All right, so again, last class we went through all the different muscles that we need to know. Today we're going to go through and we're going to talk about how muscles work, which is an even more fun topic to try and cover. Basically we're going to go through this kind of where we're going to set up every component that is needed in order to make your muscle contract.
And then we'll go through, you know, the fun 24 steps associated with that, which you do need to know for your exam. So that will be on the exam. I can tell you that right now. So that's my pep talk for today.
Yeah. Yeah. So but yeah, that's that's my way to hype up our talk today.
Not very good. Yeah, I'm not very good at hyping up these chapters, unfortunately. So, I said the lab exhale might be easier.
A lot less time. That's unfortunate. All right, let's get into our stuff for today. So let's just real quick, you know, kind of recap the different kinds of muscles that we have and some of the basic functions.
So when it comes to muscle tissues, there are three basic kinds of muscles that we have. Skeletal muscle, cardiac muscle, and smooth muscle. So where should your skeletal muscle be found? Yeah, it's a good way to describe that, right?
Kind of all over, attached to your bones, right? Where should your cardiac muscle be found? Around the heart.
What about the smooth muscle? organs and stuff. Right.
Around the organs, that kind of stuff, right? A lot of the, a lot of the viscera, that's where you're going to find your smooth muscle. The number one basic function for any kind of muscle that we have is generating force.
So muscle tension is like the number one function that we see for a muscle. And again, all we're saying here is just contracting a muscle, basically. Now, when it comes to accessory functions, again, Our skeletal muscles, they're used for movement, they're used for posture, they're used to help stabilize our joints, they're used to help generate heat.
And then when it comes to, you know, the cardiac muscles, they're used more for feeding the heart. And smooth muscles is a lot of times like allowing things to move through the body through these different hollow organs and passageways and things like that within our body. So for our talk today... We're going to spend most of that on skeletal muscle and the way the skeletal muscle work.
And then we'll have like five slides, five or six slides split between the cardiac and the smooth muscle. So it'll be real straightforward once we get through our skeletal muscles. So again, kind of to recap some of the basic histology that we see with our muscles.
When it comes to skeletal muscles, again, they tend to be very straight, long, long, straight cells. They have those striations in them, those little ridges that we tend to see, and they tend to be multinucleated. When it comes to our cardiac muscles, these tend to be shorter. They tend to be wider.
They have branches on them. And they tend to only have one, maybe two nuclei inside of them. Then when it comes to our smooth muscle, they tend to be sort of these thin, smushed together cells. It's kind of what it looks like.
They tend to be a little bit longer, not near as long as our skeletal muscle, but they tend to be a little bit longer, kind of smushed together. And they tend to only have a single nucleus. So for something like this, again, what I could ask you on the exam is, you know, if you're looking down the microscope, you're seeing muscle that's long, multinucleated, has a lot of striations. You should be able to point out that that is skeletal, something like that.
So just knowing kind of those basic characteristics for them. All right, let's talk about the properties and what each of these different properties basically mean. So muscle cells.
One property that they have is contractility, which means they can contract. Hopefully, makes sense. They are also excitable or they have excitability. That means that we can stimulate them. This is generally through an electrical signal from the nervous system.
but it can also be through other things like hormones or through just different kinds of ligands basically different kinds of chemicals and stuff like that but all around excitability just means that we can tell our muscle to perform a function conductivity means that our muscles can conduct an electrical current so we can move electricity through the muscles and that will become very important once we start talking about how our muscles actually contract. Extensibility means that they can stretch and then elasticity means that they can return to their original shape. So they can contract, we can excite them, they can run electrical currents, they can stretch, and they can return to their normal shape.
Those are the five basic properties that we see for our muscle cells. How are we feeling about that? Seems all right.
Okay. In that case, let's talk about some of the terminology that we use when it comes to muscle cells, because obviously, even though we have basically the same things inside of the cells, we couldn't keep it the same names. So when it comes to the sarcoplasm, your sarcoplasm is basically the cytoplasm found inside of a myocyte. myocytes just referring to muscle cells.
So other than that it's basically the same though, it's still cytoplasm, it's just now called the sarcoplasm. When it comes to the plasma membrane, now refer to it as the sarcolemma, because again basically the same thing, we're just going to give it another name because why not. And then one of the structures that is very different in the way that it's set up is the endoplasmic reticulum.
