Steps of Muscle Contraction: Study with Video Lessons, Practice Problems & Examples

Muscle contraction begins with a nervous signal at the neuromuscular junction, where acetylcholine (ACh) binds to receptors, triggering an action potential (AP) in the sarcolemma. This AP propagates into T tubules, stimulating the sarcoplasmic reticulum to release calcium ions (Ca²⁺). Calcium binds to troponin, exposing actin's binding sites for myosin. The cross bridge cycle then occurs, where myosin heads pull actin, shortening the sarcomere. ATP is essential for myosin's release and re-cocking, enabling repeated contractions, resulting in powerful muscle movement.

Overview of Muscle Contraction

We now want to talk about the steps of muscle contraction with the cellular and molecular level in much more detail. However, before we examine these step-by-step processes, we just want to step back and look at an overview of what's going on here. So, we're going to start out by saying that muscle contraction involves two major things that need to happen. First up is the transmission of a nervous signal. Skeletal muscle contracts when it receives a signal from the nervous system. So, how is that signal received? How is that signal spread throughout the entire muscle fiber? Then, we also have to think about the contraction of the sarcomere. Now, we said the sarcomere is the fundamental unit of muscle contraction, and so far, we mentioned that the myosin pulls on the actin to make that happen. But we want to talk about, at the molecular level, in much more detail, what's going on in the sarcomere. Now, as you look here, you'll notice we have three boxes we're about to fill in, and we've just talked about two major processes. That third box is going to be about linking these two things. How do we get from an electrochemical signal to the mechanics of contraction? Alright. To start, we're talking about the transmission of a nervous signal, and we're going to talk about the neuromuscular junction. The neuromuscular junction is where the nervous system meets a muscle fiber. We're going to say at the neuromuscular junction, a muscle cell is stimulated by the nervous system, and that's going to result in the initiation of an action potential. An action potential is this wave of electrochemical signal that's going to spread down the muscle fiber through the sarcolemma, the muscle fiber cell membrane. Now, to illustrate this, we can see here we have the axon terminal, the end of this nervous system cell, releasing neurotransmitters into the synapse, the small space between the two cells. They're binding to receptors on the cell membrane, and that's going to start this action potential that's going to flow down the sarcolemma. I have just gone through all those steps quickly. Don't worry. We will go through those steps later on in more detail more slowly. Alright. We now have this action potential, and it's spreading down the sarcolemma, but we need to get it down into the sarcomere to get to the mechanics of contraction. That link, we're going to talk about as the excitation-contraction coupling. We're going to say that that starts with the action potential spreading or, in more technical terms, it propagates along the sarcolemma and enters the t-tubules. Here we can look at our image. We can see the edge of the muscle fiber. We have the sarcolemma here, showing this action potential spreading down, and it's going to dive down into this pink t-tubule, which surrounds like a ring around this myofibril. Alright. That gets that electrochemical signal down deep into the muscle fiber. You also notice right up in close connection with that t-tubule is this blue structure that is the sarcoplasmic reticulum, that highly specialized endoplasmic reticulum of the muscle fiber. When that signal goes down through the t-tubule, that's going to signal the sarcoplasmic reticulum to release calcium ions, and I'm going to write that in shorthand here as Ca2+. Alright. It's going to release the calcium ions, and those are going to go into the myofibril sarcomeres, and that is our link. Those calcium ions are going to result in the myosin binding sites becoming exposed. Here we can look at our image again. We're zoomed way in here. We see in pink, these are the calcium ions coming in. They're going to bind to the troponin. The troponin is going to open the binding site by moving this tropomyosin, this green filament surrounding the actin. We can see the myosin binding sites there on the actin. Those are going to become exposed. Alright. Now we can talk about the mechanics of contraction. Once those myosin binding sites are exposed, the myosin is going to bind to the actin. We're going to call that binding a cross bridge. Once bound, that myosin is going to pull on the actin, and we call that pulling motion the power stroke. Alright. We can see that here. We see the myosin is bound to the actin, and it's pulling the actin that way. Okay. Again, for all of these, we've talked about many steps. We're going to go through all those steps much more slowly and in more detail coming up. I'm looking forward to it, and I hope you are too.

Steps of Muscle Contraction Example 1

Our example tells us that below is a list of structures that are found in the muscle fiber, and we need to mark the structure with a t if its primary role is involved in transferring a signal through the cell, mark the structure with an r if it's directly involved in regulating whether the sarcomere contracts, and mark the structure with a c if it's directly involved in the mechanics of contraction. Alright. So we have this big long process, and we started by breaking it up into these groups, transferring a signal, regulating contraction, and then actually contracting. So let's look at our structures here. We're going to start off with the actin. Which group would you put that in? The transferring a signal, regulating contraction, or actually the mechanics of contraction? Well, actin, I'm going to mark it with a c. The actin gets pulled on by the myosin, and that's what causes the sarcomere to contract. That is directly involved in the mechanics of contraction.

