all right everybody welcome back this is our second lecture on the muscular system and we are covering chapter 10 of our textbook where we will be continuing to look at muscular tissue previously we looked at the anatomy of muscles and muscle tissue um both at the macroscopic and microscopic level so now we're going to be looking at the functionality of that muscle tissue seeing the physiology of how muscles contract so as always let's begin with our warm-up questions there's quite a few today but we're going to um be tying these into the lecture so we'll see them come up throughout so first where is calcium stored when it is inside of a cell why is calcium stored in something when it's inside of a cell and what is a sarccomir what are the two primary proteins found at a sarccomir and finally how is an action potential passed from one neuron to the next so go ahead and pause your video to try to answer those questions to the best of your ability like I said they're going to tie into today's lesson quite a bit so hopefully you've paused the video and tried to answer these and let's take a look to see what the correct answers are so first where is calcium stored when it's inside of a cell remember that calcium when it's inside of a cell which typically it's not but when it is it's not just free floating so it must be stored inside of the smooth endopplasmic reticulum but once um since we're talking about muscles remember muscles and nerves both we use different terminology here and when we're talking about those cell types um they're different terms so in a muscle cell a myioite instead of the smooth endopplasmic reticulum we call it a cycloplasmic reticulum or SR next why is calcium stored inside of something when it's inside of a cell well because calcium likes to bind to things and as a general rule we don't want that calcium is something that likes to bind to things kind of like oxygen did but we don't really want that to happen so calcium is packed away to where it can't bind to anything next what is a sarcimeir remember a sarcimeir is the functional contractile unit of muscle both skeletal and cardiac and so cardiac muscle and skeletal muscle both use sarcimeir and sarccomirs are a functional contractile unit of muscle cells next what are the two primary proteins found at a sarcimeir there were quite a few proteins that make up a a sarcimeir um but the two primary ones were actin and meosin and we'll be looking at those quite a bit today and then finally how is an action potential passed from one neuron to the next okay so remember we've got the uh syninnapse we get to a syninnapse where one neuron meets up with another neuron and there was that gap called the synaptic cleft and so it was difficult because you can't pass an electrical current across an open gap so the neurons had to use transmitters those chemicals and those are released from the sending neuron and they travel across that space that gap and when they bind to things on the receiving neuron and then cause some sort of either excitation to the second neuron or inhibition in the second neuron and so the two neurons could still communicate that way across the gap using neurotransmitters okay so just kind of a quick refresher in our previous lecture we looked at the structure of skeletal muscle and we saw those myophibbrals we looked at um those myophibbrals are inside of the muscle cell and then those myophibbrals themselves contain sarcimeir and a sarccomir runs from the zigzag the zisk to the next zigzag or the next zisk and so everything in between those two zisks is that one sarcimeir and then they repeat and repeat on down the entire myof so they're end after end after end for the length of the entire muscle cell and once again we say that those sarcimeirs are the functional contractile unit of muscle and so this is where contraction actually takes place so even though the whole muscle is contracting um it's at that myophibbral specifically the sarcimeir level where contraction is actually occurring and so up at the top in this image we can see an actual microraph which is a picture through a microscope of some muscle cells and those striations that really make that skeletal muscle stand out and those we said were caused by the psy the sarcimeir um those different areas of the sarcimeir so we have that light and dark areas that we see uh throughout this pattern and so we end up looking a little more like this or this in the microraph so here is that artist rendition where we've pulled out this myofal and we are looking at that and then down here at the bottom we have the actual sarcimeir drawn by the author and so what is it that's happening at the sarcimeir to cause muscle contraction so we sum it up by something called the sliding filament theory and the sliding filament theory says a few things but first it says that all of these proteins that we learned about both of which um we just talked about but also uh the meosin and actin um there are other proteins so they do not get smaller you might think that they would because when we talk about contraction we said muscle contraction meant that the muscle was shortening but it's not that the proteins are getting shorter so the actin and meosin do not get shorter instead they slide past each other so that is the sliding filament theory and