hello class this is Professor Mariah Evans BSC 2085 human anatomy and physiology one and this is muscles part three or as it's listed here part C all right so we are talking about or had been talking about in part two some common-sense things that you realize about the force of a muscle contraction that if you put a stronger and stronger stimulus then you'll get a stronger and stronger contraction and that's until you reach the max once you reach the max it doesn't matter how much more stress or tension you put on it you're at your max we talked about the motor units and we talked about the size principle so we know that there are small motor units and medium motor units and large motor units we also talked about the recruitment principle right the bigger the job is the more motor units are going to be recruited to get the job done we also talked about the fact that the faster that you apply the stimulus the higher and higher you can get the contractions to go because the contraction happens faster than the relaxation and so if I add a stimulus I get my contraction and then before it completely rests I add another stimulus it'll give me a higher contraction but that's called a Trappe effect so trip a tre PPE and then of course there's the degree of muscle stretch which is new so we've talked about the first three bullet points here but the last one is this degree of muscle stretch and the reality of the situation is this we can exert the most force when skeletal muscle is between eighty and a hundred and twenty percent of its normal length so between eighty and a hundred and twenty percent of its length is where we exhibit strong forces so this is everything that I just said before about muscle fibers right the more we recruit than the stronger force the the larger the size the more force the frequency increased frequency more force and then this is the tension and length relationship the fibers will give the most force when they're between 80 and 120 percent of their normal resting length as I said so now let's talk about things that influence the velocity the speed of a contraction or the duration which is how long a contraction lasts so we have the muscle fiber types and we have the load that we are putting there and then we have that recruitment principle like I was stating before so the muscle fiber types there are different types of fibers they're slow and there's fast if we're classifying based on speed but then there's metabolic requirements oxidative would be aerobic which means they need oxygen glycolytic would be anaerobic remember glycolysis is the breakdown of glucose into pyruvic acid but we don't need oxygen for that to occur so these are slow and fast right based on speed and then metabolic is oxidative and glycolytic so we have three different types of fibers we have slow oxidative fibers fast oxidative fibers and fast glycolytic fibers now if we were meeting face-to-face what I typically do is I stop and I ask students this question based on these three fibers slow oxidative fast oxidative and fast glycolytic knowing what you know about aerobic or oxidative use of making ATP and glycolytic which is anaerobic right making ATP which of these three fiber types do you think would resist fatigue the best which of these three types of fibers would resist fatigue the best so slow oxidative that means they're moving nice and slow but using oxygen fast oxidative moving fast or working fast and using oxygen or fast glycolytic fibers so if your gas was the ones that would resist fatigue the best if your answer was slow oxidative fibers you're correct they would resistor running out of ATP stores better they would resist running out of their oxygen stores better because they're slow in oxidative therefore the fast glycolytic fibers these are the ones that would fatigue the easiest of these three that are listed fast glycolytic ones because they're moving very fast which means you will probably increase your chances of running out of your oxygen and you're using an anaerobic source already so you're gonna have that pyruvic acid buildup so these would fatigue the easiest okay and when fYI how you get your fibers it's genetically related so yeah genetic predisposition there so there are people who it's in their genes to be able to run marathons alright so where we know again about the recruitment so faster contraction is going to increase the duration of the contraction we are aerobic respirators right so we know that and aerobic exercise is extremely beneficial because it increases muscle capillaries capillaries are the vessels that deliver oxygen to muscle it increases the number of mitochondria mitochondria is where ATP is synthesized and it increases myoglobin and myoglobin is where the oxygen is bound and muscle so if I have oxygen that means I'm going to be able to do aerobic exercise for a longer period of time if I have mitochondria I'd like to make my ATP aerobically so that oxygen helps and then oxygen is delivered to the muscles through blood vessels capillaries so these things right here are benefits of doing aerobic exercise and as a result of that then you'll get a greater endurance you'll have more strength and you'll be resistant to fatigue better and by doing aerobic exercise you can convert those fast oxidative fibers the ones that are most likely to fatigue first into fast oxidative fibers so you're still working fast but you're using an aerobic pathway to do so resistance exercise is typically an aerobic exercise and muscle hypertrophy this means an increase in size this is what happens when you build your muscle mass and increase mass is going to give you increase