Alright. Let's look at the calcium ions. Which group would you put the calcium ions in? Oh, I'm going to mark the calcium ions with an r. Calcium ions get dumped into the myofibril, into the sarcomere, and that results in the binding sites on the actin opening. So if the calcium's in the sarcomere, there can be contraction. If the calcium's not in the sarcomere, there can't be contraction. That's directly involved in regulating. Next, we have the myosin. What do you think about the myosin? Well, if I marked actin with a c, then myosin's getting a c as well. Myosin holds on the actin, and that's how the sarcomere contracts. That's directly involved in the mechanics of contraction.

Next, we have the sarcolemma. Which group would you put the sarcolemma in? Well, I'm marking the sarcolemma with a t. The sarcolemma is the cell membrane of the muscle fiber, and it spreads that action potential throughout the muscle fiber, spreading that signal so the entire muscle fiber knows to contract at the same time. Alright. Next up, we have the sarcoplasmic reticulum. Which group would you put that in? Well, this is the one that gives me a little trouble. I can see arguments for 2 groups, but I'm definitely marking it with an r for regulating contraction. When the sarcoplasmic reticulum gets the signal, it's going to release the calcium ions. The releasing of the calcium ions is what signals the muscle to contract. That's what opens the binding site and allows the myosin to pull on the actin. Now I can see an argument for putting it in the transferring a signal, section, because transferring a signal to sarcoplasmic reticulum reticulum gets the that action potential, and that action potential signals the sarcoplasmic reticulum to release the calcium ions. But again, because it's releasing the calcium ions, I think it's better placed in the regulation group.

Alright. That brings me to the troponin. Which group would you put the troponin in? Well, I'm marking troponin with an r. Troponin, we said troponin opens the binding site. So if it's involved in opening the binding site, that's allowing whether the contraction can occur or not. When the calcium binds to the troponin, that troponin kind of changes shape, and that opens the binding site. Next, we have the tropomyosin. Well, if the troponin is a regulating group, then the tropomyosin is in that regulating group as well. The troponin moves the tropomyosin, because remember the tropomyosin is there saying no to the myosin. It's this filament that's there blocking the binding site. So if the tropomyosin is blocking the binding site, the myosin can't bind. The cell can't contract. Once it moves, contraction can occur. And then finally, we have the T tubule. Alright. The T tubule, I'm marking that with a t. The action potential moves down the sarcolemma, and then it goes into those tubes, the T tubules, which are these extensions of the sarcolemma, which dive deep into the cell and surround in a little bit of a ring around the myofibrils. That action potential down through the T tubule then tells the sarcoplasmic reticulum to release the calcium ion. So it is definitely there transferring that signal deep within the cell. Alright. Understanding these roles is going to be really important going forward. We have more practice problems to follow. I'll see you there.

True or False: if false, choose the answer that best corrects the statement.

The events of excitation-contraction coupling involve converting the electrochemical signal to the mechanical movement of contraction.

• A. True.
• B. False, excitation-contraction coupling involves the reception of the nerve signal at the neuromuscular junction.
• C. False, excitation-contraction coupling involves the movement of actin by the myosin power stroke.
• D. False, excitation-contraction coupling involves propagation of the signal through the sarcolemma and T tubules.

