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Muscle Physiology - Science topic
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Questions related to Muscle Physiology
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
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
I wanted to gather detailed evidence and mechanisms on their effects on hypertrophy and how we would apply this in practice.
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.
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.
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?
When humans are allowed to choose their work rate, they tend to lower it under greater heat stress.
Nice study, very practical.
Some studies pointed the incidence of higher levels of tetranectin in muscle fibres after training.
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?
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!
Third head of Biceps Brachii muscle.
What is the consequences of oxygen dept on muscles how it causes fatigue?
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
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!!
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?
Settings and methods for EMG examination of smooth muscle
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?
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.
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.
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?
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?
to find any molecular changes in old adults and to known reason of shaking in old adults.
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.
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.
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.
If muscle decline in sarcopenia, may it have effect in VMO or VL ?
How is the balance between VMO VL in aging?
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:
- 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.
- 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
Article What is somatics?
Chapter The Mammalian Startle Response
How can I record the lower limb muscles activity (EMG) in pool?
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.
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:
- time of afferent conduction (Ta),
- central delay (Tc)
- 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
- i had obtained EMG fatigue results for welding operators arm and forearm. can anybody explains what the graphs infers??


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.
Melatonin signal transduction in skeletal muscle during aerobic exercise and Prevention of DNA damage in The elderly?
Comparing the isometric strength abdominal and adductors ratio's
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
I need information about type of muscles that would active on manual lifting task
If muscle fatigue increases do the MPF increase or decrease?
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.
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!
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.
I found many studies about core training but I cannot find any definition of it.
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!
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!
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.
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?
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.
I am specifically interested in research papers dealing with the problem rather than in the abstracts or unpublished studies.
I had read and practised external palpation of pelvicfloor muscles ,but had no scientific articles supporting it,can someone help me with it?
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.
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
Is or has anyone conducted any studies investigating the neurophysiology of stretching or foam rolling? I am curious as to your methods. Thanks!
I need the biochemical protocol for skeletal muscle creatine kinase (ck-mb) estimation.
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...
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.
relationship between muscle contraction with muscle length and velocity
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?
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.
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?
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?
Working on my dissertation. Muscle dysmorphia related. Any assistance would be greatly appreciated.
Does muscle activity improve by either laser or stimulation?
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?



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,
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.
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.
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.
Please suggest me some books that are standard references.
There is discrepancy in the literature regarding skeletal muscle fiber type distribution in pulmonary arterial hypertension (PAH) compared to healthy control. For example, Mainguy back in 2010 found a difference for type I, but not for type II with 10 patients and 10 controls. Batt found a difference for both type with 12 patients and 10 controls while we (Potus and Malenfant) did not find any difference for both type with 18 patients and 19 controls. In view of those results, where could this discrepancy come from?
I wonder about the need of MVC record if I'm going to register EMG signal during 60 m race walking trials. Is there a better method to normalize muscle activity while performing such dynamic movements?
I would like to stain muscle fibers of multiple species of fish for SDH activity to help determine differences in oxidative capacity. My problem is that the biopsy will be taken in the field and not in a lab setting so directly freezing them in liquid nitrogen or cooled isopentane is not very feasible. How can these samples be preserved to look at enzyme activity? Would placing them on ice and then in a -80°C freezer be sufficient? Any suggestions or comments are greatly appreciated!
When should patients after hypoglossal-facial-jump nerve suture start with the exercises? How should the treatment be structured? And which exercises are most effective?
I'm standardizing the protocol for isolating muscle fiber, but am having trouble adjusting the time I leave the muscle in the solution of type I collagenase 0,2%, my muscle is being degraded. Another question is whether during the period of incubation in collagenase solution I should leave stirring or not?
I want to image z-disks (only) on a fluorescent microscope.
Is there the possibility to modulate a stimulus (by changing frequencies and duration) and set a direct relationship between that stimulus and a certain muscle AP? Telling it otherwise, applying the same stimulus (maintaining the same frequency and duration), again and again, on the same alpha neuron, I will have the same effector contraction (with plenty of time to relax between stimulus)? If the answer is yes, it is possible to build a matrix with different stimulus and correlated muscles AP's?
We use more than two potassium channel blockers simultaneously, does mixing of these blockers affect the activity of aortic rings in organ bath study? I mean that these blockers can destroy the structure then function of rings.
I would like to know who ever stained NADH-tetrozolium reductase enzyme on cyrosections for muscle viability detection? Which concentrations of acetone and how long of incubation with each concentration of acetone need to remove unused tetrozolium reagents?
All methods to remove aortic endothelial cell and which one are the best?
I'm testing the effect of denervation on muscle fibers' area and due to skewed distribution I understand the median is a better estimate for this parameter in each subject. Any suggestion on how can I then move to obtain group data and to compare between groups using the median muscle fiber's area of each subject?
