Health and medicine
Check out how the amount of Myosin that is tugging on your heart can change depending on your activity level! Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- What is the z-disk made of?(9 votes)
- The Z-disc (or Z-line, as he says at3:15) is made up mostly of a protein called alpha-actinin. I got this out of my undergrad textbook (Marieb & Hoehn 2013), but this is not something undergrads are expected to learn.
I hope this helps.(9 votes)
- doesn't the SA node stimulate the heart to beat at approx. 120 bpm? Yet resting HR is approximately 60 bpm. What is the mechanism in which the Parasympathetic nervous system keep the heart at approx. 60bmp at rest?(3 votes)
- The parasympathetic nervous system slows down the heart rate through the release of acetylcholine by vagal nerve. It hyperpolarizes target cells by opening potassium channels that would require more calcium ions to enter the cells to keep HR at 120 bpm. The calcium release is induced by norepinephrine during sympathetic stimulation (such as stress, anxiety, or exercise). In the absence of such stimulation, the heart rate is at about 60 bpm at rest.(6 votes)
- What happens to the Ca2+ after a muscle contraction? What makes it leave the cell - or go back inside the sarcoplasmic reticulum?(3 votes)
- There is a pump in the membrane of the sarcoplasmic reticulum called the Ca+ ATPase. It uses energy to sequester Calcium back into the Sarcoplasmic reticulum.
As a secondary Calcium transport mechanism, there is also an antiporter in the muscle cell plasma membrane that uses the electrochemical gradient of Na+ (eg: lets sodium flow into the cell) in order to pump calcium out of the cell. This Na+ that flows into the cell must then be extruded back out of the cell using the plasma membrane Na+/K+ ATPase.(6 votes)
- Does adrenaline affect this process in any way?(5 votes)
- The main effect of adrenaline on the heart is increased rate. Norepinephrine (or noradrenaline) is the hormone (neurotransmitter) involved here because it increases force, which is a function of this kind of muscle cell (this is the part in the video at1:10where he says: "to be clear, this is a ventricular heart cell"). When you get deeper into it, you have to start learning about corresponding receptor sites and their effects in different parts of the body.(5 votes)
- Is there a video where Rishi explains what norepinephrine is and how it works with sympathetic nerves?(4 votes)
- Not Rishi, but there's probably a video that will help you in the neurology section:
- When the Z-Disks are pulled together (3:27), this causes cell contraction, correct? So is this what ultimately causes the muscle that the cells are part of to contract, or I am misunderstanding?
If this is correct, and Myosin is working more when you are more active (7:00), is this why your heart beats more when you are walking or running rather that sitting? Also, calcium is being used in this process, especially when you are more active; does this mean you need more calcium when you are being active than when you are not?(4 votes)
- In some earlier video there was an explanation that actually Ca2+ that is going to the heart cell throught t-tubules is binding some receptor that will make Ca2+ realesed from sarcoplasmatic reticulum. So I am wondering if the force that pushes heart cell to work (respectively amount of myosin heads binded to actin) is not the same at all situation (active vs nonactive) and what differs is time when cell reach some critical level of Ca2+ that will lead SR to release more Ca2+(3 votes)
- The strength of a muscle contraction (including that of the heart) ultimately depends on the amount of Ca2+ in the cytosol: more calcium exposes more binding sites on actin for myosin, which in turn allows more crossbridge cycling to occur. The autonomic nervous system regulates the heart muscle by modulating the frequency and force of heart muscle contractions.
If you increase the frequency of action potentials, then this will in turn increase the amount of Ca2+ that is released from the SR and will result in increased cardiac output. Therefore, the force of the cardiac muscle is driven chiefly by the neural system but is strongly influenced by hormones. For example, epinephrine increases action potentials which increases heart rate. Thyroid hormones, insulin and glucagon primarily increase the force of myocardial contraction, but glucagon also promotes increased heart rate.
