Cardiac Muscle Contraction

hi everyone in this video we're going to talk about cardiac muscle contraction and in order to do so we need to review and expand upon our previous discussion of cardiac muscle tissue so this drawing should look a little bit familiar what I'd like to do is take a cross-section of the cell and draw in some of the structures so that we could start to see them in three dimensions so first we have our sarcolemma which is the cell membrane of a muscle cell and inside of the cell is many many myofibrils and myofibrils are bundles of filaments particularly actin and myosin and surrounding the myofibrils are the sarcoplasmic reticulum which is comparable to endoplasmic reticulum in other cells but in muscle cells we call it sarcoplasmic reticulum and it's really notable for storage of calcium we also have these structures called t tubules and the t tubules are basically like tunnels that are that are sort of threw out then the muscle cell and then we also have abundant mitochondria so let's just draw the myofibril and we'll sort of organize the filaments that are contained within the Maya fibril so we can become a little bit more prepared to talk about what happens during muscle contraction so in orange we have myosin fibers and the myosin which we mentioned before as a protein has these little sort of heads that come off of off of it on either end of the myosin and eventually we're going to use the Masen head to interact with the actin so we'll use that structure to allow for muscle contraction the green is actin and actin is basically there are multiple forms of actin and I like to think of actin as kind of like a bead of pearls and in this drawing I only drew one sort of chain but actually a gene is sort of two intertwined chains of pearls and then it's surrounded by in blue tropomyosin and attached to tropomyosin is troponin in red we see Titan Titan is another a protein that actually sort of anchors the myosin to itself and then also connects to actin along what we call the Z line so the myofibril is actually very long and we sort of break it into segments and we actually divide the segments by Z lines so between one z line in another Z line we call that a sarcomere and so that's basically like the functional unit of the myofibril and so we can sort of think of the muscle shortening based upon this particular organization from z line to z line now the m line is like the midline of the of the myosin and then we have several bands and so the H band is basically the space between the actin filaments so it's just made of myosin and then there's an AI band and the AI band is the space between the myosin filaments where there's just actin and then the H band is kind of an adult little category because we actually sort of see an alternating pattern in between all the I bands is a band in a band contains the h band but basically it's from this from the point of overlap of the actin myosin where that begins all the way till it ends for the the myosin filament so basically it's like the entire length of the myosin the mouse and fibers and so we see this alternating pattern I bend a band I've in a band and so on and so what I just want to point out is that if we were to we'll just draw this a little bit smaller up here we can actually see that the as the IB end and the Abyan sort of alternate we get this sort of pattern and it actually looks like stripes so you notice that in this picture the filaments actin-myosin are in the horizontal direction but the stripes are actually in the vertical direction and so the stripes is what actually we refer to as striations and that's where we get our strategy appearance of cardiac muscle tissue okay so now let's draw the myofibril again in this drawing I want to talk a little bit more about the t tubules that we saw in the previous drawing and so in in cardiac muscle we see we are still organized by sarcomeres and then in between each of the sarcomeres is sarcoplasmic reticulum and that basically surrounds myofibril it's cylindrical in its conformation and then we'll just draw in the cell membrane and we'll see that the t tubules sort of extend along the Z line and so it's a little bit difficult to depict in this particular drawing but I want to sort of convey that the the t tube you will sort of encase that particular section of the myofibril but also extends to the cell membrane so technically everything that's sort of within the t tubulin is extracellular fluid okay so now let's just sort of pretend that we're taking a slice along the Z line we'll just draw a cross-section so we can look sort of at it head-on so we can see multiple mile five rolls in this particular cell and the myofibrils are surrounded by the t tubules only get basically is the sort of network of tunnels so i just want to reiterate that because this is a cross-section at the T tube you'll if we were to take a cross section at a slightly different place we wouldn't see exactly this picture we would see something slightly different so this is this is just sort of one view at the point in space where we decide to take this to make this drawing now let's take this same original drawing and let's actually slice it right down the middle it's almost as if we cut right into the middle of the myofibril so you can see the t tubules still extends above and because we cut a cross section here we're not able to see that the T tube you would actually sort of come out of the page and then still surround the the Z line of the mouth fiber book since it's no longer three-dimensional we're just trying it flat will destroy the Z line right in the middle and then we have of course our myosin filaments and our actin filaments and also just take sort of a cross-section of our sarcoplasmic reticulum so it's kind of like a web-like structure and so just sort of envision everything that's kind of within the purple lines is going to be sarcoplasmic reticulum and then within the bases in the middle be ECF and um so this'll above a cartoon drawing but I'm just hoping that will kinda get the point across so I really want to convey more than anything in this picture is the proximity of all the structures the t-tubules to the sarcoplasmic reticulum and then also to the myofibril and that's going to become important as we explore the relationship between each of each of these structures and