Insights on Muscle Physiology

So obviously skeletal, cardiac, and smooth muscles like nervous tissue, these tissues are able to change their membrane voltage and we're going to look at how they do that and what that then causes, how that causes changes instead of their behavior. We're not going to really do a whole lot with smooth muscle but we will get into more specific details about cardiac muscle. and the action potentials that occur in the SA node and in the myocardium itself in Unit 4 after break. Some important terms related to skeletal muscle cells. Okay, make sure you know what the term, what I mean when I say muscle fiber. That's a cell because it's long, they're elongated. And during embryonic development, they start as very, very small cells that fuse together. to form these very very long cells that's why they have many nuclei per cell and those cells that they're derived from are called myoblasts there's some terms there you need to be aware of as they relate to muscles and muscle cells terms that were in your packet sorry in the in the book so they go on and talk about cellular structure the connective tissue structure i am really not all that concerned that you know those connective tissue that are part of a muscle as an organ. So the epimysium, the paramysium, and endomysium, I'm not real concerned about that. We're focusing on the physiology of the fiber itself and what happens to cause the contraction, ultimately shortening that organ muscle as an organ. So some terms. Thin filaments and thick filaments. I would imagine you probably talked a little bit about that in Biology 152. Did you use those terms at all? Okay, so we're going into the details this semester. Okay, I guess I'm not going to be writing on the screen today. So I want to make sure that you understand that when we talk about the thin filament, sometimes it's referred to as actin, but that's one component of it. The thick filament is myosin. And when we look at a myosin molecule, I'm going to have to use my pencil here, my regular mouse. is that myosin is the thick filament but there's kind of some multiple parts and you can see that the thick film has these little what we call cross bridges these little heads that come off there it's kind of like two golf clubs with the golf club shafts intertwined and they're what we call the heavy chains and the light chains of light chains you might have heard a term similar to that before Remember when we talked about the beta receptors and beta receptors are inhibitory and they adenylate cyclase stimulates the production of cyclic AMP. And what did I say that cyclic AMP did, Justin? It's going to inhibit what's called myosin light chain kinase, which is an enzyme that adds a phosphate to the light chains, which then stimulates the contraction. of those. Well, this occurs in smooth muscle, but it's very similar. Okay. Anyway, so you've heard that term before. So all those are part of it. And when the myosin head contracts or when the, yeah, I guess when the myosin head contracts, it's going to pivot at this little pivot point down here. All right. And that's when we get into what's called the sliding filament theory and how the sarcomere shortened. I believe for homework I assigned some labeling exercises and one of those was a sarcomere. So if we look at this diagram here, while it's not listed under terms, you do need to be familiar with the sarcomere and the parts of the sarcomere because it does relate to what happens during contraction. That sarcomere is going to change. One of the key things about muscle contraction Skeletal muscle contraction, especially, is that the cells get shorter when they contract, but the individual proteins don't change their length. Now, those thick and thin filaments are... called myofibrils, grouped together into what we call myofibrils, little bundles of filaments. So myofilaments and myofibrils are different. The fibril would be a bundle of thick and thin filaments. And that sarcomere shortens. And what we'll see is that that H zone is going to get smaller because these thin filaments slide over. the thick filaments. See if I got a picture somewhere. Yeah, so I know I'm getting ahead, but ultimately what happens is when those cross bridges cycle, which is something we're going to talk about, notice how the length of the sarcomere changes. The proteins aren't getting smaller, the sarcomere is getting shorter because we're overlapping. Okay, we're overlapping. We'll get to all that. So some terms related to the thick and thin filaments, specifically cross bridges, regulatory proteins, and contractile proteins. Do you remember troponin and tropomyosin from biology 152? No? Okay. Well, let's talk about it then. I'm sure you read about it. So when we look at that thin filament, we have these little globular proteins called actin that form and join together to form like a string of beads. In fact, it's really like two strings of beads that are kind of intertwined and twisted together. Also, part of this thin filament are two regulatory proteins, tropomyosin And troponin. Troponin is actually a calcium receptor. Please make a note of that. That's really important. Troponin is actually a calcium receptor. You haven't read about that yet. The other is called tropomyosin. Tropomyosin is the blue one in the picture. It's a long fibrous protein. It is physically connected to the troponin and its job is to cover up what we call the myosin binding sites. Let's jump ahead real quick to this picture here since we're talking about it. Page 139, slide 21. So you can see larger now that there's troponin, the tropomyosin, and see on those actin filaments, those little spherical globular things, there's that little dark spot kind of in the middle. You can see on my hand-drawn diagram here, that is what we call the myosin binding site. If I can... Try this. I feel helpless without being able to write on the screen. Well, maybe this is why. Because I didn't... click that? I don't know. Nope. So what I've drawn on the bottom then would be just those actin proteins without the tropomyosin. So it would look like this. If this red line represents the tropomyosin, notice how it's covering those binding sites. So these little circular are the myosin binding sites. Yeah. There are some molecular forces that are holding the tropomyosin to the actin, but at the same time, if you look at the troponin, there's three proteins to