Neurotransmitters & Action Potentials

We said the first steps of muscle contraction are going to be all about how the muscle fiber receives a signal from the nervous system, and then how it spreads that signal throughout the entire cell. So, to understand how that works, we need to talk about neurotransmitters and action potentials. Now, neurotransmitters and action potentials, we're going to talk about in a lot more detail when we get to the nervous system. But to understand how the muscular system works and to be able to answer some questions about it, you need to know the basics. So, neurotransmitters, they're going to be these chemical messengers that are used at a synapse. And a synapse, we're just going to say, is a really small space between the axon and the muscle. And so, if we look over here, we have the small image here. This is the axon, that end of a neuron, that highly specialized nervous tissue cell, and it comes down, and this is going to be our membrane of the muscle fiber there. And you can see that there's a small space between the two. They don't actually quite touch. So to get a message across that synapse, the neuron dumps these neurotransmitters into the synapse. You can see all these little dots in here. It's dumping those neurotransmitters into the synapse. They're going to diffuse across the synapse, and they're going to bind to receptors in the membrane of the muscle fiber. Now when enough of them bind, that'll stimulate an action potential. Now, before we get to the action potential though, we just need to know that acetylcholine is the neurotransmitter of the neuromuscular junction. In the nervous system, there's all sorts of different neurotransmitters that are used, but there's only one neurotransmitter that is used to stimulate muscle fibers, and that is acetylcholine. Alright. So, we pass the message on to the muscle fiber. Now it's spreading. It's going to spread through an action potential. An action potential is going to be this wave of electric signal that moves along a membrane, and in this case, our membrane is the sarcolemma, or the membrane of the muscle fiber. And to understand how this works, we need to know that muscle fibers are polarized. And by that, we mean that they have a negative charge inside and a positive charge on the outside. Polarized means they have a separation of charge. And an action potential is just going to be this really brief, and by brief, I mean milliseconds change of polarization, and it's going to be caused by the movement of two ions, sodium and potassium. The ions Na+ and K+ ions. And I really suggest that you just remember that sodium is Na+ and K+ is potassium if you don't know that yet. It's a really important ion for anatomy and physiology. Okay. So let's see how this works. We have some illustrations here. We're going to start with our polarized cell here, and this is our muscle fiber at rest. We have all these sodium ions, Na+ ions on the outside of the cell, and we have a lot of potassium ions K+ in high concentration on the inside of the cell. And that results in the cell being positively charged on the outside and negatively charged on the inside. Now one way to remember this, we can say that the cell is swimming in a salty sodium sea. That's something that we're going to say again in the nervous system. Your cells are swimming in a salty sodium sea, and the sodium is positively charged, so you have a positive charge on the outside of the cell. Now what confuses people sometimes a little bit, this potassium, you'll note, also has a positive charge. Don't worry about that too much. We're just talking about net charges. There's a lot of other stuff going on here, and so we really just want to remember the sodium's on the outside, potassium's on the inside, positively charged outside, negatively charged inside. So we said we want to flip that charge. So when we flip it, we're going to look at this image here. We are going to call that depolarization. So, to first depolarize the cell, we said we have a really high concentration of sodium on the outside. It's swimming in a salty sodium sea. So we open the sodium channel, and this high concentration of sodium causes the sodium ions to diffuse into the cell. As the sodium, or as I'll write here, Na+ moves inside the cell, well, it's going to bring along with it its positive charge, and that's going to cause the inside of the cell to become more positive. So, we've now flipped the charge. It's become just a little bit more positive on the inside and negatively charged on the outside. But the action potential, we're going to flip it and then we're going to flip it back. So to flip it back, we're going to talk about repolarization. Well, the sodium came in to make the inside of the cell positive, so now we're going to open the potassium channels. We have a really high concentration of potassium inside the cell, so when you open that potassium channel, that high concentration is going to cause them to diffuse out of the cell. So I’m going to write here the K+ moves outside the cell, and with that, it's going to bring its positive charge with it. It's going to turn the outside of the cell positive and the inside negative, and the charge is restored. Alright. So that flip and flip back of the charge, that's the action potential, and it's going to be passed in this wave down the cell membrane. It's going to go really fast. Fast enough that essentially your entire muscle fiber, which can be inches or, in some cases, longer than a foot long, is going to basically all start contracting at the same time. Alright. Again, we're going to go into all of this in a lot more detail in the nervous system, but for the muscular system, you should be familiar with it at about this level. We'll practice it some more in the example to follow. I'll see you there.

Steps of Muscle Contraction Example 2

Our example here tells us that the membrane potential inside a cell during an action potential is graphed below. So before we go on, I just want to orient myself to the graph. Alright. On the x-axis, we have time, which is measured in milliseconds, so this is really fast. And on the y-axis, we have membrane potential, which ranges from negative 90 millivolts up to 0 and then on to positive 30. Now we don't really need to worry about those values or the units. We just know that we're starting negative. We're going to cross 0 and we're going to end up slightly positively charged, again, inside the cell.

Now what it's asking us to do is to identify which part of the graph refers to depolarization and which refers to repolarization. And we have this image here showing our potassium ions and our sodium ions and our positive charge outside the cell and negative charge inside the cell that we've talked about already just to use as a reference. Alright. So as we go along here, we're going to follow this line. We see that it starts at negative 90 millivolts, so we're negatively charged inside the cell. Then the sodium channels are going to open. Remember, our cell is swimming in a salty sodium sea, so those sodium channels open and the sodium flows inside the cell because it's in high concentration outside of the cell, so it's going to diffuse to the inside and with it, it's going to bring its positive charge.

As the sodium flows into the cell, the inside of the cell gets more and more positive. It comes up to 0 and even passes 0 until it's slightly positively charged inside the cell. Well, if we started out polarized, this shift in charge, or bringing the charges on the other side, we're going to call that depolarization. Depolarization occurs when this curve increases up to the 0 mark and even overshoots it just a little bit. Now, once we've overshot it, the sodium channels are going to close, so no more sodium can enter the cell and the potassium channels are going to open. Remember, the potassium is in high concentration inside the cell, so the potassium is now going to flow out of the cell. As it flows out, it takes its positive charge with it. It takes positive charges out of the cell, so the charge on the inside of the cell is going to start falling. It's going to fall and fall, and then, the sodium channels are going to close until it levels out right where it started again. So we depolarized, and now we're getting this charge to fall back to where it started, and we're going to call that repolarization.

Again, depolarization and repolarization are key processes. This, you're going to see in much more detail when you talk about the nervous system. Following these ions, sodium coming into the cell and potassium moving out of the cell, and how they bring their charges with them is going to be really important for understanding how an action potential spreads this message through the sarcolemma. We're going to talk all about this and how it specifically refers to the muscle fiber, coming up next.

During an action potential, the phase where ___________ moves into the cell results in depolarization while the phase where ______________ exits the cell results in repolarization. 

• A. Na$^+$: K$^+$
• B. Ca$^2$$^+$: Na$^+$
• C. Na$^+$: Ca$^2$$^+$
• D. K$^+$: Ca$^2$$^+$

A. Events at the Neuromuscular Junction

We said that the first major step of muscle contraction is that the skeletal muscle fiber needs to receive a signal from the nervous system, and then it has to spread that signal throughout the muscle fiber. Receiving that signal from the nervous system, we're going to call the events at the neuromuscular junction. To remind ourselves that this is the first of 3 major steps, we have it labeled here as a. So the neuromuscular junction, that's the connection between the nervous system and the motor end plate of the muscle fiber. Now remember the cell membrane of the muscle fiber we call the sarcolemma, and there's going to be one small region of the sarcolemma that's going to be specialized for receiving this signal from the neuron.

