Transcript for:
Muscle Contraction and Anatomy

hello class it's professor Mariah Evans this is BSC 2085 human anatomy & physiology 1 and today we are going to talk about muscles whoo-hoo all right so I posted an announcement in mus four muscles with videos for muscle contraction muscle contraction is considered the sliding filament theory and the reason why they call it that is because there is actin and myosin actin another name for it is the thin filament myosin is the thick filament and those two filaments actually slide past each other to get a muscle to contract now there are four actions within that process of muscle contraction the excitation and that's because skeletal muscle must receive a nerve impulse okay so excitation then there's an excitation contraction coupling and that's because the excitation is gonna be a neurotransmitter by the way but the excitation that comes from the nerve cell now has to meet with the muscle cell and that takes place at the sarcolemma which is the membrane of a muscle cell then you get the actual contraction itself and that is when the two filaments actin and myosin slide past each other and then since muscles don't stay in a constant state of full contraction they have to relax so relaxation is a part of the muscle contraction process so for actions and excitation excitation contraction coupling the contraction itself and then the relaxation now what I've done is if you purchase the book if you have an e-book or if you have the lab manual or if you have a textbook so remember our lab manual and our textbook is written by the same author and so in the lab manual there's information about muscles and muscle contraction that would help you with lecture if you never purchased a lecture book but the reason why I'm saying that is of course I do my powerpoints and I do them from you know the publisher but I add my own things in here so this is not in the textbook so if you have an e-book you are not going to find this I took this from something else and I liked it because it was step by step so so those four actions the excitation the excitation contraction coupling the contraction itself and then the relaxation these are broken down into several steps so that you understand what's happening so the first thing it says here is that this is the excitation so step one right of this process and it just says here that a nerve signal so if we read the bottom like you know like it's a caption and then we look at the picture then we get an understanding and that's why I did these and then I course added videos as well in an announcement so we get a nerve signal and that nerve signal stimulates voltage-gated calcium channels now my assumption is is that you don't know what a voltage-gated calcium channel is so I'm going to tell you voltage-gated ion channels calcium or potassium or sodium or whatever but voltage-gated ion channels are channels that don't open unless there's been a change in charge and the way that a change in charge occurs is that we get a flow of ions across the cell's membrane so remember I have two types of ions cations which are positively charged anions which are negatively charged so here we have calcium and calcium is diffusing into the axon terminal when it diffuses into the axon terminal then it's going to cause this release of acetylcholine so see this it says an X I ptosis of acetylcholine ACH is the abbreviation for sido coaling so these little tiny green dots that you see here that is the neurotransmitter acetylcholine okay now your question should be well now that calcium has diffused into the axon terminal and that caused the release of acetylcholine what is that acetylcholine going to do well this is where we get to the excitation contraction coupling because it's going to bind to the sarcolemma a muscle cell now if you look here you can tell that the sarcolemma is the cell's membrane and the reason why is because it says sarcolemma and then if you look closely what you see is the phospholipid bilayer see the phosphate heads and then the two lipid tells the phosphate heads two lipid tells so this is the membrane of a muscle cell acetylcholine so remember that abbreviation ACH acetylcholine bound to its receptor on the sarcolemma and then what that did was it opened up voltage-gated ion channels so I'm sorry not voltage chemically gated ion channels chemically gated ion channels are a little bit different than the voltage-gated ion channels because chemically gated ion channels will only open when a chemical in this case acetylcholine binds to the receptor now what happens when this ion channel opens if you follow the arrows you'll see that potassium leaves the cell and you'll see that sodium goes in to the cell so when acetylcholine binds to the sarcolemma it opens up sodium and potassium channels sodium goes in and potassium goes out and that causes an event to occur that event is called an end plate potential now I'm assuming that you don't know what an end plate potential is so I'm going to tell you what an end plate potential is an end plate potential is a localized change in charge so all that means is is that the inside of the cells are what we call polarize they're negatively charged inside and when ion channels open the flow of ions can cause the inside of the cell sorry can cause the inside of the cell to become positive so whenever there is a flow of positively charged ions to the inside of a cell that's negative then the cell becomes positive and that's called the depolarization that word depolarization is going to come up