Hello class, it's Professor Mariah Evans. This is BSC 2085, Human Anatomy and Physiology 1, and today we are going to talk about muscles. All right, so I posted an announcement for muscles with videos for muscle contraction. Muscle contraction is considered the sliding filament theory, and the reason why they call it that is because there is actin and myosin. Actin another name for it is the thin filament.
Myosin is the thick filament. And those two filaments actually slide past each other to get a muscle to contract. Now, there are four actions within that process of muscle contraction. The excitation, and that's because skeletal muscle must receive a nerve impulse. Okay, so excitation.
Then there's an excitation contraction. coupling, and that's because the excitation, it's going to be a neurotransmitter by the way, but the excitation that comes from the nerve cell now has to meet with the muscle cell, and that takes place at the sarcolemia, which is the membrane of a muscle cell. Then you get the actual contraction itself, and that is when the two filaments, actin and myosin, slide past each other, and then since muscles don't stay in a... constant state of full contraction, they have to relax. So relaxation is a part of the muscle contraction process.
So four actions and excitation, excitation, contraction, coupling, the contraction itself, and then the relaxation. Now, what I've done is if you purchase the book, if you have an ebook, or if you have the lab manual, or if you have a textbook. So remember our lab manual. and our textbook is written by the same author. And so in the lab manual, there's information about muscles and muscle contraction that would help you with lecture if you never purchased a lecture book.
But the reason why I'm saying that is, of course, I do my own PowerPoints, and I do them from, you know, the publisher, but I add my own things in here. So this is not in the textbook. So if you have an ebook, you are not going to find this.
I took this from something else and I liked it because it was step-by-step. So those four actions, the excitation, the excitation, contraction, coupling, the contraction itself, and then the relaxation, these are broken down into several steps so that you understand what's happening. So the first thing it says here is that this is the excitation. So step one, right, of this process. And it just says here that a nerve signal.
So if we read the bottom, like. like, you know, like it's a caption. And then we look at the picture, then we get an understanding.
And that's why I did these. And then I, of course, added videos as well in an announcement. So we get a nerve signal and that nerve signal stimulates voltage gated calcium channels. Now, my assumption is, is that you don't know what a voltage gated calcium channel is.
So I'm going to tell you, voltage gated ion channels, calcium or potassium or sodium or whatever, but voltage gated. ion channels are channels that don't open unless there's been a change in charge. And the way that a change in charge occurs is that we get a flow of ions across the cell's membrane.
So remember, we have two types of ions, cations, which are positively charged, and ions, which are negatively charged. So here we have calcium, and calcium is... diffusing into the axon terminal.
When it diffuses into the axon terminal, then it's going to cause this release of acetylcholine. So see this, it says an excitosis of acetylcholine. ACH is the abbreviation for acetylcholine. So these little tiny green dots that you see here, that is the neurotransmitter acetylcholine. Okay.
Now your question should be, well, now that calcium has diffused into the axon terminal. and it caused the release of acetylcholine, what is that acetylcholine going to do? Well, this is where we get to the excitation-contraction coupling, because it's going to bind to the sarcolemia of a muscle cell. Now, if you look here, you can tell that the sarcolemia is the cell's membrane. And the reason why is because it says sarcolemia.
And then if you look closely, what you see is the phospholipid bilayer. See the phosphate heads and then the two lipid tails? phosphate heads, two lipid tails. So this is the membrane of a muscle cell.
acetylcholine, so remember that abbreviation, ACH, acetylcholine bound to its receptor on the sarcolemia, and then what that did was it opened up voltage-gated ion channels. So, I'm sorry, not voltage, chemically-gated ion channels. Chemically-gated ion channels are a little bit different than the voltage-gated ion channels because chemically-gated ion channels will only open when a chemical, in this case, acetylcholine binds to the receptor. Now, what happens when this ion channel opens? If you follow the arrows, you'll see that potassium leaves the cell, and you'll see that sodium goes in to the cell.
So when acetylcholine binds to the sarcolemia, it opens up sodium and potassium channels. Sodium goes in and potassium goes out, and that causes an event to occur. That event is called an end plate potential. Now, I'm assuming that you don't know what an end plate potential is. So I'm going to tell you what an end plate potential is.
An end plate potential is a localized change in charge. So all that means is, is that the inside of the cells are what we call polarized. They're negatively charged inside.
And when ion channels open, the flow of ions can cause the inside of the cell, sorry. can cause the inside of the cell to become positive. So whenever there is a flow of positively charged ions to the inside of a cell that's negative, then the cell becomes positive, and that's called a depolarization.
That word depolarization is gonna come up a million times. Our cells have a resting membrane potential. That resting membrane potential is that cells are negative on the inside when they're at rest. When ion channels open and they become positive, then the cells are going to carry out some type of action.