troponin. One is connected to tropomyosin, one is connected to the actin. And when calcium binds to this, it stimulates a change and it causes this, and I don't know all my physics, but it creates a pulling action and it's going to pull that tropomyosin away from those binding sites. So you would get something like this. So the tropomyosin is kind of held by intermolecular forces and by the troponin, but it's loosely held because we need it to be able to shift away. So again, myosin binding site. And remember on the thick filament, they had those little golf club heads, the cross bridges. Well, what happens is those will actually reach up and form a bond with that myosin binding site on the active. I'm getting a little ahead of myself, but that's what the purpose of those myosin binding sites are. Now what happens after that, I'm going to save. Maybe we'll get to it today, maybe not. So the role of troponin is to act as a calcium receptor. When it changes its shape, it's going to pull on the tropomyosin, shifting that tropomyosin out of the way. And I will repeat this. We're going to look at this again. So that's what I mean by regulatory proteins. Because if we don't move the tropomyosin out of the way, we can't have muscle contractions, skeletal muscle contractions. And then the whole purpose is to shorten that sarcomere. Now this would be a cross-section through a myofibril. And within that myofibril, we have the individual myofilaments, the little purple ones. are the thin filaments and the other ones are the thick. And they kind of form this hexagonal arrangement and all the myosin heads would be kind of around those like in a spiral. In fact if you look at the picture just above of the thick filament you can see those myosin heads are kind of spiraled around and notice the angle of orientation. You got some of these myosin heads that are kind of pointing this way and on the other side of that M line they're pointing the opposite direction because what happens in contraction is that those thin filaments slide inward over the thick and so those cross bridges have to be positioned in such a way that when they pivot so the cross bridges that's not a good one That's not a good one either. They have this pivot point, kind of this here. And what's going to happen is that myosin head, when it's attached to the thin filament, is going to move on both sides, and that's going to cause that sarcomere to shorten because the thin filaments are being pulled inward. So that arrangement is really important to make sure that we're producing the tension that we need and that there's enough spots for those myosin heads to attach to, those cross bridges to attach to, so that we can shorten those sarcomeres. Are you familiar with the micro anatomy? Did you have that in biology 152? So the t-tubules and the terminal cisterna, the sarcoplasmic reticulum, all that terminology. You want a refresher? You didn't? Okay, so this would be a muscle fiber, a cell, and you can see that on the sarcolemma, which is just another term for the cell membrane or plasma membrane of the fiber, is that we see these little holes here. And they've cut away the plasma membrane and a few other structures to kind of reveal the internal structure. Those little holes, those little openings, and they're all over the membrane are called transverse tubules. They open up into this tubular network here. This is just membrane that's kind of been enfolded and pushed inside. So I always use the analogy, if you're walking along... the surface of that cell and you saw this little hole here you could drop down into it and make your way through and come out in a different part of the cell it's like a little wormhole that's going to be really important for how that action potential how the change in voltage that occurs during excitation can actually get down deeper into the cell these cells don't have axons Neurons did, and we know that with that action potential was regenerated down those axons to get the neurotransmitter to be released. You can look at this as kind of like the axon that transmits that action potential down into the cell, and that relationship between the T-tubules and the sarcoplasmic reticulum, which is all this blue stuff, is really important. So those T-tubules are what... Bring that action potential into the deeper portions of the cell. What do we find inside the sarcoplasmic reticulum? What's stored there? Calcium ions. So this is smooth endoplasmic reticulum. We know that rough endoplasmic reticulum has ribosomes all over it. It's important for protein synthesis and modification. This is a form of smooth endoplasmic reticulum, source calcium. So if you look at all these tiny thin blue lines in here, that network, that's all smooth ER. But notice how wedged in between two different T-tubules here that I've just kind of drawn in these red circles or red lines, we have these enlarged areas. You notice that? That's called, each of those is called a terminal cisterna. It's still smooth ER. It's still sarcoplasmic reticulum, except this is the part where the calcium channels are that are going to let the calcium leave the sarcoplasmic reticulum and go into the sarcoplasm, which is really the cytosol. So terminal cisterna are smooth endoplastic reticulum. They're just in large, larger diameter portions that have a physical connection to the t-tubules because there's channels in the terminal cisterna that directly respond to the action potential that's moving down that t-tubule. We also have a lot of mitochondria here. Why? What do you think that's important for? Think form and function. Huh? Muscles need ATP to contract. And so we need a lot of mitochondria to be able to provide the ATP necessary for muscle contraction. Is that good enough to review? We talked about motor units in lab last week. And how a motor unit is a single somatic motor neuron that innervates skeletal muscle cells, and every time we have an action potential on one of these cells, all of those muscle fibers are going to have action potentials too. Let's think back to lab last week. What did we say about increasing the strength of the stimulus? What is that going to do to the number of motor units stimulated? It's what? It's going to increase. So as we increase the strength of the stimulus artificially as we demonstrated, you're going to stimulate more motor units. We measured the m-wave which was a collective change in voltage