Understanding Muscle and Nerve Cells

Now remember one of the biggest things that muscle cells and nerve cells have in common is unfortunately they don't go through mitosis. So we don't get more of these cells. This is crucial in understanding how your muscles get bigger. When you are doing weight training or trying to get all buff, you don't get more muscle cells. That's not how it works. Because remember, muscle cells don't go through mitosis. You're born with all you're ever going to have. But what can happen is... the individual muscle cells, which is what I was trying to draw here, can get bigger. So I'm a child of the 80s and there was this like trash bag commercial that was like, hefty, hefty, hefty, wimpy, wimpy, wimpy. They should bring it back. So some of you that are young have absolutely no idea what I'm talking about. You older people, you'll find that hilarious. So the point is bulkier muscle cells, bulkier muscle fibers are going to contract a lot more intense than thinner. So when you start weightlifting, your individual muscle fibers. get bigger. What you can get more of is more golf clubs and necklaces, more actinomycin. Actinomycin are proteins, and that's why bodybuilders eat a lot of protein, because it helps them build those golf clubs and necklaces inside their cells to make their cells bigger. So you don't get more muscle cells, you can get more myofilaments, actinomycin. So atrophy versus hypertrophy. If you're forcefully enlarging your muscles, and so this is showing Arnold back He doesn't look like this now. Hypertrophy means that you've increased your muscle size. You didn't change the cell number. These cells don't reproduce. They don't go through mitosis. But you got more actinomycin, so you got more force, and the individual muscle fibers themselves get bigger. So that's why we say hyper, hypertrophy, because it gets bigger. Atrophy is the opposite. When the muscle size, the overall size shrinks because the individual muscles. cells or fibers shrink. This can happen from just lack of use. If you've ever lifted weights and then stopped, it only takes a few months for you to lose all that you gained. It's so depressing. It's kind of like making my bed every day. I just don't have the patience. I don't have the patience for working out because you're never done. You have to keep doing it. So the muscles decrease in size because you use it or you lose it. It's kind of like the skeletal system. You've got to lift weights to keep your bones strong. You've got to use them or your body goes, why bother? Same things with muscles. So if you're using your muscles, you get more blood, you get more ATP, they get bigger. But atrophy is from a disease, certainly, or just becoming a couch potato, you start wasting blood. The capillary goes, you know, why should I keep feeding all these muscle cells? You're not using it anyway. So if the capillaries decrease, you're not getting as much blood, you're not getting as much sugar, you're not using as much ATP, the actin and myosin filaments decrease. Why would you waste protein, which is expensive and hard to come by, making actin and myosin, making golf clubs and necklaces that you're not even using? So the overall muscle weakens. Now, to record a muscle contraction, we can use little machines called myograms. And we don't use this at DAC just because we don't do these kind of higher-up physiologists. labs, but you can take a little muscle from a frog leg and zap it and watch it contract, but frankly I like frogs, so I think that's fine. But the point is there are different types of contractions. So we can contract the muscle fibers and the whole overall muscle. The two types of contractions are similar. We call them isometric and isotonic, which we've had in lab. Isometric is you're increasing tension, but you're not shortening the muscle. An isometric contraction is like pushing against. against a wall. You're still doing effort, you're still using ATP, you're still fatiguing that muscle, but the wall wins. So your muscle's not changing in length because it has nowhere to go. Versus an isotonic contraction, where the muscle changes length, it shortens during contraction. So isotonic, like I said in lab, is what we think of as muscle contraction. So isometric, you're holding that and she looks like a little wimpus. She can't possibly move that, what, two-pound dumbbell there, poor baby. But isometric. the muscles are contracting at the cellular level but the weight of the load is pushing against it. So you have tension you have a workout you're still burning ATP but the filaments can't slide together where I was isotonic she's able to move that little dumbbell she moves the load We have this picture in lab so we're just kind of reviewing hopefully some of this stuff. An isotonic contraction is A and B where the muscle is changing shape. Isometric is C, you're pulling on that bar that's attached to the wall, it ain't going nowhere. But if you think of a bicep curl, you have the biceps brachii