we're going to look a lot closer at it but in order to u look a little bit closer at some of these other things that the theory says um but just to sort of sum it up actin and meosin do not shorten they just slide past each other and so we can kind of look at got a few videos to clip in today um this picture video so here these thicker blue lines so here we're looking at just the sarcimeir and one sarcimeir one unit is going to shorten by this the actin and mison sliding together so here the thicker blue line that represents the meosin or those thick filaments and the thinner red line is that actin the thin filament and we can see in the middle the M line um we can see the A band but most importantly if we look at those Z disks on the sides the left and the right side what are they doing right that's where everything anchors and that is the boundary of kind of what our sarcomir is so the area between the Z disks is our sarcomir and you can see that area between the zisks is getting shorter so the z disk is moving towards the mline on both sides so the mline of each sarcimeir the z disks is moving towards the mline on each side of the sarccomir the actin is moving towards the mline on each side and then down at the bottom we can see the eye band and the eye band is marked by that kind of blue area um and the eye band is getting shorter so this is the area where there was no measin so there's no thick filaments there's only thin filaments and so um this uh area is shortening because the zisks and those thin filaments are moving or sliding towards the endline so this is the sliding filament theory that's what we uh see when we talk about the sliding filament theory and muscle contraction so if we go back to our sarccomir here the other things that the sliding filament theory says is that um the proteins don't shorten so actin meosin don't get any shorter that the thin filaments of each sarcomir so all of the blue lines um here on the left and then all of the blue lines over here on the right the thin filaments of each sarccomir they get pulled towards the mine and that's what we just saw in that video clip so except they were red in that image but they're getting pulled towards the Mline and the eye band shortened remember the eye band was the area where there's no thick filament it's the area between the ends of the thick filament of one sarccomir and the thick filament of the next sarccomir where they're end to end and then the H zone which is around the Mline so we've got the Mline here and here's our H zone so that was the area in the uh with thin filaments of a single sarcimeir the Mline runs down the middle of the H zone so the H zone shortens right but depending on how strong of a contraction it is not only does the H zone shorten the H zone may completely disappear entirely um so if this left and right side moves close enough to the Mline we might see that H zone completely disappear if it's a not very strong contraction and it's not going to move all the way in then we'll still have some H zone but it's possible with a strong contraction that we would see that H zone completely vanish okay so the distance between one Z disk and the next um so really the length of the entire sarcimeir gets shortened because this Z disk is also moving towards the Mline and this Z disk is moving towards the Mline so the distance between the two is going to shorten and so if we go back to that video um here is one Z disk on the left another Z disk on the right and we can see the distance between them is shortening okay so the A bands um so those thick filaments that length the length of the A band from one end of the meosin to the next end of the measin within one sarccomir the A bands are going to move closer together that does not mean that the specific A band is going to move closer together it means that the A band of this sarcimeir and the A band of the adjacent sarcomir are all going to move closer together so this sarcimeir and this sarcimeir those A bands are all going to move in as this one moves in and so the distance between the thick filaments of this sarccomir and the thick filaments of the one next to it are all going to move closer together as the distance between them shrinks and then lastly the sarccomir are shortening and that means that the myophibbrals are shortening and so if the myophibbrals are shortening that means the muscle cell is shortening and the muscle cell is shortening that means the entire muscle is shortening because remember that um the length of the muscle is the length of the the muscle cell sorry the length of the muscle cell is the length of the facasicle which is the length of the muscle and so if any one of those shrink or shorten or contract it's going to shrink shorten or contract the length of the entire muscle okay and remember that we had that protein called distrophen and that distrophen anchored the sarccomir to the connective tissue of the muscle which is what allowed us um when the sarccomir shrank or when they contracted that caused the muscle itself to contract so here is our sliding filament theory in action but what is it that actually causes these filaments to slide past each other so we have to kind of approach that from a different angle and we can see here um and this is also another microraph a photo taken through a