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Can anyone suggest a good marker for muscle damage, in addition to creatine kinase and lactate dehydrogenase, for evaluations of acute resistance training sessions?
I am writing a scientific project, and I want to include some biochemical markers rather than CK and LDH to identify possible skeletal muscle damage after resistance training session with different overloads.
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I agree with Mathias, that there is no single best marker. But I'd recommend a marker of force loss (MVC perhaps) as it gives you a holistic insight into the changes. Plus, if you're looking at this from an applied perspective (e.g. sport/exercise performance), then force changes underpin this. If you're looking for some sort of blood marker, then you'll need to think about what you're trying to get an insight into (e.g. sarcolemma disruption, inflammation, time-course of change etc) and then tailor the marker to this. Unfortunately, for the blood markers I don't believe there is a single best one.
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Dear all,
I encountered some problems when using the ABAQUS CDP model. Could you please give me some suggestions?
I did a monotonic uniaxial test using a single 3D solid element (C3D8R) and the CDP model. As shown in the picture attached, if tension damage is defined the maximum principle stress vs maximum principle strain relation shows strain hardening compared to the input data, while the stress and strain curve matches the input value if tension damage was not introduced. This is kind of strange as material damage should not have an effect on the stress and strain relation under monotonic loading.
Moreover, when the plane stress element (CPS4R) is used, the stress and strain relation is identical for cases with and without damage as it should.
I have also attached the input files for both the 3D and 2D models. I will be grateful if you could give me some advice.
Regards,
Delon
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Md. Mahmud Sazzad Thanks for your reply. I think the boundary conditions should not be an issue as I just did a simple tension test with a single solid element.
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I'm trying to identify muscle reinnervation after a nerve injury. For that I want do inject some traccer on the muscle to identify which nerve is reponsible for the reinnervation.  Which is the bast traccer, can BDA or DiI work in a short period of time?
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I agree with Thomas Wooten
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Hi all,
If anyone is aware of a study that has selected magnitude-based inferences as their statistical analysis, but used it to assess two independent groups across various time points?
An example of this would be the comparison of two recovery strategies following a muscle damaging protocol (pre, post, 24-h, 48-h, etc).
Thanks in advance.
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Probably not because if you compare groups across time they are no longer independent. Suggest you see this link:
Best wishes, D. Booth
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can someone explain about of effect of this both training model on muscle activation and muscle damage? moreover what effect they have on the muscle hypertrophy?
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eccentric -> mostly in force there is contribution of passive elements, and less of active elements (cross-bridges). Because of lengthening the "damage", which is more in reality sensing of receptors leads to, generallly, addition of sarcomeres in series. So lengthwise the muscle cell will grow, and in parallel some addition can be done because there is some activity of myosin-actin.
In case of drop set, there is more fatigue, and you keep training with lower intensity or load, but because of higher fatigue, you keep on getting more higher or highest threshold groups. Also there is both eccentric and concentric work done, so more addition of parallel sarcomeres (at least in theory).
With the eccentric training the question remains how soon or how many highest threshold groups are involved as the passive elements can contribute a lot towards the force production. It might be that less high(er/est) threshold groups are activated. Eccentric training can be done with overload, as in very heavy weights only eccentric, with less voluntary control. Or with for instance a bit more load which can still be controlled.
Eccentric has more muscle damage related to intensity, because of higher loads, while drop sets have less high loads and more fatigue, so there would be in the first, hypothetical more mechanical damage, and in the second more metabolic damage. However, the question is open if muscle damage contributes to HT in the first place.
So drop set with controlled eccentric movement in the exercise might be better for overall hypertrophy as you train both eccentric and concentric.
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Skeletal muscle damaged by injury or by degenerative diseases is able to regenerate new muscle fibers?
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Skeletal muscle possesses considerable regenerative capacity. This is attributed primarily to stem cell-like cells, i.e., satellite cells, that reside in the muscle tissue. They lie between the basal lamina and the sarcolemma of a fiber. Satellite cells can fuse with injured muscle fibers to repair those fibers and can fuse with other satellite cells to replace irreversibly-injured fibers. Muscle regenerates well from injury except for injuries in which the extracellular matrix is severely disrupted, e.g., as in when there is a traumatic loss of tissue such as an IED blast. Muscle regenerates well from injuries induced by exercise/work, eccentric contractions, freezing, toxin injection, ischemia/reperfusion, etc. It may take a month or so but the muscle usually recovers. However, age, impaired inflammatory response, etc. can impair the recovery.
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I have been trying to find articles regarding the use of phototherapy in muscle injury in vivo. All I can find are studies that have worked with exercise-induced muscle damage and in vitro studies. Any help would be greatly appreciated!
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Thanks a lot guys, I appreciate it!
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Cardiotoxin from Naja mossambica mossambica is commonly injected into skeletal muscle to induce experimental muscle.  It appears that this product was sold exclusively by Sigma-Aldrich.  The product has unfortunately been discontinued.  I would be grateful for advice on suitable alternatives to induce experimental muscle damage in rodent models.  Thank you!