which is your top muscle and you have the triceps which is on the back of your arm. Well when you're doing a bicep curl, The muscle that's doing the contraction is the bicep. We call that the concentric muscle. So I always remember that concentric because it's doing the contracting. It's shortening and doing the work. But if you think about opposing muscles, the bicep shortens while the tricep on the other the back of the arm has to lengthen. It's like a pulley. You pull on one side of the rope, the other side goes up. You pull on the other side, the other side goes up. It's a give and take. It's a yin and a yang. If your tricep does not stretch, the bicep can't contract. So during a bicep curl, the concentric muscle is the bicep. The eccentric is the muscle that increases in length. That would be the tricep. So he's not actually causing the object to move, but if he doesn't stretch, the object can. So we call this agonist and antagonist. We have a lot of opposing muscle groups. For example, the bis and the tris or the brachialis and the tricep. The brachialis is just under the bicep. An agonist is the prime mover. So when you're doing a bicep curl, the bicep is the agonist. It's the one doing the contraction. The antagonist is the opposite. Like in a story, the agonist is the hero. The antagonist is the evil villain because his goal is completely opposite. So the agonist contracts, the antagonist contracts, the antagonist antagonist relaxes, so he opposes the prime move. Synergists. Synergists are muscles that help out. So a synergistic effect is like drugs and alcohol have a mixture together. They have a more powerful effect together than independently. So you have lots of muscles that are there to help, just like if you piss me off, my best friend's probably going to be there to yell at you too. So when you flex your elbow, the main mover is the brachialis, which is this kind of middle muscle in your arm. If you haven't started studying your muscle, muscles yet you should. Whereas the synergist would be the bicep because he's just helping the brachialis out. But the point is muscles work together. Just like if you're moving things, you have people help you out. Origin versus insertion. If you've looked at the muscle list, you're depressed because origins and insertions are pretty difficult. Now the origin for lecture, we need to just know the definition of origin versus insertion. In lab, you have to know the origin and insertion for the muscles that are listed on that table. The origin is the point of attachment for a muscle that doesn't move. So it's on a stationary part of the skeletal. Like you have all of these origins for the biceps and they're all in your shoulder. Insertion is the more movable part. So a lot of your insertions are in the elbow for your arm muscles because you can move your elbow a lot more than your shoulders. The point is they can't be on the same bone. The muscle can't stop and end on the same bone because what happens when it contracts? It would just snap that bone in half. Now, we talked about muscle fibers, but there's actually two different types of muscle fibers, and they vary in their velocity, which is speed, and their duration, which is their amount of contraction. Now, we're only going to focus on the first two, slow versus fast, or... red fibers versus white fibers. Technically there are intermediate fibers, but that kind of makes it confusing. So we're just sticking because this is an intro class with our first two. Muscles have mostly one type or the other, but all muscles have both. They have a mixture and we'll come back to that. That's important when we talk about function. So if we look at red fibers, red fibers if you think red you think blood. These are the slow twitch fibers. The reason why they're called red fibers, they're really rich in myoglobin. That stuff remember that holds blood. So they get lots of blood which is going to have lots of oxygen and lots of sugar. They also have lots of mitochondria so they can make ATP really really fast because they have that benefit. So because Because of that, they can contract for a long time without getting tired. So their contraction speed is pretty slow, like your back muscles. You can contract your back muscles for a really, really long time without them being tired. Or your leg muscles, or your butt muscles. So this is another instance where training can affect your physiology. Long distance runners have 90% of their muscle fibers have become red fibers, where they have lots of blood, lots of mitochondria. Or if you think of birds, dark meat, which is kind of gross, but now that you've taken this class. and especially once we get the cadavers out, you'll look at meat in a totally different way now. But like Thanksgiving, my mom's always like, do you want white meat or dark meat? I'm like, white meat, because dark meat kind of skeeves me out, especially when you can see the big blood vessels in it. But if you eat duck or if you eat geese, if you eat these