microscope of something called the neuromuscular junctions and so what we're seeing here are these black lines these are the axons and they come to an end at an axon terminal and the axon terminal has those axon bhutons remember that's where the neurotransmitters are stored and so that's what these little black circles or ovals um are so the neuron is coming down from the top of this image kind of off the screen right so it's coming down begins to branch at those ends of the terminals and then we have our terminal bhutons and in all likelihood this is one neuron whose axon we're seeing uh the axon terminals were where they kind of branch out and then at the end of each one there's those terminal bhutons and we can't really see if this is one single axon because it's up off the top of the screen but there may be a couple it's probably just one and um what we're seeing here is just the branching at the end and that axon terminal so we're going to be paying very close attention to those neuromuscular junctions which is exactly what it sounds like so it would be neuro neuron nerve cell and then we have muscular muscle cells and we see here skeletal muscle cells so a neuromuscular junction is where a neuron meets or joins with a muscle cell and so this is an actual image um but here is an artist's rendition something you might have seen before hopefully if you've been paying attention along the way um here is the axon terminal and here it is at that terminal bouton and so we saw this when we were looking at the syninnapse um back in the nervous system um and so inside we have these neurotransmitters inside those vesicles that's our acetylcholine those green dots inside of the vesicles so just like before those neurotransmitters um now here is our synaptic clft just like we saw before and then across the synaptic clft down here we have a membrane and along this membrane is uh we have our lian gated or chemically gated channels that acetylcholine can bind to but what's different in this image than what we saw before when it was a neuron uh the synaptic clft and it was a neuron communicating to another neuron um and so here we're going to say we have a neuron communicating with the surface of a muscle cell and so the events are going to be exactly the same as what we saw when we drew this out before when we looked at syninnapse um the only difference is it is a neuron talking to a muscle cell instead of another neuron and we're going to um not really get much of a graded potential because this guy right here this voltage gated sodium channel um and we know that that's what he is because he has that little wrecking ball looking thing and so when we send the action potential to a muscle cell we're going to get an action potential to develop in the muscle cell and we don't have to wait for the entire muscle to get to threshold or something we kind of um like we did in the neuron you know we had that axon hillic and that's not the case here and so right next to this syninnapse um there's that voltage gated sodium channel which is what we had in the axon hillic that allowed that action potential to keep going and so this is much easier to cause the action potential in a muscle cell because this guy is right here so we said this is a neuron we have our synaptic clft and we have a muscle cell so this is a syninnapse this is a syninnapse a neuromuscular junction is just another type of syninnapse and this type of syninnapse is called a neuromuscular junction so this is what we just saw um that photo microraph of and we're not going to draw this out or anything because we've already drawn it out back in the nervous system but let's talk through what's just happening here and so an action potential is traveling down this axon remember all along this membrane we have all those proteins u that we drew and we don't see them here but they are there and so when we get to this terminal bhuton uh we now have the voltage gated channels we have voltage gated calcium channels they're going to open up at threshold calcium which is high outside the cell and non-existent or packed away when it's inside the cell um but what does calcium do when it comes into the cell like we see here it's going to bind into those vesicles and when calcium binds into the vesicles what does it do it causes them to travel to the edge of the cell and get um they exocytose and then they release those neurotransmitters and whatever is in them um to the outside of the membrane so then they're out here in the synaptic clft and then it diffuses across that clft and it binds with our lian gated channels that are specific and so here we have acetylcholine that traveled through the vess the vesicle through um the membrane exocytos into the clft and now it's going to diffuse through these acetylcholine specific like andated channels and so they open and then just like we saw at the neuron what's going to happen that causes this depolarization that sodium rushes in right so when sodium comes into the muscle cell it's going to start to depolarize and it doesn't take much we only have to get to this little area right here to reach threshold and so that happens really easily because this guy's so close and so as soon as we get to threshold here that voltage gated sodium channel opens and now an action potential begins in the muscle