That specialized region is going to be the motor end plate. Alright. Now remember, these don't actually connect to each other, they have this real small space between each other that we call the synapse. So to get this signal across the synapse, we need to use a neurotransmitter, and the neurotransmitter used for muscles is acetylcholine, or as we're going to write here, ACh. So I'm going to write ACh going forward just because it's easier, but whenever you see ACh, just know that means acetylcholine.

It's the neurotransmitter used at the neuromuscular junction. Alright. So let's go through this step by step. First up, the action potential is going to arrive at the axon terminal. Alright.

The axon is the extension of the neuron, that highly specialized nervous tissue cell, and neurons send these electrical messages using action potentials, that flipping of the charge, using the sodium and potassium ions. So this action potential is going to arrive at the terminal, and we can see here in yellow is our axon terminal, and we see this action potential coming in with those arrows there. Now the word terminal just means the end of something, but the way I remember that this yellow structure here is called the terminal, is that if I get off a train, I get off at a train terminal. How do we get the message off of the axon? The message gets off the axon at the axon terminal.

Alright, so we've gotten this electrical signal down into the terminal. What that's going to do is cause voltage-gated calcium channels to open, and we can see that here in our image. We have the calcium on the outside here, and we can see these channels here. And when that action potential comes in, that's going to open the channels, and the calcium is going to flow into the axon terminal. Now you may remember in the sarcomere, calcium entering the sarcomere is going to cause the sarcomere to start contracting.

So, in both cases, an action potential is going to stimulate the release of calcium, and the release of these calcium ions is going to start the process we're talking about. In this case, the release of the calcium ion as they enter the axon is going to release that acetylcholine, ACh. It's going to release it into the synapse. So you can see here in our illustration, we have all these vesicles, and in these vesicles, you see these little sort of blue dots. That's the acetylcholine.

This calcium enters the axon terminal and these vesicles sort of dump by exocytosis this acetylcholine into the synapse there. That acetylcholine is just going to sort of diffuse across the synapse. It's going to diffuse across the synaptic cleft, that's just another word for the synapse, and it's going to bind to the receptors in the sarcolemma. And we can see that here. This sort of pinkish membrane here is our sarcolemma.

It's sort of this wavy membrane at this neuromuscular junction. And you can see here we have these receptors that are going to bind to the acetylcholine. Now when the acetylcholine binds to the receptors, the sodium ion channels are going to open in the sarcolemma. Alright. So that binding of the neurotransmitter acetylcholine causes sodium ion channels to open.

Now you remember, opening sodium ion channels, that's how we start an action potential. So the action potential is going to start. Those sodium ions are going to enter the sarcolemma. They're going to bring their positive charge with it. That's going to depolarize the membrane.

We're then going to have the potassium ions leave, that'll repolarize, and that's just going to happen like a switch flipping back and forth, going down like a wave down the membrane. Alright. So I'll just show here that's going to cause this action potential to go out and spread in both directions down the muscle fiber and that's going to be the signal in the muscle fiber to start contracting. Okay. But we have this acetylcholine now in the membrane, and we got to get rid of it because if this acetylcholine just keeps binding to these receptors here well, if it keeps binding then the muscle is just going to keep getting action potentials and it's just going to keep contracting.

So there are 2 ways that we get rid of the acetylcholine. First off, the acetylcholine can just sort of diffuse out of the synapse, and some acetylcholine will do that. But more importantly, the acetylcholine is going to be broken down by an enzyme, and that enzyme is Acetylcholinesterase. Acetylcholinesterase is going to be in the synapse and it's going to just be breaking down acetylcholine into acetic acid and choline, and when that happens, when that acetylcholine is gone, the signal stops. Now that choline actually gets taken back up by the axon terminal.

It gets recycled into more acetylcholine so that we can do this whole process again. But for our purposes, we started an action potential. That was our goal. Our membrane's now excited, and now we have to figure out how do we couple that excitation to the contraction. That's what we'll be talking about next, but first, we have an example in practice problems.

Give them a try.

Steps of Muscle Contraction Example 3

Our example tells us that interfering with the function of acetylcholine at the neuromuscular junction will interfere with muscle function and can even lead to death. Two ways to interfere with acetylcholine function are to block the acetylcholine receptor or to inhibit the enzyme acetylcholinesterase. We need to predict how each will affect muscle function, and we have this image here for a reference. We've seen this before. We see the axon terminal here in yellow. We see the sarcolemma here, and we can see the acetylcholine being released into the synapse, these little blue molecules, and they're going to bind to these receptors in the sarcolemma. Alright. So, what do you think would happen if you block the acetylcholine receptor? Well, what I think will happen, you're going to release this acetylcholine into the synapse. That's the signal to contract, but it can't bind to the receptor because it's blocked. That means the action potential in the sarcolemma can't start. If the acti

What is the role of the calcium ion in the signaling of an action potential at the neuromuscular junction?