And in this case specifically, this action is about to be the contraction of skeletal muscle cells. All right, so let's go back just for a second. I get calcium, which is positively charged, diffuses into an axon terminal, which is the end of a nerve cell. That causes the release of acetylcholine.
Acetylcholine binds to the sarcolemia. When it binds to the sarcolemia, it causes ion channels to open. Sodium comes in and potassium goes out, and it results in an end plate potential, which is a localized change in charge. That means right here, right here locally where the event occurred, the inside of the cell now is becoming positive.
Now, adjacent, that means next door, the ones that are close to, adjacent voltage-gated ion channels now open. So again, remember what I said about voltage-gated ion channels? They only open when there's been a change in charge, and an end plate potential is a localized change in charge.
So what happens is the voltage-gated ion channels that are close to where the event took place, the EPP, those open. So here it says, voltage change in that end plate potential opens up the... nearby, right, the neighboring voltage-gated ion channels.
And then they don't tell you, but I need you to know this, that causes more sodium to come rushing into the cell. And when that happened, it causes an action potential. Now, end plate potential was a localized change in charge.
That means it stayed close to where it was initiated. And action potential moves. So action, like it's on the go. And that action potential is headed somewhere, which is going to be this next part.
Because remember, we're talking about the contraction of the muscle now. So the action potential, it propagates. So it moves. And it moves down these T-tubules. That doesn't mean anything to you right now.
But T-tubules are where calcium is housed inside of muscle cells. And if you remember from the bone chapter. We know that calcium is so important, right?
We need calcium for skeletal muscle to contract, like here. We need calcium for nerve impulses, like the beginning of this, step one. We need calcium for our blood to clot.
We need calcium for cardiac muscle and smooth muscle, so all muscle, not just skeletal muscle. But we need calcium. We will steal calcium from our bones. because it's so important to other things.
So inside of the muscle cell, these T-tubules are holding the calcium. But when this action potential, which is a change in charge, when it propagates in them, it causes the calcium to be released, which should indicate to you that there is a voltage-sensitive gated channel that's holding the calcium. Remember, voltage-gated channels only open when there's a change in charge, and action potential just happens to be a change in charge.
and it's in change and charge that doesn't stay localized. It moves, okay? So now, oh, look, voltage-gated channels in the T-tubules causes calcium to be released. Now, question is, what happens to the calcium that's being released from the T-tubules?
Well, it binds to troponin, and troponin in this case is this little yellow type of, I don't know, it looks like a snowman with only two parts to it, but this is the troponin. And calcium binds to the troponin. And when calcium binds to that troponin, it causes this tropomyosin complex to open. And when the tropomyosin complex opens, we can see those active sites on actin. So it makes those active sites on actin available to react with myosin heads.
So remember I started this whole lecture saying that muscle contraction is the sliding filament theory. And I told you that actin, which is the thin filament, is going to slide past myosin, which is the thick filament. This is where we are now. We're about to have our contraction. The only thing is, is even though the active sites on actin are available, the head is not ready to bind yet.
So the head has to be cocked. I don't know if you've ever shot a revolver where you have to, you know, cock it back and then pull the trigger. So in order for myosin to react... with these active sites on actin we have to cock the heads and the way that we cock the heads is this enzyme that's called ATPase it breaks down ATP so if I break down ATP I break it down into ADP and pi and that's how I get my head cocking so here it says myosin ATPase so the enzyme that breaks down ATP which is attached to the myosin is going to hydrolyze or break down ATP, and it causes the head to cock. Once the head cocks, then it can bind with the active site on actin, and when actin and myosin come together, it's called a cross bridge.
So the formation of the cross bridge between actin and myosin takes place now. Remember, sliding filament theory. So I've attached the myosin head to the active site on actin. And the next step is going to be this power stroke.
The next step is going to be the pull where actin is pulled past myosin. So the power stroke happens to require ATP. So if you remember organelles, right, ATP, you'll say sometimes they say that the mitochondria is the powerhouse of the cell. So power ATP.
So the power stroke requires ATP. And luckily for us, we just... happen to have ADP and that inorganic phosphate.
And we add those back together, now we have ATP. So that's all they're showing is that ADP and phosphate, that was from this step here where ATPase broke it down, then they're going to join back together, and this is ATP, that breaks the cross bridge and pulls the power stroke, is pulling the actin past the myosin. So that power stroke is the...
actual contraction. It's the sliding of myosin, the thin filament over, excuse me, actin, the thin filament over myosin, which is the thick filament, okay? Now, there are in this picture just one myosin head, and you can see the active sites of actin, but the reality is that we have, oh my gosh, it's just so many, millions, trillions, bazillions, I don't even know how many, but we have... so many of these myosin heads and we have all of these active sites on actin that if I'm trying to get a muscle to contract, I get head cocking when ATP is broken down into ADP and pi.
