Lecture15 Muscle Physiology

hi everyone this is lecture 15 muscle physiology so today we're going to talk about skeletal muscle we're going to begin with reviewing a bit about skeletal muscle anatomy we're going to then talk about the activation and response in a muscle through excitation contraction coupling part of which is the sliding filament theory and then we will talk about how to get stronger muscle contractions through the mechanics of muscles and how the metabolism of muscles being so active is supported with certain specializations so I want to remind you that skeletal muscle is not the only type of muscle in the body we also have smooth muscle and cardiac muscle smooth muscle and cardiac muscle are both involuntary and smooth muscle is found in the majority of organs and also in the blood vessels some examples of smooth muscle are control of blood vessels Airways digestive tract urinary tract and then cardiac muscle is found in the heart so cardiac muscle is responsible for pumping blood through the chambers of the heart the atria and the ventricles when we talk about muscle muscle in general we're talking about skeletal muscle so for the rest of this lecture we'll be talking about skeletal muscle which is the voluntary movement of the body and in that process it also can generate heat we'll give you some more functions in a second so some examples of skeletal muscle are muscles that attach to the limbs and move the limbs muscles that attach to the jaw and move the move the jaw for chewing muscles that are aiding in breathing so some very important functions of muscles I also want to briefly remind you of the difference in histology for these three types of muscle so both skeletal and cardiac muscle when we look at them under the microscope and look at individual cells skeletal muscle here's one individual cell here there are these very elongated rectangular cells that have these striped appearance so this striped appearance these dark bands and light bands are called striations here you will have nuclei of which muscle cells have multiple skeletal muscle cells have multiple nuclei cardiac muscle also has dark and light bands it also has striations but it is unique in the sense that it is more branching and then it also has these dark staining regions here which actually are gap junction containing structures card called intercalated disks and we'll talk more about those when we get to cardiac muscle smooth muscle is not striated so it does not have the striped appearance of skeletal and cardiac muscle and it's muscle cells look sort of more pinnate or sort of worm-like they're pointed at the ends and they have single nuclei so to focus now on skeletal muscles so the major functions of skeletal muscle are movement that's the main one and it's a voluntary movement muscles will attach directly or indirectly to the bone and they will then pull and move the bones or sometimes tissue such as the skin when they contract so this is why you guys had to learn so much in anatomy about origin insertion and action because where the muscles attach to tells you first where the muscle is braced to be held on to and second what the muscle is pulling on to move muscles also maintain posture and body position there are some muscles in our body that are continuously contracting to make adjustments muscles also stabilize joints there are some tendons that are crossing joints and muscle tone provides the stability to some of those joints also as muscles are active during contraction that activity generates heat so muscles as a secondary function can also create heat or work with thermogenesis so we know that we we shiver when we get cold and the the importance of that is not the actual contraction or the movement of the body the importance of that is the heat generation that comes after the contraction so let's look then at skeletal muscle anatomy I'm sure that you guys did this in your regular anatomy course but let's look at it briefly so here your textbook has a picture of a whole muscle but for example your bicep muscle and I want you to think of the whole muscle as an organ so each muscle in your body is like its own tiny organ and if we slice that muscle open we will see several different bundles those bundles we call fascicles and then if we look within the fascicles an individual fascicle will have several muscle cells a muscle cell is the same thing as a muscle fiber those words are used interchangeably so muscle cell muscle fiber same thing so then we look inside at a muscle cell here the muscle cell is so densely packed with contractile organelles that you almost can't see any other organelles within the cell so each one of these little cylinders is a tiny organelle called a myofibril and the myofibrils then are packed with contractile proteins that are arranged in a circle mirror so there's your muscle there's your individual muscle cell of which many are bundled inside a single muscle and then there's your muscle cell or muscle fiber which has many many contractile organelles or myofibrils and those myofibrils then have a certain protein arrangement we call the sarcomere there's a larger picture and then here we go the muscle cell with the sarcomere focused in so i want you to notice there are many circle mirrors per-mile fibril many myofibrils per muscle cell or muscle fiber so the major contractile proteins within a muscles muscle cell within these myofibril organelles are called myosin and actin myosin makes up the thick filaments and actin makes up the thin filaments the myosin and actin are arranged in a very specific overlapping pattern that creates those striations that you see when you look at skeletal muscle histology so we are going to draw out the