strength okay so increase mitochondria like I said before it's gonna be ATP and then if you are using ATP aerobic Li right that's your energy then you can increase your muscles strength because you've increased its size so the best plans right as far as weight loss and and you know being healthy the best plan is to alternate aerobic and anaerobic exercise so weight training and cardiovascular training okay now overload principle for those of you who may work out and try to are trying to build your muscle mass your overload principle just means your muscles are going to respond to the stresses that you put on them so the more stress and tension you put on muscle the bigger the muscles will get it's the same idea about your bones remember we talked about that the more tension you put on bones than the thicker the bone will be because it's remodeling so the overload principle says that if you force your muscles to do work right then you can increase their strength but muscles adapt to those demands so if you want your muscles to get bigger you have to add more weight add more weight add more weight at more weight and that's the overload principle to get you those further gains additionally if you don't rest right because you're overloading your muscles if you don't rest properly before you go and you know this is why people alternate between leg days and arm days if you don't rest then you can actually injure your muscles and then like I said the best programs are going to alternate aerobics so this is that cardiovascular part with anaerobic which is the weightlifting okay so if you don't use them you will lose them that applies to muscle it applies to a lot of things but it definitely applies to muscle so atrophy is when they get smaller and smaller and smaller so hyper tree was when they got bigger right so muscle gain and what happens is is that if you are not like if you're bedridden your muscle strength can decline by five percent each day that you're bedridden without being able to move and then if there's no neural stimulation your muscle can atrophy to about one-quarter of its original size one-quarter of its original size and then unfortunately fibrous connective tissue will replace the contractile tissue and rehabilitation will be impossible so that you won't be able to rehab and learn how to walk again or use your muscles again now skeletal muscle we compared our skeletal muscle to smooth muscle to cardiac muscle right the three types of muscle now smooth muscle does not have striations smooth muscle is involuntary and smooth muscle lines all of our hollow organs except for our heart which is also a hollow organ but the heart is made up of cardiac muscle so there's two layers of smooth muscle longitudinal and circular and what they did is they took a piece here of the intestine and then they magnified it for you so that you could see the two types of muscle layers and then they magnify those again so that you could see the longitudinal layer and then the circular layer and this is smooth muscle this is what we looked at underneath the microscope and in the lab when we look at it underneath the microscope the individual cells look like spindles spindle means that they are pinched on each end so pinched like on the ends that's what they mean by spindle shape and they have one nucleus they don't have the connective tissue sheaths that we were talking about so when we were talking about skeletal muscle we talked about the epimysium which was one the outside and then we talked about the Paramecium which was around the fascicles which are bundles of muscle fibers and then we talked about the endomysium which is directly around the muscle fiber and smooth muscle all they have is the end of my cm now there are some differences of course between the structure of smooth muscle because it functions differently than skeletal muscle so the sarcoplasmic reticulum is not as well developed as it is in skeletal muscle and then we have these caviola and these caviola are where the calcium is and so instead of t tubules we have Cabul i so no t tubules instead caviola and then again we talked about the two layers longitudinal and circular and they alternate and that's how peristalsis propels our food through the lumen which is the opening of those hollow organs so when you masticate which is chewing then you swallow you have your fairness which is made up of skeletal muscle and the reason why you know the fair Nick's is made up skeletal muscle is because if I asked you right now to swallow you could and if I asked you to swallow and you didn't it's because you consciously chose not to so that means that it is under voluntary control of skeletal muscle once it gets past the fair Nick's then it gets into the esophagus and the esophagus is made up of smooth muscle and smooth muscle courses involuntary so then it goes to the stomach and the stomach is smooth muscle and from the stomach it goes to the small intestine which is also smooth muscle and in the large intestine which is also smooth muscle and all of these have the layers of longitudinal and circular smooth muscle that allows the propulsion of the foodstuff all the way down until it gets to our poop chute so out the anus we've seen this picture already skeletal muscle compared to cardiac muscle compared to smooth muscle we've seen this picture as well again just comparing what you see as far as the connective tissues and and sarcoplasmic reticulum not as well developed in and smooth muscle and also there are no there are no tutti Beauty tubules we have the cabbie Olli instead now also and smooth muscle there's no neuromuscular Junction because remember