• A. Calcium moves across the synaptic cleft to relay the signal to the muscle tissue.
• B. Calcium causes the muscle cell to depolarize propagating the action potential.
• C. Calcium is important for contraction in the sarcomere; it does not play a role at the axon terminal.
• D. Calcium entering the axon terminal triggers the release of Acetylcholine into the synaptic cleft.

True or false: if false, choose the answer that best corrects the statement:

The motor neuron is in contact with the sarcolemma in order to efficiently pass the electrical signal to the muscle fiber.

• A. True.
• B. False: the axon terminal touches the endomysium.
• C. False: the motor neuron forms a synapse with the muscle fiber at the neuromuscular junction.
• D. False: the axon terminal touches the sarcolemma passing on a chemical signal.

B. Excitation-Contraction Coupling

As we continue talking about the steps of muscle contraction, remember the events at the neuromuscular junction ended with an action potential spreading out or propagating through the sarcolemma. We now want to link or couple that excited membrane, the sarcolemma, to the actual steps of muscle contraction, and we call this excitation-contraction coupling. And to remind ourselves that this is the second major step we're talking about, we have it labeled here B. So excitation contraction coupling. What we're trying to do here is to connect an action potential. And sometimes you can see here, we just write the action potential as AP. We're trying to connect that action potential with a muscle contraction. Now, we're going to break this up into 5 steps here, but before we dive in, I want to look at these first two steps and just step back and look at this in 3 dimensions in the muscle fiber in a little animation here. So, as we look, we're going to see this sarcolemma, the outside membrane, and this action potential spreading down. And you can see that that action potential spreads down into the transverse or the T tubules. Those t tubules are these tunnels that dive in from the sarcolemma and surround these myofibrils. Now, you see that these T tubules are in really close association with the sarcoplasmic reticulum. They come up really tight together, and where they meet the sarcoplasmic reticulum is referred to as the terminal cisternae. And the 3 there, the terminal cisternae and the T tubule, form what's called the triad. Now, this sarcoplasmic reticulum is filled with these calcium ions. And as this action potential is going to come down, it's going to stimulate this voltage gated channel that's going to open up, and those calcium ions are going to rush out into the sarcomere, into the myofibril, and that's going to lead to the muscle contracting, as you see here. Alright. So let's return to our notes and write this down. So we're going to say that the action potential, or the AP, spreads down the sarcolemma and into the T tubules. In our image here, you can see-we have this section of the muscle fiber with parts cut away. You can see all those myofibrils here. The action potential is going to come down the sarcolemma, it's going to dive into these T tubules here, these pink sort of tunnels that are running down, and this is going to carry that excitation deep within the cell and it's going to stimulate the sarcoplasmic reticulum. The sarcoplasmic reticulum, you can see it in really close association with those T tubules there. So next, we're going to say that the voltage gated channels of the sarcoplasmic reticulum are going to release the calcium, or ₂, these calcium ions into the sarcomere, and that's going to be our signal to contract. Alright. So now let's remember exactly how this happens. Before we fill in our notes here though, let's look at another animation. So we have here, we have the myosin on the bottom and we can see that actin filament. This calcium comes in, the calcium is going to come in and bind to that troponin. The troponin is then going to move the tropomyosin, and when that happens the binding sites on the actin are exposed and that myosin can bind. Now it's ready to contract. Alright. Let's look at that one just one more time. So remember here we have the calcium is going to enter in and it's going to bind to the troponin. And remember, the troponin, we said, is there to open the binding sites. It opens the binding sites by moving the tropomyosin. Tropomyosin's normally there saying no to the myosin, but when it moves the binding sites are open, our myosin can bind, and we're ready to contract. Alright, so we'll go back to our page here. And we see here we're going to say: 3, the calcium ions binds to the troponin, and that moves the tropomyosin. In our image here we can see these calcium ions coming in. We can see the troponin here in blue. We see this tropomyosin right now is going to be blocking those binding sites on the actin, so the myosin head can't bind. But once it binds, it's going to move and the myosin binding sites on the actin are exposed. And we can see that down here. Right now, this tropomyosin is out of the way and these actin binding sites are open. If those actin binding sites are open, well, now the myosin head is going to bind to the actin, and that's going to create what we call a crossbridge. Alright. And we can see that here. The myosin head has come up, it's bound to the actin, and now it is ready to pull and do that power stroke. We're not going to talk about that yet. Alright. Finally here, I just want to note, right, we've dumped this calcium into the sarcomere. It's not going to stay there forever. We'll go into all this later on, but I just want to note here that the calcium is only there for a little while. It's going to start leaving the sarcomere, And when the calcium ion exits the sarcomere, gets picked back up, or reenters the sarcoplasmic reticulum, that's going to cause that tropomyosin to move back, and the binding sites will now be blocked. So if the calcium's in the sarcomere, you're going to have contraction. If the calcium all gets picked up and it's removed from the sarcomere, the contraction's going to stop. Ah, forgot the unblockEd. Alright. We're going to talk about the cross-bridge cycle and how this myosin actually pulls on the actin, coming up next. But first, we have an example and some more practice problems. Give them a try.