sarcomere to remind you guys of its anatomy so let's draw this out okay so for a sarcomere remember that there are several of these within a single myofibril and then several myofibrils within a single muscle cell and we start by denoting the ends of the sarcomere and a region we call the z line so from Z line to Z line is one single sarcomere so this whole thing and will be one sarcomere and then attached to the Z line are the thin filaments which are made up of actin so here we have thin filaments made up of acting then at the center of the sarcomere we have a central line that we call the M line so that denotes the center of the sarcomere and then stretched across the center we have our thick filaments so the thick filaments are made up of myosin and myosin contains these head groups that want to grab on to the actin I'm not going to draw all of them here it would take forever but you guys get the idea right so myosin has the head groups makes up the thick filaments then we have some regions of the sarcomere that are denoted by overlapping or non overlapping regions of the actin and myosin reach are acting the myosin thick and thin filaments so where we have only myosin this is the H zone or the H band where we have only actin and stretching across to the next sarcomere is the I band so we will also have an i bend on the other side here where we have just actin on either side and then the region that contains both actin and myosin is going to be the AV end so we have I a I and then we have the H zone at the center so again we can do it this way here's your H zone then we have a band which contains the H zone and the actin and myosin overlapping regions and then we have the I band which is on either side with just actin so why are we doing this that we're doing this because the sarcomere is the contractile unit of the muscle cell and we're going to see how it changes as we study the contraction of the muscle so let's look in a little bit more closely at the individual proteins that we're talking about so myosin forms the thick filaments and you can see the head groups here on the myosin so it looks kind of like a golf club with head groups the myosin contains binding sites for actin and the myosin wants to grab on to the actin the myosin heads also contain an ATP a's site which can activate the myosin multiple myosins group together to form a whole thick filament where you will have lots of myosin heads sticking out reaching towards the actin actin then forms the thin filaments actin molecules contain myosin binding sites to where myosin wants to grab on to the actin that's what's shown here in these sort of dark green sites here so actin protein binds together to make the thin filaments and they're sort of arranged in this twisting helix pattern there are also two regulatory proteins found on active so this one that looks like a rope stretching across and blocking all of the myosin binding sites is called tropomyosin and then this one here that's in the lighter tan color is holding on to the tropomyosin and locking the tropomyosin on to the actin so I say that tropomyosin and troponin ponent at the lock are like a chastity belt so the myosin head wants to bind onto the actin but tropomyosin prevents that binding site from being available so tropomyosin wraps around and then troponin is like the lock that locks the chastity belt close so that the actin is not available because the tropomyosin is locked on by the troponin so again myosin with the myosin heads and then actin with its helical pattern making the thin filaments blocked by tropomyosin and troponin held on by troponin and then here are just some pictures for your reference to see the sarcomere pattern I also want to show you the histology and how these different bands and zones of the sarcomere are named so the eye band is the light band that a band is the dark band the EM line forms at the center and then the Z line is a dark line in between the eye bands and then there's the histology again okay so again we're doing this because the sarcomere is the contractile unit so when a muscle cell is relaxed its individual myofibrils are also relaxed and you'll see that that actin is stretched further away and you have a large h zone when the muscle cell is relaxed when you contract a muscle the individual proteins will change and the actin is going to move closer towards the EM line making the H zone very very small by nature of that that also makes the eye band shorter so everything moves in closer to the center during contraction overall that means that contraction is literally shortening of sarcomeres that are within the myofibrils and the total shortening of the muscle style itself so the sarcomere changes during contraction this makes the H zone smaller the eye band smaller and it moves the Z lines closer together the a band and the M line do not change why because the myosin stays in place so it is only the zones that have actin that change and the a band only encompasses the end of the myosin to the end of the myosin so the dark band stays the same the light band gets smaller okay now that we understand a little bit about the anatomy within the muscle cell let's talk about excitation contraction coupling so muscle contraction is caused by activation of the muscle cell in other words depolarization from the nervous system and then it responds by contracting so the steps of excitation contraction coupling are these we start with an accent action potential which comes from the nervous system that causes calcium release that activates troponin that's the lock that releases tropomyosin that's the rope or the chastity belt tropomyosin is pulled off of the myosin binding sites on actin and then the myosin heads