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I know when you see me, the first thing that goes in your mind is holly cow look at his muscles. They are breath-taking. I know. While true, it isn’t just the incredible definition that makes them so awesome. It’s the ability to contract and that’s just due to some weird ballet of molecular events.
Muscle contraction has fascinated scientists for quite sometime. I mean the sliding filament theory came out as a way to explain how muscles are able to shorten and generate force, is one of the first detailed of molecular events well supported than explained in physiology.
Because of that it’s become one of those classic things that they’ll ask questions about on test. I’ve seen it appear in the AP biology essay section more than once. To start this off though you need to understand the basic terms used to refer to the different parts of a muscle cell. Once you got that down, we’ll take a look at what the heck is a sarcomere, the basic contractile unit of a muscle cell. And then describe in general sliding filament theory.
Then, with the big picture under your belts, we'll go and look at what are those molecular events in muscle contraction.
My incredible muscles are an example of what’s known as skeletal muscles. There is three kinds of muscles in your body, the skeletal muscles, the one that go under your skeleton. The cardiac muscle cells or cardiac muscle tissue that is the walls of your heart. And then the smooth muscles, or something that’s called visceral muscles. Which are the ones that line things like your intestines, or make up the muscles of your eyes, in the iris they at least that can open or shut adjusting that light coming in.
Generally when people are talking about muscle they are actually referring to skeletal muscles. So let’s discuss some of the structures of a skeletal muscle cell. Otherwise known as a skeletal muscle fiber for stupid historical reasons.
Skeleton muscles, the muscle cells can actually extend. Pretty much they lengthen one entire muscles. They are really long. Because of this, this requires that they have lots of nuclei both to ensure proper control and to make all the proteins that are within a skeletal muscle fiber.
Let’s take a quick look at this YouTube video. We’ll go ahead and make it big. And so here we have a skeletal muscle. So what’s going to happens is, skeletal muscle is made of these bundles called fascicles or fasciculi. Each one of these is numerous muscle cells. Let’s pause it here.
Do you see this outer layer? This outer layer is the plasma membrane or cell membrane of a skeletal muscle cell. Because of, again stupid historical reasons, it’s given its own special name. It’s called a sarcolemma. Sarco is a root that means flesh and because people are first doing these dissections on essentially meat or flesh, that’s why they started using sarcola. The sarcolemma is kind of a special membrane. It’s similar to the membrane of a nerve cell or a neuron. Because it can send along the length of this membrane, it can send special kinds of nerve signals called action potentials.
We are going to go ahead we are going to peel away the sarcolemma. And underneath it we see all these other structures. Let’s pause it there.
And here we still see that sarcolemma. These things labeled transverse tubules, those are connections those are actually part of the sarcolemma. They have been in-folded. And remember that I talked about the sarcolemma can send very fast signals. well those signals have to travel along a membrane. To ensure that the membrane signal, the action potential can get deep inside of the cells. So that the entire cell contracts all at the same time. That’s why you have these transverse tubules. T stands for transverse.
Wrapped around of the transverse tubule, on either side of that is, are these sacks of modified and endoplasmic reticulum called sarcoplasmic reticulum.
Can guess what are called the cytoplasm of a muscle cell as sarcoplasm. So anyway, the sarcoplasmic reticulum is the specialized part of the ER, like I said that stores up calcium. When an action potential zips along the transverse tubule, it triggers the release of calcium from the SR. Which is short for sarcoplasmic reticulum deep into these bundles here.
These bundles here are clusters that contract all proteins called niacin and actin, that are grouped together in what are know as myofibrils. Myo is another root word that means muscle, and if a big muscle cell is called a fiber, a little bundle kind of like a muscle cell but it’s not. It’s called a fibril, which means little fiber.
So you have myofibrils making up the protein engines of contraction. Each one has sarcoplasmic reticulum wrapped around it with transverse tubules connecting them to the sarcolemma. This allows first communication. There you go, the structure of the skeletal muscle fiber.
