hi everyone i hope you're doing well today let's get started with our skeletal muscle unit so there are actually three different types of muscle tissue that we can see in illustration of here so we have cardiac muscle skeletal muscle and smooth muscle for the location of cardiac muscle it's pretty self-explanatory in the sense that it's located in the heart smooth muscle on the other hand is going to be located in most hollow organs our circulatory vessels and the digestive tract just for a few examples our focus today though is on skeletal muscle so this is the kind of muscle that we typically think of when we're referring to a muscle in general so the muscles that attach to bones to allow the movement of the skeleton though our emphasis for this lecture is on skeletal muscle it's important that you're able to distinguish between the different types of muscle tissue so let's dive into that a little bit smooth muscle has a distinctive appearance under the microscope in comparison to the other two because it is smooth or is lacking striations so skeletal muscle and cardiac muscle have striations where smooth muscle does not some other notable features here are these little purple dots which we can see on all three of them so this is the nucleus or pleural nuclei skeletal muscle is going to be multi-nucleated meaning that it has multiple nuclei per cell and we can see that in comparison to smooth muscle which is uninucleated cardiac muscle can be a little wonky in the sense that it can be both uni or bi-nucleated meaning that it can have either one or two nuclei per cell another distinguishing feature about the nucleus that we can point out is that with smooth and cardiac muscle the nucleus is going to be more centrally located whereas with skeletal muscle the nuclei are peripherally located meaning that you'll see them located around the edges of the muscle fiber or muscle cell last thing to point out is that cardiac muscle and smooth muscle are both involuntary meaning that their contractions are controlled by the autonomic nervous system so this just happens automatically or independent of voluntary nerve activity skeletal muscle is kind of cool in the sense that it can be both voluntary and involuntary so some muscles do have an involuntary component an example of this is the diaphragm so our diaphragm is a dome-shaped muscle separating the thoracic and abdominal cavities and it's critical for respiration or breathing so most frequently the diaphragm is going to contract and relax on its own by the autonomic nervous system meaning that it is primarily involuntary so i don't have to think about inhaling or exhaling all day but i can choose to take voluntary control over the diaphragm if desired so i can choose to hold my breath and stop its relaxation if i want to so that's a good example of a skeletal muscle that is both voluntary and involuntary but when we think about scalp muscles in general they are typically voluntary moving forward for the remainder of today's lecture though we'll be learning specifically about skeletal muscle so let's first look to see how the skeletal muscle is organized we attach skeletal muscles to the skeleton by tendons a common mistake is confusion between tendons and ligaments so tendons attach muscle to bone whereas ligaments attach bone to bone as far as the organization goes you'll see it's kind of like bundles within bundles so starting at the outermost layer we have the epimysium the prefix epi is a greek root word meaning on so that would make sense that it is on top of or on the outermost region so the epimysium is the connective tissue layer around the entire muscle group within each muscle group the muscle fibers are separated into bundles so we can see that here this is one bundle this is another bundle this is another bundle and these bundles of muscle fibers are called fascicles so surrounding each fascicle is the perimysium perimysium is another word root meaning around so the perimysium goes around the fascicle can go a step further to pull out one single muscle fiber or muscle cell and we'll see another connective tissue layer called the endomysium last word root for you endo means within or inside so we typically see endos as the innermost like like the endothelial cells that line the innermost of our vessels or the endometrium lining the innermost region of the uterus or endomysium which is what we see here an important clarification that i want to point out is that you'll frequently hear me say muscle fiber or muscle cell so that is the same thing those two words can be used interchangeably so a muscle fiber is a muscle cell and we can see that right here so one of these little sticks right here is a muscle fiber or a muscle cell looking at the histology of a skeletal muscle tissue in a typical semester i have the microscopes out so you can view the histology slides for yourself but these images will have to do what we are remote learning when you are drawing these for your lab report it'll just be a nice review for you to illustrate the location of these layers and bundles so you can get creative with it if you want to we have two different views here so for this one we have a cross section which would be if you chop the muscle like as seen here so this is a cross sectional cut that we see with the cross section we can see the arrangement of the fascicles really nicely with all the appropriate connective tissue layers so the epimysium the perimysium and the endomysis looking at the longitudinal section then this would be like cutting the muscle lengthwise so kind of