grab on to actin once the myosin heads grab onto actin they move the actin in a power stroke and then everything needs to reset so let's go through these steps one by one okay step one the action potential reaches the muscle cell membrane now if you are having trouble understanding the action potential you may want to go back and review the prior nervous system introductory lectures where we talked about membrane potential and action potential but the ultimate outcome of the action potential is that electrical activity travels down the motor neuron and reaches the neuromuscular Junction so that contacts the muscle and acetylcholine is released onto the muscle so the neurotransmitter is released on to the muscle here so here is a motor neuron in blue coming from the spinal cord going out the ventral root of the spinal cord and traveling to the muscle fibers that it innervates this particular one has four muscle fibers for the blue neuron here's a red motor neuron traveling out of the spinal cord out the ventral root and going to the muscle fibers that it innervates and each little contact that a motor neuron makes at the muscle cell is a neuromuscular Junction so the action potential reaches the muscle cell membrane through the acetylcholine release at the neuromuscular Junction remember how synaptic activation happens so here's the motor neuron here's the action potential traveling down the motor neuron there's the neurotransmitter being released in this case it's acetylcholine and traveling across the synaptic excuse me traveling across the synaptic cleft and then attaching to or binding to the acetylcholine receptors these receptors acetylcholine receptors are ion channels so when the neurotransmitter binds to the receptor it opens up ion channels and sodium rushes into the muscle cell membrane when sodium rushes into the muscle cell membrane that then causes electrical activity or action potential traveling into the muscle cell itself that action potential in the muscle cell is then going to make changes within the muscle cell so that specific change that is made when the depolarization of the muscle cell membrane is caused is calcium so the depolarization of the muscle cell membrane causes calcium release the depolarization spreads into the membrane in these invaginations of the membrane we call t tubules so here's the muscle cell membrane here in red so the depolarization or the excitation of sodium traveling down the membrane will then be transmitted down the t tubules so the depolarization goes down the T tubules which are really just membrane that has dipped down into the muscle cell so down the T tubules and then it reaches the structure that's drawn here in green which is the sarcoplasmic reticulum the sarcoplasmic reticulum is a modified endoplasmic reticulum so it's a branching network of membranous organelle that stores calcium so the sarcoplasmic reticulum is holding onto calcium and waiting for the depolarization to travel down the t tubules once the depolarization travels down the t tubules then calcium will be released from the sarcoplasmic reticulum so depolarization spreads down the T tubules that sends a signal to the sarcoplasmic reticulum and then the sarcoplasmic reticulum dumps calcium on to and see right here this cylinder is the sarcomere so let's look a little bit more closely here so we have depolarization of the muscle cell membrane depolarization spreading down the t tubules and then causing activation of the sarcoplasmic reticulum that then is going to dump calcium all over the myofibrils of which they are wrapped around so here's the myofibril and now you can see if we remove the sarcoplasmic reticulum you can see just below that that's where you're going to have your myosin here in red and then your actin in blue just waiting for that calcium signal so what the calcium does is it activates troponin so it unlocks the key so calcium binds to here in yellow is the troponin calcium binds to the troponin and the troponin unlocks and releases from tropomyosin once the calcium releases from tropomyosin tropomyosin which is this rope-like protein that was remember it was stretched on top of and bound to the myosin binding sites on actin now tropomyosin that's what these arrows are showing tropomyosin is now moved out of the way so the acting binding sites are available and now the myosin heads are able to find specifically to the actin because the tropomyosin is not blocking anymore so tropomyosin is released freeing the actin the next step is that the myosin heads will bind to the actin and when the myosin head fine to the actin we form what's called a cross bridge so that binding is cross bridge formation so here's your myosin head binding to the actin then step six is that the myosin has moved the actin so they bind to the actin and now they're gonna like a ratchet move the actin inwards towards the EM line this movement is called the power stroke and it requires ATP the last step then is that myosin detaches from the actin so the myosin was bound to the actin in the cross bridge it moved the actin in a power stroke now the myosin has to detach and reset and get ready for another contraction that detaching and resetting also requires ATP after that calcium is returned to the sarcoplasmic reticulum so there are calcium pumps located in the start sarcoplasmic reticulum stop the calcium signal and that resets the calcium also to prepare for the next contraction so I think we should probably take a second to draw out these three steps so let's go back to the one through six and draw these out okay so for excitation contraction coupling you okay excitation contraction coupling we have the neuron coming down and contacting the muscle cell