smooth muscle doesn't necessarily need a nerve impulse so there's no neuromuscular Junction however there is a place where neurotransmitters are released and the place where neurotransmitters are released are called varicosities so the varicosities release the neurotransmitter to the smooth muscle sheet and there's no neuromuscular Junction like we have in skeletal muscle and then when we get the release of that neurotransmitter then it can and will cause changes in the cell perhaps depolarizations or hyperpolarization Stu pending on which ions are flowing in and out so varicosities and then the neurotransmitter but no neuromuscular Junction so so far we know that smooth muscle doesn't have t tubules instead it has the caviola make sure remember that we also know that smooth muscle doesn't have a neuromuscular Junction instead it has Mirko cities and then the third thing and there's other things but the third thing that I'm gonna highlight about smooth muscle is that when calcium is released in smooth muscle it binds to calmodulin but in skeletal muscle the calcium binds to the troponin so those are the three things that I need you guys to recall as far as comparison between smooth muscle and skeletal muscle structure skeletal muscle has a neuromuscular Junction smooth muscle has varicosities skeletal muscle has t tubules smooth muscle has the caviola and then skeletal muscle calcium binds to troponin and in smooth muscle calcium binds to calmodulin and that word is going to come up in the slide or two so this is a sheet of smooth muscle these are the varicosities they magnify them for you you can see the synaptic vesicles this is where the neurotransmitters are housed el here it is here so smooth muscle it still has acted in myosin all muscle has actin and myosin except for in smooth muscle the calcium binds to like I said to the command line and then skeletal muscle and cardiac muscle it binds to the troponin okay so those are the three main differences again there's these are a few more differences between smooth muscle they don't have smooth muscle doesn't have the the Z disk or the z lines instead they have these little dense bodies that are there but I've already emphasized the three that that are the most important for me and that's because of course I'm my own test so smooth muscle resists fatigue so smooth muscle contracts very slow it has slow working ATP ASE's and so it resists fatigue which is good smooth muscle as we talked about does not need that nerve stimulus so this is the self excitatory right so it can depolarize without a stimulus and you know that's kind of cool as well and then we have pacemakers in your smooth muscle and the pacemakers do exactly what it sounds like it sets the pace it sets the pace for the contraction it sets the pace for the contractions to take place now like I said all muscle whether it is skeletal muscle or cardiac muscle or smooth muscle all muscle has actin and myosin and actin and mice and still still still slide past each other to allow the muscle to move so actin and myosin sliding filament theory of course actin being the thin filament myosin being the thick filament and then the final trigger for muscle contraction while there's skeletal muscle smooth muscle or cardiac muscle that final trigger is calcium and calcium binds to calmodulin in smooth muscle but binds to troponin in skeletal muscle okay and and cardiac muscle as well troponin all it says here is that calcium comes from the sarcoplasmic reticulum and extracellular spaces when we talk about smooth muscle all that means is that when calcium comes from extracellular spaces it's what allows the release of calcium intracellularly and then of course ATP is needed because it is still muscle contraction and then here it's kind of the same idea that calcium has to bind to come Agilent to get acted in mice and the slide past each other and you don't have to know the steps of this like you had to know the steps for skeletal muscle but again just to walk through it so you understand the similarities so calcium binds to calmodulin and collage illan then activates a myosin kinase and that phosphorylation so it kinase has any enzyme that has the ability to phosphorylate something so that phosphorylates and then activates the actual myosin so the kinase is going to take a phosphate and activate the myosin once myosin is activated then it can cross bridge with actin so remember those same active sites on actin and then if I want smooth muscle to stop contracting then it's going to do so in response to low intracellular calcium levels so again what does this mean about muscle contraction rather it's smooth muscle cardiac muscle or skeletal muscle you have to have calcium for it to contract and then if you want it to relax you have to take the calcium away so calcium is needed for muscle contraction and then of course again just this again this comparison between skeletal muscle cardiac muscle and smooth muscle it's there's there nice little charge to go back and and look over and kind of help yourself remember the information but recall the three major things because I write my own test recall the three major things that I told you about smooth muscle and skeletal muscle so smooth muscle doesn't have neuromuscular junctions but skeletal muscle does right and smooth muscle instead of the neuromuscular Junction and has the varicosities okay then smooth muscle doesn't have t tubules like skeletal muscle does instead it has the I'm just drew a brain fart but and so that the the t tubules it has oh my gosh I'm really just I had a brain fart I'm so sorry so caviola so sorry anyway so no t tubules