like if you were to take a deli slice off the top one thing to point out on the longitudinal section that we can see really nicely is the nuclei so just a reminder for us that skeletal muscle is multinucleated in that there are multiple nuclei per cell and they're peripherally located meaning that you'll see them here along the edges with the longitudinal section our striations appear beautifully so we can see these alternating light and dark bands so this striated or striped appearance comes from the arrangement of protein filaments within a muscle cell and we'll talk a little bit more about that on the next slide with the sarcomere okay so let's take a moment to recap real quick the striated appearance comes from how our myofilaments are arranged within a myofibril just to clarify some terminology here remember that a muscle fiber means the same thing as a muscle cell so within each muscle fiber there are myofibrils within each myofibril we have our myofilaments the myofilaments are contractile proteins like actin and myosin a myofibril is composed of repeating segments called sarcomeres so that's what we're looking at here a myofibril and then zoomed in even further so we can see the details of one sarcomere the sarcomere is the functional unit of a muscle which means that it's the most basic unit of muscle contraction this is like the real business end of what makes a muscle move a sarcomere is going to extend extend from z line to xen so that defines the boundaries of one sarcomere we can see our actin filament here in green sometimes called the thin filament and then this purple rope-like structure that's wrapping around the actin filament is called tropomyosin and these little purple dots here here here and here these little purple dots are troponin and we will explore the significance of those more in depth in a few slots this thick gold filament is our myosin filament and we'll see these bulb-like structures here as our myosin heads the sarcomere has some important bands and zones that you need to know so let's talk about those we already know the boundaries are defined by xenons so this is a z line this is a z line straight down the middle we have the m line so you can just think m for middle it's this protein myomesin structure right here the i band is located right here and it's the region that's composed of actin only our a band is going to span the length of the myosin filament so it's composed of myosin and then whatever overlapping actin we have there so a band is the length of myosin plus overlapping acting and then we have the h band sometimes called the h zone that's the same thing the h band is composed of myosin only we'll see as the muscle contracts these myosin heads are going to grab on to actin and pull it inward so it'll pull the z lines closer together which causes the sarcomere as a whole to shorten so the filaments themselves the actin and myosin don't structurally change their length at all they simply increase their overlap which makes the whole thing shorten or contract so that's why the sarcomere is called the functional unit because it's the most basic unit or most basic structure that we have that actually performs the contraction on a microscopic level so every time we contract a muscle this happens in billions really trillions of sarcomeres throughout the body this slide just has the same information basically but laid out in text for those of you that prefer that style of learning written versus auditory so we know that myosin is the thick filament actin is arthritis and then this slide here is for our visual learners with an image showing more details and descriptions here we can see what a sarcomere looks like in a relaxed state versus a contracted state with the z lines being pulled closer together as actin and myosin increase their overlap so you can study this in whatever way you learn best i personally recommend a mix of all three as you go throughout the class first with listening and trying to understand the audio of my recording and then translating studying that with the text written text and then icing on the cake reviewing the visuals and images but it's totally up to you okay so moving on we're going to dive deeper into how the muscle actually contracts on a cellular level so let's set the stage for that here we've isolated a single or an individual muscle fiber muscle cell and around this muscle muscle cell will notice the plasma membrane in general we refer to the plasma membrane of a cell as the plasma lemma but since we're talking specifically about a muscle plasma membrane it's going to be called the sarcomere so just quickly to review the layers starting with the outermost going inward we have the epimysium the perimysium the endomysium and then beneath that is where we are right now at the sarcoma so if we were to cut past that we would notice our peripherally located nucleus and we'll see that a bunch of myofibrils taking up most of the space inside of our cell our myofibrils are composed of the myofilaments actin in myosin and so these are what will perform our physical contraction this right here just shows you what it would look like if you cut open one of those myofibrils so we can see the details of the sarcomere with our bands and zones inside in addition to that we have other important organelles like mitochondria located in the periphery and then this mesh-like structure laying over top looks kind of like a netting this is our sarcoplasmic reticulum which is just an elaborate smooth endoplasmic reticulum with its interconnectedly interconnecting tubules