Source: Principles of Human Physiology, Cindy L. Stanfield, 5th edition.(3 votes)
- Are there a certain amount of myosin heads her myosin molecule?(2 votes)
We're going to do a little comparison. I'm going to draw three different people here-- or it could be the same person, I suppose-- in three different situations. So you've got the first person just kind of sitting and maybe they're watching a YouTube video on their laptop. And you've got a second person who's actually going for a little walk. Let's see if I can draw this person walking. And you've got a third person who's-- let's say this person is actually really active and they are running. So they are actually in full stride, running. And maybe they're late for a test or something. So-- oh, let me actually change that so their arm does not look broken. So there have these three people. And they're running and walking and sitting, right? So you can imagine if you were to take a look at their heart cells they might be doing different things. In fact, let's draw all three's heart cells and show you what they might be doing. So we've got our heart cell. And in this case I'm actually going to draw also a nerve. This is going to be the sympathetic nerve. I'll write an s, for sympathetic nerve. And the heart cell, just to be clear, is going to be a ventricular heart cell. So this is a-- I'll write ventricular heart cell here. Just so that we know we're not talking about some pacemaker cell or some other cell in the heart. This is a ventricular cell. And now, just to remind us of a couple things we know, this ventricle cell is branched. And it's got two little nuclei. And it's got some receptors on its surface waiting for, potentially, norepinephrine from that sympathetic nerve. Right? Now inside of that heart cell, if we were to dive inside of the heart cell, you might see some actin. And you'd see that at the ends of the actin. It's a Z-disk, right? So we've got a Z-disk with our actin. And I've drawn this far too close together. Let me actually make a little bit of space in here. But you get the idea. You've got our actin kind of like little ropes. And in the middle you've got our myosin. And our myosin, you remember, is basically going to have a whole bunch of myosin heads. And these heads are going to want to do work. They're going to want to pull the actin and yank that Z-disk closer to the middle, right? That's what they want to do. So these myosins are hanging here, waiting to do work. And their trigger for work, of course, is going to be calcium binding the troponin C and pulling tropomyosin out of the way. So this is our actin and myosin. This is our actin up here. And we've got our myosin in the middle. And then finally, I'll draw one last thing and that is the titan. And the titan, remember, is a protein that basically is going to attach the myosin to the Z-disk. Remember, our Z-disk is this thing at the end. This is our Z-disk over here. Let me just kind of draw it in for us. This right here is our Z-disk. I've been calling it a Z-disk. Sometimes you see Z-line. That's kind of interchangeable. But this is our Z-disk right here. And it's basically tethered by those actin ropes, you can think of them as. And we're going to use those ropes to pull the Z-disks together. So this is basically the set up and what it looks like. And now I'm actually going to just take this and cut and paste it a couple of times so that we can actually use this for our two other situations. We've got one there. And we can actually do it again and have it like so. So now you can see our three situations side by side and our three setups with our actin, myosin, and our Z-disks. So what would happen in situation one? Well in situation one you're just hanging out. You're happy. You're maybe watching something kind of funny on YouTube. And you don't have much sympathetic drive. You don't have any stimulation coming from your sympathetic nerves. You're not running or you're not frightened, let's say. So you have-- you know, your normal amount of calcium comes into the cell when it's time to contract. And so you get a little bit of calcium in here. Looking over at the other side, when the calcium comes in, you have a low amount of calcium, let's say. Because not much is coming through the channel. You're not activating that channel in any way. So that calcium, let's say, it binds here and it binds here. And let's say a little calcium binds here and here. And when I say binds remember I mean it binds the troponin C. Remember that. So the calcium binds there. And what do you get? Well let's draw a little table on the side of-- this is, let's say, the proportion-- I'm trying to make sure I phrase it correctly-- the proportion of myosin heads that are working. And if you count them up, if you count up all the little purple heads-- you can do that right now-- you'll see there are 20. So this is the proportion of myosin heads that are working. And what would you get for this first situation? Well, at four spots the calcium has bound, right? And it doesn't bind forever. At some point the calcium is going to be kind of taken back into the sarcoplasmic reticulum, or thrown out of the cell. But for the time that our heart is contracting, for that brief bit of time, how many myosin heads are working? Well we've got this guy over here. This guy. And we've got this guy down here. And we've got this guy and this guy. So four of them are working. And that means that 16 are not working. So 4 out