a million times ourselves have a resting membrane potential that resting membrane potential is that cells are negative on the inside when they're at rest when ion channels open and they become positive then the cells are going to carry out some type of action and in this case specifically this action is about to be the contraction of skeletal muscle cells all right so let's go back just for a second I get calcium which is positively charged diffuses into an axon terminal which is the end of a nerve cell that causes the release of acetylcholine acetylcholine binds to the sarcolemma when it binds to the sarcolemma it causes ion channels to open sodium comes in and potassium goes out and it results in an end plate potential which is a localized change in charge that means right here right here locally where the event occurred the inside of the cell now is becoming positive now adjacent that means next door the ones that are close to adjacent voltage-gated ion channels now open so again remember what I said about voltage-gated ion channels they only open when there's been a change in charge and an end plate potential is a localized change in charge so what happens is the voltage-gated ion channels that are close to where the event took place the epp those open so here it says voltage change in that end play potential opens up the nearby right the neighboring voltage-gated ion channels and then they don't tell you but I need you to know this that causes more sodium to come rushing into the cell and when that happen it causes an action potential now endplate potential was a localized change in charge that means it stayed close to where it was initiated an action potential moves so action like it's on the go and that action potential is headed somewhere which is going to be this next part cuz remember we're talking about the contraction of the muscle now so the action potential it propagates so it moves it moves down that these two t these t tubules that doesn't mean anything to you right now but t tubules are where calcium is housed inside of muscle cells and if you remember from the bone chapter we know that calcium is so important right we need calcium for skeletal muscle to contract like here we need calcium for nerve impulses like the beginning of this step one we need calcium for our blood to clot we need calcium for cardiac muscle and smooth muscle so all muscle not just got all to muscle but we need calcium we will steal calcium from our bones because it's so important to other things so inside of the muscle cell these t tubules are holding the calcium but when there's action potential which is a change in charge when it propagates in them it causes the calcium to be released which should indicate to you that there is a voltage sensitive gated channel that's holding the calcium remember voltage-gated channels only open when there's a change in charge an action potential just happens to be a change in charge and it's a change in charge that doesn't stay localized it moves okay so now oh look vil tidge gated channels and the t tubules cause the skels going to be released now question is what happens to the calcium that's being released from the t tubules well it binds to troponin and troponin in this case is this little yellow type of I don't know it looks like a snowman with only two bars do it but this is the troponin and calcium binds to the troponin and when calcium binds of that troponin it causes this tropomyosin complex to open and when the tropomyosin complex opens we can see those active sites on actin so it makes those active sites on actin available to react with myosin heads so remember I started this whole lecture saying that muscle contraction is the sliding filament theory and I told you that actin which is the thin filament is going to slide past myosin which is the thick filament this is where we are now we're about to have our contraction the only thing is is even though the active sites on actin are available the head is not ready to bind yet so the head has to be cocked I don't know if you've ever shot a revolver where you have to you know it back and then pull the trigger so in order for myosin to react with these active sites on actin we have to the heads and the way that we cocked the heads is this enzyme that's called ATPase it breaks down ATP so if I break down ATP I break it down into adp and pi and that's how I get my head cocking so here it says myosin ATPase so the enzyme that breaks down ATP which is attached to the myosin is going to hydrolyze or break down ATP and it causes the head to once the head then it can bind with the active site on actin and when actin and myosin come together it's called a cross bridge so the formation of the cross bridge between actin and myosin takes place now remember sliding filament theory so I've attached the myosin head to the active site on actin and the next step is going to be this power stroke the next step is gonna be the pull where actin is pulled past myosin so the power stroke happens to require ATP so if you remember organelles write ATP you'll say sometimes they say that the mitochondria is the powerhouse of the cell so power ATP so the power stroke requires ATP and luckily for us we just happen to have ADP and that inorganic phosphate and we we add those back together now we have ATP so that's all they're showing is that ADP and phosphate that was from this step here where ATPase broke it down then they're going to join back together Nisus ATP that breaks the cross bridge and pulls the power stroke is pulling the actin past