then lastly let's just zoom in on the t2 Buhl and the sarcoplasmic reticulum and one thing I want to mention is that we know already that calcium is in high concentration in the ECF so there is a high concentration of calcium in within the t2 Buhl and within the sarcoplasmic reticulum there's also a high abundance of calcium major function of the sarcoplasmic reticulum is storage of that calcium and that's actually because we need the calcium for muscle contraction so let's go ahead and draw a couple channels in the membrane so there is a voltage-gated calcium channel in the membrane of the t tube you'll and this voltage-gated calcium channel is is is sort of associated with several receptors including the dihydropyridine receptor or d h PR and one thing that we really haven't talked much about yet is the the potential for a voltage-gated channel to be blocked in some way so we've mentioned you know that there could be an agonist or an antagonist that could block a ligand gated channel but we really haven't mentioned how that because this could happen in a voltage-gated channel so what it will be easiest to envision is this channel is is you know more or less cylindrical or three-dimensional in structure and so there's a sort of a tunnel in the middle it's not different just because it's a voltage-gated channel and so somewhere within the inside of that channel is actually a receptor and that receptor if something binds to it will I mean there's a couple of sort of ways to look at it one is that there's now physical obstruction that's preventing the ion to pass through and then also the sort of thing to consider is that how it binds it could stabilize the the particular channel in an inactive State and so therefore it just isn't really able to open in response to depolarization or hyperpolarization whatever the particular channel is is sensitive to and so in this particular case they really mention this receptor because this is the receptor that's blocked by certain types of calcium channel blockers including diltiazem now we also notice a second voltage-gated calcium channel that's present in the membrane of the sarcoplasmic reticulum and this particular voltage-gated calcium channel is associated with the ryanodine receptor and the ryanodine receptor is of particular interest to us because in skeletal muscle so it's not true so much for cardiac muscle and skeletal muscle certain types of patients might have a mutation in the Reina D and receptor where they have a significant increase in the calcium that's able to follow out account of stimulation and this is what leads to malignant hyperthermia so that's the disease process that is discussed you know in conjunction with certain medications such as succinylcholine all right so now we also want to draw in a couple of transporters in the different membranes so let's draw in a transporter for calcium in the membrane towards the sarcoplasmic reticulum so the this particular transporter is atp-dependent and so we'll put ATP in the middle it transports calcium it is a pump so it's moving calcium against its concentration gradient from the cytosol into the sarcoplasmic reticulum and this transporter is actually called circuit stands for Sarco endoplasmic reticulum calcium atpase but it's really just think of it as a calcium pump that pumps a calcium back in and so this is important because when we pump the calcium back in we make the calcium available for the next contraction so we want to affect the rate of contraction in the heart what we would do is we would utilize medications that will cause a number of effects including faster reuptake of cows so that we can get faster depolarization and contraction the next time around we also have a just plain old calcium ATP pump that comes the calcium out of the cell into the ECF we have a sodium potassium pump which we are already familiar with and last we have NC excess sodium calcium exchanger so the this particular transporter does not have does not utilize ATP instead it actually functions by secondary active transport so the sodium gradient is a high concentration of sodium outside of the cell low concentration of sodium inside the cell so the sodium is able to move down its gradient we're actually moving in three sodium for every one calcium that's exchanged in the in this particular transporter so as the three sodium ions move in one calcium ion is moving out and so it's harnessing the energy from the movement of sodium in from that data from from down that gradient in order to transport the calcium out okay so now let's talk about what happens during depolarization so we know that cardiac muscle cells are connected by intercalated disks which contain gap junctions and so the way the cardiac muscle cell is going to be depolarized is by way of sodium movement through the gap junctions from one cell to the next so we can see the sodium that moves in along the membrane and as the sodium reaches the first voltage-gated calcium channel in the T 2 Buell we can see that the voltage-gated channel will be activated and calcium will be able to move in to the cytosol down its gradient and then the calcium now is increasing the positive charge in this vicinity which is also near the second voltage-gated calcium channel that is present in the sarcoplasmic reticulum membrane and so we have a process called calcium induced calcium release meaning as the calcium is moved through the red voltage-gated calcium channel in the T tube you'll it activates the voltage-gated calcium channel in the sarcoplasmic reticulum which involves more calcium movement in the cytosol so sort of like a cascade of reactions calcium release causes more calcium release but from a different source so it's called calcium induced calcium release and so what happens after the calcium is in the cytosol is it floods its way down to the myofibril and it's actually going to associate with troponin which is present on actin and so the calcium is basically one of the two major components that allow for muscle contraction to occur we're going to explore that a little bit more in a moment what I want to mention is that we said we have all of these transporters cerca the calcium pom the sodium potassium pump and ncx all present and they their job is to remove the calcium from the cytosol and transport it either back into the sarcoplasmic reticulum