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Muscle Structure and Physiology for Orthopaedic Exams
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Muscle Structure and Physiology for Orthopaedic Exams
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Upload Date:
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Language: EN.
Segment:0 .
We recording. OK good evening, everyone. Welcome again to this Fox teaching webinar. Topic tonight is about muscle structure and physiology. I hope you can all hear me well.
The presentation done tonight by Saad memon, who is a senior registrar from Wales. He has recently passed the exam in November, so he has lots of a wealth of knowledge that he could embark on us and his recent knowledge and recent experience with the exam, which is, as you know, all extremely valuable.
As I saw him, I'd also been like all of you, member of this group, and he's done a lot of practice, attended a lot of these teaching sessions. I'll be moderating the session, I'm fearless slap no other faculty members attending. We have Abdullah Hanoun was also one of the mentors here, and he will be supporting us. Just housekeeping points again, please, guys, if any questions, put it on the chat box or raise your hand simple.
We will keep questions to that. We will keep questions coming and we'll get you get them answered by the mentors, and after the session, there will be a couple of Viva practice questions. So if anyone is interested, please let me know as soon as you can. So it's first come, first served basis. Anyone who attends will be eligible for a CPD certificate, so please let me know if anyone needs one.
And again, this will. The video will be edited and published on YouTube channel, along with the previous teaching sessions program called postgraduate orthopedic fellowship, of course. for now, we welcome everyone again, and I'll leave you with sight to welcome slap and please go ahead. Good evening, everybody.
Can you all hear me? I'm sure. Yes, thank you. We can't hear it yet. So let me start with the slightly intro about the topic. This is the schedule. Muscle and nerve are the two most important topics in the basic sciences. As you all probably know, the basic science is a significantly dry topic in general.
It does require a lot of dedication to remember and to go through the topics in clear detail so that when you are able to present, it provides you a really solid marks. It is not much to go further in this topic, and you probably would be able to cover it easily. What the reason I've actually put a few things in there, which are slightly over the 7 and 8 mark. Most of people might agree, might not agree there at some point in bivariate.
There will be asked questions which are probably beyond the level, but when you come to the actually the basic sciences. This is the one table. You can square it very easily if the facts very well from the point of view as this topic, as you know, skeletal muscle. I will try to actually input a lot of physiology in it because this is mainly based on the physiological concepts.
I try to actually go very slow because since the topic is quite dry and it's a lot of material is there. I would rather go into a more of a conceptual basis of the topic in more detail, and I would go slowly if any point, please actually the amount of mementos around, they will be able to answer your questions. We will keep the questions for the end. And first of all, what exactly the skeletal muscle is, what is actually the structure?
What is this basic unit, which is called sarcoma? What are the filaments involved in this? How does the synapse actually works? What is actually an action potential, a brief description of that, which is a very important concept to concur. A muscle injury and then types of the muscle contraction, I'll go very briefly into them. So this is what we are covering today. I will slow, nice and easy at any given point.
Actually, you feel like I'm going to first just let the initialism know and then we take it from there. So it's good to muscle is a specialized connective tissue, provide a contractile elements to the support and facilitate human locomotion. It provides homeostatic storage for the electrolyte. Glucose, amino acids and fatty acid and is an instant source of energy.
And the body requires it to do any activity. It protects the internal organs of obviously, you know, that types of the fibers are usually that is a classification. A very, very fondly asked by the examiners is type I and type two, which is red and white fibers. The red fibers are actually called slow oxidative fibers or red ox. They are called.
Because they are red and have got oxygen component to it and type 2 fibers, other fast fibers, which are actually the White fibers, which has got less of a oxidative stuff, i.e. mitochondrial because the mitochondria is of a powerhouse of the cell. It has got a high is a very low quantity of that because the instant energy source of energy is available glycogen or glucose at the time when they utilize it.
The main elements involved are actin and myosin, as you would know. And these are actually the smallest component of that. This piece filaments make them a basic work unit of the skeletal muscle, which is called sarcoma. The this is a detailed diagram of the actin and myosin on your left is actin, which has got the chains which are intermingled or in the helix base.
And there are main three components of the actin is affecting top of myosin and top on in complex. However, the Mason parliament is a heavy chain composed of the two heavy chains and the two light chains. You can see this structure and this slide presentation will be available for you on our YouTube channel. You can see that these two heavy chains is making a helix, which is actually going up to the end, and they are connecting with the light chain, which would be involved in the contractile activity, which would be showing its next.
So this is a sarcoma. This is electron micrograph picture of the muscle. You can see these are the bends on this level, at the level of electron microscopy. You can see there's two types of dark bend one a light bends and in which they are actually that is the lines which we'll be describing it further in details.
The events, or N isotropic band means it is a darker band is the component which actually is sitting down as a Black band that I bet is a lighted band or isotropic band. The hatch ban is a heavy chain band, which is hitting the center, and the Z line is usually a line which is actually is holding the actin filaments, which goes toward the iPad. The M line is a myosin line, which is a main central component of the myosin band.
If I can, I just say this is very, very interesting, actually. I don't know if want to repeat it for people to take note of, because if you know what, all the m and and m and and h bands, what they are mean what they mean. There's a lot easier to remember, isn't it? Yeah, so just remembering random letters, you put it to those letters, which I think of many people will know.
Yeah so the darker band is an isotropic band, so it is actually taking the light which cannot pass through the ID completely. So it's a dark band, is a band. The lighter bend is isotropic bend. And the hedge bent is a heavy chain band, which you can see in the area, which is more hardened on the sides. The deadline is usually aligned.
Don't ask me the spelling for that because it's a German word, but that's actually the main line which actually connect the actin filaments. In a sense, it's a deadline. This is a main protein which goes down all the way, and the actin elements are connected to it. The bend is a myosin line or myosin band, which goes down to the center of it, where the heavy chain is actually connected to each other in the three dimensional structure.
Thank you. So you can see this subcommittee is in slightly more detail, this picture in the center is the most important picture for this topic. If you can't take away anything but anything, this picture, I'm sure you can see my mouse going around it. It's actually the sarcomere. This is you. All you have to do is make a diagram of you need to know it by heart.
So this is sarcoma, which is between the 2z lines. This is a structural unit of the skeletal muscle where the contractile elements work. So this is the. So this is the Z line and these are the actin filaments, which are 10 filaments which goes down from the sides. OK then there is a myosin back myosin filament, which is sitting down the center. On which the act elements come in between intervene between each other.