surrounding each myofibril our sarcoplasmic reticulum is important when we're trying to understand muscle contraction because this is where we'll have the storage of calcium ions that will be released when the muscle is stimulated or receives an action potential to contract one other thing to point out is the transverse tubules or the t tubules so we have these little spots right here right here and right here and we'll see how it's like a continuation of the sarcolemma to extend inside of the muscle fiber so these t tubules are extensions of the cell membrane into the interior of the cell the reason this is important is because in order for our muscles to contract the cell membrane has to depolarize so we want to make sure that that depolarization reaches all of the different myofibrils not just the ones that are located on the exterior so these specialty tubules will carry the action potential to the entirety of the muscle fiber okay so excitation contraction coupling this is where it gets a little complicated so to state it simply excitation contraction coupling is the process that pairs the depolarization of a neuron with the depolarization of a muscle cell so let's talk about the neuron first a nerve cell that innervates muscle fibers is called a motor neuron and the spot at which the nerve ending and the muscle fiber meet is called the neuromuscular junction so we can see that here with the axon terminal coming down to match up with a sarcolemma of a muscle cell at the neuromuscular junction so first thing that will happen is an action potential is going to be produced in the neuron and that's going to be propagated down the axon this nerve impulse stimulates the release of a neurotransmitter called acetylcholine so they're gonna we're gonna release acetylcholine into the synaptic cleft so going back to cellular physiology we know that neurotransmitters are most often released by exocytosis so that is what is happening here so acetylcholine is released from the synaptic vesicles of our neuron at the axon terminal and it will diffuse across the synaptic cleft of our neuromuscular junction where it will bind to receptors on the sarcolemma and this binding induces an impulse that's going to excite our muscle cell so that impulse is going to be propagated along the sarcolemma down to depolarize the t tubules so it's going to go so it comes across here at the neuromuscular junction it'll go along this way down to depolarize those t tubules which trigger calcium channels to open so we'll have an increase in intracellular concentration of calcium within the cytoplasm so in order for a muscle contract we must have the presence of calcium in the cytoplasm so it's available to bind to troponin so that kind of picks up right here and we have individual slides for the rest of this so make sure that you read through all of this is just a general overview of the process but i'm going to explain in further detail over the next few slides okay so going from so i just covered from here to here and then from here to here is we're going to cover that in the next two slides so calcium has now been released from the sarcoplasmic reticulum into the cytoplasm and that is what we want for contraction to occur so when calcium is present contraction can occur if the intracellular calcium concentration is low then contraction cannot occur so this calcium is going to bind to a special protein complex called troponin so looking at this picture here is these little purple dots these this is troponin you'll see is a polypeptide complex with subunits tnc tni and tnt we are going to focus our energy on tnc because that's what binds calcium we aren't going to get into tni in lab uh but just if you're curious just so you know it's an inhibitory subunit that can be measured in a clinical setting as a physiological indicator for damage to the heart so an elevated troponin is often seen with patients who've had a myocardial infarction which is just the fancy science way of saying that they've had a heart attack and then tnt it helps bind to japonen so you can think t for i'm sorry it helps bind the troponin to tropomyosin so you can think t for tropomyosin but again we're going to focus our energy on tnt speaking of tropomyosin though so it's going to be this rope-like protein that wraps around actin in the previous picture it was purple but in this image it's this rope like blue structure that's wrapping around actin and an important thing to know about tropomyosin is that it blocks the myosin binding sites on actin so the myosin heads have a special spot where they bind on actin so they can't just readily bind whenever they want to because we have tropomyosin here blocking it or standing in its way actin and myosin have a natural affinity for one another so they're like magnets myosin so desperately wants to bind to actin so you can think about this troponin as like the chaperone at the high school dance like making sure that actin and myosin don't touch each other keeping them six feet apart kind of thing the fun part though is when calcium binds to your opponent that causes troponin to change shape and in doing so that will roll tropomyosin away exposing those myosin binding sites so as soon as myosin gets the chance it's like game time right the myosin heads will grab onto actin as soon as the opportunity presents itself so once calcium binds to troponin tropomyosin will move out of the way that will allow for the interaction of actin and myosin which brings us to some even more exciting stuff with the sliding filament theory so the sliding filament