And in a muscle cell, we just call it the sarcoplasmic reticulum. But other than that, again, really other than the sarcoplasmic reticulum, the sarcoplasm and the sarcolemia, they're fairly standard compared to other cells. So we're filling in our new terms.
Fun stuff. Okay, so let's talk about one muscle cell and the way, again, that basically one muscle cell set up. And this is, again, in reference to skeletal muscles. That'll be what we'll focus on really until I'd say that we switch to.
cardiac or smooth muscle. So when it comes to one muscle cell, again, we generally just call them muscle fibers, and they are surrounded, all of them are surrounded by their endomysium. So we'll kind of look at that whole breakdown again in a little bit once we start talking about all the small parts inside of our muscle cells. When it comes again to our skeletal muscle, the fibers, they're very thin cylinders. They can be about 30 centimeters long, which is very, very large.
for a single cell. 30 centimeters is a standard ruler. So 12 inches, that's pretty long for a cell. Does anybody know what type of cell we have in the body that's longer than that? Neurons, right?
So our nerves, the neurons again can go quite a bit further than that, but still huge, huge for... that type of cell. Again, they're only about 100 micrometers in thickness, so they're very, very thin, but they are very, very long cells.
So again, you know, as an example, the red blood cells, they're only about 7.5 micrometers in diameter, so very, very tiny. So that kind of gets us into the breakdown of a muscle. And you should know, basically, if I were to tell you to go from like the biggest structure that we have from a muscle all the way down to the smallest structure that we have in a muscle.
So the biggest structure that we can have in reference to our muscles are what we call compartments. And compartments is basically where we house functionally related muscles within a deep fascia. So an example of that could be that, you know, the flexor muscles in your arm, all the muscles that kind of perform flexion. that would be one compartment in the upper arm and all the ones that do extension could be another compartment.
Then you have all the flexors in the forearm, that would be another compartment and all the extensors would be another compartment. Does that kind of make sense? So it's just multiple muscles that all perform a similar function.
If we then look at the individual muscle itself again, our muscle is wrapped by an epimysium. So it's not labeled on here, it was labeled in our last chapter, but... just epi and then mysium.
So it's wrapped by epimysium and within each of our muscles, we will then have our fascicles, our fascicles being wrapped by the paramysium. And then we actually, within each fascicle is where we get down into the cell level, where we have to unique muscle fiber and our muscle fibers are then wrapped by the endomysium. Now, inside of our muscle fibers are where we're going to have the myofibrils.
And within the myofibrils is where we have the myofilaments. And that is the basic outline as we're going from large to small. So compartment, muscle, vesicle, fiber, myofibril, myofilament.
That would kind of be that outline as we're going down through. How are we kind of feeling about those steps? So the big talk that we're going to be talking about today is basically the myofilament level. That will be the part that we're going to be focusing on the most.
But how's everybody feeling about kind of going from large to small? beat those all right absolutely so compartment again is the first one then you just have a muscle then a fascicle then a muscle fiber then a myofibral and then a myofilament everybody good on those So I guess I should say right now, what we're doing is we're kind of familiarizing ourselves with every part to a muscle fiber. So that when I start talking about how electrical currents move through the muscle, we'll actually know where everything is.
And we can figure out how, again, the specific muscle contracts. So if anybody is kind of lost along the way, let me know, because if not, once we get to all the steps, it won't make any sense at all. So everybody good on this part here? All right. Then let's talk about some of the components to our sarcoplasmic reticulum and the way that it kind of is set up.
So what we have is that we have these transverse tubules or T-tubules. It's kind of this sort of beige looking structure. And these are basically deep inwards extensions of our sarcolemia. So they sort of go in. And they just kind of extend it down in between all of our myofibrils.
Around our T-tubules is where we have what we call the terminal cisternae. So it's these sort of bulging projections that we have around those T-tubules. And this constitutes a major portion of our sarcoplasmic reticulum.
And collectively, we call one T-tubule and our two terminal cisterna a triad. So the triads, again, they're going to become really important once we start talking about the way that certain ions are going to be moving in order to make our muscle contract. So again, T-tubules, they extend down, basically allows us to feed currents down deep into our muscle, our terminal cisterna. they're going to provide basically the stuff to help contract our muscle. And that's sort of all again, that sarcoplasmic reticulum that we have.
One T-tubule, two terminals of sternum, that gives you your one triad. We'll kind of again, look at that triad structure here in a minute and the way that it works with contracting the muscle. All right. How are we feeling about these kind of three terms here?
