are evidence troponin and other cardiac injury marker such as CK-MB, NT Pro BNP, etc elevated after prolonged endurance exercise. Some studies show that it happens 30% or even almost 90% of participants in marathon, ultha marathon, long distance cycling, thriathlon and other kind of sports. According to your knowledge and your experiences is it pathological or physiological process?
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If the subject is a fully trained stamina athlete such as a long distance runner, he/she may have cardiac hypertrophy that I regard as a pathological condition, but my colleagues above may consider physiological!
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what could cause roundation and hyalinization of muscle fiber like this ?
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Dear Arwa: I will recomend you, if possible, to make cryostat sections and stain with HE. This method might not be easier than that you used, but artifacts in preparations will be much more lessened. good luck! T.K.
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Settings and methods for EMG examination  of smooth muscle
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Peter,
I have many years of experience.  Can I help you?  RE Garfield
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I'm recently working on the Gomori's trichrome staining on adult mouse limb. The whole lower limbs (skinned) were fixed in 4% PFA at 4C , decalcified in EDTA, embeded in OCT and cut as 20um sections. The morphology  was pretty good in freshly cut sections. However, when I fixed them in Bouin's solution at RT overnight, the skeletal muscle in the sections shrank severely while the bones and connective tissue were fine. So anybody has any idea what went wrong in the Bouin's fixation?
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If the Bouin's fixation is not necessary for your staining procedure, the problems you got might  be solved nicely. However, there are several reasons why parts of skeletal muscles shrunk frequently. To keep adhesion on slide glasses, what kind of liquid did you use for coating slide glasses before staining ? The adhesion of frozen sections is important to get good results. T.K.
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Dear all, I know there are several ways for us to connect the single muscle fiber to the test machine when we want to do the research about the contractile properties of single muscle fiber. I guess T-clip is the easier way for me, but my problem is wher could I purchase the T-clip? Anyone who has an idea? Thank you.
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Dear Shafagat,
Thank you so much for your information. Actually, I already know these links, but I don't know where could I buy the T-clips.It is said only a small company has that product, while I am not sure which company it is.
Sincerely,
Gaoyan
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I am designing a study to investigate neuromuscular function in two different muscle groups in untrained individuals; one that is predominantly fast twitch, and one that is a similar mix of slow and fast twitch. The quadriceps seem to be a good option for latter, but struggling on the former. I have seen authors state that the Triceps Brachii are predominantly fast twitch but can't find many references specifically documenting this. Can any body recommend some good references documenting the mean +/- SD of fiber types of different muscle groups in untrained (not sedentry) humans? I appreciate SD will be fairly large for most muscles.
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Not to be self serving, but we ran MHC distribution on human limbs along with collagen and titin isoforms.  Bottom line is that humans are more like elephants than mice.  Check this out:
J Exp Biol. 2012 Aug 1;215(Pt 15):2551-9. doi: 10.1242/jeb.069385.
Human skeletal muscle biochemical diversity.
Tirrell TF1, Cook MS, Carr JA, Lin E, Ward SR, Lieber RL.
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I am dealing with a 19 year old, male patient with transient, unilateral swelling of the temporalis muscle. First episode took place in 2009. The patient is diagnosed with migraine. Patient reports that muscle becomes swollen during stressful situations that he „can’t put his glasses on”. The swelling is painful and disappears in about an hour. MRI revealed small nodule in the affected temporalis muscle. It is also visible in USG as hypoechoic lesion. Doppler USG did not reveal blood flow. The lesion is palpable and painful during palpation. However, I am not if it is a myofascial trigger point. Is it possible that the swelling is caused by temporalis muscle/fascia dysfunction?  What other possible causes should be considered?
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I know that this might sound a little weird, but try to check pelvic floor on the opposite side. in many cases I treat pelvic floor issues, mandible and relevant muscles react in compensation. look especially for opposite piriformis m. (but - the "internal" part - meaning: palpated vaginally or analy - depends on patient's sex)
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In 1940 pudendal analgesia was quite popular to reduce the tonus of the pelvic floor muscles to avoid injuries. Does anybody know new studies about pudendal block and perineal protection at birth?
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Dear Peggy we are practicing pudendal  block for operative delivery only   
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to find any molecular changes in old adults and to known reason of shaking in old adults.
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Dear Kaniaw,
The following publication entitled " The Loss of Skeletal Muscle Strength, Mass, and Quality in Older Adults: The Health, Aging and Body Composition Study" by Bret H. Goodpaster et al. published in J Gerontol A Biol Sci Med Sci (2006) 61 (10): 1059-1064 describes a study conducted on 1880 older adults for three years and the methods used to determine muscle loss or/and decline:
Background. The loss of muscle mass is considered to be a major determinant of strength loss in aging. However, large-scale longitudinal studies examining the association between the loss of mass and strength in older adults are lacking.
Methods. Three-year changes in muscle mass and strength were determined in 1880 older adults in the Health, Aging and Body Composition Study. Knee extensor strength was measured by isokinetic dynamometry. Whole body and appendicular lean and fat mass were assessed by dual-energy x-ray absorptiometry and computed tomography.
Results. Both men and women lost strength, with men losing almost twice as much strength as women. Blacks lost about 28% more strength than did whites. Annualized rates of leg strength decline (3.4% in white men, 4.1% in black men, 2.6% in white women, and 3.0% in black women) were about three times greater than the rates of loss of leg lean mass (∼1% per year). The loss of lean mass, as well as higher baseline strength, lower baseline leg lean mass, and older age, was independently associated with strength decline in both men and women. However, gain of lean mass was not accompanied by strength maintenance or gain (ß coefficients; men, −0.48 ± 4.61, p =.92, women, −1.68 ± 3.57, p =.64).