theory is like a cycle so you can pick up wherever you want because it's just going to circle back around i'm going to pick up right here because this is where we left off on the previous slide so here myosin is ready it's just waiting for the opportunity and then once the opportunity presents itself we're going to move to the next step where we have a cross bridge being formed so a cross bridge is just when the myosin head attaches to actin so tropomyosin has moved out of the way that's what myosin was waiting for the chaperone has left the room kind of thing and myosin grabs on to actin to form a cross bridge the next step is called the power stroke so we can see our previous atp we see atp here our previous atp has been broken down into adp and an inorganic phosphate so that with our power stroke that phosphate group goes flying off release of energy this myosin head is going to pivot or bend so it just does like a little mini bicep curl which pulls the actin filament towards the inline so this is how we get the sarcomere to shorten or contract by pulling by myosin pulling the actin filament towards the in m line which will bring those z lines closer together so we can see that that adp is also released down here the next part cycling background here to the top is a critical step so you can see it cycles looking at this part it's important to note that myosin is still attached so if we look down here i'm sorry if we look down here we can see myosin is still attached so this is still in a con in a contracted state but the question i have for you is how do we get myosin to let go right so cycling back around to the top once another atp binds to myosin the link between actin and myosin is weakened and that myosin head detaches we break that cross bridge between the two so we have to have atp present in order to to break that bond between actin and myosin when it is attached so next the myosin head will assume the cocked position so it's already getting ready to go it's going to hydrolyze that atp into adp and inorganic phosphate which we saw earlier so now myosin is prepared to start the whole process over again with myosin binding to actin we have our power stroke release of energy bison is going to pull that actin filament inward we'll have another atp bind break that original that original cross bridge so we can prepare to do it all again so to say it very simply this pulling of actin by myosin with our sliding filament theory results in the overall muscle shortening and the generation of force so this is like the nitty-gritty of muscle contraction okay so let's talk about motor units the motor unit consists of one motor neuron so one nerve and then all the muscle fibers that it innervates so those two things taken together are called a motor unit the whole reason why we refer to it as a motor unit is because when that single motor urine neuron fires all the associated muscle fibers that it innervates will contract as a unit so that's how we get motor unit sometimes we'll have one a motor neuron innervating like 60 muscle fibers sometimes it's innervating only six fibers but the size of these motor units is important because it'll tell us the kinds of movements that we are able to perform so if a neuron innervates only four or five muscle fibers think about it for a minute what kind of movement do you think we'll be able to produce so if it innervates just four or five fibers do you think it will be able to perform a very precise action or a very gross movement very precise right so you'll have one nerve controlling a very small number of fibers so you can be really meticulous and precise with that movement however not all muscle movements we need to perform are very fine so large motor units ones that innervate several hundred muscle fibers are going to elicit gross movements which if you don't know what i mean when i say fine versus gross so fine is something precise like our eye movements or writing whereas something gross is typically a large movement something like walking or running a really cool thing about our motor units is that the body displays this property known as recruitment so this is a wonderfully designed way to keep us efficient so equipment essentially refers to the process of activating smaller motor units before activating larger ones so let me give you an example let's say that there is a box on the floor in front of you and you have no idea what's in it or how much it weighs it could be a box of feathers or a box of cement you don't know but i'm asking you to pick it up so if this is a box of feathers and your body doesn't display recruitment so instead of activating smaller motor units first let's say that you jump straight to activating the larger motor units if you lift that box with too much strength or too large of motor units it's going to go flying right like if you pick up that box with the same amount of muscle involvement as you would if it were a box of cement you'd end up just like throwing it or flinging it to the ceiling so fortunately that doesn't happen so the body will recruit just the right amount of motor units to perform or accommodate the action so we'll start with the smaller and we can call on more if additional strength is needed for our muscle actions there are two main categories that we can split these into isometric and isotonic i love our latin greek root word so let's use those here the prefix iso means same and then metric just like referring to measurement or length so if you perform a muscle action in which the muscle stays the same length right so an isometric