03.04 Muscle Contraction

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Outline

Overview

  1. Micromechanics of muscle cell contraction
    1. Sliding filament theory
    2. Stretched muscle cell
      1. Z-lines further apart
      2. Filaments do not change dimension
      3. A band doesn’t change
      4. I band gets longer
      5. H band gets longer
    3. Maximally contracted
      1. Z lines get closer (sarcomere shortens)
      2. Filaments do not change
      3. A band doesn’t change
      4. I band disappears
      5. H band disappears

Nursing Points

General

  1. Micromechanics of muscle cell contraction
    1. Sliding filament theory
    2. Stretched muscle cell
      1. Z-lines further apart
      2. Filaments do not change dimension
      3. A band doesn’t change
      4. I band gets longer
      5. H band gets longer
    3. Maximally contracted
      1. Z lines get closer (sarcomere shortens)
      2. Filaments do not change
      3. A band doesn’t change
      4. I band disappears
      5. H band disappears

References
Betts, J.G., et al. (2017). Anatomy and physiology. Houston, TX: OpenStax, Rice University. Retrieved from https://openstax.org/details/books/anatomy-and-physiology?Book%20details

See Animation of Contraction

Transcript

All right in this lesson we’re going to take a look at muscle contraction and their mechanics.

The first thing we want to look at it something called the sliding filament theory. And what the sliding filament theory is is it proposes that the that the filaments aren’t shortening but that they’re actually passing by each other. And you’ve got two different types of element groups with this that we’re going to look at you. You’ve got thin and thick and the thin filaments are actin, troponin and tropomyosin and the thick filament is myosin. And we’re going to talk about that here in a second but that’s what I want you to remember is that they don’t shorten they actually just pass by each other.

When you’re looking this, we need to go over a couple things here so this is your a band right here, and you’ve got the I-Band and you got your M line which is your midline which houses is your H-Zone. “S” actually stands for a sarcomere which is the functional unit that were actually talking about here. And then there’s the Z-Line, which are your edges of your sarcomere And when your muscles get stretched out, think about it, we want to try to make this as long as possible. And what happens is that your Z lines go out and they get further apart, your I and H bands get longer and then you’re A-Band doesn’t change note between stretch and maximally contracted you’re a man isn’t going to change at all it’s that you’re going to have changes within your I and H band. So if we look at the other one go the other way in maximally contract a muscle, what we’re going to find is that your I & H bands essentially disappear and your A-band is the same but you’re Z bands get closer. They go in or the Z-lines get closer so this is something I want you to think about when we were talking about the myofilament as they actually shift past each other to create a shortening of the entire muscle cell. Before we do that we have to understand how we get the impulse from the nervous system.

So we’re going to look at something action potential. What the action potential is that it’s basically the nerve impulse to where whatever destination we’re going to. So in this instance what we’re looking at as we’re looking at something called a neuromuscular junction or something that I’ll call later the nmj. And when we’re talking about the neuromuscular junction we’re talking about the nerve impulse going from the nerve to the muscle fiber. And this is how it happens. We need to look at some quick anatomy though. This is the end foot, this is the end of the axon. And then you have your synaptic cleft which is the gap or the space between the neuron and the muscle fiber and then you’ve got the motor end plate which is part of the sarcolemma which is the the cell membrane of the muscle. What happens is we want to get the nerve and want it to continue. So you got this gap and so we basically want to say hey we need to continue this nerve impulse down from the nerve all the way to the muscle fiber to get it to do what we need to do. So you get your action potential that comes down the nerve and it hits this end foot where you had this influx of calcium. And this calcium enters the end foot and stimulates these. These are vesicles and the vesicle stimulates the release of acetylcholine into the synaptic cleft, and they kind of move down this way and attached. And then they release the acetylcholine across the synaptic cleft and they cross here and basically bridges the gap here. And then the acetylcholine binds to these receptors in the motor end plate and then what happens is it promotes the action potential down the muscle fiber. And when that happens it passes over the sarcolemma end of the T tubules and you get this influx in calcium, which is what we want because calcium is required to go into the myofibril and cause contraction.

So what does that look like?

Before we figure out what it looks like we have some conditions that we have to meet. The first thing we want to look at is something called the all-or-none principle. You cannot have one or two muscle cells contract with a nerve stimulus. Basically all muscle cells contract or none at all. So that’s something that you need to be mindful of. The other thing we need to think about is normal temperature. In order for optimal muscle contraction you can’t have excessively high or excessively low temperatures. Also a muscle contraction is not going to happen normally in the presence of fatigue substances so things are carbon dioxide, lactic acid or ADP.