Conclusions. Although the loss of muscle mass is associated with the decline in strength in older adults, this strength decline is much more rapid than the concomitant loss of muscle mass, suggesting a decline in muscle quality. Moreover, maintaining or gaining muscle mass does not prevent aging-associated declines in muscle strength.
In addition the following link contains a number of studies on mechanisms and countermeasures of muscle mass decline  in aging and neuromuscular disorders:
Finally, the following is a review article entitled "Human neuromuscular structure and function in old age: A brief review " by Power et al. published in Journal of Sport and Health Science Volume 2, Issue 4, December 2013, Pages 215–226 which focuses on motor unit loss associated with natural adult aging, age-related fatigability, and the age-related differences in strength across contractile muscle actions:
Abstract
Natural adult aging is associated with many functional impairments of the human neuromuscular system. One of the more observable alterations is the loss of contractile muscle mass, termed sarcopenia. The loss of muscle mass occurs primarily due to a progressive loss of viable motor units, and accompanying atrophy of remaining muscle fibers. Not only does the loss of muscle mass contribute to impaired function in old age, but alterations in fiber type and myosin heavy chain isoform expression also contribute to weaker, slower, and less powerful contracting muscles. This review will focus on motor unit loss associated with natural adult aging, age-related fatigability, and the age-related differences in strength across contractile muscle actions.
Hoping this will be helpful,
Rafik
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what will be the effects of latissimus muscle stretching on symptoms in patients with chronic mechanical low back pain???
need the supported evidence
because as per my clinical observation the latissimus dorsi tightness is common the chronic patients of mechanical low back pain.
thats why we want to investigate the issue by a research study.
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Dear Shakil,
that's an interesting topic. What kind of research are you thinking about?
As my previous colleagues already said, you should define the condition of shortened lats. How do you test for this? You con probably find some help in the work by Shirley Sahrmann and by Kendall& Kendall (Muscle testing and function). LBP due to tight and shortened fascia thoracolumbalis and this again due to a short lats, that's quite tricky to show. You may think of intervening with a lats stretch (which has to be addressed specifically) compared to stretching of other muscles which also attache into the fascia thoracolumbalis.
Good luck for that study, I'm already interested in your methods and results
Markus
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I'm looking for a prediction equation of segmental muscle mass? I've searched in PubMed and others bases but i didn't find.
Please, if somebody know one send me the paper or the link.
Thank you.
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You can use this book:
Hamill, J., Knutzen, K. M. Derrick, T.R (2015). Biomechanical basis of human movement. Lippincott Williams & Wilkins. chapter 11 Angular Kinetics, p 404)
 Exemple: Leg weight =
Thigh = 0.127 BW – 14.82
Leg = 0.044 BW – 1.75
Foot = 0.009 BW + 2.48 (Hamill et al. 2015)
• Add thigh, leg and foot weight to get leg weight
• Body weight (BW) is in Newton (N)
• Convert Newton to Kilogram (1kg = 9.806N)
Goud luck
Mohamed Arbi Mejri
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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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I'm looking for explanations from the points of view of  neurophysiology, neuropsychology, and related fields on the question of why people experience a sensation that is colloquially described as being “tense”. (My background is in computing science, dance, and somatic practice.) It seems to be such a simple question but I haven't really found an answer that satisfies me. The closest I've come to is Hanna's "sensory-motor amnesia" theory, which the rest of this post focuses on.
Here's what I understand so far: Anxiety is known to chronically activate muscles (Hazlett, McLeod, & Hoehn-Saric, 1994), and the feeling of tension is likely to be the phenomenological equivalent of this activation of the muscle tonus (though this needs a bit of elaboration). But what causes increased muscle activity? Why do our muscles “get tense” when we are stressed?
Repeatedly triggered physiological reflexes leads to chronic muscular tonus: Hanna's sensory-motor amnesia theory
In his books Somatics, Thomas Hanna asserts that “our sensory-motor systems continually respond to daily stresses and traumas with specific muscular reflexes” that when “repeatedly triggered create habitual muscular contractions which we cannot—voluntarily—relax” (1988, pp. xii–xiii). He calls this “habituated state of forgetfulness” sensory-motor amnesia (SMA).
He suggests three types of sensory motor responses that, when continuously triggered, lead to SMA: a “red light” reflex, a “green light” reflex, and the trauma reflex. The red light reflex is basically the mammalian startle response a withdrawal response that activates the a series of muscular reflexes. These include jaw contraction, eye blinking, brow contractions. activation of trapezius muscles to raise shoulders and bring head forward, flexion of the elbow, pronation of the lower arms, and abduction of the upper arms (Davis, 1984)The green light reflex is the Landau reflex (which primarily activates the extensor muscles) in babies. It is an assertive reflex that is “essential for the erect carriage of the body in standing and walking” (Hanna, 1988, p. 65). But, Hanna suggests, it can be triggered past the point when the reflex has served its purpose in babies and children, and instead is triggered all the way through adulthood: “Adults must make a living and be able to take care of themselves—whether they want to or not… The muscles of the back, [though] now totally mastered, are [still] being activated increasingly towards the responsibilities of life. The more responsible one is, the more often the back muscles are triggered.” (Hanna, 1988, p. 65)
Hanna only names three reflexes, although perhaps there are others that contribute to Hanna's theory of sensory-motor amnesia. For example, Bracha et al (2004) summarise human reactions to acute stress as “freeze, flight, fight, or fright”. Freezing is the state of hypervigilance, flight is characterised by an attempt to flee, fighting needs little elaboration, and fright is the state of tonic immobility. A fifth state, “faint” (flaccid immobility), can accompany acute fear or stress (Bracha, 2004; Gellhorn, 1965).