Now this is two dimensional structure, but there is pictures available for the three dimensional structures. Now this is a central line, which is emlyn, which connect the myosin line as we saw it in the electron micrograph picture. The actin filament you can see now, this a band which is an isotopic band is actually the myosin molecule or my myosin filaments overlapping the actin filaments.
This area is called a band, which is nice to be called dark band, because these epimysium are the very heavy chain molecules. That anisotropic bend is start from the hair goes down to the next up to the second Mason line, which you can see in the later pictures. You can see these in a slightly more detail that you have got actin filaments coming down on the sides.
And then these are heavy myosin chambers. They're multiple heads around that area. OK this is a difference between the relax muscle and the contracted muscle. That's how you see it in a schematic diagram how actin actually overlap on the myosin. You can see a Z lines of fall apart. And here they are, come together to become a contracted muscle.
The most important thing, which we think actually is myosin bent, but actually actin is much more important component of this. It has got the three main areas filament, actin or actin. Rapamycin and the draconian complex. Which can bring contents of CIA binding sites. In greater detail, you can see there's an actin filament down here.
You can see there is a site on the Acton effect of Acton, which is covered by the troponins complex. But to epimysium is a sheet of filaments which goes on the area of the myosin binding site. These are the type of sites, these are target sites around that area where they are covered by the troponins complexes.
To make it story is to start with the kind of how the contraction happened. You got to get the calcium to come and connect with the sea component of the troponin complex. It induces the conformational change. The PT component actually drag the triple and tropomyosin away from the target site. And allow the Mason had to come on the target site to be attached.
Coming to the sign-ups now, this is another concept which is very favorite concept for the thing in my basic science is Survivor. This whole topic is what you discuss in significant detail. It was five minutes, but it was very, very chop, chop, chop chop business. So you need to know this very well. And he should be able to make a schematic simplest possible diagram for this area.
This is very complex. It is material. You have to make it very, very super simple diagram. Now, sign-ups is the area where the nerve ending comes in contact with this skeletal muscle or any target organ. You can see here in the first picture there is Exxon, which is coming down with this nerve endings and landing up down onto the surface of the muscle and the muscle cell has got its own nuclei, has got the pits available down that area where the nerve endings actually end coming in contact, the blood cells, which are cells to connective tissue cells to support this area in terms of connective tissue.
You can see the myelin sheath on the top. This is obviously you can see there's a lot of synapse is connecting to the lot of skeletal muscle to provide a neutral ending to target organ and skeletal muscle. This is the area where you can see there's this nerve endings. Coming down and the surface of the skeletal muscle, I've got a terminal. And you can see a lot of mitochondria are rumbling around to actually make this actually quite an active muscle, especially the fine muscles of the hand have got a lot of nerve endings available for months.
They were smaller muscle unit in a final muscle activities. These are the synaptic vesicles, and this is actually the pit I will go into slightly more detail into this because this is important for few, few and few questions, which is very, very important to understand this. So what happens here is that you have got this muscle nerve ending. You have cottage cheese is a muscle.
So the nerve endings and got a muscle membrane around that area. You can see that these vesicles comes in attach to the surface. Release their style choline in the pits available to down there. There is a subdural cleft where they go and attach down that area. There there are a few versions of the structure, whatever you make it as simple as possible.
So this is an area where you have got acetylcholine, acetylcholine, which which basically is responsible to just remember the static images because we will talk about it a little later. The circle in the synaptic vesicles they released in the pit where it comes down and attached to the disk that circle interceptors. These are the chemically activated chemical activated channels which increase the sodium permeability in the membrane and hence activate the voltage cable channels later on to activate further.
Now, this is a concept, it is quite a heavy picture, but it is very simple concept that what do you mean by all this action potential business? This is very important concept, it has to be known by everything, everyone, because this is actually the basis of the nerve conduction and the muscular activity. Here you can see what are the levels inside and outside?
We have got available on the surface on the cell. So the sodium is 142 million Allen per liter on the outside and about 14 million inside. The potassium is excellent. On the outside the bag, about 240 of the 42 and then the 14 chip inside and potassium is totally excellent on the outside and 140 equaling per liter on the inside. This is to maintain the resting membrane potential across the cell membrane.
So you have got a high concentration of the sodium outside the cell and low concentration of the population outside the cell. And conversely, inside the cell. Now, you always have in every single cell, a leaky channels which keep letting the sodium come out so they can diffuse in and out all the time. However, there are sodium and potassium ATPase pumps available, which keep that resting membrane potential to the levels or does not get excited.
In simplest terms that the body or the cell has to stay in the resting membrane potential or the voltage where it cannot get activated unnecessarily. This is maintained by the most important function is sodium. Potassium ATP is pumped. Now, on the right side of the image, you can see there are visual changes on the surface membranes. The sodium is basically trying to get in, but the activation slows.
Then these are the voltage gated channels, there's not chemically activated channels. They are voltage gated channels. These are two types of the channels, sodium voltage channels and sodium activated channels here. Once that there is the sodium permeability due to the leaky channels arrived at level, which cannot be maintained or all the voltage across the membrane can change. These are get activated and the sodium channels opened up, and then the sodium rushes in very quickly as quickly as possible.
The moment they get enough sodium inside the inner side, gait closes and the sodium can stop happening to translate it as happened in the way to translate that into action potential. We have got a normal minus 90 millivolts volt resting membrane potential. Your leaky can slightly get up, but is constantly maintained at the level of arresting human potential by the sodium potassium pump.
Until we come to the stage when you have either acetylcholine comes in and a chemical gated sodium channel activated. The sodium started to rush in and because the end across the membrane that is a polariton one side, the significantly positive on the other side is significantly negative. Now, this polarity is not dropping, just the polarizing. So it's deeply polarized, the polarization is starting to finish, and it's getting the voltage to the equivalent on the zero.
However, it is a kind of fragmented time component into that until it actually get to all the channels get closed down. As you can see, the second gait of the sodium channel closes that lead to the potential much more positive and hence the inner gait of the sodium channel closes down. Then, because the gait channels are activated at the level of the zero, they started to actually start to become leaky.
When they become leaky, they lashes out, hence that they start regaining the polarity. Back in the system. And if they get down to the level of any of the testing on potential now at this level, we have got the biggest problem available to the cell that the whole polarity is completely reversed. Now there is a function of the sodium and potassium ATPase pump to regain that polarity back in position.