cell and an action potential along an axon um is the exact same so all of those things that we drew before when we were drawing the action potential down the axon is happening along this surface of the muscle cell and the only difference is um the resting potential is90 in a muscle cell okay so remember in a neuron it was -70 RMP or resting um resting membrane potential was -70 but we also said that even though it's negative every cell in the body um different cells have different resting potentials and so in the case of a muscle cell resting potential is 90 so an action potential comes we get to threshold voltage gated sodium channels open we depolarize same exact thing we get up to positive 30 voltage gated sodium channels inactivate and then the voltage gated potassium channels open we repolarize as we repolarize and those voltage gated potassium channels close we do not get that hyperpolarization so if we think about that for a second why not okay because remember what hyperpolarization went to about990 which is our resting potential here it's our resting uh place for a muscle cell so we don't go below that because we're already at990 and so that is the action potential of a muscle cell almost identical to the action potential graph of a neuron the only difference is90 is that resting potential so we don't have the hyperpolarization because here resting is90 okay so here's that neuromuscular junction again this is what we just saw in that cartoon form um the picture that we had seen previously and so action potential is traveling down the axon gets to these terminal bhutons and then even though we can't see it this is where all that acetylcholine would be released onto the muscle cell and then an action potential develops and then travels along the muscle cell so um action potentials travel down the axon get to the axon terminal calcium rushes in acetylcholine is dumped out and opens those liand gated channels action potential develops travels along the surface of the muscle cell and so let's take a look at this video here uh it's going to kind of show that for us and I've sped it up just a little bit to a speed we can get through our whole lecture today just a little fast so hopefully that's not too bothersome also apologize in advance if the ads pop up can't do anything about that right now nerve impulses also known as action potentials travel from the brain or spinal cord to trigger the contraction of skeletal muscles an action potential propagates down a motor neuron to a skeletal muscle fiber the site where a motor neuron excites a skeletal muscle fiber is called a neurovvascular junction this junction is a chemical synapse consisting of the points of contact between the axon terminals of a motor neuron and the motor end plate of a skeletal muscle fiber the events at the neuromuscular junction occur in seven coordinated steps step one an action potential travels the length of the axon of a motor neuron to an axon terminal voltage gated calcium channels open and calcium ions diffuse into the terminal step three calcium entry causes synaptic vesicles to release acetylcholine via exocytosis step four acetylcholine diffuses across a synaptic ple and binds to acetylcholine receptors which contain ligated cation channels step five these liengated cation channels open step six sodium ions shown here in red enter the muscle fiber and potassium ions shown here in blue exit the muscle fiber the greater inward flux of sodium ions relative to the outward flux of potassium ions causes the membrane potential to become less negative step seven once the membrane potential reaches a threshold value an action potential propagates along with sarcoba neural transmission to a muscle fiber ceases when acetylcholine is removed this removal occurs in two ways one acetylcholine diffuses away from a synapse two acetylcholine is broken down by the enzyme acetylcholine eststerase to acetic acid and choline choline is then transported into the axon terminal for the resynthesis of acetylcholine liberty Mutual is all she talks about since we saved hundreds by bundling our home in auto insurance that's pronouncing Liberty liberty might get only pay for what you need all right so we had our action potential pass from one neuron to a muscle cell that it formed a syninnapse with this is a neuron which has four main parts back to our slides right so now we've seen that it causes that depolarization and we go through the full action potential the action potential spreads okay it travels down that muscle cell it goes in all directions but now we're going to find out how does the action potential cause anything to actually happen so remember all along the surface of that muscle cell where we have that muscle cell membrane sarmma there were those openings where we said there was an extension that went through the muscle cell and so here's that image that we had so we have all along this membrane there were the openings and that plasma membrane folded inward and traveled um through the muscle cell as it branched and it did so and it was wrapping around each one of these myophibbrals and this was called the T- tubule and the T- tubule has on either side of it and that part of that cycloplasmic reticulum and here it's called the terminal and so one T- tubule and both The terminal sister on