In general, the SMA theory seems to rest on two assumptions:
  1. Physical reflexes (whether they be the mammalian startle reflex, the Landau reflex, hypervigilance, tonic immobility, etc.) are activated (to some extent) in response to everyday situations that cause stress and anxiety.
  2. Repeated activation of these responses cause habitual muscular contractions, and these is what we feel and refer to in everyday terms as “tense muscles”.
My questions
  • How does sensory-motor amnesia theory fit with what is accepted in psychology and neuroscience?
  • If assumption 2) above is correct, is this related to “associative learning”?
  • What do you make of the suggestion that the Landau reflex—through its association with the development of more complex skills such as standing and walking—can then be further associated with other activities in which an individual is required to assert their presence in the world, such as taking on responsibilities in adult society?
  • Where else should I be looking or what keywords should I be using to find the answers to my questions? Any other comments or ideas?
Sorry for the length of the post. Thanks a bunch! 
References
  • Bracha, H. S. (2004). Freeze, Flight, Fight, Fright, Faint: Adaptationist Perspectives on the Acute Stress Response Spectrum. CNS Spectrums, 9(09), 679–685. http://doi.org/10.1017/S1092852900001954
  • Bracha, H. S., Ralston, T. C., Matsukawa, J. M., Williams, A. E., & Bracha, A. S. (2004). Does “fight or flight” need updating? Psychosomatics, 45(5), 448–449.
  • Davis, M. (1984). The Mammalian Startle Response. In R. C. Eaton (Ed.), Neural Mechanisms of Startle Behavior (pp. 287–352). Boston, MA: Springer US. Retrieved from http://link.springer.com/10.1007/978-1-4899-2286-1
  • Gellhorn, E. (1965). The Neurophysiological Basis of Anxiety: A Hypothesis. Perspectives in Biology and Medicine, 8(4), 488–515. http://doi.org/10.1353/pbm.1965.0058
  • Hanna, T. (1988). Somatics: reawakening the mind’s control of movement, flexibility, and health. Cambridge, MA: Da Capo Life Long.
  • Hazlett, R. L., McLeod, D. R., & Hoehn-Saric, R. (1994). Muscle tension in generalized anxiety disorder: Elevated muscle tonus or agitated movement? Psychophysiology, 31(2), 189–195. http://doi.org/10.1111/j.1469-8986.1994.tb01039.x 
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Hello Diego. You can check this papers for a actual point of view about the topic (Also the example of Gilles de la Tourette Syndrome):
-Larsman, P., Kadefors, R., & Sandsjö, L. (2013). Psychosocial work conditions, perceived stress, perceived muscular tension, and neck/shoulder symptoms among medical secretaries. International archives of occupational and environmental health, 86(1), 57-63.
-Nielson, K. A., Wulff, L. L., & Arentsen, T. J. (2014). Muscle tension induced after learning enhances long-term narrative and visual memory in healthy older adults. Neurobiology of learning and memory, 109, 144-150.
-Spencer, M. L. (2015). Muscle Tension Dysphonia: A Rationale for Symptomatic Subtypes, Expedited Treatment, and Increased Therapy Compliance. SIG 3 Perspectives on Voice and Voice Disorders, 25(1), 5-15.
-Burns, J. W., Gerhart, J. I., Bruehl, S., Peterson, K. M., Smith, D. A., Porter, L. S., ... & Keefe, F. J. (2015). Anger arousal and behavioral anger regulation in everyday life among patients with chronic low back pain: Relationships to patient pain and function. Health Psychology, 34(5), 547.
I hope this info be useful in some way to your work.
Bests, David 
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How can I record the lower limb muscles activity (EMG) in pool?  
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Dear Saeed,
The following publications describe a method to record EMG under water:
1-
Electromyogr Clin Neurophysiol. 2009 Mar-Apr;49(2-3):103-8.
A novel signal processing method using system identification for underwater surface electromyography.
Uehara S1, Muraoka Y, Tanabe S, Ota T, Kimura A.
Author information
 
Abstract
PURPOSE:
Currently, to record underwater surface electromyography (EMG), electrodes are covered with waterproof tape. For short-term measurement, waterproof tape prevents electrical leakage. However, during long-term measurement, water or sweat can contact the electrodes, changing the measurement conditions and gradually affecting the EMG data. The purpose of present study was to devise a novel method for prolonged underwater EMG recording, which estimate dry-land EMG from underwater EMG recorded by non-waterproofed electrodes using system identification techniques.
METHOD:
One healthy male participated in this study. System identification was used to convert underwater EMG signals to the estimated dry-land signals. Transfer functions were derived using two pairs of surface recording electrodes on the same muscle in parallel. System input was the EMG recorded using non-waterproofed electrodes; the output was the signal recorded underwater using waterproofed electrodes (supposed to be the same as dry-land signals). To examine the validity of the present method, three experiments were conducted.
RESULT:
There was a high positive correlation between the estimated dry-land EMG based on the non-waterproofed electrodes and the EMG obtained using waterproofed electrodes. To test the validity of long-term recording using the novel method, the estimated dry-land EMG signals were measured during 30 minutes of underwater stepping and were stable.
CONCLUSION:
The novel method using non-waterproofed electrodes with system identification techniques eliminated the effect of changes in measurement conditions and appears effective for long-term, underwater surface EMG recording.