In that case, let's talk about our myofilaments. So when it comes to the filaments themselves, we have myosin, we have actin. Myosin is also called our thick filament and actin is called the thin filament. The basic goal for our muscle for it to contract is simply to slide the thin filament over the thick filament.
We'll talk a little bit more about how that works in just a minute. But if I want to contract my muscle, all I want to do is basically take this thin filament on both sides and move them closer towards the middle. Again, we'll kind of discuss how that works in more detail in just a minute. So our myosin or our thick filament, it has kind of this really sort of big middle portion to it, and then a whole bunch of little myosin heads on it.
And then on our thin filament, again, our actin, it has what we call troponin and tropomyosin. Basically, our myosin heads... always wants to bind to actin, but they cannot do that if tropomyosin sits on the myosin binding sites.
So troponin, this little yellow guy right here, basically if we add the right ion to it, it will pull our tropomyosin off a bit and that will cause our myosin to bind to it and basically our muscle to contract. So that's kind of why we have again the myosin heads. We've got our trypomycin, our troponin, and then these little binding sites on reactive.
Yes. I'm sure he's probably got the same question, but in MS, we often refer to troponin when we're talking about cardiac amounts, specifically with myocardial infarctions or cardiacs. I guess typically those people have what we call an elevated troponin.
Do we, at some point in time, have a correlation between the two, or is that something that's... That's not something I'm super familiar with. but it has to do with essentially ischemia of the heart or dead muscle tissue. I've heard it before.
I've heard my wife talk about it before. Let's see. Well, that's not writing at all. Okay.
I'll try to look it up, see what I can find, and then kind of get back to you on that. antitroponin. I don't know because I'm definitely, I know that my wife had talked about it before.
I can't remember if it's a thing, like this is a wild guess, where that, again, if we have a heart attack, that looks like an H. If you have a heart attack with a dead tissue, it like releases them. And because of that, I can't remember. Yeah.
because they're released they're like your blood levels go up or something like that but again that's a wild guess i'm gonna look into it more to see if i can find like an actual answer for that so all right um but structure wise how are we feeling about our thick and thin filament the thick filament wants to always grab onto the thin one but it can't do that as long as that little blue band is in the way basically so that's kind of one of the big regulators of whether or not muscle contraction is going to happen All right, that gets us into the sarcomere then so that we can actually discuss the way that the sarcomere works. When it comes to a muscle, the actual portion of the muscle that is going to contract or the functional portion of your muscle is the sarcomere. So this is your unit of contraction. And basically the way that this works out is the more sarcomeres that you contract inside of a muscle, the more your muscle will shorten. How's everybody kind of feeling about that?
I'm not getting the most confident vibes from you guys at this point here. So basically one sarcomere extends from one Z disc to one C disc. So one Z disc to one C disc.
And these are normally somewhere around like two to three micrometers in length. But if I shorten them from three micrometers, let's say down to two, my muscle has now gotten one micrometer shorter. Considering that most sarcomeres or most muscles, they're going to have about 2,500 of these per centimeter.
If we do that out of something like our biceps, which is about 20 centimeters long that gives us about 50 000 sarcomeres per muscle fiber So I could shorten my muscle technically 50,000 micrometers, and that would make my muscles shorter. Now multiply that out by the roughly 250,000 muscle fibers we have within the biceps, and you get something, what was that, 12.5 billion tachymeters, something like that inside of there. So you can shorten it quite a bit, basically. But how are we kind of feeling about that concept there?
You have a whole bunch of these inside of your muscles. The more of those that you shorten, just a tiny little bit, the more your muscle shortens, the more you're contracting. Seems to make sense.
All right. Let's talk about the different parts to the sarcomere. So, again, I'll give it different definitions and you do need to know these definitions again for your exam.
Again, so sarcomere, we define it as the unit of contraction and it basically extends from zetus to zetus. So it's degenerative contraction and it extends from Z disc to Z disc. So from this guy right here, all the way over to this guy over here. All right.
We already talked about the thin and the thick filaments again. Thin filament is actin. Thick filament is myosin. If we talk about a Z disc just on its own, it is the attachment point for the thin filament.
So your Z disc, it is the attachment point for the thin filament. That's kind of the definition we give for that one. Wait, what did you say? The Z disc, it is the attachment point of the thin filament. All right, then we can use the M line.