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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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also info on musculo-tendinous tears versus tendon-bone insertion versus muscular tears
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Awesome, thanks
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It will be performed on the lower limb and using eccentric exercise. We were wondering whether 50 max repetitions at 120 degrees per second would actually cause enough damage? 
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I serve as a clinical instructor for Biodex and have seen a number of dynamometers that use what is called "reactive eccentric" modes. The problem with the reactive eccentric mode is the necessity of producing 5 - 10% of the peak torque set for the exercise to activate the dynamometer. This is problematic since the force velocity relationship clearly demonstrates that eccentric torque is greater than concentric or isometric torque. I know studies of intact muscle have sometimes reported less torque with eccentric dynamometry, but in using it with numerous patients in therapeutic settings I have observed that this is only the case when the velocity setting exceeds the capacity of the patient to perform at the given velocity.
The theory of eccentric muscle damage with eccentric muscle actions is based on studies using supramaximal loads in true eccentric muscle actions (the subject could NOT move the resistance using a concentric muscle action). The best way to do this using the Biodex is to set up the test in "Passive Mode." This doe not require the subject to provide a counter-torque to start the movement, and therefore they can resist the movement throughout the entire ROM of the test. For the knee, set up the ROM for the test. For your question of influence with cycling, I would seek to determine the velocity of movement for the performance. If that is considered too fast, I would do a spectrum from about 90 d/s to 180 d/s but this may require some learning because the change in direction occurs very rapidly. For the passive mode of a Biodex, you will be able to set a maximum torque for each direction, this should be set to exceed the maximal concentric torque of the subject at that velocity by 50% to insure they do not STOP the movement.
At velocities of 90 - 180 d/s it will take between about 20 and 10 seconds to perform 10 repetitions; 40 - 20 seconds for 20, respectively. Again you need to look at the specific aspects of performance you are attempting to study or modify through training to set up the protocol. The dynamometer should be set for REPS however, not time, when setting up the END BY mechanism.
If you have further questions you can contact me here.
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We are looking for a way to assess "muscle damage" without an invasive method. Since muscle damaging protocols lead to increased biomarkers (e.g. CK, CRP,...), we need a method to proof that the impact of our exercise protocol induces a real local muscle damage, without taking blood samples. 
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what about the use of ultrasonography?
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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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I am looking for an exercise type enable focusing a high tension to vastus medialis muscle only (or on vastus lateralis if that appears easier to realize) in order to induce muscle damage mainly on this quadriceps head. Do you know some exercise characteristics (e.g. hip angle, specific knee range of motion, leg rotation) to get that? Thanks
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It might be possible by changing joint angles etc.. it is said that the medialis is mainly used near full extension.  However the easiest way is to use local electrical stimulation.  Use relatively small electrodes, place the cathode over the muscle you want to damage and stimulate at about 30-50Hz to develop an isometric contraction and then, whilst still stimulating forcibly flex the knee. Alan Donelley used electrical stimulation like this to cause major damage to the whole quads but he was using large electrodes that stimulated all, or most, of the muscle.
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I am interested in research that explains the causes of DOMS. Specifically is it the muscle damage that causes the pain or is it the associated inflammation and ROS's that cause the pain? Thanks
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Dear Dieter and Alexandre, 
thank you for your answers. I do agree , as I stated before, there is no direct proof that lactate is major cause of DOMS, and that current literature mainly states structural damage as the cause. However, I believe that lactate is much more than just waste metabolite of anaerobic metabolism. We now know that it is important intracellular messenger and therefore I am not ready to discard its possible involvement in this type of tissue damage. It may not be most highlighted by current research, but I didn't want to except it. 
Regarding lactate, some of the facts that could help explain why I think it has much greater role that it is commonly thought. First of all, oxygen availability is not only mechanism that is in control of lactate prodution. That hypothesis has been thrown away long time ago but it is somehow stuck in exercise physiology and similar fields. Regarding exercise, there are other more important factors to consider when thinking about lactate production than oxygen. Second, lactate has important regulatory functions, and it is therefore possible that it could be involved in fast recovery of structural damage (eg.stimulation of fibroblasts). Lactate also has antioxidant properties and is directly involved in ROS production (commonly stated as probable cause of DOMS). Lactate can control cell migration (immune cell migration is important in DOMS on various levels). Lactate can iduce neovascularization. Lactate is probably involved in muscle adaptation to exercise (and adaptation of many other tissues). Moreover, lactate can change activity of neuronal ion channels thereby changing potential of sensory neurons to transfer pain signals.
As I said, I am not trying to convince anybody that lactate is main cause of DOMS, but I want to add that, having current literature in mind, it has much more to do with metabolism than it is commonly thought (so I think it is also much more involved in DOMS that commonly thought. Just my opinion though.) 
I will add two more interesting reads:
Best regards,
Jan Homolak
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I wanted to know if there are any flexibility tests I should be looking at to specifically identity if weight-bearing activities (carrying a heavy backpack all day) relates to muscle stiffness, such as lumbar and hamstring muscles. 