2-Journal of Neuroscience Methods 134 (2004) 37–43
A method for positioning electrodes during surface EMG
recordings in lower limb muscles
A. Rainoldi a,b,∗, G. Melchiorri b,c, I. Caruso b,c
a Electronic Department, Bioengineering Center, Polytechnic of Turin, C.so Duca degli Abruzzi, 24. 10129 Torino, Italy b Physical Medicine and Rehabilitation, University of Tor Vergata, Rome, Italy c Don Gnocchi Foundation—Onlus, Rome, Italy
Received 4 July 2003; received in revised form 24 October 2003; accepted 27 October 2003
Abstract
Purpose: The aim of this work is to provide information about the degree of inter-subject uniformity of location of innervation zone
(IZ) in 13 superficial muscles of the lower limb. The availability of such information will allow researchers to standardize and optimize
their electrode positioning procedure and to obtain accurate and repeatable estimates of surface electromyography (sEMG) signal amplitude,
spectral variables and muscle fiber conduction velocity. Methods: Surface EMG signals from gluteus maximus, gluteus medius, tensor faciae
latae, biceps femoris, semitendinosus, vastus medialis obliquus, vastus lateralis, rectus femoris, tibialis anterior, peroneus longus, soleus,
gastrocnemius medialis and lateralis muscles of ten healthy male subjects aged between 25 and 34 years (average = 29.2 years, S.D.= 2.5
years) were recorded to assess individual IZ location and signal quality. Results: Tensor faciae latae, biceps femoris, semitendinosus, vastus
lateralis, gastrocnemius medialis and lateralis showed a high level of both signal quality and IZ location uniformity. In contrast, rectus femoris,
gluteus medius and peroneus longus were found to show poor results for both indexes. Gluteus maximus, vastus medialis obliquus and tibialis
anterior were found to show high signal quality but low IZ location uniformity. Finally, soleus muscle was found to show low signal quality
but high IZ location uniformity. Conclusions: This study identifies optimal electrode sites for muscles in the lower extremity by providing
a standard landmarking technique for the localization of the IZ of each muscle so that surface EMG electrodes can be properly positioned
between the IZ and a tendon.
© 2003 Elsevier B.V. All rights reserved.
Keywords: Electromyography; Electrode positioning; Lower limb muscles; Innervation zone; EMG variables; Standardization
3- Monopolar electromyographic signals recorded by a current amplifier in air and under water without insulation
ARTICLE in JOURNAL OF ELECTROMYOGRAPHY AND KINESIOLOGY 24(6) · SEPTEMBER 2014 
ABSTRACT
It was recently proposed that one could use signal current instead of voltage to collect surface electromyography (EMG). With EMG-current, the electrodes remain at the ground potential, thereby eliminating lateral currents. The purpose of this study was to determine whether EMGcurrents can be recorded in Tap and Salt water, as well as in air, without electrically shielding the electrodes. It was hypothesized that signals would display consistent information between experimental conditions regarding muscle responses to changes in contraction effort. EMG-currents were recorded from the flexor digitorum muscles as participant’s squeezed a pre-inflated blood pressure cuff bladder in each experimental condition at standardized efforts. EMG-current measurements performed underwater showed no loss of signal amplitude when compared to measurements made in air, although some differences in amplitude and spectral components were observed between conditions. However, signal amplitudes and frequencies displayed consistent behavior across contraction effort levels, irrespective of the experimental condition. This new method demonstrates that information regarding muscle activity is comparable between wet and dry conditions when using EMG-current. Considering the difficulties imposed by the need to waterproof traditional bipolar EMG electrodes when underwater, this new methodology is tremendously promising for assessments of muscular function in aquatic environments.
Hoping this will be helpful,
Rafik
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Could you please identify these tissues? 
Thanks 
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1. Striated muscle.
2 Simple columnar epithelium of the small intestine, probably the villus.
3. Mucous acini and striated duct, could be sublingual salivary gland.
4. Spongy, or trabecular bone.
5. Striated muscle.
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You have to respect the Nyquist rate to avoid aliasing. As Flavio Castro said the sampling frequency must be, at least, twice the higher expected frequency of the signal. If you have an electromyography instrument with a sampling frequency lower than 2000 Hz, I strongly suggest that you collect data to make a pilot study in an EMG device capable of 2000Hz of sample rate and then apply a Fast Fourier Transform. You can analyse the power spectral density of the signal and determine the minimum frequency that you will need to avoid aliasing. After that maybe will be possible to use a lower sample rate than the usual 2000Hz.
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what is reliable and valid method of measuring hamstring muscle length?
objectively.
as tool used in research to measure the outcome of interventions used for increasing hamstring length or flexibility.
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It really depends on what question you are trying to address.  You must be clear that, given the method, you could be measuring muscle-tendon unit length, muscle belly length, muscle fascicle length, muscle sarcomere length or some combination of them.  If you're just trying to establish a valid method, it may not matter.  Sorry I can't provide more information without knowing what you want to do.  
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Dear all,
We know that each reflex involves a time delay between the stimulus and the reaction. This time delay is called reflex latency and It consists of three components:
  1. time of afferent conduction (Ta),
  2. central delay (Tc)
  3. time of efferent conduction (Te).
I want to model the reflex latency of the stretch and miotatic reflexes in human upper limb (In particular,  I'm interested in biceps, triceps and brachialis muscles).
In your opinion which are the best values for Ta , Tc and Te?
After reading different papers and books, my ideas is that good values could be:
Ta= 10 msec;
Te= 10 msec;
Tc= 0.5 msec if we hypothesize that the motoneuron has just one synapse.
So, the stretch reflex latency is equal to 20.5 msec and the golgi tendon reflex latency is equal to 21 msec
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Dear Antonio,
I dont know any specific references, but I would recommend you to check work from Simon Gandevia from UNSW, Sydney Australia. He and his collegues have 100s of electrophysiological studies in humans. If you go through their papers you may find alot of usuful information.
Best wishes,
Refik
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  • i had obtained EMG fatigue results for welding operators arm and forearm. can anybody explains what the graphs infers??
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Hi Selva
If you want to make sense of these, you will need to carefully explain the experiment, including: which muscle, electrode positioning, load level (fraction of maximal), duration of the exercise, level of pain felt by the volunteer, recording of the torque generated, details of the subjects, and more. My suggestion is that look at the SENIAM guildlines for this. If you are unsure, you may also see one of my pubs on this topic - in IEEE TNSRE in 2012.
