>>This video lecture 10, we’re going to cover skeletal muscle physiology. The learning objectives are here, we’re going to focus on whole muscle physiology; talk a little bit about fiber types, how muscles generate different amounts of force, then finish up with a little bit about muscle injury and fatigue. So, the first learning objective is to distinguish between the skeletal muscle fiber or cell types, so remember a fiber equals a cell and when we look at skeletal muscle it turns out that all the different fibers aren’t the same and actually scientists have divided up the fiber types into two different types, type I and type II. Some of them appear to twitch slowly or generate force slowly, some of them fast. They also tend to have a different fiber diameter which you might think might have to do with their muscle force and so exercise scientists, one of the things they started to do was to test these different fibers and actually pull individual fibers out of a muscle and test them in the lab in isolation and that’s a lot of how they discovered how these cells behave and how they’re different. So, if you study an isolated fiber or muscle cell you can stimulate it and you can actually look at how fast it generates force when you stimulate it much like a nerve would do with an action potential, so the type I cells that are slow to generate force or twitch they have a lot of mitochondria to make their ATP and they also notice that they’re fatigue resistant so it seems like you can stimulate them all day long, so those are the type I or slow twitch fibers. Another type of a fiber that they discovered were these fast twitch fibers, they were fast to generate force whenever you stimulated them. They didn’t have a lot of mitochondria, they have a lot of stored up glucoses, glycogen and that’s how they tended to make their ATP through glycolysis but they also noticed that they were fatigue, they fatigue quickly, they lost their force when you continued to stimulate them, so these are the classic type IIb or fast twitch muscle fibers. And then what happened as they kept studying cells, they noticed that some of them were fast to generate force so they were fast twitch fibers but they have a lot of mitochondria and they were fatigue resistant, so they sort of had a little bit of type IIb fiber qualities and type I fiber qualities so this became the type IIa fiber, so they weren’t able to just break everything down into type I or type II, it’s type I, type IIb and type IIa and type I, so those are the fiber types. You can also do other things like do histology and stain the muscle fibers for metabolic enzymes say mitochondrial enzymes and proteins and you can really see the difference in a human skeletal muscle. Human skeletal muscle is a mix of fiber types. If we look at an example muscle like the gastrocnemius in your calf, you can see that scientists have determined that about 50% of the fibers or cells are type I and the other half are type II and you can see the type IIa are more prevalent than the type IIb. So again, to summarize, we’ve got our type I or slow twitch fibers which have these properties here, they’re slow to generate force but they don’t fatigue so you can use them all day long for walking and posture and things like that versus our type IIb, they’re fast to twitch. They generate a lot of force but they fatigue really quickly, they rely on glycolysis to make their ATP and they have a larger diameter and they’re more powerful but you can only use them briefly and that’s the type IIb and then sandwiched right in the middle there are these type IIa fibers which are sort of like a hybrid or intermediate between the two. They’ve got the properties of the IIb that they’re fast and powerful but they have the properties of I in that they’re fatigue resistant and they use a lot of mitochondria. So, when we talk about fatigability or fatigue resistance or faster fatigue, we’re talking about overtime you keep stimulating that fiber it’ll decrease it’s force versus fatigue resistant will maintain their force. Some animals, actually their muscles, are not really mixed fibers, instead they’re one fiber type and you can see this in birds and turkeys and chickens in the breast type tissue is probably type IIb muscle fibers versus the thigh which is predominately type I muscle fibers and you can see some differences in the colors because type I have a myoglobin protein to bind oxygen and blood vessels, so remember breast type IIb that would be for bursts which turkeys and chickens do versus thighs are for walking around, so just an interesting thing about the fiber types. One other thing I wanted to note is a little bit about fiber type and blood supply; type I and type IIa have to have a large blood supply to supply oxygen to the mitochondria, whereas IIb pretty much rely on glycogen and glucose and glycolysis and that doesn’t require oxygen and has many blood vessels. Studies looking at fiber distribution and fiber numbers in the biceps brachii actually showed that young and old people have about the same number of cells but their cells are of a lower size, they’re lower diameter, so 