the myosin so that power stroke is the actual contraction it's the sliding of myosin the thin filament over excuse me actin the thin filament over myosin which is the thick filament okay now there are in this picture just one myosin head and you can see the active sites on actin but the reality is is that we have oh my gosh it's it's just so many millions trillions bazillions I don't even know how many but we have so many of these myosin heads and we have all of these active sites on actin that if I'm trying to get a muscle to contract I get head cocking when ATP is broken down into adp and pi and then i get the cross bridge when the head of myosin attaches to the active site on actin and then I get the power stroke which requires ATP right so pulling actin past the myosin and then I get this millions of times because there are millions and millions of heads and millions and millions of active sites on actin so if they all attached at one time meaning if all the myosin heads attach to the active sites on actin all at one time and then they all let go at one time the filaments would just slide back to where they were so at any given time half the heads are attached and the other half are free so that they don't slip back past each other alright now if I go through all of these actions and I'm gonna say it because it's redundant but I'm gonna say I get my head cocking my cross bridging my power stroke and that pulls actin please make sure you guys watch the videos then I get another head cocking cross bridging and pooling of and another head cocking cross bridging and pooling of actin eventually the muscle is fully contracted which means actin and myosin have been slid past each other right slid past each other to their furthest degree of overlap and the muscles contracted completely but muscles don't stay in a state of complete contraction as a matter of fact we have a vaccine against that very thing tetanus which is sometimes referred to as lockjaw that's when you're in a state of continuous muscle contraction we call them spasms and that could actually cost you your life okay so muscles don't stay in the state of complete contraction okay so we need to relax and since this whole thing muscle contraction model since it started with calcium diffusing into the axon terminal and causing the release of acetylcholine that opened up the ion channels that let sodium come in and potassium go out which gave us an end plate potential which was a localized change in charge then opened up voltage-gated ion channels that were next to it then that initiated an action potential and action potential is that moving change in charge and it propagated down the sarcolemma and into the t tubules causing the release of calcium then calcium bound to the troponin caused the tropomyosin complex to open revealed the active sites of actin so it can react with myosin heads but we had to the heads first so ATP ace broke down ATP head cocking cross bridging power stroking and that goes on and on and on and the muscles contracted but the whole thing started with acetylcholine binding to the sarcolemma and opening up those ion channels so look what relaxation there's two parts to relaxation one of them is we have to degrade that acetylcholine so acetylcholinesterase is the enzyme that breaks down acetylcholine and when it breaks it down it closes the ion channel when the ion channels are closed that means no more soda is going to be coming in no more potassium is going to be going out right so acetylcholinesterase is going to degrade acetylcholine and close the ion channels and that's this picture here right acetylcholinesterase degrades acetylcholine closes the ion channel the other thing is we need ATP we need ATP for muscle relaxation and that sounds confusing you're like wait ATP energy for to relax yes because ATP is needed to actively transport calcium back down into the sarcoplasmic reticulum and once it does that it's been removed from the troponin so then that tropomyosin complex goes back to covering the active sites on actin so this is the calcium being removed from the troponin being actively transported back down into the sarcoplasmic reticulum and then the tropomyosin which is like this kind of light teal green piece right here this goes back to covering the active sites on actin if the active sites on actin are covered that means they can't react with myosin heads which means the muscle can't contract anymore so that's muscle relaxation loss of calcium right results in the tropomyosin complex going back and covering the active sites on actin then the muscle fiber returns to its resting length relaxation now here's the kicker this is the most in my opinion this is the most complex of the material that we've had thus far but I'm telling you now in order to do well on exam 3 you really do have to understand that and/or understand this this muscle contraction but I also want to make a promise to you when you learn and understand what's happening here with the voltage-gated ion channels the release of acetylcholine binding to the sarcolemma opening up chemically gated ion channels causing that localized change in charge which then opens up voltage-gated ion channels which causes an action potential then you understand reality is this you will understand a bunch of systems in the body because this is muscle contraction and we have cardiac muscle smooth muscle and we have a core skeletal muscle so when we start talking about the digestive system and you are propelling food it's going to be the contraction of smooth