So now that we’ve discussed the structure of a skeletal muscle fiber,if you zoomed in on one of those myofibrils, you would start to see they form these bands. These banding pattern is called striations. And it’s one of the things that makes skeletal muscles cells and cardiac muscle cells look distinct from the smooth muscle cells. That striation, scientist when they were first studying skeletal muscle cells they start noticing that striation was this regular pattern. And they call this pattern a sarcomere.
So let’s take a look at what a sarcomere is. We’ll take a look at this pretty cool YouTube video. As you remember we had paused it here. Let’s keep it going a little bit as we extrude one of these myofibrils out. If we pause it now, let’s take a look at this. Here we can see this repeating pattern, end to end. And the entire myofibril which extends.
Like I said, previously entire length of the muscle itself will be made of hundreds, maybe even thousands of these sarcomeres. Here we can see the middle of one sarcomere. You have the structure you call the M line. It’s a group of proteins that hook together these blue things called myofibrils. Now the blue ones here are special one called myosin. The red ones are called actin. So actin and myosin are the two major protein myofilaments that can make up a myofibril.
The M line hooks together all these myosin lines so that they don’t get poured out of coordination. While here, the Z line, which is considered the end of one sarcomere, and the beginning of the next. The Z line is the similar plate of dent proteins that anchor together all the actins.
How can you remember that the Z line marks the end of one sarcomere? We’ll just think it's 'ze'line at ze' end of ze' sarcomere'. And Z is at the end of the alphabet. So let’s get rid of their labels and then we’ll go ahead and start labeling it. I have to make it small to do this. So let’s go ahead and do that.
Again this is a Z line so here to there is one sarcomere. That burning pattern that I talked about before, it's this repeating light and dark region. We kind of see this area here where we have the overlap, that’s a dark region. And so scientists call that an A band. While this lighter region here, they call an I band. So far so good. You do notice that it gets a little bit lighter in here, and that’s this region called the H zone. So some of the basic parts of a sarcomere which they could have, you will expect to be able to label it on the multiple choice section.
The basic parts are the I band, the H zone, and the A band, as well as the Z lines, that define the ages of a sarcomeres. It’s kind of hard to see on this video but actually from these myofilaments here, you have these little proteins called crossbridges. That reach up, that part of the myosin that they can actually grab a hold the actin.
When they do, on this side of the A band, the crossbridges pull this way. On this side, they pull that way. Let’s take a look at another video that will kind of show this.
So let’s take a look at this YouTube video, and we will go ahead and make it bigger. Before I get it started, I want to just remind you of where we were. So here they used red to represent the myosin and they used blue to represent the actin. But here again, we see our Z lines there is our H zone our, A band, our I band.
So let’s take a look and see how this works. So what we are going to do is, we are going to move this over. And if we pull out some of the actin in the myosin, we can see again here is our Z lines marking the end of the sarcomere. And what happens, let's pull out a few more, is that crossbridges pull inwards shrinking the H zone. If we add in more, you can see how as this happens, that one is shortening. And that entire shortening as this thing slide over each other, as this filament slide, that’s the sliding filament theory That’s the basic idea. Feel smart?
If you get an essay on muscle contraction, simply by explaining the stuff we just went over about the sarcomere and the sliding filament theory, that in of itself should get you a good two or three points on the essay. And that’s good enough to get a passing grade. But after we are done with this last stuff, you are going to be able to ace that. Especially if you toss in some other things like how skeletal muscle cells are voluntary but quick to fatigue.
So let’s take a close in look at how muscle cells actually do contract. When I mention that they are voluntary, remember, that means that your nerve cells send the signals directly to them and tell them when you want for them to contract.
Remember the action potential thing that I mentioned earlier? That zips along the neuron that goes to one of your skeletal muscle cells. Those kinds of nerve ells are called motor neurons, which just means that they sense most of the muscles. Let’s take a quick look at a video on YouTube that does a really good job of explaining or showing this entire process.
We’ll go ahead and we’ll make it larger. Before I get this started, here we see the motor neuron. Inside of the motor neuron, are these sacks filled with a chemical called acetylcholine. Remember that I said that action potential signal has to travel along membranes? See the membranes here are close, but they are not actually the same membrane. And action potentials travel along membranes. So in order to get from the motor neuron to the muscle, that’s why we need a chemical, this acetylcholine. It’s an example of a neuron transmitter. So let’s go ahead and get it started.