either side of it is what we call a triad and I said before that the triad would come back in a future lecture we had already kind of introduced it and so here's where we are now let's go back one so action potential comes down vesicles release the acetylcholine action potential develops travels along the plasma membrane of the sarmma it travels down the T- tubule because remember that T- tubule is just an extension of the sarlemma okay so it's made of the exact same stuff including all those proteins needed for action potentials and so if an action potential is traveling along the sarlemma it's also going to travel down the T- tubule which is the important part here okay so an action potential travels down the T- tubule and then here we have this very zoomed in part of this area of the triad so here our action potential is traveling along the surface of that muscle cell along the saroma and it's going to travel down the T- tubule because again it is the saroma so the action potential is traveling down the T-t tubule but scattered all the way down the length of that T- tubule we have our triads and at a triad we have a terminal cesterni on one side and a terminal cesterni on the other and so in addition to all those proteins that carry an action potential which we don't really see here u but there is another type of protein that's serving two purposes and one is anchoring that terminal to the t- tubule and then also It is a voltage gated calcium channel and it's a special type of voltage gated calcium channel and this is called a ranodine receptor or ryanodine receptor so but it is a voltage gated calcium channel so let's take a look real quick to see exactly how this triad is laid out um so here's one terminal and then here's another and they are being held together by this T- tubule at those ryanodine receptors and so if we look closely we see the the rest of this terminal it's not bumped directly against the T- tubule there is this space here there's a little bit of a gap on either side and so when that action potential gets to the ryenine receptor it causes it to change shape it opens inside of a terminal sister as part of the cycloplasmic reticulum the cycloplasmic reticulum is smooth endopplasmic reticulum um what's inside of the smooth endopplasmic reticulum calcium so the voltage gated calcium channel opens calcium rushes out and it rushes out into this gap which is the interior of the muscle cell where all those myophibbrals are found so calcium is now open inside this muscle cell and what does calcium do when it's inside of a cell it likes to bind to things so up here at the top we have this very zoomed in image of kind of the meosin head and the rest of that measin remember this part is just kind of repeating and repeating and repeating um but up here one masin head okay and then here's the thin filament just that small section of it and each of these little blueberries is an actin molecule but all of them together this is our thin filament okay so we have this long spaghetti yellow looking thing that's lying on the actin that's our tropomyiain and then holding on to that tropomyiain and the actin is tropponin droponin is holding the tropommyosin in such a way that it covers up those active sites on the actin so all those little dimples on the blueberries are covered up right now and that is um at rest okay so this muscle is at rest we go back here um muscle is at rest but we just sent an action potential now that action potential caused calcium to suddenly be present inside of this muscle cell so what does calcium do it binds to things and one thing that it likes to bind to is troponin so calcium when it's present inside of a muscle cell because of an action potential binds to traropponin and so any any time uh something binds to or is removed from a protein we've said many times now that protein will change shape so troponin is going to change shape and now that calcium binds to it it bends forward just a little bit changing shape sorry that um and when it does it's going to attach to as it bends forward it attaches to tropomyiain if troponin was holding tropomyosin in place over those active sites okay but then troponin changes shape it's going to pull tropon tropomyiain along with it so the tropo tropomyosin moves and now those active sites are exposed but back when we were first learning about actin and meosin you know I said that those active sites really like those measin heads and before measin couldn't do anything about it because those active sites were covered up but now they're not so what happens is that the measin head can actually attach to those active sites and it does so meosin those meosin heads are going to actually attach to those active sites now that they're open and when we we said when this happens this is called a crossbridge okay so this crossbridge down here has now been formed so let's quickly sum this whole thing up so an action potential comes down a muscle cell action potential travels down the T- tubule causes the reanodine receptors which is a voltage gated calcium channel to open calcium inside of the terminal cesterni on the um cycloplasmic reticulum opens calcium inside rushes out into that open space calcium is now inside of the muscle cell okay and with calcium inside of the muscle cell it likes to bind to things