muscle we have longitudinal smooth muscle and we have circular smooth muscle and they alternate back and forth to propel food through these hollow organs that we have that smooth muscle contraction you have to learn how the heart works right heart is a muscle and it also has acted in my and just like myosin just like smooth muscle has acted in myosin and so remember this class is anatomy and physiology so once you understand the physiology of muscles right how muscles function you're going to apply this that I'm teaching you right now about ions moving across membranes and about cells becoming depolarized and causing actions to occur that's gonna be applied to everything that comes after this everything it's even going to be applied to nerve impulses and that's because calcium which was positively charged diffused into the axon terminal and axon terminal is the end of a nerve cell and all cells are negative at rest so this which sounds very complicated and it is it's gonna be applicable to every single physiological process in the body every single one ok now let's talk about application so we know that we need acetylcholine for muscles to contract right that's the neurotransmitter that started the whole thing bound to the sarcolemma opened up ion channels so there's pesticides and if you're a cruel person like I am and I admit it I am a cruel person when we have a wasp or a hornet's nest I get raid wasp and Hornet spray don't get that off-brand stuff get raid I'm just I'm not trying to advertise for any particular thing I'm just saying I tried it other stuff raid works so if you're like me in your about this you read it you know and it tells you that you shouldn't you know stay around and you know you stand a certain distance and you spray it and then you know you leave the area well I like to watch them die I know I'm telling you it's cruel so if you've ever watched them though it's interesting and I'm about to make a correlation for you so pesticides have a sealant acetylcholinesterase inhibitors okay so if I inhibit acetylcholinesterase which is the enzyme that breaks down acetylcholine then that means that they are going to and this being the insects they are going to go into a state of constant contraction which means are going to have spasms so if you've watched them you sprayed them they hit the ground they go and they die and you know I'm telling the truth if you've ever watched them so basically what we did is we gave them a neural toxin we you know with them in paralysis and it caused their death it's so bad but yes so paralysis death okay now tetanus I talked about that earlier we get a vaccine for it because it's deadly i'mso tetanus is caused by a bacterium which is called Clostridium Clostridium techne is the whole name but Clostridium and basically what this does is that this causes an overstimulation of your muscles so the toxin that's associated with it causes an overstimulation of your muscles which means you are again in a state of paralysis right over stimulation that means you're in a state of contraction you can't relax and yes you can die from that just thought I put it out there then we have flaccid paralysis and if paralysis is when you're in a state of continuous contraction and can't relax then flaccid paralysis would be when you're in a state of constant relaxation and that means your muscles are unable to contract so flaccid paralysis gives to limp muscles now if you've ever had back spasms and I've never had these but I've heard people say that they get back spasms and that they hurt really bad and I know you guys know even if it hasn't happened to you when a person is having back spasms they are given muscle relaxers listen to that name muscle relaxers because the muscles are in a state of contraction which is painful so muscle relaxers some of them have this active ingredient called kirari and what kirari does is it competes with acetylcholine for the receptor on the muscle cell and if kirari gets there first then acetylcholine can't bind and if acetylcholine doesn't bind then your muscle doesn't contract and in the case of having you know problems and muscle spasms in your back being able to relax your muscle is what gives you the relief in that neat so kirari competes with acetylcholine and it binds to the receptor first prevents acetylcholine from binding and it relaxes your muscle kirari muscle relaxants okay now that membrane potential so when I go through the the whole muscle contraction model I explained you know parts of it while I'm you know talking and so I've already told you that at rest right cells are polarized that means that they are negatively charged inside and the reason why they are polarized is that they have a concentration of potassium and sodium on the inside it's different so we call sodium the major intra cellular cation that means that sodium is in high concentration inside of the cell we say I'm sorry potassium is in major intracellular cation so potassium is in high concentration inside of the cell sodium is the major extra-cellular cation and so there's more sodium outside extracellular outside of the cell so the resting membrane potential is due to those ions right in their concentrations outside of the cell so it says that the inside is negative 90 you do not have to remember that number but you do need to remember that the inside of cells are negative when cells are at rest so remember when I said an end plate potential was a change in charge and I said that that change in charge occurred when sodium came rushing into the cell and