Remember- the association of spectrum and fatigue is known, but weak. 
All the best
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Hello from Germany,
I am searching for the "Standardized Nordic Questionnaire". I was wondering if there is a validity german version available?
Thanks a lot for your help.
Warm regards and merry christmas.
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Thanks a lot!!! Thats very helpful. Happy New Year!
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Melatonin signal transduction in skeletal muscle during  aerobic exercise and Prevention of DNA damage in The elderly?
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This is a very interesting question. Melatonin has anti-inflammatory effects in different situations (see our review Mauriz et al, 2013). In aging, melatonin has anti-oxidative and anti-apoptotic effects in liver (see our papers Mauriz et al 2007, and Molpeceres et al 2007). Moreover, in exercised aging animals changes in AMK and GLUT have been described by Mendes et al (2013).
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Comparing the isometric strength abdominal and adductors ratio's
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Thanks for the reference! 
Try this paper: Lovell GA, Blanch PD, Barnes CJ. EMG of the hip adductor muscles in six clinical examination tests. Physical Therapy in Sport. 2012;13(2):134-40.
We also have a follow up paper to the diagnostic paper (Drew MK, Palsson TS, Izumi M, et al. Resisted adduction in hip neutral is a superior provocation test to assess adductor longus pain: An experimental pain study. Scand J Med Sci Sports. 2015:n/a-n/a.) It assesses EMG and a variety of other metrics which is the full paper to this abstract:
Drew MK, Palsson TS, Hirata RP, et al. The influence of experimental thigh and groin pain on the mechanical sensitivity, pain distribution and clinical tests of the adductor longus. 9th Congress of the European Pain Federation EFIC Vienna, Austria; 2015.
Should be out early next year. I try to keep Research-gate up to date so will be up when available. 
Good luck
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As works from Kaikkonen, P. et al., (2010) where Post HRV was measured, comparing exercise values with segments Post1,2,3,4 5 and 14min in the TP, HF and LF and from Saboul, D. et al., (2015) where a baseline (pre-exercise 5 to 0min pre-exercise) was compared with a Post 5 (5-10min after exercise) and Post 30 (30-35min after exercise).
A protocol carry on 10min after exercise which measured values within 5min, 30 seconds after lay down in supine position could be right?
Can We compare values between different days?
bigger values in Rmssd, HF and TP is indicative of more stressful training session?
Thanks a lot,
Santiago Sanz 
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You are welcome!
See also the studies of Rohan Edmonds for other approaches with special Olympics:
Cheers,
Daniel
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I need information about type of muscles that would active on manual lifting task
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For the task you described, a functional task evaluation would require the weight of the box since the weight of the box would determine if the task is qualified as a task performed as an occasional task (1 - 4 times/hour, 1 - 32 times per day), frequent task (5 - 8 times/hour, 33 - 66 times/day), or constant task (12 - 60 times/hour, 67+ times/day). For occasional tasks loads of 10 - 50 lbs (4.5 -22.7 kg) are considered very light - medium; loads from 50 - 100+ lbs (22.7 - 45.4 kg) are considered medium to very heavy. For frequent tasks loads of < 0.5 kg - 11.4 kg are considered very light - medium, while loads from 11.4 - 22.7+ kg are considered medium to very heavy. Tasks classified as constant involve loads of < 0.5 kg - 4.5 kg for very light to medium; and from 4.5 kg - 9.1 kg are considered medium to very heavy.
The muscles of the trunk (primarily trunk extensors) and the muscles of the lower extremity will be used for stability and moving the box across the 2 meters. The muscles of the upper extremity (shoulder girdle, shoulder, elbow/radioulnar joint, and the wrist and hand) would be used to varying degrees to lift, hold, and lift the box to sternum level and place it in its place. No single muscle would be most active. Which muscles contribute to the specific portion of the task you intend to study will depend on the magnitude of the load, the frequency the task is completed, the velocity at which the task is completed, the height differential between where the box is lifted from to the height at which the box is placed when the task is completed (since the carrying of the box in the hands across the 2 meters does not accomplish any significant work, which could be measured and quantified accurately).
The only significant difference in muscular activity in the task described is not a difference in which muscles are active but the type of muscular activity that is taking place. The same muscles will be used whether lifting, carrying, or lowering the box. When lifting the box the muscles must overcome the effects of gravity on the box, which tends to cause it to remain at knuckle level on the table or supporting surface, this is accomplished using a concentric muscle action. When carrying the box across the floor for 2 meters, the box is basically held in a stable, static condition. The legs provide a propulsive force but the resistance to movement is at the foot/floor interface and no useful work is done to the box, therefore the muscles responsible for controlling the box and its contents are active in an isometric contraction, where the muscle produces a force exactly equal to the force of gravity to maintain control of the box while carrying it across the 2 meter space. When placing the box in its final position, the upper extremity muscles and possibly the trunk and lower extremity muscles will again produce a force greater than the resistive force provided by gravity using a concentric muscle action, just as they did when originally picking up the box. Finally when lowering the box to its final resting position, the same muscles that used a concentric muscle action to lift the box would utilize an eccentric muscle action to allow the box to be safely lowered to its final position.
So your problem is really one of adequately defining the movement or movements you are going to be studying, because the global nature of your current question is too large to provide a specific answer like you appear to be seeking.
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If muscle fatigue increases do the MPF increase or decrease?
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We need more information. One, is the "signal" an electromyographic signal?  If so, what kind of electrodes are being used, indwelling or surface? Is "MPF" median power frequency or mean power frequency or neither? What is happening to the amplitude of the "signal"? What is the work task? One with a constant power output? What muscle group is involved? Is the "signal" from one or all muscles in the muscle group?