kind of gamey meats, and they have lots of dark meat, because I forget how fast it is that a Canada goose can fly, but it's something ridiculous, like 40 miles per hour. And they can fly for thousands of miles without taking a break, because they're mostly dark meat. So they can contract for a long period of time. period of time without getting tired because their muscles get lots and lots of blood. White meat comes from chicken. Chicken, or the majority of a lot of chickens, are white meat because if you've ever been around chickens, they're pretty lazy. Like they flap around all excited like, oh my god, I'm a chicken, and then they take a nap for like two hours, which is kind of my life. So we call it white meat because white fibers don't have as much myoglobin, so they're not as reddish looking or brown, I guess. They don't have as much blood. They don't have as much mitochondria. So they're not very good at making ATP through cellular respiration, but they're pretty good at anaerobic glycolysis, which is the first. first step where you just get the 2 ATP. So if I'm only getting 2 ATP, I can contract pretty fast, but I'm going to get really tired because I'm going to get all that lactic acid built up. So this is how like the muscles that move your eye function because you can dart your eyes around pretty quickly, but they fatigue really easily. Like if you sat there and just rolled your eyes and round and around and around and around, you can't do that for very long compared to contracting your back muscle. So you can see where most muscles would have both red and white, but muscles have a dominant one. Now, for the rest of the muscle contractions, we just stay very, very general because we focus on skeletal muscle contraction because this is AMP1. But we will see next semester smooth muscle contraction. The difference are we still have actinomycin but we don't have troponin. We have calmutalin which binds calcium. You don't need to know that detail. There's no transverse tubules. There's no sarco-well, there's sarcoplasmic reticulum but it's not as developed. So the calcium just kind of diffuses into the cell. Thanks. We still see acetylcholine, we also see norepinephrine, adrenaline. They can contract for longer than skeletal muscle with the same amount of ATP because they're not contracting as intensely. I mean smooth muscles to like move through food through your digestive system. It doesn't work as hard as say your leg muscles. Can change length without changing tautness. What that means is it doesn't lose its strength even when it stretches and this is important because your bladder, your uterus, your stomach, your intestines expand all the time and we don't want them to get worn out. Cardiac muscle remains contracted longer than skeletal because we don't want, we want just nice contracted relaxing, we want that nice rhythm to pump the blood. A more extensive transverse tubule system, lots more mitochondria. In fact, most of the mitochondria in your body are found in your heart muscle. But if you think about it, it never gets a break. 100,000 beats a day versus your leg muscles certainly get a break. Not a very developed sarcoplasmic reticulum, but why would there be because your constant needing that calcium so what's the point of locking it away just to get it back out just to lock it away just to get it back out but calcium is way more important for your cardio and so you're very sensitive to calcium so hypercalcemia we need to know this hypercalcemia is too much calcium hypocalcemia is too little too much calcium you may get prolonged contraction well in the heart that's bad hypocalcemia you can't get contraction to begin with Again, in the heart, that's bad. I mean, if your leg muscles go through a period where you can't contract them, or they're too relaxed, or they're too contracted, who cares? You know, you just rest your legs. But your heart, you'd obviously die. So irregular heart rhythms are often treated with calcium channel blockers because that will block excess calcium, and so your heart won't work as hard. But you don't need to know that. You just need to know hypercalcemia and hypocalcemia either increases the heart rate or decreases. But remember, it's about homeostasis. homeostasis. We want the perfect amount. Also remember the gap junctions, those little intercalated discs in heart muscle allow for functional synctium. If you're working in sync with somebody, you're together. We've got to have these little gap junctions, these little intercalated discs, so the individual cardiac muscle cells can pass ions to each other. Otherwise, you have part of your heart pumping one way, part of your heart pumping the other, and you die. So cardiac muscle, remember, is self-exciting and rhythmic, about 60 to 100 beats per minute, involuntary. All or none contraction, but it remains refractory until contraction is completed. We do not want tetany. We don't want the muscle to seize up. And it's also affected by acetylcholine and all.