Hence, what the sodium potassium pump does is bring through the three sodium out and bring the two potassium in with every stroke of ATPase. And repeat it, the three sodium things for them out and bring the two potassium in, not only destroying the chemical gradient, but also getting the polarity back onto the track. Now, this is the diagram that you have to make it in the Viva.
So you started as a minus 70 because the skeletal muscle in the nerve, it is minus 90. It goes up to 55 is a threshold from where all this voltage gated open, they continue up to that level and you can see the down here, the membrane permeability of the sodium and potassium channels. At what level the activity and hence you, as I describe this happen. Another important concept and this is what is the absolute and what is the relative refractory period?
The definition of the refractory period is that the nerve fiber or the muscle cannot be reactivated during that phase. So there is absolutely no possibility of the membrane cell can be reactivated again, i.e. opening this voltage gated sodium channels until it regains its normal resting membrane potential. That's an absolutely effective period, the period between that potential action potential and another coming on action potential.
Is between that period is a relative, a relative reflective of where the sodium potassium pump is, try to regain the polarity back into the system here. There's very much possibility if of the impulse comes in, it can get activated. Now, once this information is arrive on the surface membrane, what actually happens, so this actually is like a roller coaster.
You start walking around on the surface of the membrane unless you're got a mile and sheet with it. Find the next available based on the surface membrane to jump. This is called tightly conduction. All of the action potential here. I to say that these are the kind. This is the muscle fibers you can see on the side, Colima or this or the muscle membrane. And then you have got a tip.
It goes right inside there. It's a big imagination of the surface membrane. You can see that there is actually is a sarcoplasm reticulum, which is collecting the calcium inside down there. It has got a calcium pumps inside. Now what happens when the sodium is get accumulated? The calcium channels are very small gated channels. They start bringing the calcium in the cytoplasm of the cytoplasm of the muscle.
You can see this actin mushroom filament are onto each other. And if you come down to it area and you can see this on the surface membrane of the plasma reticulum, how the calcium release is basically, when the calcium get inside the membrane, it attaches on the surface of the protein called this is slightly complex concept. Now this is for the 7 and 8. So the calcium comes in is actually attached to the protein and then it actually is done, though this also is the system.
The same system occurs in the vesicles as well synaptic vesicles as well. So this area is very important in the concept of how does the botulinum toxin work? So in the sign-ups, because the question comes inside attached to the classic Putin protein, and that brings a vesicle on the surface of it. If you provide onabotulinumtoxin around that area, it deactivate the system called synaptic Brevin protein complex, which is stop the vesicle to allow it to attach to the surface of that or allow it to release the vesicle into the system and into the sand and declare the same system actually works within the cytoplasm reticulum as well.
Now, this is how the botulinum toxin work. This is a sign up to con concept. Guys, this is a very complex area, but I'm just making simple for it that this is a sign up to Brevin protein complex, which attaches to the synaptic vesicle and does not allow us to chemical in to release acetylcholine in the system. Hence, the struggling cannot be released and it could get blocked completely.
Coming to the walk along theory or the other contraction theory there you have got you can see down here there's the acting job, which you described earlier on the effect of acting there comes down here and actually make these lists acting component and these are myosin chain. Now these are the light chain of the myosin, which actually make the myosin head.
And you remember I was talking about the calcium coming in addition to the top iron and steel making it a conformational change drag out of Mason away from the binding site, Mason head comes in contact attached to down that area and walk along the membrane. This is slightly more detail why what exactly happens? So basically the initial deployment comes down here, it can attach down to the 80 pump down area to the ATP, which is attached touchdown area Mason had contact the ATP converting to ATP and enter the phosphate molecule and then only the contraction happened.
The most important concept here is that until the ATP is not available, this myosin head will not come off. So if you have the ATP blockade anywhere, this will not detach from the myosin binding site. Hence, you maintain the tone without using any energy at all. So this is the best conservation of energy mechanism in a God has provided us.
So if our muscles are contracted, we maintain our torn off of a muscle by making the myosin head attached to it unless the ATP is not available. And it is ready to decompose or hydrolyze ATP in five. It will not let the muscle myosin to go away to the next slide. So that's how you maintain your tone. So anyway, ATP binds to Mason had the judges, there is a nesting component.
It comes actually down to the deep end, comes in at the next available myosin binding site that becomes available. The bison the light chains go in attached to the myosin binding site. And the ATP, tenotomy, ATP and pi. This Mason attaches to it and then the myosin head pivots and bends and allowing the ATP to buy component again, the process and constantly there.
Hence the whole walking along theory happen. And this is actually the way how it happens. Myosin climate action surface active binding site Mason head comes in attach. It hinges on ATP a system, and it does work along with every power stroke every time. Now, to describe this in the exam, I just made this little chart of flow chart where you can actually talk about in greater detail why, if you remember this chart, it tells you exactly what happens.
So that's all you need to remember for the photo to talk about the walk along theory. And this is another similar kind of a corresponding diagrams accordingly, so that you can make your like slightly more clearer. Now this is now coming to the clinical applications of these concepts. One of the concept is what is threatening.
The tenotomy is actually then you have got the hypercalcemia, so a lot of actually I was asking exam at some point when we are told how come the. Can get any happens via hypercalcemia. Make our muscles to go into a constant contractile stage. And that's why you actually got into the contractions. What actually happens in this picture, if you look at the sodium channels, they are negatively charged sodium channels.
It has got a question because they are negatively charged. A lot of them are lined by the calcium channels, the calcium molecules. Because these are lined by the calcium molecules, the space between them is very, very narrow to allow to sodium come in. That's a normal state. Of the girls. When the calcium goes down, this calcium would get mobilized out of these channels linings.
Making the hole much more clear than normal. Leading to the constant contractile states are constantly happening because calcium molecule is not making the channels narrow enough to close completely, so they constantly the voltage gated sodium channels become leaky channels and allow the contractile states to constantly happen. That leaves to constant contraction of the muscle and leads to tightening and hence the stimulated bull or hyper stimulant channels is available.
That's why you've got to gymnastics sign, which you tap the facial nerve and it contract and all that sort of signs for the hypercalcemia. Then comes another important concept refractory period, which you talk about myasthenia gravis is a condition where he's got antibodies against the colon is. The obstacle in this case is the enzyme which sits down the synaptic cleft here, where the acetylcholine is released in the system, in the cleft.