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I am currently working on a research project in which I injure the legs with downhill running.  I am interested in whether there is a way to verify that the arms are uninjured so that I could verify whether any changes in arm strength are due to some sort of central process.
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I agree with Ingred in that you first have to decide if you can get biopsies.  That said, saying a muscle is "uninjured" is nearly impossible.  It is tough to even get general agreement on what "injured" means.  This has been debated for decades in the eccentric contraction literature (see, for example, Yu JG, Carlsson L, Thornell LE.Histochem Cell Biol. 2004 Mar;121(3):219-27).  Once you decide the level at which you will study this, we can provide you with more specifics.  At the ultrasound or MR level, you will simply be "deciding" what injured or noninsured means but it will not be generally acceptable.  Good luck
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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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Has anyone a procedure of skeletal muscle fiber bundles mechanical separation recorded (respirometry, Oroboros)? I am looking for tips and tricks on that (separation techniques and final separated form). I cannot get a response after adding ADP during the protocol. It probably means that I damaged the fibers during the separation process or I do not separate them enough to get them permeabilized. Anyone?
Thanks.
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Hi Robert,
How do you currently separate and permeabilize fibers?  Also, what species are you studying?
Regardless, I would recommend watching this JoVE video for how to separate fibers:  http://www.jove.com/video/2431/respirometric-oxidative-phosphorylation-assessment-saponin
The Oroboros website (http://oroboros.at) is also an excellent resource for both protocols and theories relating to respirometry.
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I found many studies about core training but I cannot find any definition of it. 
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Dear Raul a few resources to help you may be as follows:
In an article Core Stability Exercise Principles, they define it as "The so-called core is the group of trunk muscles that surround the spine and abdominal viscera"
In "Muscles of the core", they define it as "The major muscles that move, support and stabilize your spine are called the muscles of the core or trunk"
In "The myth of core stability", they say "In essence the passive human spine is an unstable structure and therefore further stabilisation is provided by the activity of the trunk muscles. These muscles are often referred to in the CS approach as the ‘‘core’’ muscles, assuming that there is a distinct group, with an anatomical and functional characteristics specifically designed to provide for the stability"
In "Core Training: Evidence Translating to Better Performance and Injury Prevention" they say "These muscles act to stiffen the torso and function primarily to prevent motion. This is a fundamentally different function from those muscles of the limbs, which create motion. By stiffening the torso, power generated at the hips is transmitted more effectively by the core"
I think it would suffice. Best of luck!
Aamir
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Could any one point me in the direction of research papers that examined the fiber type distributions in humans? I am putting together a paper on fiber type distribution and its potential application to weight training and more specifically, hypertrophy. I have been looking quite a bit and I can't find exactly what I am looking for. Every article that I do find is from the 70s and does not have the full article available. Any help is greatly appreciated!
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Dear Tyler Thomas, 
Some addition to the comments, following papers may help:
Muscle fiber type
Muscle fibre type distribution, muscle cross-sectional areaand maximal voluntary strength in humans
The influence of variations in muscle fibre composition on muscle strength and cross-sectional area in untrained males.
Effects of exercise training on skeletal muscle fiber type distribution in chronic heart failure patients
Contractile Properties and Fiber Type Distribution of Quadriceps Muscles in Adults with Childhood-Onset Growth Hormone Deficiency
Fiber Type Transformation in Human Skeletal Muscle
THE RELATIONSHIP OF BODY COMPOSITION, MUSCLE FUNCTION, AND MUSCLE FIBER TYPE TO LOWER BODY PHYSICAL PERFORMANCE IN OVERWEIGHT AND OBESE OLDER ADULTS
Relationship Between Muscle Fiber Type and Reactive Balance: A Preliminary Study
Aamir
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I am looking for information about any method using microdialysis to assess skeletal muscle protein breakdown. There is a paper (Tesch et al 2008) using microdialysis and assessment of 3-methylhistidine, but this technique may present some limitations. Anyone knows a better one?
Looking forward to more information,
Thanks!
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Human models
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I wish to do a study pertaining to lateral epicondyle and whether a vibration dampener ( a small button placed on Tennis Rackets that reduces residual string vibration from ball impact) can be used as a preventative measure against this condition. I want to have something I am able to measure quantitatively on a sample size of about 30 or so individuals. 
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The gold standard is resonance imaging. You can do that using US too, but the evidence in literature for this procedure are very poor. Finally, you can use a doubly indirect ways as maximal voluntary strength, ROM, or even seric markers as CK, lactate deydrogenase and Mb. Some researchs have used a visual analog scales for pain.
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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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I'm comparing two muscle types using subtractive hybridization in order to evaluate differentially expressed genes and the protocols I'm looking at say to perform a second self-subtraction. Im not sure what they mean by self-subtraction and to me it seems counterintuitive to isolating differentially expressed sequences.
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Do as you see fit. Explain your thought colleagues.
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I had read and practised external palpation of pelvicfloor muscles ,but had no scientific articles supporting it,can someone help me with it?
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Hello Ponmathi
I used to do this for the majority of woman who I saw, with pelvic floor symptoms; I used the method that Jo Laycock and colleagues designed and validated. I don't know if you've seen this method - I was introduced to it by Jo, and never changed from this.
Laycock, J., & Jerwood, D. (2001). Pelvic floor muscle assessment: the PERFECT scheme. Physiotherapy, 87(12), 631-642.
Part of this is available from ResearchGate:
You might want to read a previous ResearchGate Question/Answer where other members also made suggestions:
The other paper I mentioned in this answer was:
Jeyaseelan, S. M., Haslam, J., Winstanley, J., Roe, B. H., & Oldham, J. A. (2001). Digital vaginal assessment: An inter-tester reliability study. Physiotherapy, 87(5), 243-250.