So what are the resting conditions that need to be in place before we actually have a muscle contraction? Well a couple things going to happen first off. Your tropomyosin needs to be covering the active sites on the actin molecule. You have this thing that looks like this – this is your actin molecule. It looks double-helical and then you have this other thing which is your tropomyosin. And in its normal spot it covers the active sites. The other thing is you’ve got your myosin filament, your thick filament, and you’ve got your myosin head. And it has to have a ADP plus inorganic phosphate attached. It can’t be ATP because that means it’s in its resting position. That means it’s all the way forward. What happens is it when you have ATP attached it pulls it back it’s like cocking a gun. The other thing that you have to have is low calcium in the sarcoplasm. If you have high calcium you have a whole cascade happen, which I’ll explain in a minute. But when you have a low calcium that means it’s resting. When you have the influx of calcium that triggers a muscle contraction.

So what is a muscle contraction look like? Well, we’re going to show this in an animation in just a second but I want to walk you through the process.

First off you have an action potential that releases calcium. You’ve got to have calcium first then calcium binds to troponin and that causes the tropomyosin to to expose the active sites on the actin filament. When that happens the activated crossbridge combined with the expose act and one with that essentially means is that the myosin then has a way to attach to the head or that the myosin head attaches to the actin and then basically binds to it. And then the myosin deactivate and slide that process over or slides to filament in over and that shortens the sarcomere.

So we’ll go through it again you’ve got an influx in calcium. Then it binds to the troponin; it causes the tropomyosin to expose those sites. Then you have the myosin crossbridge activation and then when the myosin and deactivate it slide it over and it shortens a contraction and shortens the sarcomere and that means you have a contraction. So then what happens well ATP comes back and attaches backs that myosin crossbridge. Well this part is a little bit counterintuitive because you think you need ATP for energy. Well in this case what happens is normally the myosin head is here with ADP. ADP plus the inorganic phosphate but the problem is we need it to go backward. Well it requires energy for that process to happen so that you can basically come back and push that filament forward again. So in order to do that you need to get it in this position and that requires ATP. So in relaxation what happens is it comes and the ATP comes in and it moves his head down and it disconnect any actin and reactivate it and returns it to this resting position. Calcium returns to the sarcoplasmic reticulum so you get that decrease in a calcium. The tropomyosin goes back and recover his act of those active sites and then you get the thin filaments returning to their resting position

So I know you’re looking at this going oh, hold on what is that?! All right so let’s let’s start from the beginning and look at what we have. So you’ve got the myosin complex here which is what we’re looking at which this is this guy. Then you’ve got your actin helix and tropomyosin. So this is your actin right down here and then your blue there we’re looking at is the tropomyosin. The troponin which is important here is the purple and then you got your calcium. So remember the process. Calcium comes in first, you have action potential that says hey we need a muscle contraction. Calcium comes in and attaches when it does the troponin, it activates the tropomyosin which exposes the active sites. When that happens then is kind of the next phase. Which is you have to have all those things happen before you can even get myosin to do his thing. When that happens the myosin is immediately attracted to it. Then you have this many have if you look you’ll see the ATP the green ball right here it comes in. And it comes on when it does the myosin head, it lifts up that’s because of ATP is putting it is basically putting back in that position to slide it forward, slide it forward and then moves up and relaxes. You may also see this this little gray pyramid triangle thing comes in and basically what that does is that helps to facilitate the process of converting ATP to ADP plus inorganic phosphate which is required to be in that resting position. So I encourage you it’s a lot to study this process, to think about what we talked about

So let’s recap.

Remember you’re contraction components. You need myosin, actin, troponin, tropomyosin. You also need calcium and ATP in order to make contraction happen. Myosin this is your thick filament and these other ones are your thin filaments. These makeup your i-band and the thick filament is your a band.

Remember your action potential goes from the input of the axon to the motor plate via the synaptic cleft and the reason it happened is because of acetylcholine. You get that acetylcholine that crosses it and it continues to action potential down the neuromuscular junction, across syndrome muscular junction, down a muscle fiber

You got your normal contraction and the things that you need for normal contraction. Don’t forget that you need your normal temperature and you have to be absent of those fatigue substances like CO2, so carbon dioxide, ADP, and lactic acid

Remember that we’re talking about the the sliding filament theory that the sarcomere shortens because the thin filament passes the thick filament.

And then finally ATP and calcium. Just like we talked about here are required to create motion from that myosin head and to reveal those active sites.

I know this lesson was a lot thank you guys for hanging in there. Make sure you check out all the resources attached to this lesson. Now go out and be your best selves today and as always happy nursing.