caviola and then the third thing is that the calcium binds to calmodulin and smooth muscle and in skeletal muscle the calcium binds to the troponin alright and let's see so there we go there we go I'm sorry brain fart I'm tired you guys alright and so this is a picture of a figure showing this muscle contraction model basically and it's extracellular calcium that comes in and then initiates the release of intracellular calcium that binds to the commode Yulin and then there's a phosphorylation of the myosin which activates the myosin so the kinase there and then we get the cross bridging of the myosin heads because they're still as you see myosin heads the cross bridging of the myosin heads to the active sites on actin and then myosin pulls the actin past it so it's still a sliding filament theory all right now like I said smooth muscle contracts slower so it resists fatigue better so it's slow to contract and slow to relax but maintains for prolonged periods of time with little energy cost so its energy efficient it has slowed ATP ASE's which i mentioned when we were talking about it contracting slow and then relaxation requires the detachment of calcium from calmodulin in smooth muscle just like relaxing relaxation of skeletal muscle and cardiac muscle requires removing calcium from the troponin okay so the calcium regulation is a big deal and you guys know this already right because calcium is what's needed to get a nerve impulse and nerve impulses are needed for skeletal muscle contractions calcium's needed for every type of muscle skeletal muscle cardiac muscle and smooth muscle chicken track so we regulate rate contractions and it is about calcium so calcium regulation which you learned about in the muscle I mean in the bone chapter is huge right and you learned that even calcium regulation was done by hormones so hormones are chemical signals and they regulate a lot of things in the body so in our case the regulation of contraction could be hormones or chemical changes like neurotransmitters or nerves remember some of our muscles like smooth muscle and cardiac muscle can be self excitatory but here's what the kicker is the big deal is all cells are polarized at rest which means they're negatively charged inside so if they're negatively charged inside and I get this influx of calcium which is positively charged I can get a potential what yeah so graded potentials are local sound familiar in skeletal muscle we call them end plate potentials and they were local and then we get action potentials and an action potential is an action potential regardless to whether it happens in skeletal muscle or if it happens in smooth muscle or if it happens in a nerve cell an action potential is a moving change in charge so the response to contraction is going to depend on the neurotransmitter that's released and the type of receptor that's on that molecule and then hormones right some smooth muscle cells don't have that nerve supply so remember some of them can depolarize spontaneously or without a nerve impulse so their self excitatory and in this case right here these would respond to chemicals chemicals like neurotransmitters or chemicals like carbon dioxide or chemicals like hormones or chemicals like pH so let me kind of explain to you this effect of carbon dioxide specifically on the smooth muscle that's associated with your lungs so respiration if a person is hyperventilating that means that they are breathing excessively right a person is hyperventilating if you see them breathe so they are breathing really really fast but they're not getting the oxygen that they need what we do for that person is we give them a paper bag we give them a paper bag and we cover their mouth and nose and we have them breathe in the paper bag and so what happens is is that the paper bag catches the carbon dioxide this right here at this chemical it catches the carbon dioxide and when it catches the carbon dioxide they breathe it back in and it slows down respiration so see this regulation of contraction could be hormonal or could be chemical when a person's hyperventilating that's excessively breathing carbon dioxide inhibits that slows it down that's kind of cool fYI if your blood which has a ph of 7.4 if your blood becomes acidic then you could go into cardiac arrest that means that a decrease a decrease in pH would cause an inhibition of heart muscle which means you could go into cardiac arrest so these two examples I give for hyperventilation and then for cardiac arrest so decrease in pH in your blood could cause you to go into cardiac arrest you'll learn more about that in 2086 and then hyperventilating breathing in the carbon dioxide is going to inhibit or slow down the breathing so these things again regulating and that case it's good smooth muscle and cardiac muscle specifically and then there is a stress and relaxation response and smooth muscle just like there is attention and and tension and length relationship in skeletal muscle and so it's really cool because smooth muscle can stretch and when it stretches it still maintains its ability to contract that's a big deal think about your bladder if you don't go to the bathroom overnight then your bladder increases in size right it's being stretched and then when you finally do get up in the morning to go to the bathroom then it still contracts so that you can expel the contents and your stomach is like that as well so your stomach and your bladder they stretch to meet the you know the to accommodate whatever it is that you're taking in your inner food and then it stores those contents and then it contracts right to expel them in the case of your stomach it's