And then I get the cross bridge when the head of myosin attaches to the active site on actin. And then I get the power stroke, which requires ATP, right? So pulling actin past the myosin.
And then I get this millions of times because there are millions and millions of heads and millions and millions of active sites on actin. So if they all attached at one time, meaning if all the myosin heads attached to the active sites on actin all at one time, and then they all let go at one time, the filaments would just slide back to where they were. So at any given time, half the heads are attached and the other half are free so that they don't slip back past each other. All right.
Now, if I go through all of these actions, and I'm going to say it because it's redundant. but I'm going to say I get my head cocking, my cross bridging, my power stroke, and that pulls actin. Please make sure you guys watch the videos. Then I get another head cocking, cross bridging, and pulling of actin, and another head cocking, cross bridging, and pulling of actin. Eventually, the muscle is fully contracted, which means actin and myosin have been slid past each other, right?
Slid past each other to their furthest degree of overlap, and the muscles contracted completely. But muscles don't stay in a state of complete contraction. As a matter of fact, we have a vaccine against that very thing. Tetanus, which is sometimes referred to as lockjaw, that's when you're in a state of continuous muscle contraction. We call them spasms, and that could actually cost you your life.
Okay, so muscles don't stay in the state of complete contraction. Okay, so we need to relax. And since this whole thing, muscle contraction model, since it started with calcium diffusing into the axon terminal and causing the release of acetylcholine that opened up the ion channels that let sodium come in and potassium go out, which gave us an end plate potential, which was a localized change in charge then. opened up voltage-gated ion channels that were next to it. Then that initiated an action potential.
An action potential is that moving change in charge, and it propagated down the sarcolemia and into the T-tubules, causing the release of calcium. Then calcium bounded the troponin, caused the tropomyosin complex to open, revealed the active sites of actin, so it can react with myosin heads. But we had to cock the heads first, so ATP... ACE broke down ATP, head cocking, cross bridging, power stroking, and that goes on and on and on and the muscles contracted. But the whole thing started with acetylcholine binding to the sarcolema and opening up those ion channels.
So look what relaxation. There's two parts to relaxation. One of them is we have to degrade that acetylcholine. So acetylcholinesterase is the enzyme that breaks down acetylcholine.
And when it breaks it down, it closes the ion channel. When the ion channels are closed, that means no more sodium is going to be coming in. No more potassium is going to be going out, right?
So acetylcholinesterase is going to degrade acetylcholine and close the ion channels. And that's this picture here, right? Acetylcholinesterase degrades acetylcholine, closes the ion channel.
The other thing is we need ATP. We need ATP for muscle relaxation. And that sounds confusing. You're like, wait, ATP, energy for it to relax?
Yes, because ATP is needed to actively transport calcium back down into the sarcoplasmic reticulum. And once it does that, it's been removed from the troponin. So then that tropomyosin complex goes back to covering the active cyzonactin. So this is the calcium being removed from the troponin, being active. actively transport it back down into the sarcoplasmic reticulum.
And then the tropomyosin, which is like this kind of light teal green piece right here, this goes back to covering the active sites on actin. If the active sites on actin are covered, that means they can't react with myosin heads, which means the muscle can't contract anymore. So that's muscle relaxation.
Loss of calcium, right, results in the tropomyosin complex going back and covering. the active sites on actin, then the muscle fiber returns to its resting length, relaxation. Now, here's the kicker. This is the most, in my opinion, this is the most complex of the material that we've had thus far. But I'm telling you now, in order to do well on exam three, you really do have to understand that and or understand this, this muscle contraction.
But I also want to make a promise to you. When you learn and understand what's happening here with the voltage-gated ion channels, the release of acetylcholine binding to the sarcolemia, opening up chemically-gated ion channels, causing that localized change in charge, which then opens up voltage-gated ion channels, which causes an action potential, then you'll understand reality is this. You will understand a bunch of systems in the body. Because this is muscle contraction.
And we have cardiac muscle, smooth muscle, and we have, of course, skeletal muscle. So when we start talking about the digestive system and you are propelling food, it's going to be the contraction of smooth muscle. We have longitudinal smooth muscle and we have circular smooth muscle. And they alternate back and forth to propel food through these hollow organs that we have.
That's smooth muscle contraction. You have to learn how the heart works, right? Heart is a muscle and it also has actin and myosin, just like smooth muscle has actin and myosin. And so remember this class is anatomy and physiology.