25% reduced fiber area. If you want to sort of generalize about how does fiber type affect performance, well obviously if different muscles have different types of fibers or different percentage of fibers or different people do, perhaps that will affect our performance. So again, slow or type I fibers they’re going to be ideally situated for tasks that we do for a long period of time like posture and walking around. Interestingly, the fiber types make different myosin and heavy chain proteins, that’s the little protein in the myosin head that we used for contraction and so that’s one of the reasons these fibers behave differently is they actually make a slightly different myosin protein. Those slow type fibers have lots and lots of capillaries, so they’d be great for running marathons. If you were an Olympic powerlifter and you wanted to just do bursts of activity, you’d want a lot of type IIb fibers because they can do short bursts of high power and high force, again, remember they use glycolysis to make their ATP but the fatigue really fast so you can only use those in bursts and then, of course, the hybrid would be great the IIa fibers if you needed to do explosive but yet endurance type things like most athletic activity, even just running and things like that rely on these IIa’s because they’re powerful but they’re also fatigue resistant. So, one of the things exercise scientists noticed, of course, all of these cells have the same instruction book, same DNA but when they turn out to make that ImRNA and then translate mRNA it turns out that each one of the cell types tends to make a different myosin heavy chain protein, we call I MHC and so by making different myosin proteins it actually helps contribute to their ability to generate force in some their characteristics. Some people suggest that the neural pattern of activation determines how these fibers sort of behave and which type of myosin protein they make. So, if you go inside the cell down at the very, very small level and look at the different proteins that each of the fiber types makes, it turns out that that little myosin head or myosin heavy chain is slightly different between the fiber types, and again, that’s a protein that protein is dependent on the information that comes from the DNA as mRNA. What about making ATP? So, it turns out the little fiber types also differ in their ability to make ATP best when you exercise, so if you need more ATP or cash energy for muscle cell, where does that ATP come from? And so just as a review, we can make ATP from glycolysis which doesn’t require oxygen it really just needs glucose and you make pyruvate and a little bit of ATP, but most of our cells use mitochondria take the pyruvate in fatty acids to make lots and lots of ATP. That requires oxygen, so again, glycolysis can make some ATP but mitochondria can make much, much more. So, it turns out that fiber types are different in how they make their ATP. The type I and type IIa at rest, they don’t have much activity so they use a little bit of glycolysis and some of their mitochondrial activity to generate their ATP and then if you decide to exercise you’re going to need a ton of ATP really fast and so we have a source of almost instant ATP called creatine phosphate but that’s very limited and it only will supply ATP for a few seconds. Then we can rely on up regulation of glycolysis for a couple minutes, it’ll be able to supply all the ATP we need but eventually we’ll need to get those mitochondria revved up in gear making more ATP and that can last minutes, hours there’s just a little bit of lag time. So, typical for your type I and IIa the fatigue resistant fiber types. Of course we have things like glycogen and fats and things for our muscles to use to make that ATP. What about IIb? IIb need ATP when we activate them, again, they can use the creatine phosphate to generate ATP for a few seconds and they love to use glycolysis. They use the stored glycogen to liberate glucose and they can make ATP again for a few minutes to sustain their muscle contractions but they don’t have a lot of mitochondria and so they can’t sustain muscle contraction very long, so that’s why they’re fatigued, they’re fast to fatigue, the type IIb. Again, the source of new ATP in our muscle cells is going to be during exercise it’s going to tend to be for a few seconds creatine phosphate, glycolysis for a few minutes and then eventually we got to get those mitochondria kicked in, again, at rest we tend to use in all the cells of our body glycolysis and mitochondria. Alright, let’s switch gears and talk about how a whole muscle in your arm or in your leg can generate different amounts of force and so we call that summation or recruitment and that also relies on fiber types, so sometimes you’re going to lift something really heavy like a weight and sometimes something light like an apple, how does the body really the brain decide how much force? Well, the first thing that brain can do is decide how many action potentials or signals to send down to a fiber and so by varying the number of action potentials that reach a fiber it changes how much calcium is