This is responsible to leave the acetyl and choline and get picked up back into the vesicle system. And that will. So you can see that process happening down that this area. So they constantly consumers. And that's what comes out in the system, and it just gets picked up by the going East and is designed to control.
This has actually been blocked by the antibodies which are working against going East and hence disease called Mason of the people who are actually about Bollywood. Amitabh bachchan has the myasthenia gravis is always on treatment for anti-coal. It creates enzymes for it. Botulinum toxin we talk about that does not allow the vesicles to come out, the other important concept is Duchenne muscular dystrophy.
How does the dystrophin protein is actually deficient to make the patients to go into the muscular dystrophy? Our skeletal muscle are connected by our activities, which are in the skeletal muscle. If you can see the effect and is connected to the dystrophin protein, which this complex, which is called dystrophin serko, Black and Black and complex, this is a glycolipid collects connected with a dystrophin.
So glycol collects is actually is a Y shape v-shaped glycoprotein, which which looks like a post on the cell membrane. This get connected with the dystrophin protein and that get connected with the activity of a filament actin, which is a part of the skeletal muscle. When this connection is destroyed, the dystrophin is destroyed. There is no ability of the skeletal muscles to anchored upon the cycling muscle membrane.
And hence, the muscle activity happened within the muscle. They cannot make the whole skeletal muscle and contract as one unit. This leads to this leads to the significant amount of the muscular insufficiency and hence the patients actually die at the age of 20 to 25 because there is they start losing their respiratory muscle slowly and gradually because of the abnormal gene mutation of the dystrophin protein, which is here.
So Glaxo collects dystrophin affecting. These are three things we have to remember this complex is destroyed because of dystrophin connection is not there. Muscle injury. This is the simplest you can actually tell your examiner, how does a muscle get injured and repaired? So the physical trauma happened, inflammatory mediators comes in exactly like a bone damaged several components, inflammatory cascade.
I'm just giving you a simple terms to talk about them reduces the proteolytic enzyme reactive oxygen intermediates leading to the ATP dependent failure. Failure of the mechanism raised intracellular calcium concentration. This is different in the muscle. So this system, which normally maintain the resting membrane potential down in the cell membrane enough, they're actually making the accumulation of the calcium within the system.
This calcium activates the enzyme like proteases, possible phospholipids and in turn, damage the muscles from within. This leads to the macrophage to infiltrate psychosis that damage protein muscle fibers, eventually leading to a deposition since the muscles do not regenerate. Only a limited amount of regeneration happen and the proliferation of the residual mild blast, which are very, very rare occurrence.
Coming down to the how can we detect a muscle injury? And what are the muscle components we do the imgs electromyography? In electromyography, you put the needle in the Allen, the nerve endings in the muscle, and you will get this potential. This is because of the way in a normal muscle you get this motor unit action potential.
When you have got a dinner, it no, you basically have got this what we call a simple tribal nations and we never did. Much like you get to see the complexity which comes each in this position and this sort of configuration. What actually happened in innovation, the spontaneous activity due to the increased sensitivity of the still cooling lead to the shock waves and hence in the chronically it becomes Kessler, which are uncontrolled.
Because now the muscle itself is actually becomes a center. It's leaking the sodium out, getting it activated by himself. Like when a heart actually is, when there's a heart block is there, the cardiac muscles automatically stimulate itself and try to contract. These are the first circulation in the skeletal muscle when this innovation happened, because there's too much acetylcholine is available, there's no nerve endings coming up from there.
It is not connected in acute denervation. There's a sharp face because all they're still available comes in one go and get activated chronic denervation, which has actually been the all antagonistic. And now the muscle become its own stimulant or the epitome of the whole havoc and the constantly contracting and try to become coordinated one when this muscle get to innervated.
There's initially there is a reduced amplitude modulation potential and you have got a larger, longer duration of the motor unit action potential. But because there's a poor recruitment of the muscle component with the amplitude the low. But in the data component, the larger amplitude comes in because now it is more stable, consistent firing of the action potential. And hence you get the recruitment of the unit, which gives the physics signals.
And the innovation is a physics signals in the late, more stable amplitude modulation unit action potential. You have got to Polish the signals, which tells you where the nerve is a more or less the basic sciences section should be like that we should be teaching. The examiner on the basic sciences section, I think that you covered that really, really well.
It's like you, you also did the exam. Nowadays they have to put the clinical components even in the basic sciences section. So I like how you showed us the clinical application of muscle physiology, a condition like detainee and may see a gravies and toxin injection and how they all work.
I just I have nothing to add nothing to. I just want to say if someone finds this difficult like me because it's very, very hard to and obviously sidebars, you know, approach this very well. Generally, stick to the principles, highlight the buzzwords, because sometimes what can happen is as we talk and we know what you're talking about, the examiners might switch off a little bit. So the buzz words, say them loudly, repeat them buzz words like sarcasm.
Basic contractile unit is a sarcoma. Um, talk about the action potential, highlight these words, the motor units, make sure that you let the examiner know about the resting potential, that there is resting potential and that there is a threshold and there is the gated channel and the gated channel open by acetylcholine.
Make sure these buzzwords are clearly transferred to the examiner. Yeah, these will get you out of jail in these questions, the buzzwords and we'll sort of pass you and then you can obviously use all this rest of this information to get higher marks. We will pay off. So thank you very much, sir.
This is a very difficult topic. You, you discussed and you explained it very nicely to us and we haven't covered in any previous teaching it. A lot of us when might find it difficult because we don't discuss this very much in meetings or in rooms or trauma meetings. So it is a dry topic, but you managed to make it very interesting. So thank you very much.
I hope for some potential the sarcomere. And I just want you to just remember now I think is unfortunately, this doesn't cover everything about the muscles. We still have the tendons, obviously the insertions of tendons, we have the topics of muscle contraction and things. So it's possibly another hour to cover the whole physiology about the different types of muscle, contractor, et cetera and then the open chain, closed chain and all of that.
So they can start from talking about basic science and then they move to physiology and then they move to physiotherapy. And then they can do that. They do that, and they do that. I mean, my question was about different exercises and types of exercises and in chain and all of that. So they can start from one end and move to the other. And also, yeah, the muscle metabolic systems and things like this, which side was touched on also.
Thank you. So I thank everyone again for attending. This will be the end of the presentation. Next is the Viva session. So we had the pleasure of having 59 of you registered today for the teaching. So thank you, everyone. Please get in touch with me if anyone's certificate. So we'll end the teaching now and the next will be.