action with a muscle staying the same length that would be something like i don't know like trying to like flip a car or something so i can definitely get my hands under the bumper right and i can try like i can really put a lot of effort and contract my muscles as i'm trying to flip the car but the force generated does not overcome the load so as i'm trying to flip a car though my muscles are contracting right like i'm actually putting forth effort there's definitely tension there but it's not enough to overcome the load and actually succeed in flipping the car so that would be like an isometric action another example of an isometric action less extreme would be like carrying a box in front of you so in that example you'll have the weight of the box pushing down but your arms are opposing the weight with equal force going upward so your arms are neither raising or lowering so they're contracted but they're staying the same length on the other hand we have isotonic actions here tonic is referring to tension or tone so in an isotonic contraction will have the same tension but you're able to change the length of the muscle fiber because you can overcome the load so this an example of this would be like picking up uh your cup of water to bring it to your mouth so you have to contract muscle fibers as you move it up to your mouth and then back down to the table and you're changing the length of those fibers but the tension in the muscle resulting from the weight of the cup stays the same there are two different types of isotonic actions so a concentric action is when the muscle contracts and shortens and an eccentric action is when the muscle contracts and lengthens so a concentric action would be like the upward movement of a bicep curl as you contract and shorten those fibers curling the weight upward an eccentric action would be like the downward movement of a bicep curl so as you're lowering the weight back down the muscle has to stay controlled or contracted otherwise the arm would just like go limp and fall straight down which is not the proper way to do a bicep curl so as you bring that weight back down you're lengthening the muscle however it's still contracting to keep that downward movement nice and controlled so sticking with our bicep curl example then we can point out the agonist or the primary prime mover as the bicep right the antagonist or the muscle opposing that would be the triceps and then the synergist is like a helper muscle something like the brachioradialis in this example okay so we can classify skeletal muscle fibers into three main types and you may have heard of these slow twitch and fast twitch muscle fibers before in relation to athletics so an athlete we often think of when we're referring to slow twitch muscles is like an endurance athlete a distance runner maybe and for athletes requiring a fast twitch muscle movement we often think of movements happening very rapidly so like a basketball player going in for a layup or like a sprinter so i know these bullet points here look like there is a lot of stuff to memorize but it's actually really easy to figure everything else out just on a few key characteristics of each type so with slow twitch muscle fibers these cells produce the majority of their energy from aerobic respiration so in knowing that we can infer that they're going to need a lot of oxygen so they'll have a large number of oxidative enzymes they'll have a lot of mitochondria present they'll have a dense capillary network so they can have a ready supply of blood to receive more oxygen a myoglobin is the oxygen my binding molecule in muscle so like hemoglobin in blood we have myoglobin in the muscle so because they rely so much on their ability to undergo aerobic respiration they're going to be really rich in this myoglobin so all of these things together make them highly efficient and resistant to fatigue so just by using one hint like oxygen you can piece the rest together so it should make sense to you why these things fall in line for their short or for their slow shortening velocity that just means that they don't produce large amounts of fourth force so if i want to lift something very heavy i can't wait for the whole process of aerobic respiration krebs cycle stuff i can't wait for that to happen if it's something very heavy i'm just going to lift it in one quick explosive movement so for our slow twitch fibers they have a very slow shortening velocity just means that they don't produce very significant or very high large amounts of force so if the type 1 fibers can't produce large amounts of force what do you think their cross-sectional area will be you think it will be big or small hopefully you said small right because typically when you have a larger cross-sectional area of a muscle you'll be able to produce more force and that should make sense if you go back to our example athletes so if someone is very dominant in slow twitch fibers so they have a very high ratio of type 1 to type 2 then they're going to make an excellent endurance runner and if you think about our typical endurance runner they are typically muscular like tones but they're often very thin and lean so they aren't jacked right so the cross-sectional area of their muscle are usually pretty small in comparison to let's say a weight lifter let's talk about the weight lifter though so for our fast twitch muscle fibers there are two subdivisions we have type 2x and type 2a i like to think of type 2x as extreme so these are the super super fast ones an example of this would be like our 100 meter sprinter