That's not how it works. Because remember, muscle cells don't go through mitosis. You're born with all you're ever going to have. But what can happen is... the individual muscle cells, which is what I was trying to draw here, can get bigger.

So I'm a child of the 80s and there was this like trash bag commercial that was like, hefty, hefty, hefty, wimpy, wimpy, wimpy. They should bring it back. So some of you that are young have absolutely no idea what I'm talking about. You older people, you'll find that hilarious. So the point is bulkier muscle cells, bulkier muscle fibers are going to contract a lot more intense than thinner.

So when you start weightlifting, your individual muscle fibers. get bigger. What you can get more of is more golf clubs and necklaces, more actinomycin. Actinomycin are proteins, and that's why bodybuilders eat a lot of protein, because it helps them build those golf clubs and necklaces inside their cells to make their cells bigger.

So you don't get more muscle cells, you can get more myofilaments, actinomycin. So atrophy versus hypertrophy. If you're forcefully enlarging your muscles, and so this is showing Arnold back He doesn't look like this now. Hypertrophy means that you've increased your muscle size. You didn't change the cell number.

These cells don't reproduce. They don't go through mitosis. But you got more actinomycin, so you got more force, and the individual muscle fibers themselves get bigger. So that's why we say hyper, hypertrophy, because it gets bigger. Atrophy is the opposite.

When the muscle size, the overall size shrinks because the individual muscles. cells or fibers shrink. This can happen from just lack of use. If you've ever lifted weights and then stopped, it only takes a few months for you to lose all that you gained. It's so depressing.

It's kind of like making my bed every day. I just don't have the patience. I don't have the patience for working out because you're never done. You have to keep doing it.

So the muscles decrease in size because you use it or you lose it. It's kind of like the skeletal system. You've got to lift weights to keep your bones strong.

You've got to use them or your body goes, why bother? Same things with muscles. So if you're using your muscles, you get more blood, you get more ATP, they get bigger.

But atrophy is from a disease, certainly, or just becoming a couch potato, you start wasting blood. The capillary goes, you know, why should I keep feeding all these muscle cells? You're not using it anyway.

So if the capillaries decrease, you're not getting as much blood, you're not getting as much sugar, you're not using as much ATP, the actin and myosin filaments decrease. Why would you waste protein, which is expensive and hard to come by, making actin and myosin, making golf clubs and necklaces that you're not even using? So the overall muscle weakens.

Now, to record a muscle contraction, we can use little machines called myograms. And we don't use this at DAC just because we don't do these kind of higher-up physiologists. labs, but you can take a little muscle from a frog leg and zap it and watch it contract, but frankly I like frogs, so I think that's fine.

But the point is there are different types of contractions. So we can contract the muscle fibers and the whole overall muscle. The two types of contractions are similar. We call them isometric and isotonic, which we've had in lab. Isometric is you're increasing tension, but you're not shortening the muscle.

An isometric contraction is like pushing against. against a wall. You're still doing effort, you're still using ATP, you're still fatiguing that muscle, but the wall wins.

So your muscle's not changing in length because it has nowhere to go. Versus an isotonic contraction, where the muscle changes length, it shortens during contraction. So isotonic, like I said in lab, is what we think of as muscle contraction. So isometric, you're holding that and she looks like a little wimpus.

She can't possibly move that, what, two-pound dumbbell there, poor baby. But isometric. the muscles are contracting at the cellular level but the weight of the load is pushing against it.

So you have tension you have a workout you're still burning ATP but the filaments can't slide together where I was isotonic she's able to move that little dumbbell she moves the load We have this picture in lab so we're just kind of reviewing hopefully some of this stuff. An isotonic contraction is A and B where the muscle is changing shape. Isometric is C, you're pulling on that bar that's attached to the wall, it ain't going nowhere. But if you think of a bicep curl, you have the biceps brachii which is your top muscle and you have the triceps which is on the back of your arm.