released and changes the amount of force, so if you send more signals you’ll get more calcium, you’ll get more force. The brain can also send signals to more or less fibers so we call this recruitment, right, if you recruit or activate more muscle cells or more fibers, more fibers will contract, you’ll get more force so we call that recruitment and then finally, fiber type it turns out that the brain can decide which fibers, type I fibers, type IIa or IIb fibers it wants to activate; type I fibers generate less force, type II fibers generate more force, so the brain is pretty complex in the way it does summation or recruitment and recruitment of fiber types in order to generate the perfect amount of force. So, it’s very complex but it’s kind of cool how the brain is able to determine that. Okay, so for summation, again, just to summarize. The number or action potentials reaching our muscle fiber coming from that motor neuron changes the activation and number of action potentials in the muscle cell and if you send more action potential as you get more action potentials you release more calcium from the SR, more actin and myosin interact, more myosins grab on and you get more force, so again, I think of it as stimulation frequency for summation; they send more signals, you tend to get that little muscle cell to generate more force. What about recruitment? Recruitment is probably the easiest one to grasp, right, if you want more force your brain activates more fibers, more cells and these motor neurons go and activate different numbers of cells and so if you need more force you just recruit more fibers, if you need less force you recruit less fibers. Let’s make sure we’re clear on what a motor unit is. A motor unit is defined, motor unit is defined as a neuron and all the fibers it controls, so that’s a motor unit and so here we have two motor units, motor unit 1 and motor unit 2. Motor unit 2 activates 2 fibers, motor unit 1 activates 3 fibers, so every time that neuron is activated it’ll activate all of the fibers and it’s motor unit. So, if you activate motor unit 1 you’ll get a different amount of force cause you activate a different number of fibers and so on. If you activate all the motor units in that muscle or muscle group then you’ll get even more force. So, let’s look at some examples of recruitment. So, here we have a motor neuron coming from our spinal cord and going to say muscles in our quadriceps and in this case it looks like this motor unit is made up of 1 neuron activating 3 fibers, so most motor neurons will control more than 1 muscle cell, but a thing to keep in mind is each muscle cell is only activated by 1 single neuron. So, each fiber is controlled by only 1 motor neuron, alright, if you activate that motor neuron all of those cells are always activated all the time and we can draw in another motor unit and if the motor unit is not activated, none of the muscle cells in that motor unit will contract. The other thing that’s interesting, motor units are also arranged by fiber type, so if this motor unit, this neuron will activate all type IIa fibers versus the second activate all type I muscle fibers, so in that way the brain can actually know whether it’s recruiting type IIa or IIb or type I, again, if you activate the type I motor unit you’ll get less force versus if you activate the type IIa or IIb motor unit. So, when your brain wants to do a burst it will recruit the IIa’s and IIb’s, when it wants to maintain your posture it will recruit that type I’s, so type I’s tend to be recruited first all the time and type IIb and IIa will be recruited only when needed especially the IIb, they’ll only be recruited when you need a quick burst. Predict the training adaptations in muscle due to aerobic versus resistance training, this is learning objective 3. So, when you lift weights versus you go running, how is the or what type of adaptations will our muscles undergo in order for us to perform better? So, if we look at resistance training one of the most obvious adaptations is the muscles, the muscle cells or fibers actually get larger in diameter. They don’t get longer they just get thicker and we call that hypertrophy. The reason the hypertrophy is when those muscles cells are stressed they actually buildup more myofibrils of actin and myosin. If you have more myofibrils packed in your cell it looks bigger and hypertrophy but it also can generate more force, so even if you’re Arnold Schwarzenegger you have the same number of cells in you biceps but the bicep cells are just larger in diameter. If you do a running type training regimen how are your muscle cells different? There may be a small amount of hypertrophy of either type I of type IIa fibers but some of the other things we see is increased capillary densities, so these are the smallest blood vessels in our body, the capillaries. This also, the other adaptation we see is increased mitochondria and so you can imagine we need more oxygen to those mitochondria so they can make ATP. So, those are all changes you would expect with a running type training pattern, and again, you can pause this and take a look at