The M line is the attachment point for the thick filament. So kind of where the middle of the arm. Our thick filament sits there. So M-line, attachment point for the thick filament. All right, then let's talk about the bands that we have.
So you're going to have an I-band, and your I-band is going to be the area of only thin filament. So where we only have thin filament, again, that's going to be the I-band. Our A band is going to be the area of thick filament. And I am very specific on the terminology there. In the I band, I said only thin filament.
In the A band, I'm just saying thick filament because there will be some overlap. Is everybody all right with how those are different? So A band is thick filament?
Yes. Okay, I thought you said thin filament. No, sorry, yeah.
So the A band is just where the thick filament is located, but your I band is where only thin filament is located. The big thing here is that whenever we start contracting, the A band will always stay the same size, but the I band will change its size. All right, then we have the H zone, and the H zone is the area of only thick filament.
So our I bands and our H zones, those are going to change, but the A band will always be the same. All right, then we have the zones of overlap, which are exactly as their name implies. It is the area of thick and thin filament. So it's where we have overlap in here.
So the zone of overlap is the area of thick and thin filament. So what makes the zone of overlap in the A band different? if the A band has overlap in it.
So it's just... Oh, because A band incorporates the M line and the overlap. Right, basically like your A band is the H sound plus the overlap.
Okay. Yeah, it's very fun and how specific some of these are so... All right, let's see, then we have elastic filament or connectin.
And I tend to use connectin. Elastic filament is also a term that's used for this, but connectin is the one that I've always used. That's which is why I kind of put it in our slides here.
Basically connectin, it prevents over contraction of the sarcomere. It's basically like a spring so that if the sarcomeres are pushing against each other too hard, it just has a bit of that resistance. It also is what provides elasticity.
Basically, again, the ability is once we've contracted, it can push everything back out. So again, it's just basically like a string or a spring inside of there. And the way that a spring would kind of help push things back. So it prevents over-contraction and provides elasticity. All right.
How are you feeling about... All the different parts to one little sarcomere. What's the iffy part about it?
Just a lot. Just a lot? Yeah. Just memorizing it? Yeah.
All right, again, this is all just term-based. This would be, you know, most likely. It's been a while since I wrote the exam, but, you know, on the exam, if you were to see this, this would probably be a matching question.
You know, like, here's an area of the sarcomere. match the definition into it kind of thing all right so we're feeling okay on this part though okay to move on all right and again this is kind of to show how some of these different uh parts can change so again your a band again is going to stay the same but all around when the sarcomere contracts your eight stone is going to get smaller your eye bands will get smaller just because there is a greater zone of overlap Okay, so so far we've kind of talked about all the structures, we've talked about the parts to the sarcomere. Do we have any questions before we start kind of getting into a little bit more of the electrical and the chemical side of things?
Two minutes. We just need a little break. Yes, let's do that.
We'll take just a quick little intermission here. All right, so we are back. Let's see here. All right, and I did just look up the proponent thing. And yeah, basically what ends up happening is the more damage there is in the heart, the more those proteins are released into the blood.
So the higher the level, the more patients screwed, basically, kind of thing. Well, I guess it would probably help if I unfreeze the heat. projector okay um but any questions about kind of the stuff that we've talked about so far with like setting up the anatomy of the way the things are going to be running inside of a muscle nope we're all super stoked to move on and start talking about more stuff i'm gonna go with the yes answer so all right uh let's talk about our our first ENP in the real world which is Degene's Muscular Dystrophy.
Degene's Muscular Dystrophy or DMD is basically a degenerative muscle disease. We see this mostly in males, really more boys, just because it's pretty fatal honestly. I know I'm really cheery today.
Basically It's an X chromosome disorder. And when you look at a lot of genetics, men only having one X chromosome, it's they either have it or they don't. Women have to have two faulty copies in order to actually get the disorder, which is why it's much more common in men than it is in women. But basically, the way that this one works out is that we actually have another protein inside of our muscle fibers called dystrophin. And you can sort of think of.
dystrophin as an anchoring protein. So all those little sarcomeres and all those myofibrils, they're basically anchored in place by this dystrophin. And that's very nice because it prevents them from rubbing against each other, which causes a lot of friction.
So in muscular dystrophy, what we end up seeing here is that you do not have dystrophin. And because you do not have dystrophin, that means your muscles are rubbing against each other a lot. And because of that, they wear down.