Steps of Muscle Contraction Example 4

Our example says that the term excitation-contraction coupling refers to the events that turn an action potential into a muscle contraction, and we want to put the steps in order. And so, we see five steps here, and these steps, though, start with an action potential propagates through the muscle fiber, and they end with the cross bridges forming and the muscle contracting.

Alright. So the action potential propagates through the muscle fiber. What's going to come after that? Well, as I look here and I think about the excitation-contraction coupling, I'm definitely looking for something that talks about excitation. And as I look here, there's one thing that talks about an action potential. That's c. It says the action potential travels down the sarcolemma and the T tubules. Alright. That's that wave of depolarization spreading through the cell, spreading that signal, so I'm almost certain that comes next. Going to put a c there, and I'm also going to just cross it out up here for a little bookkeeping.

Alright. So we have the action potential now going down into the T tubules. What's going to come after that? Well, as I think what's going to come after that, I'm going to look for something about the sarcoplasmic reticulum, because the action potential goes down through the T tubules and it stimulates the sarcoplasmic reticulum. So look, do you see something about the sarcoplasmic reticulum? I do. D here, voltage gated channels open releasing calcium into the sarcomere. Now it doesn't say sarcoplasmic reticulum, but this is what it's talking about. That's what the sarcoplasmic reticulum does. When it gets that signal from the T tubules, it releases the calcium. So d is going to come next.

Now, where does the calcium go after that? Well, the calcium binds to troponin, so I'm almost certain a is going to come next. I'm going to write that down. And what happens when the calcium binds to the troponin? Well, remember the troponin kind of changes its shape and when it does that it pulls on the tropomyosin and pulls it out of the way. There we go. E. The troponin changes conformation, moving the tropomyosin. So that's coming next.

And that leaves me with one option. Let's make sure it comes last. So, the last option is, myosin binding sites on actin are exposed. Alright. Is that the last step? Absolutely. That tropomyosin moves, that moves out of the way of the binding sites so the myosin can bind to the actin. So B comes last. And once those myosin binding sites on actin are exposed, well, then the cross bridges can form and the muscle can contract.

Alright. We're going to go into those in a step-by-step fashion coming up, but first, we've got some more practice problems tomorrow.

Voltage gated channels respond to the depolarization of an action potential by releasing Ca$^2$$^+$. Where are these channels located?

• A. Sarcolemma.
• B. Sarcoplasmic Reticulum.
• C. Sarcomere.
• D. T-Tubule.

How does tropomyosin regulate muscle contraction?

• A. Tropomyosin binds calcium, changing the confirmation of troponin.
• B. Tropomyosin prevents myosin heads from binding to actin in the absence of calcium.
• C. Tropomyosin wraps myosin preventing actin from binding in the absence of calcium.
• D. Tropomyosin releases calcium during an action potential.

In a skeletal muscle fiber, which structure would you expect to have the greatest total surface area?

• A. Sarcolemma.
• B. Sarcoplasmic Reticulum.
• C. Sarcomere.
• D. T-Tubule.

C. Cross Bridge Cycle

To finish up the steps of muscle contraction, we're going to talk about the cross bridge cycle, and because this is our 3rd major stage of muscle contraction, we have it labeled here as C. So the cross bridge cycle, we're going to say, is the interaction of the myosin head and the actin in a way that leads to the sarcomere shortening. And that's our goal. If we want a muscle to contract, we need that fundamental unit of muscle contraction, the sarcomere, to get shorter. So we have this cross bridge cycle broken up into 4 steps here. But before we dive into this, let's just remind ourselves where we are in this process. At the end of the excitation-contraction coupling, we've dumped this calcium into the sarcomere. The calcium binds to the troponin. Troponin moves the tropomyosin out of the way. That exposes the binding site, and we said that that myosin head was just waiting there ready to go. As soon as that binding site was open, that myosin head is going to bind to the actin. So, that's where we're at. The first step is that the myosin head is going to bind to the exposed actin. And we have that shown in our illustration here. We see the actin here in sort of gold. We have the tropomyosin that's now moved out of the way. We can see those exposed binding sites and the myosin head comes up and it binds to the actin.

Now, one thing you might notice here that we haven't put in an illustration before is that bound to this myosin head we have an ADP and an inorganic phosphate. ADP and an inorganic phosphate are produced when you split or hydrolyze an ATP molecule, and ATP is that unit of chemical energy in the cell. So for this myosin head to have been ready to go, to be cocked and ready to go, ready to bind to that binding site as soon as it was exposed, it has to have already sort of loaded itself up with that chemical energy from the ATP. So before this started, this myosin head is already bound to an ATP and it's already split or hydrolyzed that ATP into the ADP and phosphate to capture some of that chemical energy, so it was waiting there ready to go. Well, now it's gone. Now it's come up. It's bound to that actin, so the next thing it's going to do, it's going to pull on the actin. We said that's all myosin really wants to do. Myosin wants to pull on that actin? Well, now it gets to. Myosin performs the power stroke. Power stroke, it pulls on the actin and that's going to move the actin and it's also gonna result in the release of the ADP and that inorganic phosphate. And so we can see that in our illustration here. Here we have the myosin head coming up, it's pulling on the actin in that way, and you can see it's releasing that ADP and it's releasing the phosphate. Now technically the phosphate and the ADP are released at different times in this process, but that's a level of detail you usually don't need to know. Usually, you just need to know that it's released as part of the powering of this power stroke.