it; resistance training has these changes, again, the hypertrophy is the obvious thing other things like glycolytic enzymes are increased expression. There may also be changes in the myosin heavy chain gene expression so that you make more as that myosin heavy chain fast protein. Again, if you look at aerobic training you’re going to see more blood vessels, more mitochondria, you may see a shift again in the myosin heavy chain protein that you make. Fibers switching from type I to type IIa and IIb seems to be somewhat controversial but there is evidence that fiber types can change type especially when you have injury and bedrest. So, one of the things I was thinking about is what’s the difference between a big tall skinny guy and a really fast powerful tall guy and is that, does that have to do with your fiber types that you’re born with or the fiber types that you get from training and it’s probably a little of both but it’s an interesting thing to think about. Use it or lose it seems like an obvious thing but if you don’t use your muscles they’ll atrophy, if you use them more they will hypertrophy especially if you do more resistance training and one of the sad things is that it takes a long time to get your training adaptations but relatively short period of time to lose them, so if you have disuse or an injury the detraining can go very fast, much faster than it took for you to train so detraining is very quick. Just as a little bit of a background, I want to talk a little bit about the types of muscle contractions. There’s isotonic and isometric contractions so we’ll talk about these. Isotonic contractions have constant tension and there’s two types there’s concentric and eccentric muscle contractions, again, the muscle shortens or lengthens and generates a constant force. Compare that to isometric contractions, in this case your muscle is contracting but it doesn’t change length and so that’s like when you hold a static position and don’t move around when you hold that position or push against an immovable wall or an immovable object that’s an isometric muscle contraction, again, the muscle contracts but doesn’t really shorten. So, we’ll look at a couple of examples of these. So, when you lift a 20 pound weight that’s an isotonic contraction when you’re actually moving the weight, when your muscle shortens and you lift the weight we call that concentric contraction. When you put the weight back down slowly against gravity it lengthens but you’re still contracting the muscle. We call that eccentric contraction, again, I like to remember eccentric contraction cause you use then often to resist gravity sort of like muscle breaking or muscle slowing, you’re contracting but the muscle lengthens, so again, concentric and eccentric are isotonic contractions. Compare that to if you picked up that same weight but you held in a static position, you didn’t move it. If you don’t move the weight you’re doing an isometric contraction, again, the muscles contracting generating force but you’re not actually moving the weight concentrically or eccentrically. So again, bicep curl, concentric contraction is when you shorten the muscle and move the barbell up; eccentric contraction is when you lower it back down the muscle is still contracting. For some reason and we’ll talk a little bit about it you may figure it out, why muscle soreness is often associated with these eccentric lengthening muscle contractions. Again, so getting into position are concentric contractions holding position or isometric contractions. The next learning objective is describe some mechanisms of injury and repair in muscles and talk a little bit about satellite cells which are muscle stem cells. So, when you overload or train your muscles, one of the things that gets hit is your connective tissue and the connective tissue obviously supports your little muscle cells perimysium, epimysium, endomysium are connective tissue collagen that helps support your muscle and when you work out really hard you can actually damage that connective tissue, so it will need to adapt. The other thing that happens when you train your muscles or load your muscles is you do somewhat intercellular stress or damage to inside the little myocyte those little actin and myosin in myofibrils made up of sarcomeres those little actin and myosin myofibrils can get damaged and as the muscle repairs them that’s one of the adaptations you’ll get to muscle training, so again, those are the actin and myosin inside the muscle cell, inside the myocyte so it’s sort of these two ways that your muscles have to adapt to stress and training is connective tissue and also the myocytes. If you ever have trauma injury like crush injury and things like that to your muscle, that’s going to actually activate some severe muscle regeneration hopefully that’s going to involve myoblasts and satellite stem cells. If you just do regular training though you can still activate those muscle stem cells called satellite cells and they may contribute to your hypertrophy, so these little satellite cells or adult muscle stem cells and they hangout kind of inactive on the outside of your muscle