If you are unable to access the full text, I have a copy  that I could send you on ResearchGate messages, for your attention only.
Very best wishes
Mary 
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Hi, I'm interested in looking at muscle regeneration in neonates animals and looking for a method to label newly synthesized skeletal sarcomeres. In adult, muscle regeneration can be detected by looking at embryonic and neonatal myosin. Since I work with neonate animals, that will not work out very great. There was an old experiment where they feed the animal radioactive labeled adenosine and detect where newly synthesized sarcomeres are added (adenosine get incorporated in actin monomers). Does anybody know of a common method to detect newly added sarcomeres, preferably without the use of radioactive materials?
Greatly appreciate your help.
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There is a good reason why the original Goldspink paper has not been followed up - it is a difficult system.  The suggestion of tritium label is probably the best way of getting high resolution data because of the short range of radiation emission but this is also a drawback because it lowers the sensitivity - in tissue most of the emission decays within 2µm, so much of the signal never gets into the emulsion from standard wax or frozen sections.  This can be improved by cutting thin sections in acrylate embedded material but this requires a long exposure and, as implied by Dr Morgan, noise is a problem that you need to minimize by keeping the exposing slides in lead boxes and by meticulous darkroom work.
The suggestion of using antibody against developmental myosins may work but I would think that it would be technically possible nowadays to produce a mouse with a conditional expression of a tagged actin, myosin, or other sarcomeric protein that could  be activated prior to eliciting regeneration.  The Pax7Cre-ERT system would be suitable for regeneration experiments. Whether you could get funding for such a system is another matter.
At a low resolution, one of my colleagues has tried to use pulsed Stable Isotope Labelling in the Mouse (SILAM) and analysis of the ends versus the middle of the muscle fibres by Mass Spec. So far, his produced very variable results.
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Previous article
Bilateral Deficit for untrained prepubertal children
Abstract
Objectives. – To prove the idea of Bilateral Deficit for pre-pubertal children.
Methods. – We chose conditions to optimise the Bilateral Deficit probability (arm flexor isometric action of 10 pre-pubertal children). Using a force investigation, we measured a systematic lack of arm flexor force during bilateral contraction. To explain this muscle disability, we investigated the electromyographical signal produced during muscle action of dominant arm.
Results. – No muscle activity fall down or typological recruitment changes are evident regard to temporal (RMS: 0.12 ± 0.04 vs. 0.14 ± 0.08 V) or spectral (MPF: 116 ± 14.1 vs. 114.5 ± 11.2 Hz. MDF: 79.1 ± 11.8 vs. 80.1 ± 8.3 Hz) electromyographical (EMG) parameters. Conclusion. – So, to explain the systematic BD, no lack of muscle activity and no recruitment adaptations are evident and we discussed
about several other explanations. © 2003 Elsevier SAS. Tous droits réservés.
Mots clés : Déficit Bilatéral ; Force ; Électromyographie ; Enfant Keywords: Bilateral Deficit; Strength; Electromyography; Child
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Perhaps I can if you are interested. I am finishing my master on BD with young and active males in extension and flexion of knee using an isokinetic dynamometer modified.
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Is or has anyone conducted any studies investigating the neurophysiology of stretching or foam rolling? I am curious as to your methods. Thanks!
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Ok thanks so much!
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I need the biochemical protocol for skeletal muscle creatine kinase (ck-mb) estimation.
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Hello Vishnu;
First, is it human or animal speciment.
If it is animal: There is no standardize protocol for CK measurement, because protocol might be significantly different and they depends from analysis and condition. Protocols depend from kit to kit. You should use the instructions, from the kit you plan to use.
Human sample: As mentioned above, any pathology lab can do this easily, and you should check with them from protocol, they might vary as well, or if you have a kit, follow the kit instructions.
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I often isolate myofibrils using a homogenization protocol, but it is very common to get bundles of myofibrils (specially from cardiac cells). I wonder why and how I could optimize this isolation so it yields higher amounts of single myofibrils. Maybe any enzyme treatment... 
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First I do need to know for which type of experiments are you trying to obtain these myofrils. Are these for functional experiments such as Force vs. pCa?
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Every year a lot of studies are published on tourniquet time and blood loss and outcome after TKA. I do not use a tourniquet at any time of the TKA procedure. I am interested in conducting a study to assess quad muscle function and outcome of TKA without using a tourniquet.
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Dear Rene Attal,
I think that article could be useful to you!
Harsten, A. 2015 Tourniquet versus no tourniquet on knee-extension strength early after fast-track total knee arthroplasty; a randomized controlled trial
Knee
Have a nice day!
Giacomo
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         In clinical setting we often prescribe core muscle strengthening for chronic low back pain or low back pain patients, because of the researches evolved there is a weakness of core muscles in this population, i just want to know is there is any standardized grading system is there to measure core muscle strength. 
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The difficulty is addressing this issue is because the idea of what constitutes “core” is not well defined. This is why answers correctly are asking about endurance vs strength , EMG etc.. 
If  “Core” is defined as the total lumbopelvic support musculature then isolated strength may be neither relevant nor appropriate. Isometric or isokinematic  Biodex back extensor or abd  testing - perhaps does not really address this so called “core” set of musculature .  The idea of bracing capability as described by McGuill comes close, but it is not the maximum capacity to generate brace force (definition of strength) that is important, but the capacity for appropriate modulation of bracing during various activities. 
In my humble opinion, the idea of capacity to maintain a neutral spine or time to return to a neutral spine following perturbation is the essence of “core – stability” 
An example of an simple isometric test might be to use a pressure device placed under the lumbar curve and with the person starting  supine legs flexed – lower straight legs from vertical and see to what angle they can lower their legs and still maintain a constant lumbar pressure ( maintaining neutral spine without  increasing lordosis)  There are other positions and activities this could be done in.  Unfortunately more dynamic perturbation testing requires kinematic and EMG data acquisition – which is not what Balamanigandan Jaganathan was asking .