and it's going to bind to troponin which causes troponin to move changes shape bends forward and that pulls tropomyosin with it exposing the active sites on actin which allows the meosin heads to attach forming a crossbridge okay so now we're going to go back and see that in action so when a neuron tells a muscle to contract we call that excitation contraction coupling and so in the previous video um that I just played in this lecture that was the excitation part we sent an action potential to the muscle this is the coupling part so in just a minute I'm going to play this u part where we watch we watch the contraction part and this is the part that actually couples the excitation to the contraction so let's take a look at it typically a single motor neuron arising in the brain or spinal cord conducts action potentials that travel to hundreds of skeletal muscle fibers within a muscle the sequence of events that converts action potentials in a muscle fiber to a contraction is known as excitation contraction coupling if we look at a single muscle fiber see that an action potential traveled across the entire sarmma and is rapidly conducted into the interior of the muscle fiber by structures called transverse tubules transverse or T- tubules are regularly spaced in foldings of the sarma that branch extensively throughout the muscle fiber at numerous junctions the T- tubules may contact with a calcium storing membranous network known as a cycloplasmic reticulum or SR where it absolut tubule the SR forms satellite bulges called terminal one portion of the T- tubule plus two adjacent terminal is known as a triad the membranes of the T- tubule and terminal are linked by a series of proteins that control calcium release as an action potential travels down the T- tubule it causes a voltage sensitive protein to change shape this shape change opens a calcium release channel in the SR allowing calcium ions to flood the cycloplasm this rapid influx of calcium triggers a contraction of the skeletal muscle fiber thus calcium ions are responsible for the coupling of excitation to the contraction of skeletal muscle fibers welcome to the 100 test which one of these two antipersperants can stand up looks like Okay you hear about how strict it is and how hard so we're going to see now that calcium causes um a contraction like it said at the end of that video okay so even though we don't see it here at rest before the masin head does anything at all attached to it is one second um sorry attached to it is that molecule of ADP that's a denisonin diphosphate and an inorganic phosphate so remember inorganic phosphate is phosphate that is not really attached to much of anything so it's kind of attached to the meosin head but it's not a true attachment so we just still call it inorganic phosphate and we will see in just a moment um but it's important to know that even though we don't see it here in this image ADP and inorganic phosphate are attached to the meosin head when it is just sitting there doing nothing at rest so we have our crossbridge formed down here at the bottom and it's formed because there is calcium present inside the cell and so what happens at this level once we have this crossbridge that allows that contraction to happen well here we go now we have our cycle we're going to work all the way through so we're going to start at the top and there's our ADP and our inorganic phosphate okay there's our crossbridge and here we're picking up right where we just left off now here we are at the crossbridge so again nothing all of a sudden it's exposed to um because of calcium the crossbridge forms and that's where we pick up so up here at number one the crossbridge is formed now some things are going to happen really quickly so let's go through this cycle as soon as the crossbridge is formed inorganic phosphate is released okay that inorganic phosphate is released and when the inorganic phosphate releases it causes this bond between measin and actin the crossbridge to get stronger so meosin attaches harder to actin when the inorganic phosphate falls off and when measin attaches harder to actin it causes the ADP to fall off and that's what this little asterk is here for i want you to add into your notes there um before we kind of follow up with that think for a moment about why those things happened okay everything we just talked about up in that first image so everything we're talking about here this actin measin troponin tropomyiain all these are proteins and so anytime you add something to or take something away from a protein it changes shape it changes shape which means it changes its properties this comes all the way back from the beginning of the semester so when meosin and actin attached to each other that causes some changes in meosin it doesn't like phosphate anymore okay the phosphate falls off when phosphate falls off it changes the meosin a little bit more now measin in that state likes actin even more than it did it attaches harder to the actin and when it attaches harder to the actin that causes it to not like ADP anymore so the ADP falls off and when ADP falls off we just removed something from the meosin and so what's it going to do it's going to change shape it's going to actually bend forward and by forward I mean it's moving in a direction toward the Mline okay