Alright, so it's now pulled on the actin, it's moved the actin, but remember I've sort of always described it as almost like a hand over hand, again and again motion. So for this myosin head to be able to pull on the actin again, it needs to release from the actin. It needs to go back, get cocked again, and do the whole process over. So to release, it's actually going to need a new molecule of ATP. So ATP, a new molecule of ATP, we're going to say binds to the myosin head and that releases it from the actin. So we can see here we have the myosin head coming down, it's releasing, and that's because this new molecule of ATP has come in and bound to that myosin head. But now it needs to get back cocked, ready to go, it needs to transfer some of that chemical energy from the ATP into the myosin head. To do that, it needs to split the ATP or hydrolyze it into that ADP or inorganic phosphate. So we're going to say here, the ATP is hydrolyzed and that myosin head now moves into that cocked position and it is ready to go again. And if that binding site is open, it's going to go up again, bind to the actin, pull on the actin, a new ATP molecule will come in, bind, it will release, it will hydrolyze it, it will get cocked, ready to go again, and if that binding site is still open, it's going to do this cross bridge cycle over and over and over again. Alright. Let's look at an animation of this so that we can sort of see this whole process through. So we have the myosin there on the bottom, the actin on the top, and you can see that the binding sites on the actin are exposed, and this myosin head is ready to go. So it's going to come up and it's going to bind to the actin, and here it's going to already release that phosphate. And now it is gonna do this power stroke. It is ready to move, and as part of that power stroke, it's gonna release this ADP, and now it pulls on the actin. And that's our movement. That's been our goal. Now though, we need to release from the actin so that we can do it again. To do that, we're going to have this new molecule of ATP come in. It's gonna bind to the myosin head. That allows the myosin head to release. But to get cocked again ready to go, it needs to hydrolyze this ATP. It needs to split it into the ADP and the phosphate. That's gonna transfer that chemical energy from the ATP into the myosin head, and it can move back. Now it's cocked, ready to go, ready to do it all again. Alright. So, let's move back to our page here and just to finish things up, I just want to remind ourselves, well here we've been looking at one myosin head. But, of course, it's not just one myosin head doing this. During contraction there are going to be thousands of cross bridges that are going to contribute to the sarcomere, to the shortening of just one sarcomere. Right? When we think of the myosomere, this myosin filament, every filament had over 300 of these myosin heads. These hands reaching out ready to grab onto that actin. The myosin filament reached out in both directions from the middle of the sarcomere. To remind ourselves of our analogy at the beginning. We had these guys pulling on a rope. But it's not just one guy facing in each direction. You have to think of thousands of hands pulling in each direction, and this sarcomere had many myosin filaments. And remember, the sarcomere then is repeated over and over again. We said in a 10 centimeter muscle, you'd have something like 40,000 sarcomeres repeated end to end. And that's in just one myofibril. In a muscle fiber, you have a whole bundle of myofibrils. The muscle fiber then is bundled to make a fascicle and that fascicle, a whole bundle of fascicles makes up a muscle. So when you think about that, how many individual myosin heads? When you think about a muscle like your bicep or your quadricep contracting, you do all that math, all that multiplication, I have no idea how many myosin heads are contributing to the contraction of your biceps muscle. But it is a heck of a lot. Sort of an unfathomable number. Each individual myosin head is just pulling on this actin just a little bit over and over again, and when you multiply that all out you end up with these very large and powerful muscle contractions. Alright. We've now talked about the steps of muscle contractions starting with the action potential in the neuron and now talking about how this sarcomere actually gets shorter with the actin sliding over the myosin. That was our goal, so good job, everybody.

Steps of Muscle Contraction Example 5

Our example explains that the events of the crossbridge cycle as they relate to actin and myosin are numbered below. Separately, events as they relate to ATP are labeled ABC, but they are not necessarily in the correct order. We need to match the steps related to actin to the steps related to ATP by matching each letter to the correct numbered step. Note that not all numbered steps correspond to a step related to ATP. So here, numbered 1, 2, 3, 4, we have those steps of the crossbridge cycle, focusing on the interactions between myosin and actin. On the right, labeled ABC, we have what's happening with the chemical energy that's powering these steps, namely the ATP, the ADP, and the inorganic phosphate.

First, we have step 1, where the myosin head binds to the actin. This occurs when the myosin head, already cocked and loaded with chemical energy, encounters exposed actin once the tropomyosin moves out of the way. This binding does not directly correspond to any of the ATP-related steps listed. I'll note this with a dash, indicating no direct correspondence.

Next is the power stroke in step 2, during which the myosin head pulls on the actin, resulting in movement. This corresponds to step C, where the ADP and inorganic phosphate are released from the myosin. While the release of these molecules may not happen simultaneously with the power stroke, they are part of powering that movement. I'll assign letter C to this line for step 2.

