episode43

043 The Details of Muscle Contraction

Leslie Samuel IBTV, Physiology, The Muscular System 267 Comments

Join Leslie as he shares this last video on muscle contraction explaining with full clarity the smallest details on how this works.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 43, I am going to go into the details of muscle contraction. This is going to be the last video in the muscle contraction series, so, enjoy! Let’s get right into it.

You can always go back to Episode 42 to refresh your memory but, we said that the functional unit of contraction is called the sarcomere and, that is what we’re looking at right now. This unit is one sarcomere. We said that we have a thick filament that is called myosin and, we have a thin filament that is called actin. We said that, when muscle contraction happens, the more the neuron releases neurotransmitter that stimulates calcium release. When that happens, the fibers slide against each other just like this. So, as the muscle fibers becomes shorter, that is the muscle contracting. And you can clearly see that in this animation.

The reason we said that this can happen is because on the myosin filaments, we have these heads and those heads extend and bind to the actin. When they bind, they kind of flex so, it moves in this direction and that pulls the actin shortening the sarcomere.

What we are going to do today is we’re going to look at the details of what is happening there. We are going to look at six steps in muscle contraction. This is another image that’s showing something similar to what we’ve looked at. We have the myosin heads. Let me do that in a different color so that you can make sure to see it because we have a lot of red there. We have the myosin heads that are binding to the actin filaments.

Here, we are going to be looking at that in more details. We have the actin. Yes, it’s a different spelling because it’s from a different language but, on the actin filaments, there are two things that are very important. We have tropomyosin as you see here so that’s this long strand here. On top of the tropomyosin, we have troponin. This is a complex that we find all along the actin filaments.

Here’s the situation. Because this is here, the myosin heads want to bind to the actin. There’s some binding sites on the actin so, let’s say this is a binding site right here. But, what’s the problem? The tropomyosin is covering that binding site so, the myosin heads cannot bind. Okay, so, we have these myosin head-binding sites all along the actin; myosin heads want to bind, we have all these myosin heads ready to do their business but, they cannot because it’s blocked by the tropomyosin.

All right so, let’s go now and look at the six steps of muscle contraction. Step number one. Calcium is released from the terminal cisternae. Remember we said that the terminal cisternae is a part of the sarcoplasmic reticulum and that is where calcium is stored. So, calcium is released. You can see here, we have this little binding site for the calcium so the calcium now comes and binds the troponin. So, here we have calcium and binding to the troponin. And then, what that does is it causes a conformational change. To put it more simply, we’re just moving the tropomyosin-troponin complex. So, that moves and, when that moves, it exposes the binding sites on the actin. That’s step number one. So, step number one: We had calcium in the terminal cisternae that is released when there’s a stimulus. The calcium ions bind to the troponin causing a conformational change in the troponin-tropomyosin complex. In other words, it’s moving out of the way. And then, the next step can happen. That step is, the myosin heads can bind to the binding sites on the actin. So, this is the one binding site. For simplification we’re just showing one myosin head but, as you know we have many myosin heads all along this actin.

In order for that to happen, we said that there’s normally ATP that’s on the myosin heads and you saw that, you saw that in the previous figure. But, that ATP has to be hydrolyzed to become ADP and an inorganic phosphate (Pi). So, we have ADP and the phosphate. All right, so, we have the myosin head that has bound to the binding site on the actin. That was step number two. Step number three. This ADP and Pi is released from the myosin head. I’m not showing that in the figure but, just imagine that being released. When that is released it causes the power stroke. In other words, it causes this guy here to flex. And when it flexes, it moves in this direction and that causes the actin to slide across the myosin.

Okay, so, calcium is released, step number one, binds to the troponin, causes this change in the troponin-tropomyosin complex so that it gets out of the way; ATP being hydrolyzed into ADP and inorganic phosphate is a state that this needs to be in for the myosin head to bind. When those are released, the myosin head flexes and we get the power stroke. That’s step number three.

Let’s go to step number four. Step number four is another one that I’m not showing but, we have ATP. So, this is an ATP molecule that comes in and binds to the myosin head. When that binds to the myosin head, the myosin head then detaches from the actin so, we no longer have that connection. That’s step number four.

Step number five. ATP is hydrolyzed which re-energizes the myosin head. So, once we have ATP being hydrolyzed like it is here, that re-energizes the myosin head and it’s ready to go again.

One more step, step number six. This calcium here needs to be gone. So, we have the terminal cisternae and it’s not shown here. So, I’m just going to draw it with my great artistic skills. We have calcium pumps in the terminal cisternae. What that does is it basically pumps that calcium back in. So, we have calcium being pumped back in that is going to cause the troponin-tropomyosin complex to go back to where it was and it’s going to be blocking… I should have done that in green to keep the consistency. Oh, I still can, why not. Okay, so we have the troponin-tropomyosin complex that is blocking once again the binding site for the myosin head.

All right, so let’s recap on that real quick. Step number one: Calcium is released, binds to the troponin. When it binds, it causes a conformational change or a shift, whichever one you want to call it, it causes that shift exposing the binding sites on the actin. Step number two: Myosin head binds to the actin. Remember that the ATP has to be hydrolyzed into ADP and Pi in order for that to take place, it has to be re-energized. It gets that from that hydrolysis process. Step number three: ADP and Pi release that causes power strokes that causes this guy to flex. Then, ATP comes in, binds to the myosin head, causes the myosin head to be released from the actin. The myosin head gets re-energized when the ATP is hydrolyzed back into ADP and Pi. Calcium ions are pumped back into the terminal cisternae and this process can happen again.

Well, that’s pretty much it. That is muscle contraction. If you have any questions, go ahead and leave them in the comments. That’s all for this video, and I’ll see you on the next one.

296 comments
Dinesh
Dinesh

what is the role of that MG2+ ion shown in the picture

Pablo Gonzalez
Pablo Gonzalez

Great teaching, I actually learned it, super simple!

Dave Seward
Dave Seward

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sagala40
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Enrika
Enrika

Hi Leslie, thanks for great videos they are so easy to understand and informative. However I did missed one think in muscle contraction video, at school in the UK we been talk about the cross bridge, can you explain me which part of the contraction called cross bridge. Thank you!!

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Lucas Cocco
Lucas Cocco

Titin is a giant protein that functions as a molecular spring which is responsible for the passive elasticity of muscle.

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Jeroen Rooman

What is the funtion of Titine on muscle contraction?

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visswaayful

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Ameen Ahmed

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Weston Stover
Weston Stover

Step 1 can be expanded on a bit: - AP traveling down T-tubule activates (Dihydropyridine) L-type Ca channels causing Ca influx - Ca influx acts at Ryanodine Ca dependent Ca channels on the Sarcoplasmic reticulum causing the release of sarcoplasmic reticulum Ca stores. - Ca then can bind to troponin C, etc, etc ,etc Other than great video!

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