Segment:0 .
We recording. OK good evening, everyone. Welcome again to this Fox teaching webinar. Topic tonight is about muscle structure and physiology. I hope you can all hear me well.
The presentation done tonight by Saad memon, who is a senior registrar from Wales. He has recently passed the exam in November, so he has lots of a wealth of knowledge that he could embark on us and his recent knowledge and recent experience with the exam, which is, as you know, all extremely valuable.
As I saw him, I'd also been like all of you, member of this group, and he's done a lot of practice, attended a lot of these teaching sessions. I'll be moderating the session, I'm fearless slap no other faculty members attending. We have Abdullah Hanoun was also one of the mentors here, and he will be supporting us. Just housekeeping points again, please, guys, if any questions, put it on the chat box or raise your hand simple.
We will keep questions to that. We will keep questions coming and we'll get you get them answered by the mentors, and after the session, there will be a couple of Viva practice questions. So if anyone is interested, please let me know as soon as you can. So it's first come, first served basis. Anyone who attends will be eligible for a CPD certificate, so please let me know if anyone needs one.
And again, this will. The video will be edited and published on YouTube channel, along with the previous teaching sessions program called postgraduate orthopedic fellowship, of course. for now, we welcome everyone again, and I'll leave you with sight to welcome slap and please go ahead. Good evening, everybody.
Can you all hear me? I'm sure. Yes, thank you. We can't hear it yet. So let me start with the slightly intro about the topic. This is the schedule. Muscle and nerve are the two most important topics in the basic sciences. As you all probably know, the basic science is a significantly dry topic in general.
It does require a lot of dedication to remember and to go through the topics in clear detail so that when you are able to present, it provides you a really solid marks. It is not much to go further in this topic, and you probably would be able to cover it easily. What the reason I've actually put a few things in there, which are slightly over the 7 and 8 mark. Most of people might agree, might not agree there at some point in bivariate.
There will be asked questions which are probably beyond the level, but when you come to the actually the basic sciences. This is the one table. You can square it very easily if the facts very well from the point of view as this topic, as you know, skeletal muscle. I will try to actually input a lot of physiology in it because this is mainly based on the physiological concepts.
I try to actually go very slow because since the topic is quite dry and it's a lot of material is there. I would rather go into a more of a conceptual basis of the topic in more detail, and I would go slowly if any point, please actually the amount of mementos around, they will be able to answer your questions. We will keep the questions for the end. And first of all, what exactly the skeletal muscle is, what is actually the structure?
What is this basic unit, which is called sarcoma? What are the filaments involved in this? How does the synapse actually works? What is actually an action potential, a brief description of that, which is a very important concept to concur. A muscle injury and then types of the muscle contraction, I'll go very briefly into them. So this is what we are covering today. I will slow, nice and easy at any given point.
Actually, you feel like I'm going to first just let the initialism know and then we take it from there. So it's good to muscle is a specialized connective tissue, provide a contractile elements to the support and facilitate human locomotion. It provides homeostatic storage for the electrolyte. Glucose, amino acids and fatty acid and is an instant source of energy.
And the body requires it to do any activity. It protects the internal organs of obviously, you know, that types of the fibers are usually that is a classification. A very, very fondly asked by the examiners is type I and type two, which is red and white fibers. The red fibers are actually called slow oxidative fibers or red ox. They are called.
Because they are red and have got oxygen component to it and type 2 fibers, other fast fibers, which are actually the White fibers, which has got less of a oxidative stuff, i.e. mitochondrial because the mitochondria is of a powerhouse of the cell. It has got a high is a very low quantity of that because the instant energy source of energy is available glycogen or glucose at the time when they utilize it.
The main elements involved are actin and myosin, as you would know. And these are actually the smallest component of that. This piece filaments make them a basic work unit of the skeletal muscle, which is called sarcoma. The this is a detailed diagram of the actin and myosin on your left is actin, which has got the chains which are intermingled or in the helix base.
And there are main three components of the actin is affecting top of myosin and top on in complex. However, the Mason parliament is a heavy chain composed of the two heavy chains and the two light chains. You can see this structure and this slide presentation will be available for you on our YouTube channel. You can see that these two heavy chains is making a helix, which is actually going up to the end, and they are connecting with the light chain, which would be involved in the contractile activity, which would be showing its next.
So this is a sarcoma. This is electron micrograph picture of the muscle. You can see these are the bends on this level, at the level of electron microscopy. You can see there's two types of dark bend one a light bends and in which they are actually that is the lines which we'll be describing it further in details.
The events, or N isotropic band means it is a darker band is the component which actually is sitting down as a Black band that I bet is a lighted band or isotropic band. The hatch ban is a heavy chain band, which is hitting the center, and the Z line is usually a line which is actually is holding the actin filaments, which goes toward the iPad. The M line is a myosin line, which is a main central component of the myosin band.
If I can, I just say this is very, very interesting, actually. I don't know if want to repeat it for people to take note of, because if you know what, all the m and and m and and h bands, what they are mean what they mean. There's a lot easier to remember, isn't it? Yeah, so just remembering random letters, you put it to those letters, which I think of many people will know.
Yeah so the darker band is an isotropic band, so it is actually taking the light which cannot pass through the ID completely. So it's a dark band, is a band. The lighter bend is isotropic bend. And the hedge bent is a heavy chain band, which you can see in the area, which is more hardened on the sides. The deadline is usually aligned.
Don't ask me the spelling for that because it's a German word, but that's actually the main line which actually connect the actin filaments. In a sense, it's a deadline. This is a main protein which goes down all the way, and the actin elements are connected to it. The bend is a myosin line or myosin band, which goes down to the center of it, where the heavy chain is actually connected to each other in the three dimensional structure.
Thank you. So you can see this subcommittee is in slightly more detail, this picture in the center is the most important picture for this topic. If you can't take away anything but anything, this picture, I'm sure you can see my mouse going around it. It's actually the sarcomere. This is you. All you have to do is make a diagram of you need to know it by heart.
So this is sarcoma, which is between the 2z lines. This is a structural unit of the skeletal muscle where the contractile elements work. So this is the. So this is the Z line and these are the actin filaments, which are 10 filaments which goes down from the sides. OK then there is a myosin back myosin filament, which is sitting down the center. On which the act elements come in between intervene between each other.