And then it's like... Very, very quick rate, basically. So normally what ends up happening is that by the time that a child is like somewhere around two, upwards to the teen years, their legs will probably give out just because you use your legs a lot. And the more you use the muscle, the faster it's going to wear down. So normally they're wheelchair bound by the time they're a teen, generally much younger than that.
And then generally before they're about 20 years old, either their lungs will give out or their heart will give out. Because either, again, the heart, you know, being a pretty important muscle, but again, it is affected in a similar way. or the diaphragm again being that big muscle that basically is associated with respiration that will give out and then the individuals you know fortunately die yes um i think i'm not 100 but my boyfriend has two persons that um how old are they um one is a sophomore in high school and one is like Do they have like this kind of like symptoms?
I think so. I go to the wheelchairs. Yeah. But I believe that's, I don't know, I could be wrong.
It's some muscle disorder. Some muscle disorder. Something like that. It's a very unfortunate disorder again, because there's not really anything we can really do about it other than just, you know, try to make the best out of the time, basically. because it's going to end up killing people very quickly just because of that wear on the body that it accelerates basically.
All right. Let's move into talking a bit about sort of the electrical and chemical aspects of the way that our muscles work. So all of our skeletal muscles, again, they are innovated. Does anybody remember? what it means to be innervated.
Nerves that basically excite them. So when we talk about a motor unit, a motor unit is a single neuron and all of these specific muscle fibers that it innervates or basically acts on. And what we're just saying here is that one neuron can act on many muscle fibers. And why would it make sense that we might want one neuron to act on a lot of muscle fibers?
why wouldn't we want one neuron for every muscle fiber that we have? We have a lot, right? Does anybody remember roughly how many muscle fibers I said was in the biceps?
About 250,000. So if our biceps is just there to basically contract, you know, or flex the arm, it makes more sense that you have a single neuron that goes down and then maybe excites like a fifth of it or something like that. And in that case... we don't have to have a whole bunch of neurons running through our body kind of thing. So they all basically interact with what we call a synapsis.
And the synapse is just this tiny little gap that we basically have between our neuron and or the axon terminal for a neuron and the muscle fiber itself. So it's kind of an interesting thing neurons actually don't touch anything. They have just this tiny little gap. And of course, next unit, when we get into the nervous system, we'll talk a lot more about the way the neurons actually work. But the basic idea is that a neuron sends an electrical signal.
It's what we call an action potential. And we need that action potential to get into our muscle because we have to run that action potential through the muscle to make it contract. Now, the problem is electrical signals, they do not jump very well across the synaptic cleft.
So in order to tell our muscle to perform a muscle contraction, we have to first change our electrical current into a chemical, and then it will become an electrical current on the muscle. How's everybody feeling about that? Not very efficient. Not very efficient, but...
When we start talking about the way that the body is set up, you can actually have electrical currents jump. Problem is they also jump backwards and that becomes even less efficient. So that's just, that's actually the way that like smooth muscle works, but they generally don't have to worry about the same like problems with that as we do with, they work to some degree like that I should say. but they don't have the same problems that skeletal muscles do. All right.
So let's talk a little bit about the way that that kind of works out. Let me describe it a little bit here first, and then we'll start getting into all the steps. So an action potential, again, for all intents and purposes right now, that's an electrical current. And we're going to expand on that in the next unit. I'm not going to worry about it today then.
What happens is if this action potential comes down, and gets to an axon terminal that will open these calcium channels. And if those calcium channels open, calcium will come in and it will bind to this vesicle and it will cause this vesicle to basically relieve our neurotransmitters. And this is this chemical that we're trying to release so we can change our muscles to whether it now will have an electrical signal.
So if these neurotransmitters are released into the synaptic cleft, they're going to bind to these receptors. And if they open up. Normally, sodium will move into our muscle cell.
And at that point, I have basically taken my positive signal that came down as an action potential, converted it into a chemical, just my neurotransmitters, and then put that through the synaptic cleft, now move positive charges into the muscle, effectively causing that to now become positive. And I've now changed the charge inside of that cell. How are we feeling about that?
Did that make any kind of sense or was that just nobody's wanting to say either way? How are we feeling about it? It occurs every single time you have traction. Kind of.
Basically, yes. because the binding is pretty much instantaneous. Oh yeah, this is incredibly fast, incredibly fast, yes.
But yeah, all these steps have to occur. But I always learn about this part again. I don't want to go too much further if we're not sure about this part because then again a lot of the other stuff will probably just not make sense down the line either. It's just to change the message sales deposit. Yeah, so yeah another good way to think about this is and action potential is positive.