Well when you're doing a bicep curl, The muscle that's doing the contraction is the bicep. We call that the concentric muscle. So I always remember that concentric because it's doing the contracting.

It's shortening and doing the work. But if you think about opposing muscles, the bicep shortens while the tricep on the other the back of the arm has to lengthen. It's like a pulley.

You pull on one side of the rope, the other side goes up. You pull on the other side, the other side goes up. It's a give and take. It's a yin and a yang.

If your tricep does not stretch, the bicep can't contract. So during a bicep curl, the concentric muscle is the bicep. The eccentric is the muscle that increases in length.

That would be the tricep. So he's not actually causing the object to move, but if he doesn't stretch, the object can. So we call this agonist and antagonist.

We have a lot of opposing muscle groups. For example, the bis and the tris or the brachialis and the tricep. The brachialis is just under the bicep. An agonist is the prime mover. So when you're doing a bicep curl, the bicep is the agonist.

It's the one doing the contraction. The antagonist is the opposite. Like in a story, the agonist is the hero. The antagonist is the evil villain because his goal is completely opposite.

So the agonist contracts, the antagonist contracts, the antagonist antagonist relaxes, so he opposes the prime move. Synergists. Synergists are muscles that help out. So a synergistic effect is like drugs and alcohol have a mixture together. They have a more powerful effect together than independently.

So you have lots of muscles that are there to help, just like if you piss me off, my best friend's probably going to be there to yell at you too. So when you flex your elbow, the main mover is the brachialis, which is this kind of middle muscle in your arm. If you haven't started studying your muscle, muscles yet you should. Whereas the synergist would be the bicep because he's just helping the brachialis out.

But the point is muscles work together. Just like if you're moving things, you have people help you out. Origin versus insertion.

If you've looked at the muscle list, you're depressed because origins and insertions are pretty difficult. Now the origin for lecture, we need to just know the definition of origin versus insertion. In lab, you have to know the origin and insertion for the muscles that are listed on that table.

The origin is the point of attachment for a muscle that doesn't move. So it's on a stationary part of the skeletal. Like you have all of these origins for the biceps and they're all in your shoulder.

Insertion is the more movable part. So a lot of your insertions are in the elbow for your arm muscles because you can move your elbow a lot more than your shoulders. The point is they can't be on the same bone.

The muscle can't stop and end on the same bone because what happens when it contracts? It would just snap that bone in half. Now, we talked about muscle fibers, but there's actually two different types of muscle fibers, and they vary in their velocity, which is speed, and their duration, which is their amount of contraction. Now, we're only going to focus on the first two, slow versus fast, or...

red fibers versus white fibers. Technically there are intermediate fibers, but that kind of makes it confusing. So we're just sticking because this is an intro class with our first two.

Muscles have mostly one type or the other, but all muscles have both. They have a mixture and we'll come back to that. That's important when we talk about function. So if we look at red fibers, red fibers if you think red you think blood.

These are the slow twitch fibers. The reason why they're called red fibers, they're really rich in myoglobin. That stuff remember that holds blood. So they get lots of blood which is going to have lots of oxygen and lots of sugar. They also have lots of mitochondria so they can make ATP really really fast because they have that benefit.

So because Because of that, they can contract for a long time without getting tired. So their contraction speed is pretty slow, like your back muscles. You can contract your back muscles for a really, really long time without them being tired.

Or your leg muscles, or your butt muscles. So this is another instance where training can affect your physiology. Long distance runners have 90% of their muscle fibers have become red fibers, where they have lots of blood, lots of mitochondria. Or if you think of birds, dark meat, which is kind of gross, but now that you've taken this class.

and especially once we get the cadavers out, you'll look at meat in a totally different way now. But like Thanksgiving, my mom's always like, do you want white meat or dark meat? I'm like, white meat, because dark meat kind of skeeves me out, especially when you can see the big blood vessels in it.

But if you eat duck or if you eat geese, if you eat these kind of gamey meats, and they have lots of dark meat, because I forget how fast it is that a Canada goose can fly, but it's something ridiculous, like 40 miles per hour. And they can fly for thousands of miles without taking a break, because they're mostly dark meat. So they can contract for a long period of time. period of time without getting tired because their muscles get lots and lots of blood. White meat comes from chicken.