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.
I'd like to determine the influence of excessive metabolite (including Pi, ADP, H+) and reactive oxygen species accumulation during exercise on the muscular function and specifically on muscle damage. To that end, I plan to perform muscle biopsies as well as blood draws right at exercise termination and at different times during recovery.
I'm looking for the most relevant biomarkers of those damages in humans. Does anybody have suggestions?
Struggling to find literature investigating the mechanism(s) behind myoglobin oxygenation
I investigated the facial muscles of a child with Moebius syndrome, and many patients with chronic facial paralysis with the help of ultrasound (paresis in part for more than 10 years). I could see that, despite the long period of paralysis still facial muscles were sonographically detectable. So, what mechanism prevents a complete atrophy of the muscles and is there a realistic potential for regeneration?
I am having trouble finding published research on strength training (or resistance training) during pregnancy. Can anyone help?
Concurrently training for strength and endurance limits the strength gains, a phenomen termed the concurrent training effect. A long held belief in the concurrent training literature has been that part of the interference has come from interference from molecular signalling pathways in skeletal muscle. However, this explanation is far from adequate. How big a role is the neuromuscular component likely to play in this phenomenon?
Does anyone know if a habituated physical activity, such as cycling to work or study place everyday as a mode of transportation, would help to save corporeal energy by adjusting the function in muscle to a level that consumes less calories?
I am writing an article on habituated active travel behavior, walking and biking, and would appreciate it if someone could suggest an article or two on the above question.
What happens to marathon runners in the same situation (i.e. do they also have long term production of opioids)?
Have there been any similar studies on human subjects yet?
Does the body react differently to acute stress (fight or flight), vs long term chronic stress?
I am working over different muscle models to compute muscle forces and most of them include the so-called "width" parameter, but it is not referenced how to compute it, nor its meaning, just a simple value on a table. I would appreciate any help on this.
I currently use 2% HS to induce differentiation, as many people commonly do, and it works very well. What mechanistic quality of HS makes it better?
Molecular signalling is often used as a surrogate measure for various outputs like glucose uptake and protein synthesis. However in the case of gluocse uptake only 30% of maximal PKB activity is required to saturate GLUT4 translocation (Bilan et al, 2009 - attached). In the case of protein synthesis, 30% of maximal S6K1 phosphorylation associates with saturated protein synthesis (Crozier et al, 2005 http://jn.nutrition.org/content/135/3/376.long). These data suggest that there is a reserve capacity built into signalling pathways. This raises the question "is this reserve capacity important and physiologically relevant?"
In feeding induced time course studies S6K1 switch off occurs more slowly than the switch off of protein synthesis (Atherton et al, http://ajcn.nutrition.org/content/92/5/1080.long) and in response to intermittent protein feeding the S6K1 phosphorylation response does not correlate with protein synthesis (Areta et al, 2013 http://www.ncbi.nlm.nih.gov/pubmed/23459753). Despite the lack of correlation between S6K1 and protein synthesis in response to feeding, the S6K1 response to resistance exericse correlates highly with hypertrophy in response to training (Baar and Esser, 1999 and Terzis et al, 2008) suggesting that it is a good read out of growth. What is the function of the residual S6K1 activity and why isn't there a correlation between S6K1 and feeding induced protein synthesis? Is this a feedforward mechanism?
How do we begin to reconcile the discordant data and do we need to develop new theories and methods to assess the molecular control of muslce metabolism and growth?
I am attempting to attain mean response times, time constants and the amplitude of vo2kinetics data, and i have sigmaplot however am struggling to gain results as i have never used the software before.
Research is mixed; most say third or fourth decades...
Recent work from the Phillips lab has shown that the hormonal response to resistance exercise plays little role in either the acute protein synthesis, signalling or the hypertrophy response to resistance exericse. Additionally a number of studies have brought into question the role of IGF-1 signalling in response to resistance exercise adaptations. However, these hormonal responses to resistance exercise are real and robust - so if they don't impact upon resistance exercise adaptations, what have they evolved to do?
Inverse dynamics are quite complicate and time consuming. So I would prefer for a rough estimation a method using EMG and perhaps cross section determination using MRI. Any suggestions?
For my further research I need to measure a muscle work. The purpose of my research is to measure the activity of muscles while riding a canoe C1.
Thank you for response
Radim Sryncl
Is force strictly determined by muscle cell calcium alone? Can the same muscle force be achieved with different intracellular calcium concentrations? I don't mean long term changes in muscle structure, of course. For example, dantrolene reduces calcium efflux from the sarcoplasmic reticulum and reduces grip strength in mice. Does a 20% reduction in peak force mean a 20% reduction in intracellular peak calcium? Can the same force be achieved with different calcium concentrations? If there are other factors, what are they? Can anyone recommend an article discussing such quantitative aspects?