So once you understand the physiology of muscles, right, how muscles function, you're going to apply this that I'm teaching you right now about ions moving across membranes and about cells becoming depolarized and causing... actions to occur, that's going to be applied to everything that comes after this. Everything.
It's even going to be applied to nerve impulses. And that's because calcium, which was positively charged, diffused into the axon terminal. And the axon terminal is the end of a nerve cell.
And all cells are negative at rest. So this, which sounds very complicated, and it is, is going to be applicable to... every single physiological process in the body, every single one. Okay. Now let's talk about application.
So we know that we need acetylcholine for muscles to contract, right? That's the neurotransmitter that started the whole thing, bound to the sarcolemia, opened up ion channels. So there's pesticides. And if you're a cruel person like I am, and I admit it, I am a cruel person. When we have a wasp or a hornet's nest, I get rayed.
wasp and hornet spray. Don't get that off-brand stuff. Get Raid. I'm just, I'm not trying to advertise for any particular thing.
I'm just saying I tried other stuff. Raid works. So if you're like me and you're cruel about this, you read it, you know, and it tells you that you shouldn't, you know, stay around and, you know, you stand a certain distance and you spray it and then, you know, you leave the area. Well, I like to watch them die. I know.
I'm telling you, it's cruel. So If you've ever watched them, though, it's interesting. And I'm about to make a correlation for you. So pesticides have acetylcholinesterase inhibitors, okay?
So if I inhibit acetylcholinesterase, which is the enzyme that breaks down acetylcholine, then that means that they are going to, and this being the insects, they are going to go into a state of constant contraction. which means they're going to have spasms. So if you've watched them, you sprayed them, they hit the ground, they go, and they die. And you know, I'm telling the truth if you've ever watched them. So basically what we did is we gave them a neurotoxin.
We, you know, put them in spastic paralysis and it caused their death. It's so bad, but yes, so spastic. paralysis. Death.
Okay. Now tetanus, I talked about that earlier. We get a vaccine for it because it's deadly.
So tetanus is caused by a bacterium, which is called clostridium. Clostridium tetanii is the whole name, but clostridium. And basically what this does is that this causes an overstimulation of your muscles.
So the toxin that's associated with it causes an overstimulation of your muscles, which means you are again in a state of spastic paralysis, right? Over stimulation. That means you're in a state of contraction. You can't relax. And yes, you can die from that.
Just thought I'd put it out there. Then we have flaccid paralysis. And if spastic paralysis is when you're in a state of continuous contraction and can't relax, then flaccid paralysis would be when you're in a state of constant relaxation. And that means your muscles are unable to contract.
So flaccid paralysis is... gives you limp muscles. Now, if you've ever had back spasms, and I've never had these, but I've heard people say that they get back spasms and that they hurt really bad. And I know you guys know, even if it hasn't happened to you, when a person is having back spasms, they are given muscle relaxers.
listen to that name, muscle relaxers, because the muscles are in a state of contraction, which is painful. So muscle relaxers, some of them have this active ingredient called carari. And what carari does is it competes with acetylcholine for the receptor on the muscle cell. And if carari gets there first, then acetylcholine can't bind.
And if acetylcholine doesn't bind, then your muscle doesn't contract. And in the case of having spastic, you know, problems in your muscle spasms in your back, being able to relax your muscle is what gives you the relief. Isn't that neat? So Kurari competes with acetylcholine and it binds to the receptor first, prevents acetylcholine from binding, and it relaxes your muscle.
Kurari, muscle relaxants. Okay, now that membrane potential. So when I go through the... the whole muscle contraction model, I explain, you know, parts of it while I'm, you know, talking.
And so I've already told you that at rest, right, cells are polarized. That means that they are negatively charged inside. And the reason why they are polarized is that they have a concentration of potassium and sodium on the inside and the outside, and it's different. So we call sodium the major intracellular cation.
That means that sodium is in high concentration inside of the cell. We say, I mean, sorry, potassium is a major intracellular cation. So potassium is in high concentration inside of the cell. Sodium is the major extracellular cation. And so there's more.
sodium outside, extracellular outside of the cell. So the resting membrane potential is due to those ions, right, in their concentrations outside of the cell. So it says that the inside is negative 90. You do not have to remember that number, but you do need to remember that the inside of cells are negative when cells are at rest.
So remember when I said an end plate potential was a change in charge? And I said that that change in charge occurred when sodium came rushing into the cell and potassium was leaving and it became, ready, depolarized. These are those terms and they're coming up again. So the inside of the cell is negative. When they're at rest, that's all cells.
That's muscle cells. That's heart cells. That's, you know, every cell that you can possibly think of. Neurons, which are nerve cells.