Now this is two dimensional structure, but there is pictures available for the three dimensional structures. Now this is a central line, which is emlyn, which connect the myosin line as we saw it in the electron micrograph picture. The actin filament you can see now, this a band which is an isotopic band is actually the myosin molecule or my myosin filaments overlapping the actin filaments.
This area is called a band, which is nice to be called dark band, because these epimysium are the very heavy chain molecules. That anisotropic bend is start from the hair goes down to the next up to the second Mason line, which you can see in the later pictures. You can see these in a slightly more detail that you have got actin filaments coming down on the sides.
And then these are heavy myosin chambers. They're multiple heads around that area. OK this is a difference between the relax muscle and the contracted muscle. That's how you see it in a schematic diagram how actin actually overlap on the myosin. You can see a Z lines of fall apart. And here they are, come together to become a contracted muscle.
The most important thing, which we think actually is myosin bent, but actually actin is much more important component of this. It has got the three main areas filament, actin or actin. Rapamycin and the draconian complex. Which can bring contents of CIA binding sites. In greater detail, you can see there's an actin filament down here.
You can see there is a site on the Acton effect of Acton, which is covered by the troponins complex. But to epimysium is a sheet of filaments which goes on the area of the myosin binding site. These are the type of sites, these are target sites around that area where they are covered by the troponins complexes.
To make it story is to start with the kind of how the contraction happened. You got to get the calcium to come and connect with the sea component of the troponin complex. It induces the conformational change. The PT component actually drag the triple and tropomyosin away from the target site. And allow the Mason had to come on the target site to be attached.
Coming to the sign-ups now, this is another concept which is very favorite concept for the thing in my basic science is Survivor. This whole topic is what you discuss in significant detail. It was five minutes, but it was very, very chop, chop, chop chop business. So you need to know this very well. And he should be able to make a schematic simplest possible diagram for this area.
This is very complex. It is material. You have to make it very, very super simple diagram. Now, sign-ups is the area where the nerve ending comes in contact with this skeletal muscle or any target organ. You can see here in the first picture there is Exxon, which is coming down with this nerve endings and landing up down onto the surface of the muscle and the muscle cell has got its own nuclei, has got the pits available down that area where the nerve endings actually end coming in contact, the blood cells, which are cells to connective tissue cells to support this area in terms of connective tissue.
You can see the myelin sheath on the top. This is obviously you can see there's a lot of synapse is connecting to the lot of skeletal muscle to provide a neutral ending to target organ and skeletal muscle. This is the area where you can see there's this nerve endings. Coming down and the surface of the skeletal muscle, I've got a terminal. And you can see a lot of mitochondria are rumbling around to actually make this actually quite an active muscle, especially the fine muscles of the hand have got a lot of nerve endings available for months.
They were smaller muscle unit in a final muscle activities. These are the synaptic vesicles, and this is actually the pit I will go into slightly more detail into this because this is important for few, few and few questions, which is very, very important to understand this. So what happens here is that you have got this muscle nerve ending. You have cottage cheese is a muscle.
So the nerve endings and got a muscle membrane around that area. You can see that these vesicles comes in attach to the surface. Release their style choline in the pits available to down there. There is a subdural cleft where they go and attach down that area. There there are a few versions of the structure, whatever you make it as simple as possible.
So this is an area where you have got acetylcholine, acetylcholine, which which basically is responsible to just remember the static images because we will talk about it a little later. The circle in the synaptic vesicles they released in the pit where it comes down and attached to the disk that circle interceptors. These are the chemically activated chemical activated channels which increase the sodium permeability in the membrane and hence activate the voltage cable channels later on to activate further.
Now, this is a concept, it is quite a heavy picture, but it is very simple concept that what do you mean by all this action potential business? This is very important concept, it has to be known by everything, everyone, because this is actually the basis of the nerve conduction and the muscular activity. Here you can see what are the levels inside and outside?
We have got available on the surface on the cell. So the sodium is 142 million Allen per liter on the outside and about 14 million inside. The potassium is excellent. On the outside the bag, about 240 of the 42 and then the 14 chip inside and potassium is totally excellent on the outside and 140 equaling per liter on the inside. This is to maintain the resting membrane potential across the cell membrane.
So you have got a high concentration of the sodium outside the cell and low concentration of the population outside the cell. And conversely, inside the cell. Now, you always have in every single cell, a leaky channels which keep letting the sodium come out so they can diffuse in and out all the time. However, there are sodium and potassium ATPase pumps available, which keep that resting membrane potential to the levels or does not get excited.
In simplest terms that the body or the cell has to stay in the resting membrane potential or the voltage where it cannot get activated unnecessarily. This is maintained by the most important function is sodium. Potassium ATP is pumped. Now, on the right side of the image, you can see there are visual changes on the surface membranes. The sodium is basically trying to get in, but the activation slows.
Then these are the voltage gated channels, there's not chemically activated channels. They are voltage gated channels. These are two types of the channels, sodium voltage channels and sodium activated channels here. Once that there is the sodium permeability due to the leaky channels arrived at level, which cannot be maintained or all the voltage across the membrane can change. These are get activated and the sodium channels opened up, and then the sodium rushes in very quickly as quickly as possible.
The moment they get enough sodium inside the inner side, gait closes and the sodium can stop happening to translate it as happened in the way to translate that into action potential. We have got a normal minus 90 millivolts volt resting membrane potential. Your leaky can slightly get up, but is constantly maintained at the level of arresting human potential by the sodium potassium pump.
Until we come to the stage when you have either acetylcholine comes in and a chemical gated sodium channel activated. The sodium started to rush in and because the end across the membrane that is a polariton one side, the significantly positive on the other side is significantly negative. Now, this polarity is not dropping, just the polarizing. So it's deeply polarized, the polarization is starting to finish, and it's getting the voltage to the equivalent on the zero.
However, it is a kind of fragmented time component into that until it actually get to all the channels get closed down. As you can see, the second gait of the sodium channel closes that lead to the potential much more positive and hence the inner gait of the sodium channel closes down. Then, because the gait channels are activated at the level of the zero, they started to actually start to become leaky.
When they become leaky, they lashes out, hence that they start regaining the polarity. Back in the system. And if they get down to the level of any of the testing on potential now at this level, we have got the biggest problem available to the cell that the whole polarity is completely reversed. Now there is a function of the sodium and potassium ATPase pump to regain that polarity back in position.