of those muscle cells, but we can actually measure the force produced when those muscles contract. We actually have a little sensor called the force transducer that we could potentially hook up and measure how changes in the strength of the stimulus affects the force produced during the contraction process. And what you'll see, not only as you increase the strength of the stimulus, it's going to result in an increase in the M-wave. But that's also going to increase the force produced. So they're all connected. And I believe that's something we address a little bit more in section 9.3. So that's something I'll talk about on Thursday. So let's get to the contraction process if there's no questions. Up to... Well, 9-1 really. Section 9-1. Yeah. Let's see if I can find another picture, if I have another picture in here. I don't think I do. Let me add another slide here. Alright, so Terminal Cisterna. These are the Large diameter parts of the sarcoplasmic reticulum, and they are responsible for calcium release. Sarcoplasmic reticulum stores calcium ions. They are released from the terminal cistern. Looks like a radiator. So these would be your terminal cisterna that I'm outlining in green. It's all sarcoplasmic reticulum. And then all of this stuff kind of in this area, that still is sarcoplasmic reticulum. It just doesn't have that large diameter. We can consider the role of those as this is how the calcium gets back in. Because when we pump, when that calcium leaves, it's got to get pumped back in, back into that sarcoplasmic reticulum. Make sure, okay, let me ask you this. How much did you go over about the anatomy of the neuromuscular junction? Anything? Did you look at a slide, microscope slide? Okay. Well, you read about it. Hopefully, you took some notes, but I want to make sure you're aware of all the parts. So we know that the neuron that is connected to the skeletal muscle cell is the somatic motor neuron. It is myelinated. which means that that action potential when it travels down that neuron travels down pretty quickly. Everybody remember the name of the conduction type? It's altatory conduction. And so it kind of hops. And then when we get to the end, the axon divides into what we call those telodendria, and then we have this enlarged area called an axon terminal. And that's kind of what we're looking at here. That's the axon terminal. And we have things stored inside that axon terminal. We have these synaptic vesicles. They contain acetylcholine. Now, knowing that, what type of receptor do you think we're going to find on the skeletal muscle cell then? Well, we got two choices, right? Nicotinic or muscarinic. Which one of those? Anybody remember? It's nicotinic, okay? It's nicotinic. All right, so those synaptic vesicles, some are pre-docked, meaning they're kind of ready, kind of already connected to the axon terminal membrane. Some of them are ready to be released or to fuse and to release by exocytosis. Acetylcholine, others are not. Some are just kind of hanging out in the cytosol of that axon terminal. Now this would be a single muscle cell down here. Now this full connection is called the neuromuscular junction, but the part where that axon terminal meets the sarcolemma of that single cell has a name and that's called the motor end plate. Notice that it's enfolded. What's the purpose of an enfolding of a membrane like that? Increases the surface area, which means that there's more space to add more receptors, ensuring the likelihood that an action potential is going to occur. So all over this motor end plate, we're going to have those nicotinic receptors. Bear in mind that this muscle cell is within a, it's in a bundle with a whole bunch of other cells, which we call a fascicle, right? They're all bundled together, connective tissues around it. And there's motor units. So there has to be a way to make sure that we're not stimulating adjacent cells if they're part of different motor units. So what there is, is there's a membrane that kind of connects this all together, and that's called the epimysium, and that electrically insulates the cells from other cells, meaning that when the acetylcholine is released, it's not going to sneak out and stimulate receptors on other cells. This is a synapse. This is not a neuron-neuron synapse, it's a neuron-effector synapse. We looked at that from a different perspective in Unit 2, from autonomic effectors, cardiac muscle, smooth muscle, or glands. Okay, this is a somatic motor pathway, and so we're looking at a somatic motor effector, which is skeletal muscle. Now, this axon terminal is not touching the motor. end plate. There's a gap called the synaptic cleft. Make sure you're familiar with that term. Notice there's lots of mitochondria kind of near the surface of the cell, lots of mitochondria in those axon terminals as well. Why? What does that tell you? There's some processes in there that are going to require energy. And we'll go over those. So that's the basic structure of a synapse. I'm not going to directly ask you a whole lot of questions about synapse anatomy, but in order to understand how it works and how the cells talk to each other and stimulate graded potentials, you got to understand the anatomy. Depends on how many muscle cells are attached to it. That kind of gets into the heart of a motor unit. Thank you for bringing that up. Is that depending on the type of muscle as an organ, you can have vastly different motor units. So some motor units can be very large, meaning one neuron and maybe thousands of cells. Or they can be small. I'm sure there's intermediate as well. Small would be maybe, and these are just to give you an example, one neuron and maybe 10 cells, or 25 or 50 cells instead of thousands. So in certain muscles like the erector spinae, which are posture muscles, the rectus abdominis. Those are muscles where you don't need a lot of fine motor control, do you? They're kind of like switches, either they're on or they're off. So these are going to have very large motor units. But when we look at manual dexterity of your fingertips and being able to write and adjust pressures or the minute micro movements that you can do with your eyes, those are going to be small motor units. So small motor units allow you finer motor control. As opposed to larger motor units, it's more gross motor control, meaning you're either contracting them or not. And you can adjust that to a degree.