potassium was leaving and it became ready depolarized these are those terms and they're coming up again so the inside of the cell is negative when they're at rest that's all cells that's muscle cells that's heart cells that's you know every cell that you can possibly think of neurons which are nerve cells all cells are negative on the inside when they're at rest okay now it says here that when we open up ion channels sodium can come in and potassium can go out and this changes the voltage so change in charge and it can cause as we know an action potential because and I'm just gonna repeat it so that you can hear it over and over again calcium diffused into the axon terminal which was the end of a nerve cell that caused the release of acetylcholine acetylcholine bound to the sarcolemma and then opened up ion channels that cause sodium to go in and potassium to go out that was an end plate potential which means right there at that event where those ion channels open the inside of the cell became positive so it went from negative to positive that's that change in charge then nearby neighboring adjacent whichever word works best for you the voltage-gated ion channels that were close to the end play potentials event those opened up and more sodium came rushing in and initiated an action potential the only difference between an action potential and an end plate potential is that an end plate potential stays put it's just localized it can't go very far from its point of initiation but action potentials can so they move they propagate and an action potential propagates down into the tea tube you'll called causes the release of calcium calcium binds to the sarcolemma and I'm sorry calcium binds to the troponin causes the tropomyosin complex to open reveals the active sites on actin so that they can react with myosin heads but I have to the heads first so ATP ace breaks down ATP and I get head cocking cross bridging that's when the myosin binds to the active site on actin and then I get the power stroke and that power stroke requires ATP and luckily for us we just happen to have ADP and pi right there and we bring them back together it's ATP that's muscle contraction and then I need the muscle to relax so acetylcholinesterase degrades acetylcholine causes the ion channels to close no more sodium goes in no more potassium goes out then I have to actively transport which means I need ATP I have to actively transport calcium back down into the sarcoplasmic reticulum which is part of the muscle cell back down into the sarcoplasmic reticulum and then the tropomyosin complex closes and it covers the active sites on actin and the muscle goes back to its resting length okay the more you go over it the more it's going to make sense the more videos you watch and like I said I provided two for you guys but the more videos you watch the more sense it's going to make but please please please understand you're going to have to understand that muscle contraction model to do well on exam three and I'm going to go back and reference the muscle contraction model to everything that comes next in the rest of this class okay all right so now there's three types of muscle tissue oh my gosh this is a shocker their skeletal muscle and cardiac muscle and smooth muscle there's prefixes that help you know that we're talking about muscle so my Oh miss encircle so remember that Circle Lima was the membrane of a muscle cell mm-hmm now skeletal muscle is where you know it's attached to bones and it's voluntary right so we move that it's also striated which you guys know cuz you've seen it in the lab it contracts very fast which means it can also get tired very quickly and skeletal muscles really strong like powerful and it requires nerve stimulation you know like for example calcium diffusing into the axon terminal axon terminal releasing acetylcholine and acetylcholine binding to the muscle cells membrane the sarcolemma right so it requires a nerve impulse cardiac muscle is also striated you know like skeletal muscle but it's involuntary unlike skeletal muscle and it can contract without the nervous system stimulation it can can crack without it and then it says more details when you get to 2086 chapter 18 is 1786 okay then we have a smooth muscle smooth muscle has no striations smooth muscle can also contract without nerve stimulation and smooth muscle like cardiac muscle is involuntary so you don't control you know how food flows through those organs when we talk about that digestive system earlier so the stomach is an example your urinary bladder eggs example your Airways so like breathing those things you don't control that it's smooth muscle it's involuntary and then here are pictures oh look skeletal muscle has striations and then look cardiac muscle also has striations and intercalated discs and then there's smooth muscle which doesn't have striations now this stuff right here is the anatomy of the muscle cell it gives you an idea of course because you guys know the class's anatomy and physiology it gives you an idea of the structure of muscle and then it helps you kind of understand how it works so this is me trying to I guess explain so the Paris iam is the outside covering of bone and this right here epimysium is the outside covering of muscle then we have Paramecium which surrounds what we call fascicles and what fascicles are are they are bundles of individual muscle cells and and so each muscle cell sorry each muscle cell has a covering around it and that's called endomysium so into my Sam surrounds each individual muscle