these fatigue pretty easily but they do generate the highest power output the type 2x fibers are going to be really rich in glycolytic enzymes because they don't have time for aerobic respiration their performance will be over by the time the body starts converting to aerobic respiration anyways so their energy comes from direct phosphorylation of adp by creatine phosphate or by an anaerobic pathway like glycolysis so who cares about mitochondria here right because we don't have time to wait for that cellular respiration type 2a however is like a mix so i like to think a for all so it has qualities of both type 1 and type 2x so it's like all of them i guess so for our example athlete this would be something like an 800 meter sprint so 800 meters is twice around a track and that's about half a mile so half a mile really isn't that far but it feels really freaking far when you're trying to sprint it right so for our intermediate fibers they aren't totally aerobic we'll definitely feel some significant fatigue there but we're still generating a lot of force to make a sprint so it's like a mix of the super slow and the super fast fibers okay we're almost there two more slides to stick with me here i love exercise physiology i have a background in exercise science and i mentioned during the cellular lecture how i'm really interested in epigenetics and exercise is one of the amazing things that can help us regulate our gene activity i get really excited about the health benefits of exercise not only physically but also mentally emotionally regular exercise will radically change your life for the better and it's not talked about enough in our society and in our medical professions in the interest of time i'm going to contain myself so we aren't going to go into all the benefits of exercise i could talk about that literally all day i'll spare you but let's just skim the surface and talk about some of the common topics first is hypertrophy and this is just a pet peeve of mine but i commonly hear this word mispronounced as hypertrophy so that is not right so just to clarify it's definitely hypertrophy so you know when you're like going to the gym trying to get in shape trying to get your summer bod whatever it is the most common muscular goal is often hypertrophy so this is just the increase in muscle fiber diameter so like getting swole increasing the muscle size and you're getting stronger and your muscles are getting bigger so you're not making more muscles that would be called hyperplasia and you actually don't want to do that you want hypertrophy or just make your existing muscles bigger so that you look more toned and an important concept to understand is the second bullet point here where it says the amount of force that can be generated by a muscle group is proportional to the cross-sectional area of that muscle so as you work out your muscles are going to go under is are going to undergo hypertrophy so they'll grow in size increasing the cross-sectional area so that you become stronger so now that you're going to the gym and working out you notice that the next day after your workout you're really sore and this soreness is called delayed onset muscle soreness so this is typically what people are referring to when they say they're sore from a workout it was previously thought that muscle soreness was a result of lactic acid accumulation but researchers have since proven that wrong that's just like another pet peeve of mine when you hear that guy you know like that guy at the gym that's like bragging oh yeah man you got to break up that lactic acid that's false that's wrong he doesn't know what he's talking about the muscle soreness you feel the day after your workout is not lactic acid it's actually many microscopic tears to the muscle fibers so we get an inflammatory response there leading to swelling pain and soreness in that area the good news though is that these microscopic tears are how we are going to go in and build that muscle back back up bigger and stronger i do want to clarify though because i always get some pushback about this delayed onset muscle soreness is the muscle soreness you're feeling 24 to 48 hours after exercise for me personally my soreness is always worse on the second day but that can be specific to the exercise or the individual so that is not lactic acid what is lactic acid though is like when you're actively exercising and you're on your last few repetitions or you're sprinting to the finish line and your muscles are on fire it's burning that feeling that is a result of lactic acid accumulation or building up within the muscle cell okay let's talk about sex differences this is another one where i could go deep into this topic but i'm going to try to keep it simple when absolute strength is compared in untrained men and women men are typically stronger so i'm hoping that that makes total sense for you most people are willing to acknowledge that men are just physically stronger than women physiologically we see that male skeletal muscles are generally faster and have a higher maximum output than female muscles men are typically stronger for a variety of reasons such as differences in energy metabolism muscle fiber type composition contractile speed obviously hormonal differences with testosterone stimulating muscle growth and protein production the effects of testosterone on growth hormone so there's a lot of reasons the most obvious one is just because men are usually larger than women so their muscles are usually bigger their shoulders are wider set and females typically carry more fat for