and the muscle cell has this striated appearance because of the arrangement of the circle here so if we zoom in on this what we see then is a synapse which is the neuromuscular Junction and the action potential coming down the sinem so this is the action potential going down the axon of the motor neuron and then reaching the muscle cell and we're now doing in really close on this to look at just the individual synapse so the action potential comes in that activates a whole cascade of neurotransmitter release go back to your nervous system lectures if you don't remember that whole cascade neurotransmitter gets released the neurotransmitter here is acetylcholine which I'm going to abbreviate with ACH that is going to reach the muscle cell membrane and bind to acetylcholine receptors when it binds to these acetylcholine receptors sodium floods the muscle cell membrane when sodium rushes in we're then going to get an action potential in the muscle cell itself so action potentials going to travel down the muscle cell and as it travels down the muscle cell it's going to traverse down the t-tubules so it goes across the muscle cell membrane and then it goes down into the muscle through the t tubules so X potential goes across the membrane and down the T tubules and the T tubules are very close to the sarcoplasmic reticulum the sarcoplasmic reticulum is storing calcium and are going to dump calcium when the action potential comes in so that calcium will be then dumped inside the muscle cell and it's going to then activate troponin so troponin will be active that's going to move tropomyosin out of the way the tropomyosin out of the way then frees up the active I'm going to draw that over here so now the actin if three and the binding sites on the actin are now available to the myosin so myosin can bind when myosin binds to the actin that is a crossbridge then the myosin is going to move the actin and that is a power stroke after that the myosin will unbind reset and everything will detach the calcium will also be pumped back to the sarcoplasmic reticulum okay so action potential comes in calcium release troponin unlocks tropomyosin moves out of the way myosin binds to actin forms a crossbridge myosin pulls the actin power stroke and then everything resets so let's zoom back forward then during the power stroke the myosin head moves the actin towards the center of the sarcomere so I wanted to show you guys this picture so you have an idea of how this works and what I always say is that the actin is like the lead singer in a rock band and he's there waiting but his security is holding him back right the troponin and tropomyosin and then the myosin are like the crazy fans that are waiting for him to crowd surf so they're like oh like wanting to grab onto him and then as soon as he's free as soon the security lets him go and he jumps into the crowd then he can crowd surf and the myosin can grab him and move him forward so the myosin grabs onto the actin and moves it forward towards the M line shortening the entire sarcomere so if we look at this sort of in three dimension here's a relaxed sarcomere with the myosin thick filaments in the center and the actin thin filaments on the edges towards the Z line and then during this process of the power stroke pulling the myosin in that pulls the myosin in towards the middle and the entire sarcomere gets shortened there is a summary figure in your textbook which you may want to review which goes over all of these steps as well so the sliding filament theory then are basically steps three through six of excitation contraction coupling so this is the mechanism of the myosin head grabbing onto the actin and sliding it towards the center so we call this the sliding filament theory and the important piece of this the calcium and ATP requirement so calcium is the excitation signal required to free the myosin binding sites this is important because this is linked to calcium homeostasis so lack of calcium are low calcium in the body and depletion of calcium in a muscle can cause muscle weakening so if you don't have calcium in a muscle cell you will not have the release of troponin and you will not have the myosin binding to the actin the muscle cell will then be unable to contract but there's also normal pumping the calcium back into the sarcoplasmic reticulum no calcium available to the troponin or being held back and stored in the sarcoplasmic reticulum no binding will occur the muscle will be relaxed there are also two parts of this process that require ATP ATP is required for the powerstroke ATP is also required for crossbridge release if there is no ATP then you will get no release so you may have heard of a state called rigor mortis where upon death due to some other mechanisms that occur essentially you get a complete contraction of the muscle which forms cross bridges but when there's no ATP being made because now the cells are dead no recycling of the ATP then there's no release of the muscle so there is a state of fixed contraction immediately after death called rigor mortis in which all muscles in the body are contracted and unable to be released over time of course then the body will start to degrade and will be relaxed because the proteins are now degrading but there is initial state after death where no ATP is available to release the cross bridges so here is the sliding filament theory and where ATP is important so first the myosin head is energized and ready to bind to actin if calcium is present then troponin is unlocked tropomyosin moves out of the way and the myosin can bind to the actin after that binding the myosin head then ratchets and moves the 8e excuse me the actin over during the power stroke another ATP then is required