Some important terms related to skeletal muscle cells. Okay, make sure you know what the term, what I mean when I say muscle fiber. That's a cell because it's long, they're elongated.

And during embryonic development, they start as very, very small cells that fuse together. to form these very very long cells that's why they have many nuclei per cell and those cells that they're derived from are called myoblasts there's some terms there you need to be aware of as they relate to muscles and muscle cells terms that were in your packet sorry in the in the book so they go on and talk about cellular structure the connective tissue structure i am really not all that concerned that you know those connective tissue that are part of a muscle as an organ. So the epimysium, the paramysium, and endomysium, I'm not real concerned about that.

We're focusing on the physiology of the fiber itself and what happens to cause the contraction, ultimately shortening that organ muscle as an organ. So some terms. Thin filaments and thick filaments.

I would imagine you probably talked a little bit about that in Biology 152. Did you use those terms at all? Okay, so we're going into the details this semester. Okay, I guess I'm not going to be writing on the screen today. So I want to make sure that you understand that when we talk about the thin filament, sometimes it's referred to as actin, but that's one component of it. The thick filament is myosin.

And when we look at a myosin molecule, I'm going to have to use my pencil here, my regular mouse. is that myosin is the thick filament but there's kind of some multiple parts and you can see that the thick film has these little what we call cross bridges these little heads that come off there it's kind of like two golf clubs with the golf club shafts intertwined and they're what we call the heavy chains and the light chains of light chains you might have heard a term similar to that before Remember when we talked about the beta receptors and beta receptors are inhibitory and they adenylate cyclase stimulates the production of cyclic AMP. And what did I say that cyclic AMP did, Justin? It's going to inhibit what's called myosin light chain kinase, which is an enzyme that adds a phosphate to the light chains, which then stimulates the contraction.

of those. Well, this occurs in smooth muscle, but it's very similar. Okay. Anyway, so you've heard that term before.

So all those are part of it. And when the myosin head contracts or when the, yeah, I guess when the myosin head contracts, it's going to pivot at this little pivot point down here. All right.