If I want to contract my muscle, I have to make it positive. And the way that I do that is by putting sodium into it because sodium is Na+. The way to put sodium into it is by opening my little channels.
In order to open the channels, I need to get that little green guy down to them. How are we feeling about that? So the acetylcholine is more like an enzyme?
It's not an enzyme. It's a neurotransmitter, which is a chemical. So it's like a chemical messenger.
Exactly. Okay. That's the goal. Are we feeling all right.
Let's start kind of going through the steps of how, so we're going to basically start moving through now the 24 steps associated with the muscle contraction because you know, fun stuff, right? Basically again, The first thing that would happen is that this action potential would move down your motor neuron. So I just abbreviated that MN. So that's our little green arrow right here.
We're moving a positive signal down through the motor neuron. Basically, what happens is, again, once that positive signal comes down, it opens to calcium channels. And these calcium channels then, you know, allow sodium or not sodium, it allows calcium to move in. Calcium will bind to the vesicles, and once they bind to the vesicles, it causes them to fuse with the axon terminal. As they fuse with the axon terminal, they then release the neurotransmitters.
The neurotransmitters are going to go across the synaptic cleft, which is our gap, and they will bind to our receptors. Once they bind to the receptors, I move sodium in. and that will cause my cell to become positive.
How are we feeling about those six steps? Again, basically what actually happens is inside of the neuron we also have a whole bunch of these types of receptors. These are just voltage-gated ones and we'll look at those on this side over here.
But we just move a whole bunch of sodium in, and that's how we actually move a positive charge down the neural. So we're just moving sodium around to move those positive signals. How's everybody feeling about this right here?
All I've done again is just move. My positive signal from the neuron using a chemical again into the muscle. Seems okay. All right.
In that case, we'll move on to some of those next steps here in just a second. So what we just looked at, right, was everything that happened kind of around this part right here. And while we have two types of receptors.
or two types of like channel proteins. These ones right here, what we call ligand-gated ion channels, meaning again, that they will only open if a ligand binds to them. In this case here, that's acetylcholine.
That's one of the very common type of neurotransmitters that we use for muscle contraction. These ones over here are what we call voltage-gated channels, basically meaning that If for some reason the voltage changes, normally that means that the voltage becomes positive, it will cause the first one to open and that pulls in sodium, which causes the next one to open which pulls in more sodium. And it's this sort of chain reaction that basically causes this positive charge now to move down the entire muscle cell. How are we kind of feeling about that?
that kind of makes sense or so the first signal that starts opening opens the first gate which adds a more positive charge which opens the second exactly it just keeps going it just keeps like boom boom boom all the way down the line basically and that's again what we're saying now that's basically what happens down through the neuron as well again we're going to expand on that a lot more next unit but because i made this area positive it causes basically the areas around it again just to now become positive one step at a time, basically. How are we kind of feeling about that? Make sense to everybody?
All right. Now, the other big thing that's going to happen is that it is also going to start traveling down through the T-tubules. And as it travels down to the T-tubules, it basically causes these calcium channels to open. and that will release calcium from the sarcoplasmic reticulum.
How are we feeling about that? Everybody arrive with that step there or are we confused on this part here? So the sarcoplasmic reticulum has calcium in it?
Yes. Just the work of it? A whole bunch of it, yeah.
a whole bunch of calcium inside of there and then again once this positive starts coming down it basically sidetracks down through all those tubules down deep into the muscle so all of your little myofibrils gets excited so they start releasing a bunch of calcium and this is where calcium becomes really important because calcium will bind to proponent and once it binds to troponin it basically tugs on our tropomyosin and it causes the tropomyosin to move away from those myosin binding sites. And now that those myosin binding sites are exposed, our myosin head can finally attach to it and we can actually start contracting the muscle. And we've thought about these two steps right here. calcium binds to a little yellow guy right here, a retroponin. Whenever it does that, again, it kind of tugs on that blue band and it forces it down so that the binding sites are now open.
Okay. And that gets us into what we call cross-bridge cycling. Now, when it comes to cross-bridge cycling, you should know these steps independently from the big list of steps as well.