for the detachment of the myosin and the re-energizing to prepare for the next step if there's no fresh ATP available then we form this rigor complex or rigor mortis in which the muscles are stuck in a contracted crossbridge power stroke state so now that we've done a bit on how we excite and how muscles respond to that activation I want to talk to you guys about how to get stronger muscle contractions so what you have seen so far it's just a tiny tiny tiny protein level contraction so if you just had a single sarcomere contraction or a single muscle cell contraction which would be many many sarcomeres within the myofibrils you wouldn't get any tension you wouldn't get any movement you need many many muscle cells to contract to actually get a successful movement so the phases of muscle contraction are first a single stimulus and the delay so it takes time for the excitation contraction to come together so you'll get a stimulus and then you'll have a delay that's called the latent period and then you'll have a period of contraction where the muscle is actually responding this is cross crossbridge cycling and tension in the muscle the amount of tension that is created is going to depend on several factors which we'll talk about and then there is a period of relaxation so as calcium is transported back into the sarcoplasmic reticulum then crossbridge cycling ends and the tension of the muscle cell will decrease so the actual timing here is approximately 30 to 100 milliseconds for a total contractile response that's very different than the timing of an action potential so a single action potential is about one to two milliseconds very fast that delay then during the latent period as the action potential is traveling to the muscle cell will then be followed by the long contractile response so the crossbridge cycling actually takes time about 15 to 50 milliseconds for a contraction phase on about 15 to 50 milliseconds for a relaxation phase so anywhere between 30 and 100 milliseconds for a single muscle contraction so within the whole muscle several muscle fibers will contract to create movement so the way I like to think about this is have you ever had a muscle twitch in your eye just like a teeny teeny little twitch very very small right so a single muscle cell activated are a single muscle contraction we call a twitch but it actually creates a lot it actually takes a lot more to apply force and actually move something so contracting the muscle creates tension but we need to contract many many muscle cells within that muscle to get a strong enough contraction that will actually move the thing that it is trying to move and is trying to move the bone so the tension creates force we need to then get enough for us to actually move that thing we're trying to move which is the bone the bone itself then and anything being held on the bone so for example if I'm talking about my bicep muscle which is bending my elbow or flexing my elbow it's there's a certain weight of just my forearm and my and that will be a normal load but I could also grab a textbook and that would be a heavier load which the bicep would then also have to create enough force to move in addition to the the weight of the phone so here's the bicep muscle which is bending or flexing the elbow and the bone itself and the weight of the hand is a certain amount and then if you're holding anything in your hand that also adds load to the muscle in order to actually move the bone hand and whatever's being held in the hand you need to create enough force using enough muscle cells and getting enough contraction within those muscle cells to actually pull with strong enough tension to move the load so there are many types of muscle contraction what we talked about so far is muscle contraction causing shortening that's called a concentric contraction there are also muscle contractions that are used as stabilizing contractions that's when the muscle actually lengthens or eccentric contraction so an example of that is when I am flexing my elbow that is a concentric contraction of the bicep because it's the biceps primary movement but then the tricep on the back is actually lengthening it is contracting while it lengthens to stabilize this movement of my elbow so the primary mover would be my biceps it's doing the concentric contraction the antagonist then will be the tricep in this bending motion and that's doing an eccentric contraction we also have isotonic vs. isometric contractions so an isotonic contraction is when the load remains constant and the muscle shortens so in other words when I'm actually able to move that thing that I'm trying to move this is a normal isotonic contraction and I haven't changed the way to that Lodi just steadily moved it if the load is too heavy or you're trying to move something that you cannot overcome this is an isometric contraction in this case the tension develops and you're trying trying trying really hard so if my text book it's too heavy and I can't actually lift it I'm trying to lift it but the bone and the load is not moved so the isometric contraction is when you're trying to move something and you are continuing to increase in force but you're not able to move it so we then want to think about how can we actually move larger and larger loads so how is it that we can get an increase in the strength of contraction and there's many ways that muscles have solved this problem so we talked about recruitment of motor units the size of the muscle involved activating the muscle more which is called twitch summation and the trap effect and then getting muscles to optimal length so first we need to define what is actually activating the muscle so all muscle fibers within a whole muscle