And that's when we get into what's called the sliding filament theory and how the sarcomere shortened. I believe for homework I assigned some labeling exercises and one of those was a sarcomere. So if we look at this diagram here, while it's not listed under terms, you do need to be familiar with the sarcomere and the parts of the sarcomere because it does relate to what happens during contraction.

That sarcomere is going to change. One of the key things about muscle contraction Skeletal muscle contraction, especially, is that the cells get shorter when they contract, but the individual proteins don't change their length. Now, those thick and thin filaments are... called myofibrils, grouped together into what we call myofibrils, little bundles of filaments.

So myofilaments and myofibrils are different. The fibril would be a bundle of thick and thin filaments. And that sarcomere shortens.

And what we'll see is that that H zone is going to get smaller because these thin filaments slide over. the thick filaments. See if I got a picture somewhere. Yeah, so I know I'm getting ahead, but ultimately what happens is when those cross bridges cycle, which is something we're going to talk about, notice how the length of the sarcomere changes.

The proteins aren't getting smaller, the sarcomere is getting shorter because we're overlapping. Okay, we're overlapping. We'll get to all that.

So some terms related to the thick and thin filaments, specifically cross bridges, regulatory proteins, and contractile proteins. Do you remember troponin and tropomyosin from biology 152? No? Okay.

Well, let's talk about it then. I'm sure you read about it. So when we look at that thin filament, we have these little globular proteins called actin that form and join together to form like a string of beads. In fact, it's really like two strings of beads that are kind of intertwined and twisted together. Also, part of this thin filament are two regulatory proteins, tropomyosin And troponin.

Troponin is actually a calcium receptor. Please make a note of that. That's really important.

Troponin is actually a calcium receptor. You haven't read about that yet. The other is called tropomyosin.

Tropomyosin is the blue one in the picture. It's a long fibrous protein. It is physically connected to the troponin and its job is to cover up what we call the myosin binding sites. Let's jump ahead real quick to this picture here since we're talking about it. Page 139, slide 21. So you can see larger now that there's troponin, the tropomyosin, and see on those actin filaments, those little spherical globular things, there's that little dark spot kind of in the middle.

You can see on my hand-drawn diagram here, that is what we call the myosin binding site. If I can... Try this.

I feel helpless without being able to write on the screen. Well, maybe this is why. Because I didn't...

click that? I don't know. Nope. So what I've drawn on the bottom then would be just those actin proteins without the tropomyosin.

So it would look like this. If this red line represents the tropomyosin, notice how it's covering those binding sites. So these little circular are the myosin binding sites. Yeah. There are some molecular forces that are holding the tropomyosin to the actin, but at the same time, if you look at the troponin, there's three proteins to troponin.

One is connected to tropomyosin, one is connected to the actin. And when calcium binds to this, it stimulates a change and it causes this, and I don't know all my physics, but it creates a pulling action and it's going to pull that tropomyosin away from those binding sites. So you would get something like this. So the tropomyosin is kind of held by intermolecular forces and by the troponin, but it's loosely held because we need it to be able to shift away. So again, myosin binding site.

And remember on the thick filament, they had those little golf club heads, the cross bridges. Well, what happens is those will actually reach up and form a bond with that myosin binding site on the active. I'm getting a little ahead of myself, but that's what the purpose of those myosin binding sites are.

Now what happens after that, I'm going to save. Maybe we'll get to it today, maybe not. So the role of troponin is to act as a calcium receptor.

When it changes its shape, it's going to pull on the tropomyosin, shifting that tropomyosin out of the way. And I will repeat this. We're going to look at this again. So that's what I mean by regulatory proteins. Because if we don't move the tropomyosin out of the way, we can't have muscle contractions, skeletal muscle contractions.

And then the whole purpose is to shorten that sarcomere. Now this would be a cross-section through a myofibril. And within that myofibril, we have the individual myofilaments, the little purple ones.

are the thin filaments and the other ones are the thick. And they kind of form this hexagonal arrangement and all the myosin heads would be kind of around those like in a spiral. In fact if you look at the picture just above of the thick filament you can see those myosin heads are kind of spiraled around and notice the angle of orientation. You got some of these myosin heads that are kind of pointing this way and on the other side of that M line they're pointing the opposite direction because what happens in contraction is that those thin filaments slide inward over the thick and so those cross bridges have to be positioned in such a way that when they pivot so the cross bridges that's not a good one That's not a good one either. They have this pivot point, kind of this here.