So when the action potential reaches the end of the motor neuron, that attracts the movement of the acetylcholine synaptic vesicles here, they start to dump their acetylcholine into this space called the synapse between the muscle cell and motor neuron.
Here we see the acetylcholine, now it’s drifting to these special proteins here called receptors, or acetylcholine receptors. They land and when that acetylcholine lands on the receptor, it causes it to undergo some changes, to allow sodium and potassium ions start moving across. We’ll pause it here for a moment.
Once the acetylcholine is on here, like I said, the sodium potassium start to pour in and this is what triggers off a the new action potential on the muscle cell. =
And with the acetylcholine there, it will just sit there sending our action potential after action potential. That would be kind of bad well because, it looks kind of freaky when I do that. Plus if I told my bicep contract, "Oh crap, it's stuck." And now if I ever need to pick up a pencil, I’m going to have to bend over the waist. And those muscles get stuck. So we need something to get rid of the acetylcholine now that we are done doing the contraction. And that’s the job of these green guys.
Let’s go ahead and get stated again. So these green guys or an enzyme called cholinesterase or acetylcholinesterase. And what they do is they break down the acetylcholine into couple parts, which gets sucked back by the motor neuron. Our action potential is going to start spreading in this process, kind of like how the waves spread in the stadium.
And as it travels on the sarcolemma, it comes to one of these guys. This is one of those transverse tubules. Like I said, it allows the signal to contract to get deep into the cell very quickly. I’ll pause it here for a moment.
I’ve talked about these action potentials but, to really understand what they are, they are this wave of sodium and potassium ions moving in and out of the cell. They can travel really high speeds. Sometimes upwards of more than 100 meters per second. And if you are travelling the length of your bicep, that’s pretty fast. When you are travelling deep inside the bicep, that’s over fast. So what is this right here? This is the sarcoplasmic reticulum. If you remember, it’s on either side of the transverse tubule. Each sarcoplasmic reticulum wrapped on its own sarcomere.
So the signals come along here, inside this. There little red guys, those are calcium ions. So let’s go ahead and get started.
Do you need to know the name of all these receptors and channels here? No, but what you do need to know is, as this happens, it triggers this channel, the opening. The calcium ions pour out in this massive rush. They are moving down a concentration gradient. They come to this here. Let’s pause it for a moment.
See this here, this is that thin filament. This blue guy up here, that’s the thick filament. This is myosin, this is actin. These little blue guys these are those things that I kept talking about called the crossbridges. Because they bridge the gap between the thick myosin filaments, and the thin actin filaments.
You may notice there is more than just one thing here. The thin filaments are made mostly of actin, but there is a couple of other molecules that are very important. And that’s this purpley guy here. You’ll notice that the crossbridge right now is kind of blocked by this purpely guy. That purpely guy controls the ability of myosin to grab. So they called it the protein that controls myosin.
Trop is a root word that talks about controlling, so tropomyosin means that it’s blocking or controlling the activity of the myosin. See this little yellow do dad, that controls tropomyosin. Now it'll be kind of silly to call tropotropomyosin. So they just called it troponin. And that’s what the calcium is going to bind to. And when it does, watch what the tropomyosin does as it changes shape.
Let’s go ahead and get started again. Let’s watch and we’ll see it rolls out of the way. And now the crossbridges can grab and start walking along the actin.
Now let’s pause it again and take a look at a different video.
So here we see that tropomyosin is out of the way, here is our crossbridge. It’s attached to the myosin binding site. As soon as that happens, here we see an ATP molecule. This crossbridge is already attached to this binding site. Now it won’t let go until we give it energy. It's kind of like a rat trap. When you set a rat trap, you store up energy and then it goes off and catches the rat.
And it’s not going to let go of the rat until you put more energy back into it. So let’s go ahead and see what this ATP molecule does to it.