are not active during every contraction so if I'm just moving my arm with no load attached to it there's only a few muscle cells that are active if I'm moving something really heavy I need to actually get more muscle cells active and the body knows that so it's not going to activate and use its full strength every time it's going to save the strength of that so there are several motor neurons dedicated to a single muscle or at a single group of muscle cells within a muscle so all muscle cells within a whole muscle are not activate activated by the same motor neuron there's several motor neurons here there's pink orange red so here is the pink motor neuron which is attaching to all of the pink muscle fibers here's the orange motor neuron which is attaching to all of the orange muscle fibers here the red motor neurone which is attaching to all the red muscle fibers all of these muscle fibers are within a single muscle and there are several motor neurons attached to them one motor neuron and all of the muscle fibers that it attaches to so for example the pink is one motor unit so here we have three motor units represented the pink motor unit the orange motor unit and the red motor unit one motor neuron and all the fibers it innervates if we want to increase the strength of a muscle then we can just recruit more neurons activate more motor neurons to activate more muscle cells so if we activate more motor neurons we will then activate all of the muscle cells it's attached to and we call that motor unit recruitment that will increase tension in the muscle as a load increases we're going to play with this in a lab so you guys can think about how motor unit recruitment works and you'll watch it in action as you apply more force to a particular muscle there's also some baseline muscle tone which says that some muscle fibers are always active to maintain muscles even when no movement is taking place here this graph is showing that the more motor units you recruit or the more muscle fibers you activate the stronger the contraction and that makes sense if you think of this like a tug-of-war so the more people that you have on the rope tugging or the more muscle fibers you have pulling within the muscle then the stronger the contraction is there is also a difference in muscle size this can be the number of muscle fibers per motor unit or it can be the size of individual massive muscle fibers so development determines the number of muscle cells the general size of a particular muscle so think of say the muscles in your leg compared to the muscles on your jaw big difference in size that's developmental we cannot affect the general number of muscle cells within a muscle but we can actually make more protein inside a muscles cell so the size of into individual muscle fibers will be increased when fibers produce more myofilaments so with training and with exercise fibers can make more actin and myosin in response to demands and that then can cause hypertrophy or increase in muscle cells size so bigger muscles have more motor fibers per motor neuron that sort of developmental so here they give an example of a finger versus a leg muscle and there's just a limit in a smaller muscle as to how much it can contract compared to a larger muscle so if you recruit five or the maximum motor units in a finger muscle versus five or the maximum motor units and a larger muscle the larger muscles always going to be stronger even if they're both maximally activated the next thing we can do is to change the amount of activation to a single muscle cell so when you see these recordings now we're looking within a muscle cell so this is a single twitch of a single muscle cell and here's an action potential stimulating that muscle cell so there's your action potential with the latent period there's your contraction phase there's your relaxation phase if you do this and use space apart the stimulation you'll have a full contraction relaxation delay new stimulus full contraction relaxation so what's happening here is that calcium enter terms and then calcium is pumped back calcium enters calcium is pumped back so repeated stimulation is actually necessary to produce sustained and longer longer duration contraction so back to this sort of eye twitching I was talking about right or if you've ever had a tiny twitch in your leg that individual single twitch is not enough to actually produce anything significant with respect to movement what we need is a long sustained and held contraction and we do that by stimulating a muscle very close in time and we stimulate a muscle very close in time calcium buildup and as calcium builds up and we don't give calcium time to go back into the sarcoplasmic reticulum we'll get summation or addition of activity addition of contractions on top of each other so this is what you would have if you space them apart and then you'll get much more if you put them very close together that's twitch summation we can do this to the extreme where we deliver very very very close together stimulation to the point where there's actually absolutely no chance for the calcium to return back to the sarcoplasmic reticulum and you just dump a ton of calcium onto the sarcomere with no possibility of relaxation when you do this with very high-frequency stimulation you will get a long smooth sustained contraction which we call it tetanus or techne you want this in skeletal muscle if you're trying to hold an action and to get any sort of sustained force of contraction it will hold them until the stimulation stops or until the muscle is fatigued so we can do this by putting electrodes on muscles and stimulating them the nervous system however is smart and knows how to do this already so the nervous