And what's going to happen is that myosin head, when it's attached to the thin filament, is going to move on both sides, and that's going to cause that sarcomere to shorten because the thin filaments are being pulled inward. So that arrangement is really important to make sure that we're producing the tension that we need and that there's enough spots for those myosin heads to attach to, those cross bridges to attach to, so that we can shorten those sarcomeres. Are you familiar with the micro anatomy? Did you have that in biology 152? So the t-tubules and the terminal cisterna, the sarcoplasmic reticulum, all that terminology.

You want a refresher? You didn't? Okay, so this would be a muscle fiber, a cell, and you can see that on the sarcolemma, which is just another term for the cell membrane or plasma membrane of the fiber, is that we see these little holes here. And they've cut away the plasma membrane and a few other structures to kind of reveal the internal structure. Those little holes, those little openings, and they're all over the membrane are called transverse tubules.

They open up into this tubular network here. This is just membrane that's kind of been enfolded and pushed inside. So I always use the analogy, if you're walking along...

the surface of that cell and you saw this little hole here you could drop down into it and make your way through and come out in a different part of the cell it's like a little wormhole that's going to be really important for how that action potential how the change in voltage that occurs during excitation can actually get down deeper into the cell these cells don't have axons Neurons did, and we know that with that action potential was regenerated down those axons to get the neurotransmitter to be released. You can look at this as kind of like the axon that transmits that action potential down into the cell, and that relationship between the T-tubules and the sarcoplasmic reticulum, which is all this blue stuff, is really important. So those T-tubules are what...

Bring that action potential into the deeper portions of the cell. What do we find inside the sarcoplasmic reticulum? What's stored there?

Calcium ions. So this is smooth endoplasmic reticulum. We know that rough endoplasmic reticulum has ribosomes all over it. It's important for protein synthesis and modification. This is a form of smooth endoplasmic reticulum, source calcium.

So if you look at all these tiny thin blue lines in here, that network, that's all smooth ER. But notice how wedged in between two different T-tubules here that I've just kind of drawn in these red circles or red lines, we have these enlarged areas. You notice that?

That's called, each of those is called a terminal cisterna. It's still smooth ER. It's still sarcoplasmic reticulum, except this is the part where the calcium channels are that are going to let the calcium leave the sarcoplasmic reticulum and go into the sarcoplasm, which is really the cytosol. So terminal cisterna are smooth endoplastic reticulum.

They're just in large, larger diameter portions that have a physical connection to the t-tubules because there's channels in the terminal cisterna that directly respond to the action potential that's moving down that t-tubule. We also have a lot of mitochondria here. Why? What do you think that's important for?

Think form and function. Huh? Muscles need ATP to contract.

And so we need a lot of mitochondria to be able to provide the ATP necessary for muscle contraction. Is that good enough to review? We talked about motor units in lab last week.

And how a motor unit is a single somatic motor neuron that innervates skeletal muscle cells, and every time we have an action potential on one of these cells, all of those muscle fibers are going to have action potentials too. Let's think back to lab last week. What did we say about increasing the strength of the stimulus?

What is that going to do to the number of motor units stimulated? It's what? It's going to increase.

So as we increase the strength of the stimulus artificially as we demonstrated, you're going to stimulate more motor units. We measured the m-wave which was a collective change in voltage of those muscle cells, but we can actually measure the force produced when those muscles contract. We actually have a little sensor called the force transducer that we could potentially hook up and measure how changes in the strength of the stimulus affects the force produced during the contraction process.

And what you'll see, not only as you increase the strength of the stimulus, it's going to result in an increase in the M-wave. But that's also going to increase the force produced. So they're all connected.

And I believe that's something we address a little bit more in section 9.3. So that's something I'll talk about on Thursday. So let's get to the contraction process if there's no questions. Up to...

Well, 9-1 really. Section 9-1. Yeah. Let's see if I can find another picture, if I have another picture in here.

I don't think I do. Let me add another slide here. Alright, so Terminal Cisterna.

These are the Large diameter parts of the sarcoplasmic reticulum, and they are responsible for calcium release. Sarcoplasmic reticulum stores calcium ions. They are released from the terminal cistern. Looks like a radiator.