All cells are negative. on the inside when they're at rest, okay? Now, it says here that when we open up ion channels, sodium can come in and potassium can go out, and this changes the voltage, so change in charge, and it can cause, as we know, an action potential because, and I'm just going to repeat it so that you can hear it over and over again, calcium diffused into the axon terminal, which was the end of a nerve cell.
That caused the release of acetylcholine. Acetylcholine bound to the sarcolemia and then opened up ion channels that caused sodium to go in and potassium to go out. That was an end plate potential, which means right there at that event where those ion channels open, the inside of the cell became positive. So it went from negative to positive.
That's that change in charge. Then nearby, neighboring. adjacent, whichever word works best for you, the voltage-gated ion channels that were close to the end plate potentials event, those opened up and more sodium came rushing in and it initiated an action potential. The only difference between an action potential and an end plate potential is that an end plate potential stays put.
It's just localized. It can't go very far from its point of initiation. but action potentials can.
So they move, they propagate, and an action potential propagates down into the T-tubule, causes the release of calcium, calcium binds to the sarcolemma, and I mean, sorry, calcium binds to the troponin, causes the tropomyosin complex to open, reveals the active sites on actin so that they can react with myosin heads. But I have to cock the heads first. So ATPase breaks down ATP, and I get head cocking, cross bridging. That's when the myosin binds to the active site on actin.
And then I get the power stroke. And that power stroke requires ATP. And luckily for us, we just happen to have ADP and pi right there.
And we bring them back together. It's ATP. That's muscle contraction.
And then I need the muscle to relax. So acetylcholinesterase degrades acetylcholine, causes the ion channels to close. No more sodium goes in. No more potassium goes out. Then I have to actively transport, which means I need.
ATP. I have to actively transport calcium back down into the sarcoplasmic reticulum, which is part of the muscle cell, back down into the sarcoplasmic reticulum. And then the tropomyosin complex closes and it covers the active sites on actin and the muscle goes back to its resting length.
Okay. The more you go over it, the more it's going to make sense. The more videos you watch.
And like I said, I provide it too for you guys. But the more videos you watch, the more sense it's going to make. But please, please, please understand, you're going to have to understand that muscle contraction model to do well on exam three. And I'm going to go back and reference the muscle contraction model to everything that comes next in the rest of this class. Okay?
All right. So now there's three types of muscle tissue. Oh my gosh, this is a shocker.
There's skeletal muscle and cardiac. muscle and smooth muscle. There's prefixes that help you know that we're talking about muscle. So myo, mis, and sarco. So remember that sarcolema was the membrane of a muscle cell.
Now, skeletal muscle is where, you know, it's attached to bones and it's voluntary, right? So we move that. It's also striated, which you guys know because you've seen it in the lab.
It contracts very fast, which means it can also get... tired very quickly. And skeletal muscle is really strong, like powerful, and it requires nerve stimulation. You know, like for example, calcium diffusing into the axon terminal, axon terminal releasing acetylcholine, and acetylcholine binding to the muscle cell's membrane, the sarcolemia, right? So it requires a nerve impulse.
Cardiac muscle is also striated, you know, like skeletal muscle. But it's involuntary, unlike skeletal muscle. And it can contract without the nervous system stimulation. It can contract without it.
And then it says more details when you get to 2086. Chapter 18 is 2086. Okay, then we have smooth muscle. Smooth muscle has no striations. Smooth muscle can also contract without nerve stimulation. And smooth muscle, like cardiac muscle, is involuntary. So you don't control, you know, how food flows through those organs when we talk about the digestive system earlier.
So the stomach is an example, your urinary bladder is an example, your airways. So like breathing those things, you don't control that. It's smooth muscle. It's involuntary.
And then here are pictures. Oh, look, skeletal muscle has striations. And then look, cardiac muscle also has striations and intercalated disc. And then there's smooth muscle, which doesn't have striations. Now, this stuff right here is the anatomy of the muscle cell.
It gives you an idea, of course, because you guys know the class is anatomy and physiology. It gives you an idea of the structure of muscle, and then it helps you kind of understand how it works. So this is me trying to, I guess, explain.
So the peristeum is the outside covering of bone. And this right here, epimysium, is the outside covering of bone. muscle. Then we have paramyceum, which surrounds what we call fascicles.
And what fascicles are, are they are bundles of individual muscle cells. And then so each muscle cell, sorry, each muscle cell has a covering around it, and that's called endomyceum. So endomyceum surrounds each individual muscle cell. A bundle of muscle cells is called a fascicle, and that has a connective tissue called the paramyceum.
And then several muscle fascicles make up the entire muscle, and the epimysium is what is the connective tissue around that. Now, down here, they're going to magnify this in a picture or two, but down here is the sarcoplasmic reticulum. Remember, sarco means muscle. And then these are the T-tubules. We've already talked about these because why?