cell a bundle of muscle cells is called a fascicle and that has a connective tissue called the Paramecium and then several muscle fascicles make up the entire muscle in the epimysium is what is the connective tissue around that now down here they're going to magnify this in a picture or two but down here is the sarcoplasmic reticulum member circle means muscle and then these are the t tubules we've already talked about these because why calcium right is in the t tubules and then when ATP comes on it pumps the calcium back into the sarcoplasmic reticulum and fYI the sarcoplasm teachables are part of the cytoplasmic reticulum this right here is just a little comparison of skeletal muscle and cardiac muscle and smooth muscle I do want you guys to know of course that skeletal muscle is voluntary and smooth muscle and cardiac muscle are both involuntary of course they all have actin and myosin so the sliding filament theory is applicable to all muscle whether its skeletal cardiac or smooth okay and they function a little bit differently but we'll talk about their their function like how we get smooth muscle chicken track we'll talk about that later all right so now these are some characteristics that muscle tissue exhibit excitability so that means that skeletal muscle can respond to a stimulus contractility that literally means that it can shorten like when the actin and myosin sigh past each other the muscle contracts and it becomes shorten extensibility means that it can stretch and the good thing about stretching muscles especially if you've over stretched a muscle before who give it some rest right you rest and then it goes back to its normal s length that's called elasticity so muscles can stretch that's extensibility but they're supposed to go back to their normal length and that's the elasticity so recoiling going back to their normal resting length now the functions of muscle is that they cause movement right because our muscles are attached to the bones right and so we move our bones that's movement but we also use muscles for stabilizing our joints and we also generate heat with our muscles and then our muscles help us maintain posture in our body position additionally muscles form valves and protect organs and control our pupil size so if you get really excited you got you have these dilatory muscles in your eye and your pupils dilate so when you get excited or you see something that's aesthetically pleasing your pupils get really big and then we have erector pili muscles and erector pili muscles are the muscles that give you goosebumps and I mentioned erector pili muscles in the integumentary system lecture all right so now things we know because of the muscle contraction model we know that muscles need energy right so they have to have a lot of energy we also know that they're supplied by a nerve right a nerve impulse so in order to get skeletal muscle to contract a nerve impulse has to come in okay now when you look at these I showed you in a picture and then they're going to be there's going to be a bigger picture that comes up for it but this right here is the epimysium which I said is that outermost covering of muscle and then I told you that the Paramecium is going to be covering chuckles and then I explained to you that fascicles were bundles they call them groups same thing so bundles are groups of muscle fibers muscle fibers arm muscle cells the only reason why they call them fibers is because the cells are really long so it's a muscle cell it's a muscle fiber those are synonymous with each other so a fascicle is a bundle of muscle fibers or muscle cells and then it has this connective tissue around it called Paramecium and then around each individual muscle cell or muscle fiber then we get the end of my cm and then they give you a larger picture of what I talked about earlier so this is the connective tissue around the entire muscle in here and they pulled one out like a fascicle but these are several fascicles that are in here so around the fascicle that's where we get the Paramecium and a fascicle is a bundle of muscle fibers so then they pull out an individual muscle fiber or muscle cell and then they show you that there is a connective covering around that one and that's end of my Sam so end of my Sam here here my Sam here and then up in my Sam here okay now we know that muscles allow us to move skeletal muscle right so we have the attachment in two places of skeletal muscle to the bone the insertion point is at the moveable bone and the origin is either immovable or less movable and then they can either be directly attached and this means the muscle to the bone directly or it can be indirectly attached which means that it could be attached to like a tendon and you guys know your Achilles tendon it actually takes the calcaneus which is your heel bone which you're learning in lab the calcaneus is your heel bone and your Achilles tendon attaches the calf muscle to the hill bone and it's sometimes the kilise tendon it's real name is the calcaneal tendon no so calcaneal like calcaneus anyway so that's an indirect attachment if it's a direct attachment then the epimysium which is that outer covering of the muscle is going to be fused with Paris diem which would be the outer covering a bone or perichondrium which is the outer covering of cartilage that would be direct so the outside tissue of muscle being bound to be or fused to the outside tissue of cartilage or the outside tissue of bone that's direct and erectus like our tendons or aponeurosis which is a sheet like connective