system knows the particular patterns of action potentials to send to a muscle to create tetiny so comparing a single twitch where you have calcium in calcium out long contraction relaxation calcium in calcium out contraction relaxation and then here's twitch summation calcium in a little bit of calcium out but not fully and then calcium in again and then calcium out that's twitch summation and then tons of calcium calcium calcium calcium calcium so much long sustained contraction with no possibility relaxation that's technique you can also get something called trap trap is what we call this staircase effect and this is increased contraction in response to multiple stimuli of the same strength this is different than summation because relaxation occurs as there's increasing availability of calcium but the calcium is able to get pumped back to the sarcoplasm but this is sort of like priming a muscle so this is one of the arguments for warming up so you calcium in calcium out for some reason the second time you do this you'll get more calcium and so contractions increase because you will get sort of an enhancement of the elastic component of the muscle and as you increase heat or you warm up the muscle the enzymes increase to make the contractions go more quickly excuse me to make the contractions stronger so calcium in calcium out but somehow with this repeated use of a muscle and increase in heat increase in calcium from the SR and more optimal elastic component then you will get this staircase effect with warming up me we need to talk about optimal length of a muscle so this comes into play mainly if you're thinking about say a patient who has strained a muscle or torn a muscle generally development is set up such that muscles are already at their optimal length but this is important to understand because it comes back to cross bridge formation so the way that a muscle normally is set in the body is that it is at its optimal length so there is where every myosin head is there is an actin nearby for it to grab on to so the optimal amount of myosin and actin interaction at optimal length if a muscle is stretched too far then the myosin is too far from the actin and even though the actin binding sites are available the myosin can't reach them to grab on so this will not provide much strength in muscle contraction if they're too close there's nowhere for the actin to go to create a change and to produce tension in the muscle so the the actin is already as close together as it can possibly get the myosin can pull on it but it's not going to make any difference in the tension so optimal length of the muscle is important for maximizing cross bridge formation so if we look at a muscle that is too short compared to a muscle that is optimal compared to a muscle that is over stretched this is what you see a resting muscle normally in the body is an optimal muscle length so your book has a diagram summarizing each of these processes and now we're going to talk a bit about metabolism so the last bit is that muscles require ATP so we saw ATP needed for the powerstroke we saw ATP needed for my ass and unbinding from the actin we also need ATP for active transport the calcium getting pumped back into the sarcoplasmic reticulum and the sodium and potassium actively transported for the action potentials to occur so ATP is the only energy source that can be used so muscles have a few metabolic pathways for getting ATP in high quantities and very quickly so muscles can do normal cellular respiration or aerobic which is also called oxidative phosphorylation but muscles can also have two alternate pathways so muscles can do anaerobic respiration muscles also have creatine phosphate available so first creatine phosphate is the one we haven't heard about yet so creatine phosphate is stored in muscle fibers it's a rapid source of energy for about 10 to 15 seconds of contraction the creatine phosphate transfers energy and a phosphate to ADP forming ATP immediately so it is basically holding on to an immediate source of phosphate bonds which can provide that phosphate to ATP when needed so it's a very quick very fast source of energy muscles can also do our anaerobic respiration in the form of glycolysis so let's go back to our cellular respiration lecture where you have glucose going through the path of aerobic respiration that first step of aerobic respiration is glycolysis which does not require oxygen glucose will then get broken down into pyruvate pyruvate can then enter into aerobic respiration if oxygen is available if oxygen is not available then pyruvate will broken down into lactic acid so we get a couple of ATP from glycolysis alone many more ATP from the full process of aerobic respiration but if oxygen is not available that couple of ATP can help a muscle cell function muscle cells also store a lot of glycogen glycogen is glucose bound together into a polysaccharide so this is an easy source of glucose for the muscle immediately available without relying on glucose from the bloodstream so oxidative phosphorylation is the aerobic respiration that occurs in the mitochondria if the main normal source when oxygen is plentiful and it is fueled first by the glycogen stores in the muscle so glycogen is stored in high quantities in muscle cells muscles can also use excuse me glucose and fatty acids delivered by the blend this can provide hours of muscle contraction for prolonged moderate activity but it is slower because it requires delivery of oxygen and glucose glycolysis then will be the primary source in the absence or in the depleted oxygen stage pyruvic acid will then be converted to lactic acid and acid can build up this will produce a small amount of ATP but it can occur very quickly