Chicken, or the majority of a lot of chickens, are white meat because if you've ever been around chickens, they're pretty lazy. Like they flap around all excited like, oh my god, I'm a chicken, and then they take a nap for like two hours, which is kind of my life. So we call it white meat because white fibers don't have as much myoglobin, so they're not as reddish looking or brown, I guess. They don't have as much blood. They don't have as much mitochondria.

So they're not very good at making ATP through cellular respiration, but they're pretty good at anaerobic glycolysis, which is the first. first step where you just get the 2 ATP. So if I'm only getting 2 ATP, I can contract pretty fast, but I'm going to get really tired because I'm going to get all that lactic acid built up.

So this is how like the muscles that move your eye function because you can dart your eyes around pretty quickly, but they fatigue really easily. Like if you sat there and just rolled your eyes and round and around and around and around, you can't do that for very long compared to contracting your back muscle. So you can see where most muscles would have both red and white, but muscles have a dominant one. Now, for the rest of the muscle contractions, we just stay very, very general because we focus on skeletal muscle contraction because this is AMP1.

But we will see next semester smooth muscle contraction. The difference are we still have actinomycin but we don't have troponin. We have calmutalin which binds calcium.

You don't need to know that detail. There's no transverse tubules. There's no sarco-well, there's sarcoplasmic reticulum but it's not as developed. So the calcium just kind of diffuses into the cell. Thanks.

We still see acetylcholine, we also see norepinephrine, adrenaline. They can contract for longer than skeletal muscle with the same amount of ATP because they're not contracting as intensely. I mean smooth muscles to like move through food through your digestive system.

It doesn't work as hard as say your leg muscles. Can change length without changing tautness. What that means is it doesn't lose its strength even when it stretches and this is important because your bladder, your uterus, your stomach, your intestines expand all the time and we don't want them to get worn out. Cardiac muscle remains contracted longer than skeletal because we don't want, we want just nice contracted relaxing, we want that nice rhythm to pump the blood.

A more extensive transverse tubule system, lots more mitochondria. In fact, most of the mitochondria in your body are found in your heart muscle. But if you think about it, it never gets a break. 100,000 beats a day versus your leg muscles certainly get a break. Not a very developed sarcoplasmic reticulum, but why would there be because your constant needing that calcium so what's the point of locking it away just to get it back out just to lock it away just to get it back out but calcium is way more important for your cardio and so you're very sensitive to calcium so hypercalcemia we need to know this hypercalcemia is too much calcium hypocalcemia is too little too much calcium you may get prolonged contraction well in the heart that's bad hypocalcemia you can't get contraction to begin with Again, in the heart, that's bad.

I mean, if your leg muscles go through a period where you can't contract them, or they're too relaxed, or they're too contracted, who cares? You know, you just rest your legs. But your heart, you'd obviously die. So irregular heart rhythms are often treated with calcium channel blockers because that will block excess calcium, and so your heart won't work as hard.

But you don't need to know that. You just need to know hypercalcemia and hypocalcemia either increases the heart rate or decreases. But remember, it's about homeostasis. homeostasis. We want the perfect amount.

Also remember the gap junctions, those little intercalated discs in heart muscle allow for functional synctium. If you're working in sync with somebody, you're together. We've got to have these little gap junctions, these little intercalated discs, so the individual cardiac muscle cells can pass ions to each other.

Otherwise, you have part of your heart pumping one way, part of your heart pumping the other, and you die. So cardiac muscle, remember, is self-exciting and rhythmic, about 60 to 100 beats per minute, involuntary. All or none contraction, but it remains refractory until contraction is completed. We do not want tetany. We don't want the muscle to seize up.

And it's also affected by acetylcholine and all.

Transcript for:Understanding Muscle and Nerve Cells

Transcript for:
Understanding Muscle and Nerve Cells