Calcium, right, is in the T-tubules. And then when ATP comes on, it... pumps the calcium back into the sarcoplasmic reticulum.
And FYI, the sarcoplasmic T-tubules are part of the sarcoplasmic reticulum. This right here is just a little comparison. of skeletal muscle and cardiac muscle and smooth muscle. I do want you guys to know, of course, that skeletal muscle is voluntary and smooth muscle and cardiac muscle are both involuntary, of course. They all have actin and myosin.
So the sliding filament theory is applicable to all muscle, whether it's skeletal, cardiac, or smooth. Okay. And they function a little bit differently, but we'll talk about their...
their function, like how we get smooth muscle to contract. We'll talk about that later. All right. So now these are some characteristics that muscle tissue exhibit.
Excitability. So that means that skeletal muscle can respond to a stimulus. Contractility.
That literally means that it can shorten. Like when the actin and myosin slide past each other, the muscle contracts and it becomes shortened. Extensibility means that it can stretch. And the good thing about stretching muscles, especially if you've overstretched a muscle before, whoo, give it some rest, right? You rest and then it goes back to its normal length.
That's called elasticity. So muscles can stretch. That's extensibility. But they're supposed to go back to their normal length. And that's the elasticity.
So recoiling, going back to their normal resting length. Now, the functions of muscle is that they cause movement, right? Because our...
muscles are attached to the bones, right? And so we move our bones, that's movement. But we also use muscles for stabilizing our joints and we also generate heat with our muscles and then our muscles help us maintain posture in our body position.
Additionally, muscles form valves and protect organs and control our pupil size. So if you get really excited, you have these dilatory muscles in your eye. And your pupils dilate.
So when you get excited or you see something that's aesthetically pleasing, your pupils get really big. And then we have erector pili muscles. And erector pili muscles are the muscles that give you goosebumps. And I mentioned erector pili muscles in the integumentary system lecture.
All right. So now, things we know because of the muscle contraction model. We know that muscles need energy. right?
So they have to have a lot of energy. We also know that they're supplied by a nerve, right? A nerve impulse. So in order to get skeletal muscle to contract, a nerve impulse has to come in, okay?
Now, when you look at these, I showed you in a picture and then there's going to be a bigger picture that comes up for it. But this right here is the epimysium, which I said is that outermost covering of muscle. And then I told you that the paramyceum is going to be covering fascicles. And then I explained to you that fascicles were bundles. They call them groups, same thing.
So bundles are groups of muscle fibers. Muscle fibers are muscle cells. The only reason why they call them fibers is because the cells are really long. So it's a muscle cell. It's a muscle fiber.
Those are synonymous with each other. So a fascicle is a bundle of muscle fibers or muscle cells. And then it has this connect. tissue around it called paramyceum. And then around each individual muscle cell or muscle fiber, then we get the endomyceum.
And then they give you a larger picture of what I talked about earlier. So this is the connective tissue around the entire muscle in here. And they pulled one out like a fascicle, but these are several fascicles that are in here.
So around the fascicle, that's where we get the paramyceum. And a fascicle is a bundle of muscle fibers. So then they pull out an individual muscle fiber or muscle cell, and then they show you that there is a connective covering around that one, and that's endomyosin. So endomyosin here, paramyosin here, and then epimyosin here. Okay.
Now, we know that muscles allow us to move. Skeletal muscle, right? So we have the attachment in two places of skeletal muscle to the bone.
The insertion point... is at the movable bone. And the origin is either immovable or less movable. And then they can either be directly attached, and this means the muscle to the bone directly, or it can be indirectly attached, which means that it could be attached to like a tendon.
And you guys know your Achilles tendon. It actually takes the calcaneus, which is your heel bone, which you're learning in lab. The calcaneus... is your heel bone and your Achilles tendon attaches the calf muscle to the heel bone.
And it's sometimes the Achilles tendon, its real name is the calcanean tendon. No, so calcanean, like calcaneus. Anyway, so that's an indirect attachment.
If it's a direct attachment, then the epimysium, which is that outer covering of the muscle, is going to be fused with peristeum, which would be the outer covering of bone, or perichondrium, which is the outer covering of cartilage. That would be direct. So the outside tissue of muscle being bound to the, or fused to the outside tissue of cartilage or... the outside tissue of bone.
That's direct. Indirect is like our tendons or aponeuroses, which is a sheet-like connective tissue. It's kind of cool. All right.
And so this is, again, just those fibers. So epimysium, endomysium, paramysium, et cetera. All right. So now, well, let me go here first. So this is a muscle cell.