You might be asked about those on the exam, just like those four steps, putting those in order as well. But basically, the way that cross-bridge cycling works, again, is that if the binding sites on the actin are exposed, again, so that tropomyosin moves away, your myosin automatically wants to grab onto it. it just naturally wants to do that so it grabs it and that's kind of that first step that we're seeing I guess it's actually kind of step number two over here, but the myosin basically grabs onto our actin. And after it does that, it has some ADP and inorganic phosphate kind of attached to it.
Those will kind of be released. And as those are released, it causes a conformational change of the myosin head and it performs the power stroke. So it basically grabs onto our actin and then pulls it forward, pulls it towards the M line. The next thing that will then happen is we attach an ATP to it and that tells it to let go.
And whenever that we attach that ATP again, we let go of it, we can then utilize the ATP, basically hydrolyze it, and that causes the resetting of the myosin head to where it goes back into its original configuration. And now it's ready to go again. It will then grab, release the ATP, perform its power stroke, we add another ATP, then let's go.
And then we hydrolyze it again into the ADP and the negating phosphate. And then it grabs power stroke, you know, all that fun stuff, just kind of repetitively over and over and over again. And every time we do that, our little sarcomere is just going to become shorter and shorter and shorter and shorter.
Oh, so that happened a lot, just in one contraction. Exactly. So generally about 20 to 40 cycles of this whole thing will eventually shorten your muscle to its max. well it will shorten that one sarcomere to its max contraction. What are we feeling about this part here?
Did that make any kind of sense or is this just kind of confusing? We got a thumbs up. All right, how's everybody else feeling? Thumbs up or...
You said you have to know these five separately? Yes, you should know those separately as well. So this is another way to kind of show again the way that this works out. Basically you're going to have your little myosin again, it's going to attach, you're going to do a little power stroke which pulls everything forward, it's going to release and then attach onto the second binding site.
and it's just going to sit there just constantly and it just causes your actin to slowly move towards each other and again of course it's not just a single myosin head that does all of this right there's a whole bunch of them that sort of grab in different orders because they were all to let go at the same time the actin would bounce back into its normal shape basically How are we feeling about this process though? Do we need to try and like re-explain it in different ways? Or do we feel like we kind of understand it well? Why is the ADP an inorganic phosphate that causes power screw? It doesn't make sense, right?
You would think it'd be the ATP? Yeah. Think about it this way. This way is the normal way that we have our myosin head. That's where it wants to be.
That's where it wants to be. So you can think of it almost like a lever. So we basically grab onto the head as we expend the ATP to pull it back and sort of lock it in place. And then once the head comes, it represents... Once it sits on it and we've removed that ATP and inorganic phosphate, that's basically what's holding it in place.
So we let go and then it sort of jerks forward at that point. That's why we then have to add more ATP to it and then pull it back again. And then when we let go of it, it jerks forward again. Okay, that makes more sense. I know.
It seems weird that the ATP isn't used to perform a function. It's sort of expended beforehand. Yeah.
All right. Any other questions kind of on that process? No? All right.
In that case, let's go through then how the muscle relaxes. And again, this is kind of part of a full muscle contraction where we will contract the muscle and then return to the original size. So for this part here, basically what we're going to do is we're just going to stop each of the steps along the way.
So if we terminate the signal going to the muscle, that means that we're not going to be putting more acetylcholine down through the synaptic cleft. And one of the things that is constantly happening whenever we release neurotransmitters, especially things like acetylcholine, we have enzymes that are constantly chewing them up. And that's why we keep having to add these neurotransmitters in there to continue having that muscle contraction.
So when we stop adding the neurotransmitters, eventually that acetylcholine esterase will basically eat away all the acetylcholine. No more acetylcholine means our little sodium channel, those receptors, they are close up. And when those close up, it means that now there's no more positives coming in.
And because there's no more positives coming in, these voltage-gated channels are going to start closing up, and then we will have basically potassium moving out. We're not going to worry a whole lot about how that works, and again, until we start talking about neurons. But basically, no further action potential means calcium channels close.
And if our calcium channel is closed, that's a trigger to get calcium back into the sarcoplasmic reticulum. And if we return again all that calcium from the sarcoplasmic reticulum, it means we have to strip it from the troponin. And if we strip it from the troponin, the tropomyosin now covers the binding sites.
And if those binding sites are blocked, our myosin cannot bind to it. How are we kind of feeling about that part there? Can we go through that part one more time? Go through it one more time, Rian? So again, what we've done, right, we send a signal down the neuron that releases acetylcholine.