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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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Certain cells have reports of different expression level of SMA. Working with certain cells I have seen significant  SMA expression while some other labs have not found any. Does culture conditions influence SMA expression? 
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The gold standard marker for SMC lineages is Myh11 (aka SM-MHC, smooth muscle myosin heavy chain).  Acta2 or SMA may be induced in a variety of fibroblasts and myeloid cells as well as glial cells and stellate cells of liver.  I also think it can be expressed in mesagial cells of kidney under stress conditions.  There is quite a literature on this subject.  My question relates to Brian's :  what exactly are you trying to do?
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I am interested in the effects of aging on the properties (e.g. physiology, histology, morphology and function) of skeletal muscles, pain perception, and central pain processing. Please recommend some classical and must-read materials at your convenience. Thank you very much.
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You can read this article
Eur J Pharmacol. 1994 Mar 11;254(1-2):97-104.
Age-induced alteration of neuromuscular transmission: effect of halothane.
Bhattacharyya BJ1, Tsen K, Sokoll MD
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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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Hi
I have a question about forces component in pennate musles.
In pennate muscles, the forces produce in muscle fibers should transform into two component of horizontal and vertical. The vertical component acts in tendon direction and will shorten the length of pennate muscle. But what is the role of horizontal component? Is this force wasted? Does it do some specific task?
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This question is certainly at the forefront of the current state of dynamic in vivo imaging and our 3D models of complex muscle architecture.  All models are wrong, and some models are useful.  That Lieber guy should be commended for acting like a scientist and relying on data to increase our understanding.  Most scientist of his stature would pronounce their previous findings as the gospel.  
Often, these muscles wrap around a joint or bony structure, and their actions cause compressive, tensile or twisting deformations of their constrained space during shortening, further complicating models of force production.  It appears they may be a career's worth of research waiting here for someone.
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We are planning to use MRI to define human skeletal muscle mass in terms of looking at muscle atrophy and struggling to find best validated tool or software to analyse the data. Any suggestion will be much appreciated. Thanks
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Thanks a lot for your advise. Much appreciated
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Does muscle activity improve by either laser or stimulation?
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Thanks
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What is the problem of the internal thoracic artery that feeds the mammary, when precontracted with NE and ANG II that leads to wobbling of the curve as you see in the attachment images.
Can anyone tell me what the problem is?
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We used to call this spontaneous activity and Dr Ward is absolutely right; it is really not a problem as long as you are able to quantify changes in vessel tone.
I remember on the other hand that mesenteric arteries (rat, rabbit, mouse, dog etc) actually show this type of 'behaviour' even at basal tone (i.e. without being pre-contracted with NE, Ang II or KCl).
Are these helicoidal strips and which physiological buffer are you using? In addition, if  you want to reduce these oscillations at least with an alpha agonist, try methoxamine instead and add indomethacin in your assay buffer. The addition of an inexpensive betablocker may also help.
Good luck
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With disuse, say bed-rest, casting or micro-gravity, within what time-frame would phenotype muscle atrophy occur that is measurable ? Measured by anthropometry or some imaging technique. Limited to humans only,
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The answer will depend on the muscle group you're interested in. Chronically-active muscles (e.g., lower-body muscles) are more susceptible to disuse.
Assuming you're interested in such muscles, the loss of lower-body lean mass appears to be around 100-200 g/wk during bed-rest (See some references below.) With this number, you can estimate the necessary duration of bed-rest if you know the resolution of the instrument you are using to assess atrophy.
Paddon-Jones D, Sheffield-Moore M, Urban RJ, et al. Essential amino acid and carbohydrate supplementation ameliorates muscle protein loss in humans during 28 days bedrest. J Clin Endocrinol Metab. 2004;89:4351–4358.
LeBlanc AD, Schneider VS, Evans HJ, et al. Regional changes in muscle mass following 17 weeks of bed rest. J Appl Physiol. 1992;73:2172–2178.
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Muscle pain, shortness of breath, and digestive problems are symptoms of anxiety and depression that can be attributed in part to chronic muscle tension. I was wondering if anyone has information regarding studies measuring range of motion in depression and/or anxious people.
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Please let me know if these two articles help:-
1. Generalized anxiety disorder: is there any specific symptom?
Faravelli C1, Castellini G, Benni L, Brugnera A, Landi M, Lo Sauro C, Pietrini F, Rotella F, Ricca V.
Compr Psychiatry. 2012 Nov;53(8):1056-62. doi: 10.1016/j.comppsych.2012.04.002. Epub 2012 May 11.
2. The relationships between measures of stature recovery, muscle activity and psychological factors in patients with chronic low back pain.
Lewis S1, Holmes P, Woby S, Hindle J, Fowler N.
Man Ther. 2012 Feb;17(1):27-33. doi: 10.1016/j.math.2011.08.001. Epub 2011 Sep 7.
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I want to investigate muscle fatigue and strain in the neck and shoulders by doing a survey. Is there a standardized survey questionnaire available for this purpose? Thank you.
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Any survey, including the BORG scale, will be pretty vague and vary a lot between individuals. Monitoring the MEDIAN FREQUENCY of an EMG signal would be more sensitive to a change in fatigue status.
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I am continuing my mathematical modelling of apnoea and escalating hypoxaemia, and I wish to include the effects of myoglobin. I appreciate that its P50 is very low, and so it would give up its oxygen only very late (and probably only locally), but I would like to include its effects alongside the oxygen stores (i) in the lungs, (ii) on haemoglobin, and (iii) dissolved in body water.
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