tissue it's kind of cool all right and so this is again just those fibers so up in my cm and in my Sam perimysium etc all right so now well let me go here first so this is a muscle cell so this is a muscle fiber that's the nucleus and then you guys of course can see those stripes I hope so the striations that are in there things we already know that must skeleton also striated so you see this little bracket that they have here and they say that this is a sarcomere well the sarcomere is the contracting unit of a muscle cell and since it's a contracting unit of a muscle cell it would make sense that actin and myosin is in there and it is so they're going to magnify that for you so a sarcomere runs from one z line sometimes it's called the z disk let's see how this goes zigzag where I'm following my arrow so that's one z line or z disk here's another z line or z disk so from one z line to another z line that's a sarcomere so that's the contractile unit now within that contractile unit like I said before it's going to be actin which is that thin filament and myosin which has the heads on it so then they magnify them so that you could see them all of these heads on myosin and then here's acted with the active sites if you go back to the muscle contraction model they showed you in the picture just one right one myosin head that is going to be cocked when ATP breaks down ATPase excuse me when ATPase breaks down ATP into a teepee a pie so you get head cocking and then you get cross bridging and that cross bridge is when the myosin head comes in contact with the active site on actin and then the power stroke is when the myosin head pulls the actin past it so see all these heads this is what I was saying before see all those heads that are there and see all those active sites on actin and this is just one row of myosin and one row of actin look how many there are in one sarcomere and then there are millions and millions of sarcomere in each of the muscle fibers so it's really cool all right so we already know the sarcolemma is the plasma membrane so it's the cell's membrane the sarcoplasm is the cytoplasm of a muscle cell so remember that prefix Sarco means bone I'm sorry hip means bone means muscle and then we have glasses ohms which store glycogen and glycogen is just a bunch of glucose molecules that are bonded together with glycosidic bonds and if we break one part that means we can get glucose and energy but no way and then myoglobin is how we store oxygen in muscle its myoglobin and muscle hemoglobin in your blood I know how cool is that anyway and then there's some other things like the sarcoplasmic reticulum so that's the SR and then those t tubules which we know have the calcium in them so this is me telling you about the sarcomeres already right it's the contractile unit that is in the muscle cell and the fact that you see skeletal muscle as striated is because of the dark bands and the light bands so the a bands and the I bands are dark bands and light bands that goes dark light dark light dark light dark like so you see stripes in it and so look dark light dark light dark like stripes skeletal muscle is striated now here's that z-disc notice how there's some things I'm not mentioning so work with me here since I write my test so here's the Z disk or that Z line that I talked to you guys about this is what separates the sarcomere so I go from one z line to another Z line and that's what they say down here the sarcomere is between two successive Z disks or Z lines and then we have the thick filament which you know is myosin because I've mentioned it and we have the thin filament which is actin and then they explain to you how they run so that you can see that they are partially overlapping each other so that's why I say when actin and myosin are pulled past each other to their furthest degree of overlap the muscle is contracted and that's because within the sarcomere within the sarcomere they're already overlapping see that they're already overlapping but when they get to their fullest degree of overlap and that would be myosin pulling the actin past it then these z lines are going to be brought closer together right and the muscle would be fully contracted okay so um let's see so the sarcomere contracting unit said that okay so animated picture I didn't have to go back it was coming up anyways so um the a band is the dark band the Iban is the light so that's why it looks striped so light dark light dark and then this is the Z line or the z disk here and here so that means from here to here is a circle Mir the thick filament is myosin which they mentioned and I mentioned already thick filament is myosin and the thin filament is the actin and then of course another magnified picture of actin and myosin the Z disk and a circle mayor okay now oh look what it says acting as the thin filament and myosin is the thick filament onew okay myosin the thick filament it has heads on it no way anyway it does have tells to and it's not that they aren't important but it's the heads that bind to the active sites on actin that costs that caused the cross bridging to occur during contraction the other thing about the heads and again if you think about the muscle contraction model these are things you know heads right are going to bind to the active sites on actin the heads also have a binding site for ATP remember ATP is ADP and pi together the heads also have an ATPase enzyme that's because this ATP ace has to break down the ATP to get the heads to in the muscle contraction model which we talked about already