cells and they’re kind of hard to see but these guys stained them so you can actually see them. So, you’ve got your muscle cell with a satellite cell, little stem cell hanging out they’re not doing anything and then you stress your muscle it activates it, it activates that little satellite cell and now it sort of maturing into a myoblast or sort of a premuscle cell and then it’s thought that they’ll actually fuse with the original muscle fiber and that will help contribute to hypertrophy and adapting that muscle cell to sort of new demands. The next learning objective is to talk just a tiny bit about something you’ve experienced called delayed onset muscle soreness, you’ve all probably experienced this where you try to do something new, a new workout or something maybe up the weights and you get muscle soreness and so especially when you do a new activity like hiking you haven’t done it in a while, you get this intense soreness and so I wanted to talk a little bit about what causes it. We call it delayed because it usually peeks a couple days after the activity. So, you do something new like say you decide to climb, hike to the top of Camel Back and you haven’t hiked in a while or maybe you haven’t even exercised in a while, it’s thought that there is myofibril damage inside the muscle cells, the actin and myosin, there’s also connective tissue damage to the supporting connective tissue of the muscle that causes this inflammation and swelling and a lot of it is your immune cells going in there to help clean up the damage and mess and that helps contribute to inflammation and swelling. So, all of this damage then activates sensory neurons which are neurons that sense pain and pain chemicals and they make it compressed from the swelling and all those pain signals go back up to your brain and it kind of hurts and it may hurt the more you move your muscles. That soreness tends to peek after 2 or 3 days and so we call it delayed onset muscle soreness. Eventually, you help repair those little myocytes and the supporting connective tissue build more myofibrils, build more collagen and then hopefully that soreness goes away gradually and even better if you continue to hike Camel Back Mountain regularly that soreness won’t comeback cause your muscles are more prepared for that activity. So, again, it’s this damage, this inflammation, the swelling and this pain you can help get rid of that by, of course, rest but also ice and drugs like Advil and aspirin can help the different pathways and help reduce the delayed onset muscle soreness. Our final learning objective is to predict some of the causes of muscle fatigue, so it’s an active area of research so you’ll see there’s quite a few theories about what causes muscle fatigue. What is muscle fatigue? I like to just think of it as when you’re trying to use your muscle for a steady period of time you can’t quite maintain the amount of force and performance over time, so even though you want to do 100 pushups after about 20 it just don’t seem like you can generate anymore force, that would be muscle fatigue. What causes it? You can see this is a complex long list but let’s look at a few that you might understand based on our physiology that we covered. One of the things that’s thought to cause muscle fatigue or contribute to it is an accumulation of extracellular potassium, so you remember potassium belongs in your myocyte and in your cells and potassium leaves every time we finish an action potential and so as you get muscle stimulation potassium is leaving and if too much accumulates outside the cells that can kind of mess up that membrane voltage that we talked about before. The other thing that I think is interesting is that buildup of potassium is thought to activate sensory neurons in the connective tissue around the muscle and then maybe that’s causing the muscle pain that your experience during muscle activity. The other thing is, contributes to muscle fatigue is thought to be the breakdown of ATP; ATP is broken down, I put ADP but it should be ADP and phosphate, so it’s thought that the buildup of inorganic phosphate and the reduction in ATP can contribute to muscle fatigue, so again, if ADP or excuse ATP is low and phosphate’s high, is thought that maybe that interrupts the ability to contract and that’s with the myosin or the actin. Lactic acid and lactate something you’ve all heard of that comes from glycolysis when you make ATP from glycolysis you make pyruvate; pyruvate can be shuttled to become lactic acid and lactate and it’s probably not as bad as people always think. One of the theories is that a low pH in your muscles could cause fatigue but the date on that is very inconsistent and also lactate doesn’t seem to be very bad either, so those don’t seem to be the culprits in fatigue. Another idea is that maybe your brain just gets tired or bored or decreases it’ output to your muscles over time, so that’s called the central nervous system theory of fatigue, so maybe your brain just stops sending those signals out and you begin to fatigue. Alright, that is all we’re going to cover for muscle physiology. I’ll see you guys in class.