So this is a muscle fiber. That's the nucleus. And then you guys, of course, can see those stripes, I hope. So the striations that are in there, things we already know that skeletal muscle is striated. So you see this little bracket that they have here and they say that this is a sarcomere.
Well, the sarcomere is the contracting unit of a muscle cell. And since it's a contracting unit of a muscle cell, it would make sense that actin and myosin is in there. And it is. So they're going to magnify that for you. So a sarcomere.
runs from one Z line. Sometimes it's called the Z disc, but see how this goes zigzag where I'm following my arrow? So that's one Z line or Z disc. Here's another Z line or Z disc.
So from one Z line to another Z line, that's a sarcomere. So that's the contractile unit. Now within that contractile unit, like I said before, it's going to be actin, which is that thin filament. and myosin, which has the heads on it.
So then they magnify them so that you could see them, all of these heads on myosin. And then here's actin with the active sites. If you go back to the muscle contraction model, they show you in the picture, just one, right? One myosin head that is going to be cocked when ATP breaks down ATPase, or excuse me, when ATPase breaks down ATP into ADP and pi.
So you get head cocking, and then you get cross bridging. And that cross bridge is when the myosin head comes in contact with the active site on actin. And then the power stroke is when the myosin head pulls the actin past it.
So see all these heads? This is what I was saying before. See all those heads that are there and see all those active sites on actin? And this is just one row of myosin and one row of actin.
Look how many there are in one sarcomere. And then there are millions and millions of sarcomere in each of the muscle fibers. So it's really cool.
All right. So we already know the sarcolemia is the plasma membrane. So it's the cell's membrane. The sarcoplasm is the cytoplasm of a muscle cell.
So remember that prefix sarco means bone. I'm sorry, it means bone, means muscle. And then we have glycosomes, which store glycogen. And glycogen is...
just a bunch of glucose molecules that are bonded together with glycosidic bonds. And if we break them apart, that means we can get glucose and energy. Well, no way. And then myoglobin is how we store oxygen in muscle.
It's myoglobin in muscle, hemoglobin in your blood. I know. How cool is that? Anyway, and then there's some other things like the sarcoplasmic reticulum. So that's the SR.
And then those T-tubules, which we know have the calcium in them. So this is me telling you about the sarcomeres already, right? It's the contractile unit that is in the muscle cell. And the fact that you see skeletal muscle as striated is because of the dark bands and the light bands. So the A bands and the I bands are dark bands and light bands.
So it goes dark, light, dark, light, dark, light, dark, light. So you see stripes in it. And so look, dark, light, dark, light, dark, light, stripes.
Skeleton muscle is striated. Now, here's that Z disc. Notice how there's some things I'm not mentioning.
So work with me here since I write my test. So here's the Z disc or that Z line that I talked to you guys about. This is what separates the sarcomere.
So I go from one Z line to another Z line. And that's what they say down here. The sarcomere is between two successive Z discs or Z lines. And then we have the thick filament.
which you know is myosin because I've mentioned it. And we have the thin filament, which is actin. And then they explain to you how they run so that you can see.
that they are partially overlapping each other. So that's why I say when actin and myosin are pulled past each other to their furthest degree of overlap, the muscle is contracted. And that's because within the sarcomere, within the sarcomere, they're already overlapping.
See that? They're already overlapping. But when they get to their fullest degree of overlap, and that would be myosin pulling the actin past it, then these Z lines are going to be brought closer together, right?
And the muscle would be fully contracted. Okay, so let's see. So the sarcomere contracting unit said that.
Okay, so animated picture. I didn't have to go back. It was coming up.
Anyway, so the A band is the dark band. The I band is the light. So that's why it looks striped.
So light, dark, light, dark. And then this is the Z line or the Z disc here and here. So that means from here to here. is a sarcomere. The thick filament is myosin, which they mentioned, and I've mentioned already, thick filament is myosin, and the thin filament is the actin.
And then, of course, another magnified picture of actin and myosin, the Z-disc, and a sarcomere. Okay, now, oh, look what it says. Actin is the thin filament, and myosin is the thick filament.
Oh, no. Okay, myosin, the thick filament, it has heads on it. No way.
Anyway. It does have TELs too, and it's not that they aren't important, but it's the heads that bind to the active sites on actin that cause the cross-bridging to occur during contraction. The other thing about the heads, and again, if you think about the muscle contraction model, these are things you know, the heads, right, are going to bind to the active sites on actin.
The heads also have a binding site for ATP. Remember, ATP is ADP and pi together. The heads also have an ATPase enzyme.
It's because this ATPase has to break down the ATP to get the heads to cock in the muscle contraction model, which we talked about already. And then we have the thin filament. And, you know, this is kind of cool how it's twisted together and great.