or into the ECF and so once this calcium floods down into the myofibril it will associate with a troponin for a little bit and then eventually all of these structures are going to pump the calcium back where it originally started and that will actually lead to muscle relaxation so arrival of calcium is associated with contraction and removal of calcium is associated with relaxation and so we think about the non pacemaker action potential we recall that there is a plateau phase it's all about calcium movement into the cell and the sources are from the t tubules and from the sarcoplasmic reticulum so that we can have this association of calcium with the myofibrils this is a really good demonstration of what's called excitation contraction coupling it's also a sort of you could think about electrical function versus mechanical function electrical function is all about the depolarization and making the calcium available but mechanical function is about calcium's job in muscle contraction and so without that first part we can't have muscle contraction both that muscle contraction we don't really have any real cardiac function so the two are invariably linked okay so now to finish up our discussion on muscle contraction let's just sort of draw the structures a little bit larger and take a better look at what happens in terms of the axon of myosin interaction so we notice that we have actin we have tropomyosin and we have troponin and those three are all connected and then we have myosin and we mentioned that the myosin has these heads that sort of extend off of it and we're drawing this muscle in a relaxed state so actin and myosin are not connected to each other but the myosin heads are holding on to an ADP and inorganic phosphate so think of an ATP that's already been split but the myosin is harnessing the energy from the split from from breaking off that inorganic phosphate and it's holding onto both these molecules and so there's one ADP and inorganic phosphate for each myosin head and so let's just remember real quick that we have calcium that's coming from the sarcoplasmic reticulum the calcium is going to bind to troponin and so when calcium binds to troponin there's a the there's a sort of a cascade of events that occur so when calcium binds the troponin tropomyosin moves off of the myosin binding site so normally at rest it covers the myosin binding site on the actin and it doesn't allow for myosin and actin to interact but when there's calcium available the tropomyosin moves out of the way and now there's a binding site on actin that's available for myosin to sort of grab on to and as soon as that happens the myosin binds to the actin and so we'll just show it again and this time we'll show the myosin actin connect it and so when the actin and myosin are connected we actually call that cross bridge so cross bridge formation is the act of binding acting to myosin and and and so once they're connected they're they're sort of we just say that the connection is a cross bridge so initially as soon as this connection is made the ADP and the inorganic phosphate are still attached but next what's going to happen is the myosin heads are going to sort of pull towards the center of the myosin so remember the heads are pointing sort of away from the center so we're going to pull towards the center in what's called a power stroke and so as they pull towards the center they're utilizing the energy that's from the ADP and inorganic seit split and so as this energy is utilized the ADP and inorganic phosphate are released I just want to draw quick analogy to the to the idea of cross bridge and power stroke just to sort of make sure that this sinks in so let's imagine like a canoe or like crew and then there's a bunch of people that are all sitting in the boat together and they're holding all their paddles and you can imagine that if you know they're going to be sort of all synchronized but they will all pick their paddles up at the same time that would be the active medicine are not connected they dig the pedals into the water at the same time that's our cross bridge and then they pull back in order to propel the boat forward and that is our power stroke and the energy is truly expended during that pulling of the water back to move the the boat forward and so that's when the energy would be released and then what they'll do next is they will pull their the they will pull the paddles back out of the water they will reach forward and then they will dig the paddle in again in order to move the boat forward once more so that relationship is exactly the same as what happens in actin and myosin except that in the case of the paddles coming out of the water in order for the myosin to separate from the actin a new ATP must arrive and the new ATP is actually going to allow the release of myosin from actin and then immediately after that as the head has moved back into place the ATP will be split into ADP and inorganic phosphate for utilization in the next time that the myosin head connects to the actin so as long as the calcium is still available the myosin heads will release and then they will reach up and they will attach again so this is like a sort of a continuous process this happens like a couple of times in a row and so we essentially are going to get shortening of the muscle so remember that the myosin when we looked at the original drawing there was sort of like a midline for Miocene and on either side are these heads and in both cases the heads pull towards them and so it actually causes the shortening of the muscle fiber I'll take gather and so this process just sort of repeats over and over and over again until that calcium is taken back up into the sarcoplasmic reticulum and expelled from the cell into the ECF and then we need a new depolarization order for the next muscle contraction to occur all right so that concludes our explanation of cardiac muscle contraction and I really recommend if if the first couple of videos haven't come together yet now that we've come full circle and seen muscle contraction it's really very important to go back and make sure that there's a clear understanding of the relationship between electrical function and mechanical function or conduction and contraction that's all for this video thanks for watching

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