So these would be your terminal cisterna that I'm outlining in green. It's all sarcoplasmic reticulum. And then all of this stuff kind of in this area, that still is sarcoplasmic reticulum. It just doesn't have that large diameter. We can consider the role of those as this is how the calcium gets back in.

Because when we pump, when that calcium leaves, it's got to get pumped back in, back into that sarcoplasmic reticulum. Make sure, okay, let me ask you this. How much did you go over about the anatomy of the neuromuscular junction? Anything?

Did you look at a slide, microscope slide? Okay. Well, you read about it. Hopefully, you took some notes, but I want to make sure you're aware of all the parts.

So we know that the neuron that is connected to the skeletal muscle cell is the somatic motor neuron. It is myelinated. which means that that action potential when it travels down that neuron travels down pretty quickly. Everybody remember the name of the conduction type?

It's altatory conduction. And so it kind of hops. And then when we get to the end, the axon divides into what we call those telodendria, and then we have this enlarged area called an axon terminal. And that's kind of what we're looking at here.

That's the axon terminal. And we have things stored inside that axon terminal. We have these synaptic vesicles.

They contain acetylcholine. Now, knowing that, what type of receptor do you think we're going to find on the skeletal muscle cell then? Well, we got two choices, right? Nicotinic or muscarinic.

Which one of those? Anybody remember? It's nicotinic, okay? It's nicotinic.

All right, so those synaptic vesicles, some are pre-docked, meaning they're kind of ready, kind of already connected to the axon terminal membrane. Some of them are ready to be released or to fuse and to release by exocytosis. Acetylcholine, others are not.

Some are just kind of hanging out in the cytosol of that axon terminal. Now this would be a single muscle cell down here. Now this full connection is called the neuromuscular junction, but the part where that axon terminal meets the sarcolemma of that single cell has a name and that's called the motor end plate. Notice that it's enfolded. What's the purpose of an enfolding of a membrane like that?

Increases the surface area, which means that there's more space to add more receptors, ensuring the likelihood that an action potential is going to occur. So all over this motor end plate, we're going to have those nicotinic receptors. Bear in mind that this muscle cell is within a, it's in a bundle with a whole bunch of other cells, which we call a fascicle, right? They're all bundled together, connective tissues around it. And there's motor units.

So there has to be a way to make sure that we're not stimulating adjacent cells if they're part of different motor units. So what there is, is there's a membrane that kind of connects this all together, and that's called the epimysium, and that electrically insulates the cells from other cells, meaning that when the acetylcholine is released, it's not going to sneak out and stimulate receptors on other cells. This is a synapse.

This is not a neuron-neuron synapse, it's a neuron-effector synapse. We looked at that from a different perspective in Unit 2, from autonomic effectors, cardiac muscle, smooth muscle, or glands. Okay, this is a somatic motor pathway, and so we're looking at a somatic motor effector, which is skeletal muscle. Now, this axon terminal is not touching the motor.

end plate. There's a gap called the synaptic cleft. Make sure you're familiar with that term.

Notice there's lots of mitochondria kind of near the surface of the cell, lots of mitochondria in those axon terminals as well. Why? What does that tell you? There's some processes in there that are going to require energy. And we'll go over those.

So that's the basic structure of a synapse. I'm not going to directly ask you a whole lot of questions about synapse anatomy, but in order to understand how it works and how the cells talk to each other and stimulate graded potentials, you got to understand the anatomy. Depends on how many muscle cells are attached to it.

That kind of gets into the heart of a motor unit. Thank you for bringing that up. Is that depending on the type of muscle as an organ, you can have vastly different motor units.

So some motor units can be very large, meaning one neuron and maybe thousands of cells. Or they can be small. I'm sure there's intermediate as well.

Small would be maybe, and these are just to give you an example, one neuron and maybe 10 cells, or 25 or 50 cells instead of thousands. So in certain muscles like the erector spinae, which are posture muscles, the rectus abdominis. Those are muscles where you don't need a lot of fine motor control, do you? They're kind of like switches, either they're on or they're off. So these are going to have very large motor units.

But when we look at manual dexterity of your fingertips and being able to write and adjust pressures or the minute micro movements that you can do with your eyes, those are going to be small motor units. So small motor units allow you finer motor control. As opposed to larger motor units, it's more gross motor control, meaning you're either contracting them or not.

And you can adjust that to a degree.

Transcript for:Insights on Muscle Physiology

Transcript for:
Insights on Muscle Physiology