Hence, what the sodium potassium pump does is bring through the three sodium out and bring the two potassium in with every stroke of ATPase. And repeat it, the three sodium things for them out and bring the two potassium in, not only destroying the chemical gradient, but also getting the polarity back onto the track. Now, this is the diagram that you have to make it in the Viva.
So you started as a minus 70 because the skeletal muscle in the nerve, it is minus 90. It goes up to 55 is a threshold from where all this voltage gated open, they continue up to that level and you can see the down here, the membrane permeability of the sodium and potassium channels. At what level the activity and hence you, as I describe this happen. Another important concept and this is what is the absolute and what is the relative refractory period?
The definition of the refractory period is that the nerve fiber or the muscle cannot be reactivated during that phase. So there is absolutely no possibility of the membrane cell can be reactivated again, i.e. opening this voltage gated sodium channels until it regains its normal resting membrane potential. That's an absolutely effective period, the period between that potential action potential and another coming on action potential.
Is between that period is a relative, a relative reflective of where the sodium potassium pump is, try to regain the polarity back into the system here. There's very much possibility if of the impulse comes in, it can get activated. Now, once this information is arrive on the surface membrane, what actually happens, so this actually is like a roller coaster.
You start walking around on the surface of the membrane unless you're got a mile and sheet with it. Find the next available based on the surface membrane to jump. This is called tightly conduction. All of the action potential here. I to say that these are the kind. This is the muscle fibers you can see on the side, Colima or this or the muscle membrane. And then you have got a tip.
It goes right inside there. It's a big imagination of the surface membrane. You can see that there is actually is a sarcoplasm reticulum, which is collecting the calcium inside down there. It has got a calcium pumps inside. Now what happens when the sodium is get accumulated? The calcium channels are very small gated channels. They start bringing the calcium in the cytoplasm of the cytoplasm of the muscle.
You can see this actin mushroom filament are onto each other. And if you come down to it area and you can see this on the surface membrane of the plasma reticulum, how the calcium release is basically, when the calcium get inside the membrane, it attaches on the surface of the protein called this is slightly complex concept. Now this is for the 7 and 8. So the calcium comes in is actually attached to the protein and then it actually is done, though this also is the system.
The same system occurs in the vesicles as well synaptic vesicles as well. So this area is very important in the concept of how does the botulinum toxin work? So in the sign-ups, because the question comes inside attached to the classic Putin protein, and that brings a vesicle on the surface of it. If you provide onabotulinumtoxin around that area, it deactivate the system called synaptic Brevin protein complex, which is stop the vesicle to allow it to attach to the surface of that or allow it to release the vesicle into the system and into the sand and declare the same system actually works within the cytoplasm reticulum as well.
Now, this is how the botulinum toxin work. This is a sign up to con concept. Guys, this is a very complex area, but I'm just making simple for it that this is a sign up to Brevin protein complex, which attaches to the synaptic vesicle and does not allow us to chemical in to release acetylcholine in the system. Hence, the struggling cannot be released and it could get blocked completely.
Coming to the walk along theory or the other contraction theory there you have got you can see down here there's the acting job, which you described earlier on the effect of acting there comes down here and actually make these lists acting component and these are myosin chain. Now these are the light chain of the myosin, which actually make the myosin head.
And you remember I was talking about the calcium coming in addition to the top iron and steel making it a conformational change drag out of Mason away from the binding site, Mason head comes in contact attached to down that area and walk along the membrane. This is slightly more detail why what exactly happens? So basically the initial deployment comes down here, it can attach down to the 80 pump down area to the ATP, which is attached touchdown area Mason had contact the ATP converting to ATP and enter the phosphate molecule and then only the contraction happened.
The most important concept here is that until the ATP is not available, this myosin head will not come off. So if you have the ATP blockade anywhere, this will not detach from the myosin binding site. Hence, you maintain the tone without using any energy at all. So this is the best conservation of energy mechanism in a God has provided us.
So if our muscles are contracted, we maintain our torn off of a muscle by making the myosin head attached to it unless the ATP is not available. And it is ready to decompose or hydrolyze ATP in five. It will not let the muscle myosin to go away to the next slide. So that's how you maintain your tone. So anyway, ATP binds to Mason had the judges, there is a nesting component.
It comes actually down to the deep end, comes in at the next available myosin binding site that becomes available. The bison the light chains go in attached to the myosin binding site. And the ATP, tenotomy, ATP and pi. This Mason attaches to it and then the myosin head pivots and bends and allowing the ATP to buy component again, the process and constantly there.
Hence the whole walking along theory happen. And this is actually the way how it happens. Myosin climate action surface active binding site Mason head comes in attach. It hinges on ATP a system, and it does work along with every power stroke every time. Now, to describe this in the exam, I just made this little chart of flow chart where you can actually talk about in greater detail why, if you remember this chart, it tells you exactly what happens.
So that's all you need to remember for the photo to talk about the walk along theory. And this is another similar kind of a corresponding diagrams accordingly, so that you can make your like slightly more clearer. Now this is now coming to the clinical applications of these concepts. One of the concept is what is threatening.
The tenotomy is actually then you have got the hypercalcemia, so a lot of actually I was asking exam at some point when we are told how come the. Can get any happens via hypercalcemia. Make our muscles to go into a constant contractile stage. And that's why you actually got into the contractions. What actually happens in this picture, if you look at the sodium channels, they are negatively charged sodium channels.
It has got a question because they are negatively charged. A lot of them are lined by the calcium channels, the calcium molecules. Because these are lined by the calcium molecules, the space between them is very, very narrow to allow to sodium come in. That's a normal state. Of the girls. When the calcium goes down, this calcium would get mobilized out of these channels linings.
Making the hole much more clear than normal. Leading to the constant contractile states are constantly happening because calcium molecule is not making the channels narrow enough to close completely, so they constantly the voltage gated sodium channels become leaky channels and allow the contractile states to constantly happen. That leaves to constant contraction of the muscle and leads to tightening and hence the stimulated bull or hyper stimulant channels is available.
That's why you've got to gymnastics sign, which you tap the facial nerve and it contract and all that sort of signs for the hypercalcemia. Then comes another important concept refractory period, which you talk about myasthenia gravis is a condition where he's got antibodies against the colon is. The obstacle in this case is the enzyme which sits down the synaptic cleft here, where the acetylcholine is released in the system, in the cleft.