reproduction a study in the journal of applied physiology found that women exhibited 40 less upper body strength and 33 percent less lower body strength on average another study estimates that females have anywhere from 37 to 30 or i'm sorry 37 to 68 the muscle strength of males so it's like pretty clear biological males are stronger than biological females in general or on average we're talking about this because you'll be using this information when you're answering a question in your lab report so in the lab you're going to get a partner and we're going to be doing some push-ups so ladies will be doing a modified version with a pivotal point at the knees and this is not like some sexist confrontational thing that we need to be upset about it's just to accommodate for the biological differences between sexes so we can even the playing field a little bit when we're comparing or competing men and women so ladies please don't get upset with me for saying this it's just our physiology conversely an interesting study found that women or female muscles are generally more fatigue resistant and a possible mechanism to explain this is that women will often recruit more motor units so we can distribute the load more evenly okay last slide clinical applications rigor mortis rigor mortis is the stiffening of your body after death so it typically peaks around 12 hours after death and you'll see in crime shows sometimes we can use the degree of rigor mortis to better estimate someone's time of death so let's talk about why this happens though so dying cells are unable to exclude calcium so they start leaking and will have a calcium influx into the cytoplasm we know that that calcium then will bind to troponin tropomyosin will move out of the way and myosin will then grab onto actin and a cross bridge will be formed so that muscle is in a contracted state so if we go back to this slide here one moment if we go back to this slide here we remember that we must have atp present in order to break that actin myosin bond and with rigor mortis we don't have atp because well we're dead and so the muscle stays in that contracted state over time though it will gradually disappear as the body starts to decompose and break down but it's just kind of cool that that happens and it can be useful in determining the time of death let's talk about what happens to our muscles as we age so sarcopenia is the age-related decline in muscle mass that occurs naturally throughout our lifetime and there are two distinct phases a slow phase beginning at age 25 holy crap right your muscle naturally starts declining at 25 yikes but it does so very slowly from 25 to about 50 losing approximately 10 percent of the original mass which really isn't that much but once you cross over to that rapid phase you're going to lose another 40 percent very quickly as you approach the last quarter of your life with this we'll see a shift in fiber types to be more predominantly slow fibers slow twitch fibers those type 1 fibers so old people move pretty slow right you don't see many 80 year olds like playing basketball or doing sprints their activities are usually more aerobic something like walking the good news though is that this can be counteracted to a degree with strength training so this 50 loss of muscle mass is what happens naturally so if you just kind of lived your life regular i guess and so what i mean by that is right now in the u.s eighty percent of americans do not meet the minimum recommendations for physical activity eighty percent of americans don't meet their recommendations so i can probably take a few educate educated guesses to figure out why we're losing so much muscle mass so rapidly but that's a tangent point is if you're intentional about your exercise and your muscle strengthening activities then you can definitely counteract this maybe not totally but it's not necessary to lose such a large percentage of your mass if you don't want to okay very last thing muscular dystrophy is a group of hereditary muscle diseases that results in the weakening of skeletal muscle so there are several different kinds but the most common is duchene muscular dystrophy and it's caused by a defective gene for the protein dystrophin dystrophin helps us maintain the structural integrity of the sarcolemma so without that the muscle is damaged very easily and we lose that regenerative capacity so the damaged cells will undergo apoptosis or programmed cell death we'll see that muscular dystrophy is common in men is most common in men because it is an x-linked recessive gene so since males are xy and females are xx if a female inherits one defective gene then it'll be recessive and she can use her other x chromosome as a backup but since men only have one x if they inherit this gene then unfortunately there is no backup this is a really grim slide to end on because the prognosis for muscular dystrophy is not good there is no cure and these individuals typically live a short lifespan as their muscles weaken the diaphragm also weakens leading to respiratory failure early in life there are some clinical trials happening now to see if a synthetic form of dystrophin can be injected sometimes steroids and immunosuppressants can help slow the progression but there is no cure for this okay well i hate to end on such a sad note but that is all i have for today so exam one will cover uh cellular physiology and then muscle physiology i am always available to you by email please don't hesitate to reach out i am here for you and i am happy to help you all right have a good day everyone do good