of 20 are working. So really we've got-- what does that work out to? 20%. That's equal to 20% of them are working. So that's not too many. But what's going to happen? Basically these myosin heads are going to pull-- let me erase the little arrows, not to confuse you. But basically these myosin heads, these four that are working, are going to pull the actin that way and that way. And this way and this way. And the Z-disks will come closer together. Let's not be confused about that point. The Z-disks definitely will come together. But it's going to take a while. Really it's like having four-- you can think of it as four of your friends pulling on a rope. It's not as effective as having 20, right? So let's go to situation number two. So in situation number two, let's say now you're going for a walk. And you're enjoying the beautiful day. But you're walking, right? And so there's a little bit of activity. And so let's say your sympathetics are firing a little bit, a little bit of a sympathetic drive here. And a little bit of neurotransmitter gets released. And so this neurotransmitter, we know, is called norepinephrine. And so a little bit gets released into that space between the nerve and the cell, the heart cell. And it binds to, let's say, one of the receptors. So one of the receptors is going to fire. And during a muscle contraction you've got calcium coming in. But because that receptor fired now you have a little bit extra calcium coming in. Meaning that channel has been activated so that it's letting more calcium in. OK so if more calcium's coming in-- let's now take a look at our diagram. Now you've got a little bit more calcium coming in and binding. And I'm just choosing them by random, in a sense. But let's say these six. And on this side let's just choose another six. Let's say four up here and maybe a couple down here are going to bind calcium. So you've got troponin C's that are binding calcium. And of course that means that those are the myosin heads that get to work. And so in total, how many myosin heads are working? Well now instead of only four total, we've got-- what is that-- 12 myosin heads out of 20 working, or 60%. So it's really gone up considerably. So just as before, you're going to have the Z-disks getting yanked in. But now the yanking is going to be much more forceful because you've got many more myosin heads actually involved in dragging that Z-disk over. So this is actually quite interesting because now you can see that you have, as a result of the sympathetic drive, more force in your contraction, your heart contraction. So you can probably guess where the last one is going to go. Now you're running. You're excited. And let's say, now instead of just a little bit of transmitter, you've got tons of neurotransmitter being released, lots and lots of norepinephrine. In fact, let's say a little bit over here. And you've got all three receptors kind of firing, right? Because all that norepinephrine is allowing lots and lots of stimulation to the cell. And so with all this norepinephrine your calcium channels are going to be really active, right? They're going to be pouring in calcium. So instead of just a little bit of calcium, now when you have a contraction you've got lots of calcium dumping into the cell, right? And this is, of course, just during the time when your contracting or squeezing. So with all this calcium now it's going to go and bind the troponin C everywhere it can find the troponin C. It's going to come and sit basically everywhere. And all these myosin heads are excited because now they all get to work. And with this full set of myosin heads working-- you have 20 out of 20 working. You have 100% of them doing their job. And as a result you can see that now you're going to have a huge mechanical force, enormous forces, yanking those Z-disks closer together. So in all three situations you do get the Z-disks coming together. But remember, the period of time that the calcium is in the heart is finite. Right? It's not like it's there forever. Because, at some point, that calcium's going to get, as we said, brought back out of the cell or into the sarcoplasmic reticulum. So while it's there, for those few precious moments that the calcium is there, you really want your heart to be able to do as much work as possible. And in this case, you're actually seeing that here at the top-- let's actually draw an arrow-- at the top this side there's really low energy use because not too many of the myosin heads are actually converting ATP to ADP plus phosphate. So remember, the myosin heads that are working-- those are the only ones that are actually converting ATP to ADP plus phosphate. And the ones that are not working are of course not doing that. So in this case you can also see that, in addition to force, the other thing that's less in this sitting situation is that it's a low-energy state. You're not really burning any energy. Whereas over here, when you're running, each one of these myosin heads is cranking through ATP. It's making lots and lots of ADP. So it's using lots of energy. It's a high-energy situation. In other words, you're using up a lot of energy here. And so of course this makes sense. Right? Because you think, well if I go for a run of course I'm going to use up energy. Whereas if I'm just sitting I'm not using much energy at all. And now you can see exactly why that's the case. Because in the running situation, all 20 of your myosin heads are burning through ATP.