This is responsible to leave the acetyl and choline and get picked up back into the vesicle system. And that will. So you can see that process happening down that this area. So they constantly consumers. And that's what comes out in the system, and it just gets picked up by the going East and is designed to control.
This has actually been blocked by the antibodies which are working against going East and hence disease called Mason of the people who are actually about Bollywood. Amitabh bachchan has the myasthenia gravis is always on treatment for anti-coal. It creates enzymes for it. Botulinum toxin we talk about that does not allow the vesicles to come out, the other important concept is Duchenne muscular dystrophy.
How does the dystrophin protein is actually deficient to make the patients to go into the muscular dystrophy? Our skeletal muscle are connected by our activities, which are in the skeletal muscle. If you can see the effect and is connected to the dystrophin protein, which this complex, which is called dystrophin serko, Black and Black and complex, this is a glycolipid collects connected with a dystrophin.
So glycol collects is actually is a Y shape v-shaped glycoprotein, which which looks like a post on the cell membrane. This get connected with the dystrophin protein and that get connected with the activity of a filament actin, which is a part of the skeletal muscle. When this connection is destroyed, the dystrophin is destroyed. There is no ability of the skeletal muscles to anchored upon the cycling muscle membrane.
And hence, the muscle activity happened within the muscle. They cannot make the whole skeletal muscle and contract as one unit. This leads to this leads to the significant amount of the muscular insufficiency and hence the patients actually die at the age of 20 to 25 because there is they start losing their respiratory muscle slowly and gradually because of the abnormal gene mutation of the dystrophin protein, which is here.
So Glaxo collects dystrophin affecting. These are three things we have to remember this complex is destroyed because of dystrophin connection is not there. Muscle injury. This is the simplest you can actually tell your examiner, how does a muscle get injured and repaired? So the physical trauma happened, inflammatory mediators comes in exactly like a bone damaged several components, inflammatory cascade.
I'm just giving you a simple terms to talk about them reduces the proteolytic enzyme reactive oxygen intermediates leading to the ATP dependent failure. Failure of the mechanism raised intracellular calcium concentration. This is different in the muscle. So this system, which normally maintain the resting membrane potential down in the cell membrane enough, they're actually making the accumulation of the calcium within the system.
This calcium activates the enzyme like proteases, possible phospholipids and in turn, damage the muscles from within. This leads to the macrophage to infiltrate psychosis that damage protein muscle fibers, eventually leading to a deposition since the muscles do not regenerate. Only a limited amount of regeneration happen and the proliferation of the residual mild blast, which are very, very rare occurrence.
Coming down to the how can we detect a muscle injury? And what are the muscle components we do the imgs electromyography? In electromyography, you put the needle in the Allen, the nerve endings in the muscle, and you will get this potential. This is because of the way in a normal muscle you get this motor unit action potential.
When you have got a dinner, it no, you basically have got this what we call a simple tribal nations and we never did. Much like you get to see the complexity which comes each in this position and this sort of configuration. What actually happened in innovation, the spontaneous activity due to the increased sensitivity of the still cooling lead to the shock waves and hence in the chronically it becomes Kessler, which are uncontrolled.
Because now the muscle itself is actually becomes a center. It's leaking the sodium out, getting it activated by himself. Like when a heart actually is, when there's a heart block is there, the cardiac muscles automatically stimulate itself and try to contract. These are the first circulation in the skeletal muscle when this innovation happened, because there's too much acetylcholine is available, there's no nerve endings coming up from there.
It is not connected in acute denervation. There's a sharp face because all they're still available comes in one go and get activated chronic denervation, which has actually been the all antagonistic. And now the muscle become its own stimulant or the epitome of the whole havoc and the constantly contracting and try to become coordinated one when this muscle get to innervated.
There's initially there is a reduced amplitude modulation potential and you have got a larger, longer duration of the motor unit action potential. But because there's a poor recruitment of the muscle component with the amplitude the low. But in the data component, the larger amplitude comes in because now it is more stable, consistent firing of the action potential. And hence you get the recruitment of the unit, which gives the physics signals.
And the innovation is a physics signals in the late, more stable amplitude modulation unit action potential. You have got to Polish the signals, which tells you where the nerve is a more or less the basic sciences section should be like that we should be teaching. The examiner on the basic sciences section, I think that you covered that really, really well.
It's like you, you also did the exam. Nowadays they have to put the clinical components even in the basic sciences section. So I like how you showed us the clinical application of muscle physiology, a condition like detainee and may see a gravies and toxin injection and how they all work.
I just I have nothing to add nothing to. I just want to say if someone finds this difficult like me because it's very, very hard to and obviously sidebars, you know, approach this very well. Generally, stick to the principles, highlight the buzzwords, because sometimes what can happen is as we talk and we know what you're talking about, the examiners might switch off a little bit. So the buzz words, say them loudly, repeat them buzz words like sarcasm.
Basic contractile unit is a sarcoma. Um, talk about the action potential, highlight these words, the motor units, make sure that you let the examiner know about the resting potential, that there is resting potential and that there is a threshold and there is the gated channel and the gated channel open by acetylcholine.
Make sure these buzzwords are clearly transferred to the examiner. Yeah, these will get you out of jail in these questions, the buzzwords and we'll sort of pass you and then you can obviously use all this rest of this information to get higher marks. We will pay off. So thank you very much, sir.
This is a very difficult topic. You, you discussed and you explained it very nicely to us and we haven't covered in any previous teaching it. A lot of us when might find it difficult because we don't discuss this very much in meetings or in rooms or trauma meetings. So it is a dry topic, but you managed to make it very interesting. So thank you very much.
I hope for some potential the sarcomere. And I just want you to just remember now I think is unfortunately, this doesn't cover everything about the muscles. We still have the tendons, obviously the insertions of tendons, we have the topics of muscle contraction and things. So it's possibly another hour to cover the whole physiology about the different types of muscle, contractor, et cetera and then the open chain, closed chain and all of that.
So they can start from talking about basic science and then they move to physiology and then they move to physiotherapy. And then they can do that. They do that, and they do that. I mean, my question was about different exercises and types of exercises and in chain and all of that. So they can start from one end and move to the other. And also, yeah, the muscle metabolic systems and things like this, which side was touched on also.
Thank you. So I thank everyone again for attending. This will be the end of the presentation. Next is the Viva session. So we had the pleasure of having 59 of you registered today for the teaching. So thank you, everyone. Please get in touch with me if anyone's certificate. So we'll end the teaching now and the next will be.
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