It binds to it and it causes it to change shape just like what you do with the rat trap, and pulls back. Let’s pause it for a moment. See what it’s done? It’s broken the ATP into adenosine diphosophate and a phosphate ion. They are still stuck to it, but the energy from the ATP has now been transferred to the crossbridge. It's changing shape. Just like if you pull back a bow and an arrow, you are transferring your energy into the bent shape of the bow. Or when I pull back my rat trap, I'm transferring my energy to the spring. Let’s go ahead and get it started again.
So now it’s a now it’s a cocked crossbridge. If there is an open binding side, it will nearly grab and fire off and pull. Letting go of the adenosine diphosphate and phosphate ion. Here comes another ATP and it keeps just grabbing and pulling, walking its way along the actin, pulling it in towards the middle of the sarcomere. Shortening that age cell. So let’s pause it again.
And we are going to go ahead and we are going to take a look now at back at that original video. So here we go and so again we are going to see our crossbridges walk their way along the actin myofilament. What makes this process stop? Remember the calcium? Here is the sarcoplasm reticulum. How do we get the calcium away from the troponin and tropomyosin so that it will block that binding sites again? We spend some more ATP. And we pump the calcium back into the sarcoplasmic reticulum. Once that happens, then we’ve carried away all the calcium. It’s now stuck inside of the sarcoplamic reticulum, the calcium that is left falls of the troponin and tropomyosin complex, and winds up in the SR.
Once an ATP molecule grabs a hold of the crossbridge, it will let go. If the troponin and tropomyocin complex has blocked the binding sites, then it can no longer grab and it stops. That’s the end of muscle contraction. Just a weird little side note.
What happens if there is no ATP? So it can’t let go. Then it stays locked in contraction. And this is something that may happen if you’ve ever heard of people who are dead being called stiffs. Ever wondered why that happens? That’s because after about 30 minutes of being dead your cells have run out of ATP. So whatever position is crossbridges are stuck in and they no longer have ATP to let go. And so you start suffering the stiffness, it's called rigomortis, stiffness of the dead.
So now you know the process of muscle contraction. If they ask you any essays about it, the first thing to do, is to toss out a little bit of your knowledge of the anatomy of the skeletal muscle cell. I mean just even saying it’s a skeletal muscle fiber, it’s likely to get you a point. Then make sure you go through the basic process. The nerve cell, called a motor neuron, will have an action potential reach its end. It will then dump out that acetylcholine or otherwise its abbreviated ACH molecule. And that drifts across to the receptor proteins on the surface of the sarcolemma, the membrane of the cell, another point.
The action potential now starts a new and spreads out across the sarcolemma going deep into the cell by means of those transverse tubules. As the action potential swoops down past the sarcoplasmic reticulum, that triggers channels to open up in the sarcoplasmic reticulum, and allow out the calcium that’s been stored.
The calcium floats to the myofibrils. There in the myofibrils, it sticks to troponin which pulls the tropomyocin out of the way. So now the crossbridges of myosin thick filaments can bind to the actin on the thin filaments. Remember, the crossbridges are like the clocked rat trap, with energy already stored in form of the ATP. That fires, pulling on the actin. On one side of the sarcomere, the actin is pulling this way.
On the other side of the sarcomere, the actin is pulled in that way, Shortening the distance between them called the age cell. Those crossbridges just keep going, grabbing and pulling grabbing and pulling. Remember they can’t let go until our new ATP provides the energy to re-cock them. And then off they go.
So comes in, comes in, comes in, this process continues until back of the synapse, the acetylcholinesterase molecule breaks up the acetylcholine. That floats back to the motor neuron. Without any more action potential sweeping the transverse tubules, the sarcoplasmic reticulum sick back in the calcium. That floats it away from the troponin. The troponin moves the tropomyosin back over walking the binding sides.
One last ATP molecule comes in to pull the crossbridges off, and the muscles now relax. That’s it. The one thing I would recommend you to do, is check out the bonus materials folder I’ve included all the videos that I used today and some others.
One quick way to review this for yourself is actually pretty useful. It’s just to watch them and then start it over, and do the narration yourself for the sound off. Do that and you will have mastered muscle contraction.