But this is the important part to me, you know, the stuff down here that's bolded. So this tropomyosin and troponin complex is attached to actin. And this troponin is where the calcium binds. Calcium binds to troponin and causes the tropomyosin complex to open, reveals those active sites on actin so that they can react with the myosin heads. And then we can get the muscle to contract.
So then, of course, again, they just show you actin and myosin. So the thick filament is myosin. The thin filament is actin. Myosin has heads. troponin and the tropomyosin.
Okay, now the sarcoplasmic reticulum is basically the cytoplasm of a muscle cell because endoplasmic reticulum, cytoplasmic reticulum, right? So sarcoplasmic reticulum. And those T-tubules are part of the sarcoplasmic reticulum and the T-tubules have the calcium. So intercellular means we're inside of a cell.
What type of cell? A muscle cell. And lo and behold, calcium is needed for muscles to contract.
So let's think about what happens. Calcium diffuses into the axon terminal, causes the release of acetylcholine. Acetylcholine binds to the sarcolemia, opens up ion channels. Sodium comes in, potassium goes out, and causes an end plate potential. An end plate potential can be described as a localized change in charge.
That localized change in charge then opens up neighboring, nearby, adjacent, whichever word you prefer. voltage-gated ion channels, and that lets more sodium in. And then when that happens, it initiates or causes an action potential.
An action potential is similar to an end plate potential in the fact that it is a change in charge. However, end plate potentials are localized, and action potentials get to move. So this action potential moves down the sarcolemma into the T-tubules, causes the release of this intracellular calcium. Then calcium binds to the troponin, causes the tropomyosin complex to open, reveals the active sites on actin so they can react with myosin heads.
But the heads aren't ready yet. They've got to get cocked. So ATPase breaks down ATP into ADP and pi, so P sub i, which is inorganic phosphate.
And then I get head cocking, cross bridging, which is when the myosin head actually binds or connects to the active site on actin. And then I get the... The power stroke.
The power stroke is when myosin pulls actin past itself. And that keeps happening until the muscle's fully contracted. How cool is this crap?
Love this stuff. All right. Hey, guess what? The T-tubules are continuous within that, you know, sarcolemma.
That's cool. They're showing you the picture here so that you can see the sarcoplasmic reticulum. Then you can see the T-tubules that are in there.
We already know that the T-tubules are going to release the calcium. If you look here, they're showing it like they removed the sarcoplasmic reticulum so that you could see. But right here is my... sarcomere.
This is my contracting unit. Remember from Z to Z, this is my contracting unit. Here is my actin and my myosin.
And then here are my T-tubules within the sarcoplasmic reticulum. So calcium's released and binds right to the regulatory protein. So troponin causing the tropomyosin complex to open. Now, things that you know, and I know it sounds silly because I'll say this a lot.
Things that you know, since we talked about the muscle contraction model, you know that a nerve cell was right there at the muscle cell, right? Because the acetylcholine released, you know, from the nerve cell and then bound to the muscle cell. The place where a nerve and a muscle come together is called a neuromuscular junction.
Let me get this straight. The place where two things come together are named for the two things that come together. What?
Who knew? Neuromuscular junction. Now... This is going to look familiar because this is how we started off the lecture.
So they magnified it. This is the axon terminal, and this is a muscle cell. And then they magnified it so that you could see calcium going in, right? Calcium goes in, causes the release of acetylcholine. So these green dots are acetylcholine.
When acetylcholine binds to the sarcolemia, so this is the muscle cell, it says sodium goes in, if you follow the arrow, right? Sodium goes in and potassium goes out. That causes that end plate potential.
They also mention here, and I'm not mad at them for doing it, but they also mention here that acetylcholinesterase can break down acetylcholine. And when it breaks down acetylcholine, it's going to close the ion channel, which we know because that's what has to happen for the muscle to relax. Oh, bigger picture. Here is acetylcholinesterase breaking down acetylcholine. So acetylcholinesterase breaks down acetylcholine, closes the ion channel.
No more sodium can go in. No more potassium can get out. They tried.
They tried, but it didn't work. All right. So at the neuromuscular junction, what do we have there?
Axon terminal, the end of a nerve cell. Acetylcholine is the neurotransmitter that's going to be released. It binds to the sarcolemia, which is on the muscle cell. I know, I know, things you already know.
So it says here that that acetylcholine is going to be released. Then it's going to cross this cleft, like a cliff is going to cross a cleft. It binds to the sarcolemia. Then we get the electrical events.
They're not being specific here, but, you know, the movement of those particles. So we're going to get the movement of those particles that generates that action potential, which is the, you know, moving change in charge that goes down into the T-tubules. Then, oops, sorry. So then we already know, hold on one second.
I'm so sorry. I'm sorry, I'm trying to pause the recording.