because they're going to move from the stomach into the small intestine in the case of your bladder of course you're gonna hear na so excreted from your body so the length intention does change and can contract when half or twice its resting size so when you talk about skeletal muscle it was between 80 and 120 percent its resting length and in smooth muscle it's about half and then twice so between half and twice its resting length is where you get the most tension now hyperplasia is when you have an excess number of cells so Hydra pee was an increase in size at repiy was a decrease in size hyperplasia is an increased number of cells so when we gonna increase number of cells somewhere it can cause that thing to grow so smooth muscle divides right mitosis divides and increases in numbers that's hyperplasia this is what we see cuz you know when a female is you know preparing for you know pre puberty thank goodness for all these lovely hormones and stuff but also during pregnant pregnancy so estrogen has the that effect of increasing the mitosis or the cell vision to increase the size of the uterus so females of course we come here you know but six seven pounds maybe eight or nine you know depending on you know how you got here but the size of the uterus is very small and as you get older and you reach puberty then you're going to have the release of hormones that increases the size of the uterus and then when you get pregnant of course it continues to grow to accommodate the fetus and then here's just again a nice little comparison of skeletal muscle smooth muscle and cardiac muscle realizing that they all have actin and myosin and that calcium binds to troponin in cardiac muscle and skeletal muscle but calcium binds to calmodulin and smooth muscle skeletal muscle contracts really fast I mean you can contracts location Terry right but it contracts very fast and then it relaxes slowly and then cardiac muscle is nice and slow and smooth muscle is nice and slow because these things go every minute of every second of every day that you're alive okay now as far as the exam is concerned I don't test you in this besa Fissel of unitary vas versus multi-unit smooth muscle but I do want you to know that smooth muscle is categorized as unitary or multi-unit and by that I mean here they give you examples of the unitary muscle and it tells you that it's all of the hollow organs so I wouldn't list them on the test or expect you to know them but the esophagus for example in the stomach for example small intestine large intestine examples but those are unitary and they are innervated at the varicosities so remember the MiraCosta these are where the neural transmitters are released and it says they often exhibit spontaneous action potential so that's self excitatory and then the multi-unit ones like the large Airways like your bronchi the bronchi are these branches that go into your lungs and then the large arteries like you know the aorta but again for the exam I'm not asking you to specify multi-unit smooth muscle from unitary smooth muscle so you don't have to know you just have to know that there are those two categories okay now these are some homeostatic imbalances or some diseases so these are when things are wrong so muscular dystrophy your muscles being destroyed and if your muscles being destroyed then of course it doesn't work so what happens is the muscle fibers atrophy so remember I told you that means that they get smaller and smaller and smaller so they degenerate unfortunately Deschenes muscular dystrophy is the most common and the most severe so that's awful the most common type of muscular dystrophy is the most severe it's x-linked so they say sex-linked but I'm going to be a little bit more specific x-linked it's associated with inheritance of the X chromosome which you can get from your mom or your dad but if you get an X chromosome with the gene for muscular dystrophy and you are male then you will have muscular dystrophy if you are a female and you get the gene on an X chromosome with muscular dystrophy and you get the other X chromosome and it doesn't have the gene for muscular dystrophy then you don't have muscular dystrophy you're just a carrier so males are more likely to get it so females who are XX right and males are XY so carried by females and expressed in males okay let's see things that happen in muscular dystrophy the sarcolemma which is as you guys recall the membrane of the muscle cell it's very fragile so it tears and that interferes with calcium entry and causes inflammation to take place and then you get drop in your muscle mass but the person usually male becomes clumsy and begins to fall and they usually die of respiratory failure in their 20s there's no cure for it prednisone which is I think most you guys know steroids right so prednisone and prove some of the muscles strength and function and then my Oblast therapy my Oblast transfer therapy was very hopeful a couple years ago like maybe three or four years ago we were all excited about trying myoblast if you remember from previous lectures and I hope you do because this matters right terminology the suffix blast means that it's secreting and the prefix mile is muscle so these were muscle secreting cells and it would make sense that they would show promise because atrophy is the muscle deteriorating but then if you transplant the muscle with my Oblast cells then it's supposed to make new muscle that was the whole idea but it was very disappointing right now they're doing other things like viral gene therapies and fusion of stem cells and some of those are showing some promise alright that is part three of muscles