then we have the thin filament and you know this is kind of cool how it's twisted together and great but this is the important part to me you know the stuff down here that's bolded so this tropomyosin and troponin complex is attached to actin and this troponin is where the calcium binds calcium binds to troponin and causes the tropomyosin complex to open reveals those active sites on actin so that they can react with the myosin heads and then we can get the muscle to contract so then of course again they just show you actin and myosin so the thick filament is myosin thin filament is actin myosin has heads actin has the troponin and the tropomyosin okay now the sarcoplasmic reticulum is basically the cytoplasm of a muscle cell because endoplasmic reticulum cytoplasmic reticulum right so sarcoplasmic reticulum and those t tubules are part of the sarcoplasmic reticulum and the t tubules have the calcium so intracellular means we're inside of a cell what type of cell a muscle cell and lo and behold calcium is needed for muscles to contract so let's think about what happens calcium diffuses into the axon terminal causes the release of acetylcholine acetylcholine binds to the sarcolemma opens up ion channels sodium comes in potassium goes out and causes an end play potential an end play potential can be described as a localized change in charge that localized change in charge then opens up neighboring nearby adjacent whichever word you prefer voltage-gated ion channels and that lets more sodium in and then when that happens it initiates or causes an action potential an action potential is similar to an end play potential and the fact that it is a change in charge however mplet potentials are localized and action potentials get to move so this action potential moves down the sarcolemma into the t-tubules causes the release of this intracellular calcium then calcium binds to the troponin causes the tropomyosin complex to open reveals the active sites on actin so they can react with myosin heads but the heads aren't ready yet they've got to get cocked so ATP ace breaks down ATP into ADP and pi so P sub I which is inorganic phosphate and then I get head cocking cross bridging which when the myosin head actually binds or connects to the active site on actin and then I get the power stroke the power stroke is when myosin pulls actin past itself and that keeps happening until the muscles fully contracted how cool is this crap love this stuff all right hey guess what the t tubules are continuous within that you know sarcolemma that's cool they're showing you the picture here so that you can see the sarcoplasmic reticulum then you can see the t tubules that are in there we already know that the T tubules are going to release the calcium if you look here they're showing it like they remove the sarcoplasmic reticulum so that you could see but right here is my sarcomere this is my contracting unit remember from Z to Z this is my contracting unit here is my actin and myosin and then here are my t tubules within the sarcoplasmic reticulum so calcium is released and binds right to the regulatory proteins so troponin causing the tropomyosin complex to open now things that you know and I know it sounds silly because I'll say this a lot things that you know since we talked about the muscle contraction model you know that a nerve cell was right there at the muscle cell right because the cetyl choline released you know from the nerve cell and then bound to the muscle cell the place where a nerve and a muscle come together called a neuromuscular Junction let me get this straight the place where two things come together are named for the two things that come together new neuromuscular Junction now this is going to look familiar because this is how we started off the lecture so they magnified it this is the axon terminal and this is a muscle cell and then they magnify that so that you could see calcium going in right calcium goes in causes the release of acetylcholine so these green dots are acetylcholine when acetylcholine binds to the sarcolemma so this is the muscle cell it says sodium goes in if you follow the arrow right sodium goes in and potassium goes out that causes that endplate potential they also mention here and I'm not mad at them for doing it but they also mention here that acetylcholinesterase can break down acetylcholine and when it breaks down acetylcholine it's gonna close the ion channel which we know because that's what has to happen for the muscle to relax Oh bigger picture here is acetylcholine esterase breaking down acetylcholine acetylcholine esterase breaks down acetylcholine closes the ion channel no more sodium can go in no more potassium can get out they try they try but it didn't work alright so at the neuromuscular Junction what do we have there axon terminal at the end of a nerve cell acetylcholine is the neurotransmitter that's going to be released it binds to the sarcolemma which is on the muscle cell I know I know things you already know so it says here that that acetylcholine is going to be released then it's going to cross this cleft like a cliff is going to cross a clef it binds to the sarcolemma then we get the electrical events they're not being specific here but you know the movement of those particles so we're going to get the movement of those particles that generates that action potential which is the you know moving change in charge that goes down into the t tubules then oops sorry so then we already know hold on one second I'm so sorry I'm sorry I'm trying to pause the recording