this can provide about 30 to 60 seconds a very high level intense activity so if we look at overall the pathways that can be used there is glycogen stored in the muscle and glucose it can come from other sources to go into glycolysis the glucose will then be broken down into pyruvate if oxygen is available then the normal oxidative phosphorylation will occur if oxygen is depleted then pyruvate will be broken down to lactate and then into lactic acid there's also ATP that is then so this provides um ATP for the contraction and ATP for the various pumps that are required there's also then creatine phosphate which is immediately available and stored when ATP and phosphate bonds are plentiful and it can be used as a quick source of phosphate bonds to provide ATP fatigue that will happen if muscles are depleted of ATP anaerobic respiration will be less efficient as lactic acid accumulates and the pH drop so is remember that as acid goes up pH goes down and muscle fibers will lose potassium as a sodium potassium pump is unable to restore the ion balance so the sodium potassium pump requires ATP and if ATP becomes depleted then it's not going to be working as efficiently so fatigue then or neuromuscular fatigue is caused by a shortage of neurotransmitters at the neuromuscular Junction so there's physiological fatigue which is lack of ATP and then there's psychological fatigue which is lack of neurotransmitter or lack of activation so the central nervous system has to activate the neuromuscular Junction that causes excitation contraction coupling which releases calcium calcium is then the contraction relaxation signaling and we can have various forms of fatigue based on central or peripheral depletion of either the stimulus which is the neurotransmitter release or the calcium and ATP oxygen debt um is then difficult on muscles and it is the amount of extra oxygen that the body must take in to restore muscle chemistry back to a resting state so the liver has to convert lactic acid back to pyruvic acid when oxygen becomes available again the glycogen stores have to be replenished the creatine has to be re phosphorylated and then the oxygen will have to return and rebind to the oxygen binding myoglobin protein in the muscle for this we can also look at different muscle fiber types and this can get super interesting there's a lot of very interesting genetic and kinesiology Studies on athletes of varying abilities and the muscle fiber types that they can actually vary in genetically so muscle fibers can differ in their methods of metabolism based on either the pathways they used to produce ATP being some muscle fibers are more oxidative some muscle fibers are more glycolytic they can also differ in how quickly their ATP AAA's enzymes work so some muscles have fast ATP ASE's some muscles have slow ATP a's enzymes and this can affect the speed of contraction so generally we talk about three types of muscle slow which will have slow ATP uses and oxidative those are type one fasts which will have fast ATP ASE's and oxidative those are type 2a and then fast fast ATP ASE's and glycolytic which are type two so slow oxidative muscle fibers are very slow to contraction but most resistant to fatigue so these are very good for endurance and continuous contraction they are very well equipped for oxidative phosphorylation what do you need for a lot of cellular respiration will you need a lot of mitochondria and you need a lot of oxygen so we can get a lot of oxygen by having a lot of myoglobin protein to store the oxygen and also a rich supply of capillaries the fast oxidative are fast to contraction but resistant to fatigue so these are also very well equipped for oxidative phosphorylation and they have fast ATP aids activities these sort of like intermediate fibers then fast glycolytic fibers are fast to contract that they fatigue very quickly so these are our power and speed athletes right so they have high glycogen reserves and they um rely mainly on glycolysis so they don't eat oxygen there and work very quickly but they can then fatigue quickly because of the lactic acid buildup there will be large fibers that can generate more force but they will have poor nutrient diffusion they will also look lighter in color because they have less myoglobin storing oxygen so they're doing mostly anaerobic respiration they will also have fewer capillaries and fewer mitochondria so your book has another summary diagram of the differences between these fibers lastly I want to talk about the effects of exercise on muscle fibers we talked about it briefly already but let's formalize it here so aerobic exercises result in more efficient muscle metabolism and resistive to fatigue it also increases capillaries mitochondria and myoglobin in addition to that it will increase the efficiency of the heart lungs general body metabolism and muscular coordination that can aid muscle function resistance exercising weightlifting and isometric type contractions with lifting very heavy loads can produce more myofilaments and myofibrils causing hypertrophy this can also increase glycogen stores and increase muscle size and strength but remember you can't get more muscle cells that's development you can only get bigger muscle cells by packing them full of actin and myosin protein okay so I hope this is interesting for you guys I find muscle mechanics and muscle physiology to be very interesting let me know if you have any questions and this will conclude everything that you need to study for unit 2 so good luck on your next exam

Channel: Physiology for Students

Views: 209,465

Keywords: anatomy, physiology, muscular system, sarcomere

Id: 6YvdLWgT5mg

Length: 63min 46sec (3826 seconds)

Published: Sat Jul 09 2016