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Hi Marina
I suggest checking out the relationship between weight-bearing and hypertrophy of muscle collagen
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My current project is looking at blood flow restriction, and we are weighing up the options of using official kaatsu bands or the use of a medical tourniquet.
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Hell Danny...
"...Use of KAATSU Equipment requires specific training and adherence to KAATSU protocols. Therefore, you must first become a Certified KAATSU Specialist before you can purchase KAATSU Equipment."
Look at it!
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Tetranectin has been suggested to play a role in tissue remodeling, due to its ability to stimulate plasminogen activation and its expression in developing tissues such as developing bone and muscle. I would like to study its role in muscle damage due to exercise, and if there is some relationship between them.
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Here are a few articles I found on the subject.
The last article (Tetranectin is a Novel Marker for Myogenesis during Embryonic Development, Muscle Regeneration, and Muscle Cell differentiation in vitro) is probably the closest to what you are looking for.
Hope this helps and best of luck in your research. 
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I am looking into the use of ice and compression garments; both are thought to reduce exercise induced muscle damage, and inflammation post exercise. I am interested in literature that explains or shows how/whether reducing this inflammation is positive or negative to recovery and adaptation to exercise. Thanks for your help. 
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Hi,
If you are focused on the inflammation aspect then you may want to take a look at some of the work by Todd Trappe, granted it is not using BFR or ice but does look at the inflammation aspect and adaptation via protein synthesis of the muscle. I also like the artilce by Fatimah Lateef as a starting point to look at the effect of ice on muscle adpatation.
Skeletal muscle PGF(2)(alpha) and PGE(2) in response to eccentric resistance exercise: influence of ibuprofen acetaminophen.
Trappe TA1, Fluckey JD, White F, Lambert CP, Evans WJ.
Post exercise ice water immersion: Is it a form of active recovery?
Fatimah Lateef
best,
karen
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We want to determine the efficacy of various post exercise treatments to improve recovery.
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Si vous vous intéressez à l'aspect biochimique et en français puisqu'il me semble que vous connaissez notre langue :
EFFET D’UN EXERCICE JUSQU'A EPUISEMENT SUR LES PROTEINES PLASMATIQUES.
APPROCHE PAR SPECTROMETRIE DE MASSE MALDI-TOF
(Seconde Partie)
D. Atlaoui1 , P. L. Bourdon2 , M. Jaquinaud3 , O. Richard1, E. Forest3 et Ph. Germain1 .
1 Laboratoire de la performance motrice, faculté du sport et de l'éducation physique, université d'Orléans
Laboratoire de physiologie animale, université d'Orléans
2 Centre de Recherche du Service de Santé des Armées, Grenoble
3 Institut de Biologie Structurale, laboratoire de spectrométrie de masse des protéines, Grenoble.
Résumé
A l’issue d’une première étude visant à identifier des protéines plasmatiques caractéristiques d’un état pathologique (infarctus du myocarde), nous avons fait l’hypothèse que par électrophorèse et spectrométrie de masse, des protéines sarcomériques entières ou fragmentées pouvaient être reconnues dans le plasma. Par la même méthode d’investigation, cette expérimentation a pour objectif de comparer les incidences d’un exercice maximal et épuisant à ceux d’une ischémie cardiaque.
La population expérimentale est composée de rats Spagues Dawley que nous avons entraînés sur tapis roulant et dont nous avons prélevé une partie de la masse sanguine par ponction directe au niveau de l’aorte abdominale. Nos résultats très comparables à ceux que nous avons préalablement exposés chez l’homme cardiaque, nous laisse supposer que la spectrométrie de masse est un outil permettant rapidement de diagnostiquer une phase de surentraînement se traduisant par une rhabdomyolyse de tissus musculaires striés squelettiques. Des études complémentaires restent cependant nécessaires, d’une part pour élargir notre population expérimentale à plus de sujets et à l’homme, d’autre part pour affiner la reconnaissance des protéines et enfin pour proposer une méthodologie accessible au plus grand nombre.
Mots clefs : Spectrométrie de masse, rhabdomyolyse, plasma, surentraînement.
Bien à vous
Philippe
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Do you know reliable α-actin antibody for Western blot to investigate skeletal muscle damage?
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You can take a look at the original article entitled Release of a-actin into serum after skeletal muscle damage from Martínez-Amat et al. (2005) in the Br J Sports Med (Western Blot was used)
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Ultra-structural damage including plasma membrane impairments and damage to the sarcoplasmic  reticulum have been observed following unaccustomed eccentric exercise (Warren et al., 1993 Friden et al., 1993., etc). My question is, is there any possibility that omega-3 fatty acids may play a role in maintaining plasma membrane integrity and the subsequent reduction in membrane permeability and Ca2+ concentration?
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Thank you very much for your answers! Highly appreciated. I am in the process of doing my literature review and I will be looking up some of your suggestions.
Kind regards,
Sallu
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How might this relationship become affected with muscle damage? Need relevant studies to support.
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I've been doing a literature review on mechanical disruption and impairments to the E-C coupling process as a result of contraction-induced injury and information from Friden et al. (1983) and Warren et al. (1993, 2001) was very insightful! Fantastic piece of research. Thank you