so up here is a zoomed in part of what we're looking at so everything on the right side is some actin from the right side of the sarccomir here getting pushed towards the mline so not very much at all but um it would not be perceptible if we were to see this on just one little bit of movement um if we just saw that one little bit of movement happen but the measin head pushes forward okay this is called the power stroke it's important the power stroke the meosin pushed the actin towards the Mline that's the power stroke so when the meosin bends forward in this state it really likes ATP and so ATP is floating around in the cell binds to measin when ATP binds to measin that provides the energy needed then to break the crossbridge and ATP the energy broke the crossbridge and when it does that splits it hydrayes the ATP into what it started as ADP and inorganic phosphate okay but when ADP and inorganic phosphate when they split from each other that the meosin head back and we say now it's put into the high energy position and so as long as there is still calcium in the cell that means the binding site or the active sites on actin are still available so we go through this again and again and again all right so one single crossbridge cycle does not visibly or even noticeably shorten the muscle but this doesn't really just happen once that would be um like the twitch that you talked about in lab um so in reality though this goes on a lot and the fact that it happens a lot means that we do get a noticeable shortening of the muscle and so I'm going to take a look at one more video just to see this actual contraction part um okay so we said that the excitation contraction coupling was really the whole process and we saw the excitation as the action potential was passed from one neuron to the muscle cell and we saw the excitation contraction coupling portion as the calcium was released but now we're going to see the actual contraction part and this uh remember how a measin filament how it appeared um it didn't just have a single head coming off in one direction when we were looking at it in the previous lecture we saw that there were lots of measin heads and they kind of stuck off in all directions and that's going to be important for what we see in this video the contraction of a skeletal muscle generates the force necessary to move the skeleton a contraction is triggered by a series of molecular events known as the crossbridge cycle in a skeletal muscle fiber the functional unit of contraction is called the sarcomir a sarccomir shortens when measin heads in thick myofilaments form cross bridges with actin molecules in thin myofilaments the formation of a crossbridge is initiated when calcium ions released from the cycloplasmic reticulum bind to troponin this binding causes troponin to change shape tropomyosin moves away from the meosin binding sites on actin allowing the meosin head to bind actin and form a crossbridge also note that the meosin head must be activated before a crossbridge cycle can begin this occurs when ATP binds to the meosin head and is hydraized to ADP and inorganic phosphate the energy liberated from the hydraysis of ATP activates the meosin head forcing it into the cocked position a crossbridge cycle may be divided into four steps step one crossbridge formation the activated meosin head binds to actin forming a crossbridge inorganic phosphate is released and the bond between meosin and actin becomes stronger step two the power stroke atp is released and the activated meosin head pivots sliding the thin myofilament toward the center of the sarcomir step three crossbridge detachment when another ATP binds to the meosin head the link between the meosin head and actin weakens and the meosin head detaches step four reactivation of the meosin head atp is hydrayed to ADP and inorganic phosphate the energy released during hydrarolysis reactivates the meosin head returning it to the cocked position as long as the binding sides on actin remain exposed the crossbridge cycle will repeat and as the cycle repeats the thin myofilaments are pulled toward each other and the sarcoir shortens this shortening causes the whole muscle to contract crossbridge cycling ends when calcium ions are actively transported back into the cycloplasmic reticulum tropponin returns to its original shape allowing tromyosin to glide over and cover the meosin binding site on actin okay okay so now we've seen excitation we've seen contraction we've seen the coupling of the two together that's excitation contraction coupling so that's what causes a muscle to contract and then we saw a little bit at the end of that video um as to how the muscle how we get it to relax again okay so when uh what happens to cause the muscle to relax well we have to first get rid of that calcium so when the action potential stops coming from the motor neuron we have no more stimulation and if there's no more stimulation then those reanodine receptors those special calcium channels are going to close so calcium stops being put into the muscle cell and there is another type of protein all along that cycoplasmic reticulum called calcestrin okay caliquestrin and it pumps calcium back into the cycloplasmic reticulum so calcium falls off of the troponin to move back into the cycloplasmic reticulum and the tropparonin