In step 3, the myosin head releases from the actin, a process necessary for the repetition of the cycle. This occurs when ATP binds to the myosin head, facilitating its release from actin. Thus, step 3 corresponds to letter A, the binding of ATP to the myosin head.

Finally, in step 4, the myosin head moves into the cocked position. This movement requires the transfer of chemical energy from ATP to the myosin head, which occurs through hydrolysis of the ATP into ADP and inorganic phosphate, denoted as step B. Thus, letter B is assigned to this fourth line.

Understanding these steps and how they are powered by chemical energy, which is then converted into mechanical energy, is crucial. Familiarize yourself with this process, and try more problems to reinforce your understanding.

Which part of the cross-bridge cycle is called the power stroke?

• A. Cocking of the myosin head.
• B. ATP hydrolysis.
• C. Myosin pulling the actin.
• D. Binding of myosin heads to actin.

What would happen if a muscle completely ran out of ATP during a muscle contraction.

• A. The myosin head would not move into the cocked position.
• B. After the power stroke, the myosin would remain bound to the actin.
• C. The myosin would bind to the actin, but the power stroke would not occur.
• D. The sarcoplasmic reticulum would be unable to release calcium.

Here’s what students ask on this topic:

What are the steps involved in muscle contraction at the cellular level?

Muscle contraction at the cellular level involves several steps:

1. **Neuromuscular Junction**: A nervous signal triggers the release of acetylcholine (ACh) at the neuromuscular junction, which binds to receptors on the sarcolemma.

2. **Action Potential**: This binding initiates an action potential (AP) that propagates along the sarcolemma and into the T tubules.

3. **Calcium Release**: The AP stimulates the sarcoplasmic reticulum to release calcium ions (Ca²⁺) into the sarcomere.

4. **Binding Sites Exposure**: Calcium binds to troponin, causing a conformational change that moves tropomyosin, exposing the binding sites on actin.

5. **Cross Bridge Cycle**: Myosin heads bind to actin, forming cross-bridges, and perform a power stroke, pulling actin filaments inward, shortening the sarcomere.

6. **ATP Role**: ATP binds to myosin, causing it to release actin and re-cock for another cycle, enabling repeated contractions.

How does the action potential propagate in muscle fibers?

The action potential (AP) in muscle fibers propagates as follows:

1. **Initiation**: The AP is initiated at the neuromuscular junction when acetylcholine (ACh) binds to receptors on the sarcolemma.

2. **Depolarization**: Sodium (Na⁺) channels open, allowing Na⁺ to enter the muscle fiber, causing depolarization.

3. **Propagation**: The depolarization wave travels along the sarcolemma and dives into the T tubules, spreading the AP deep into the muscle fiber.

4. **Repolarization**: Potassium (K⁺) channels open, allowing K⁺ to exit, restoring the negative charge inside the cell.

This rapid sequence of depolarization and repolarization ensures the AP travels quickly, coordinating muscle contraction.

What role does calcium play in muscle contraction?

Calcium ions (Ca²⁺) play a crucial role in muscle contraction:

1. **Release**: When an action potential reaches the sarcoplasmic reticulum, it triggers the release of Ca²⁺ into the sarcomere.

2. **Binding**: Ca²⁺ binds to troponin, a regulatory protein on the actin filament.

3. **Conformational Change**: This binding causes a conformational change in troponin, which moves tropomyosin away from the myosin-binding sites on actin.

4. **Cross Bridge Formation**: With the binding sites exposed, myosin heads can attach to actin, forming cross-bridges and initiating the power stroke that leads to muscle contraction.

5. **Reuptake**: After contraction, Ca²⁺ is actively pumped back into the sarcoplasmic reticulum, allowing the muscle to relax.

What is the cross bridge cycle in muscle contraction?

The cross bridge cycle is the process by which myosin heads interact with actin filaments to produce muscle contraction:

1. **Cross Bridge Formation**: Myosin heads, energized by ATP hydrolysis, bind to exposed sites on actin, forming cross-bridges.

2. **Power Stroke**: The myosin head pivots, pulling the actin filament toward the center of the sarcomere, releasing ADP and inorganic phosphate.

3. **Cross Bridge Detachment**: A new ATP molecule binds to the myosin head, causing it to detach from actin.

4. **Reactivation**: The myosin head hydrolyzes the new ATP to ADP and inorganic phosphate, re-cocking into a high-energy state, ready to bind to actin again if the binding sites remain exposed.

This cycle repeats as long as Ca²⁺ and ATP are available, leading to muscle contraction.

How does ATP contribute to muscle contraction and relaxation?

ATP is essential for both muscle contraction and relaxation:

1. **Contraction**: ATP binds to myosin heads, providing the energy needed for the power stroke. The hydrolysis of ATP to ADP and inorganic phosphate energizes the myosin head, allowing it to bind to actin and pull the filament.

2. **Detachment**: A new ATP molecule binds to the myosin head, causing it to release from actin, which is necessary for the myosin head to re-cock and prepare for another cycle.

3. **Relaxation**: ATP is required to actively pump calcium ions (Ca²⁺) back into the sarcoplasmic reticulum, reducing Ca²⁺ levels in the sarcomere and allowing the muscle to relax.

Without ATP, muscles would remain in a contracted state, known as rigor mortis.