moves back into its initial shape pulls the tropomyosin back over the active sites on the actin and now meosin can no longer form a crossbridge and the titan remember that springy protein at the end of those thick filaments um it pulls everything back to its original position and so that's how we get relaxation after contraction but let's take a look at a little bit of a special case rigor mortise okay rigor mortise is the contraction of muscle following death and that's something that naturally occurs so sometime after death the muscles of the body will become very contracted and in some cases it can cause dead bodies to noticeably move which if you've you know ever kind of had the unfortunate experience of of seeing that it can be a little bit unsettling because you know even if you know to expect it it's a little unsettling because movement from a fully dead body but what is it that's happening there so if we look at all of those events that we just saw okay those are chemical reactions and none of them require any energy except for breaking the crossbridge so let's go back to our crossbridge cycle so even though there are no neurons sending signals like if we're dead or maybe they're paralyzed and there's nothing there we're dead um we can still get a little bit of action and so after death the muscles go completely limp and remember when you are alive even when your muscles are relaxed there's still something called toness or muscle tone and you saw that in lab and so that was a constant state of contraction not a full contraction but this is like even when you're asleep um even when you're at your most relaxed your nerves are always sending that little bit of background signal to your muscles and so your muscles are always contracting a little bit but once you're dead or if you're paralyzed and then your muscles go completely relaxed there's no stimulation to those muscles so if you've ever you know had that unfortunate experience of moving a recently dead person or a pet or any kind of body something like that that um you know is a completely different feeling than moving someone who's just asleep when someone when something is dead there's no stimulation of those muscles and it feels completely different because of that pure relaxation and that stays that way for quite a while depending on the environment you know it can take a few or several hours um but at some point when that happens protein starts to break down those reanine receptors start to break down that cycloplasmic reticulum itself starts to break down and the result is that inside of the muscle cell begins to flood with calcium and even though the person is not alive chemical reactions can still happen right chemical reactions can happen in a glass jar and so if calcium is present it's going to bind to things including tropponin and when it binds to troponin it's going to go through all of these steps we're going to have the tropomyosin pulled out of the way we're going to have that crossbridge form and we're going to go through the cycle and so when we get down to that bottom image there's still ATB present in the muscle we're going to go through these crossbridge cycles where we get contraction and then the muscles are going to stiffen right they're contracted they're going to um get contracted until we run out of ATP and that's because um even though these other chemical reactions do not require life right making ATP does so because now we're not breathing so we don't um make any more ATP we use up the ATP that's there and then we get stuck um we get stuck in that position where the crossbridge is formed so we get stuck in that contraction phase we can't break the contra the crossbridge because there's no ATP so the muscles contract and then they stay contracted and that's what rigger mortise is okay so um rigor mortise takes a while it'll be in that contracted state until enough time passes and the proteins those filaments begin to degrade so the actin the meosin the troponin the tropommyosin all of those begin to decay at which point the whole thing just kind of deteriorates and then the muscles are relaxed again and so that's how you can kind of tell um how long it's been since someone has died so based on things lots of things like temperature location all that kind of stuff has to be taken into account um but if you do take that into account that there's a certain amount of time after death when muscles are completely limp and then there's a certain time during rigor mortise when muscles are contracted and then there's a time after rigor mortise when the muscles deteriorate and relax again and so that's what's happening during rigger mortise okay so that's where we will stop today i know that this was a very long lecture compared to most of the others that we've had um but it's very important a lot of information here so in bio139 when you get to the cardiac system and you look at cardiac muscle it's also going to follow this crossbridge cycling and you'll be expected to know this um but for now this is where we will end today we will have one more lecture in this muscle portion talk about things in chapter 11 and things that influence muscle contractions and so we will talk about that next time i hope you enjoyed this lecture this was a fun one I think i'll see you next time take care