As long as acetylcholine is being released, our muscle is positive. If it is positive, we release calcium. Calcium pulls away the tropomyosin when it binds to a component.
We're doing muscle contraction. So now... No more signals means no more acetylcholine.
That means acetylcholine esterase eats away all the acetylcholine and basically breaks it down. Where does the acetylcholine esterase come from? So it's just naturally hanging out in the synaptic cleft.
It basically just kind of hangs out there. It's just an enzyme that's made by, you know, one of the neighboring cells and then they spit it out, basically. And then they just kind of hang out there.
And again, they sort of regulate. that positive level by eating away the acetylcholine. So again, if we're not continuously inputting acetylcholine, they will eventually eat all of it. Once they eat all the acetylcholine, no more positives coming into the muscle means the muscle will eventually become negative.
Once the muscle becomes negative, that closes the calcium channels. That triggers calcium to be returned. That means tropomyosin blocks your myosin binding sites. You can't grab the thin filament anymore. and then it's going to just return to its normal shape.
So that's basically kind of what these last parts to it are kind of going to. So return of troponin again to its original shape that blocks your actin myosin binding sites and because of that now we can no longer again perform that power stroke. So your muscle will eventually return to its original position due to that elasticity that So that connecting kind of pushes everything back the way it's supposed to be. All right.
So my question now is. Are we feeling okay with this enough that we want to move on or do we want to go back and kind of look at it again? We can always try to draw it out step by step and kind of explain it that way.
What are we feeling like doing? Again, this is one of the more detailed concepts that we're going to cover really in this class as a whole, so we can kind of take our time with it. Can you go through the whole thing one more time?
Just kind of go through the whole...do we want to like draw it out as we're going through? Yeah. Let's do that. Okay. So I'm just kind of going to explain the steps as I go along.
I won't write them all out because I don't have them all memorized word for word. And if you were to see this on the exam, it would be word for word out there. Well, you're going to see it on the exam.
But I don't want to give you the wrong set of like, it won't be the right order. It just might not necessarily be word for word. So I want to make sure that we just kind of explain the process.
I mean, this is going to be a big portion of our lecture exam this time, like the 24. I think it's only like five points if I remember right. Because it is one of those things, like if you get one step wrong, then the rest of it will be like not good. So it's not one of those things where it's like, oh, yeah, this is going to be like 50% of your grade.
And then, you know, you mess up one thing and then you just fall in the exam. So no. So a portion of it, but not like a huge portion of it. Okay. So if I have, again, a muscle cell and I have my neurotransmitter or not my neurotransmitter, my neuron that I'm supposed to touch my neuron kind of coming down like that.
So the first thing that I'm going to do again is that I want to basically get this positive charge and I want to move it into here. That's my goal. Basically, as this positive charge is sort of traveling down through my axon terminal, when it eventually starts sort of traveling across the edges, this is where that we would have our calcium channels.
And again, I'm going to try to stick with the colors that we're using in our diagrams to kind of keep it consistent. But these calcium channels, again, simply allows calcium to move into my cell. And that's, again, kind of this first step of converting a positive charge into a chemical, into a positive. So after I've done that, again, inside of here, I have my vesicles.
And my vesicles have those neurotransmitters in them. And if a calcium binds to my vesicle, it triggers it to fuse with the membrane itself. Okay, so we're just, there we go. Not going to work for some reason. And when they fuse, it allows me again to basically release my neurotransmitters.
Does anybody remember what that process is called? That was like unit one stuff, like exocytosis, right? When we spit stuff out, that whole fun thing, right? But basically, once my neurotransmitters have been released, I'm going to have a whole bunch of sodium kind of floating around in my synaptic cleft. You know, purple ones, that's the color that they're used.
And should my neurotransmitter again bind, onto the sodium channel, now sodium moves in. If I get enough sodium inside of here, again, now my entire structure out here gets a nice big positive. I'm sure you probably mentioned the surface, sodium's already refloating.
Yeah. It's just waiting for the... Just waiting to go, basically.
So there's a whole bunch of sodium basically floating around in there, ready to go whenever those things open. by a concentration basis they're going to move into the cell. So once that happens again, then down the line I would have a whole bunch more of these little sodium channels and because this part became positive that means that guy opens up and sodium moves in. That then causes my next one to open because now this part of my cell is positive so sodium moves in. We continue that process again down through the muscle.
We just go and go and go and down through the muscle. So kind of along the way again, we're going to end up with, I'm just going to raise a little bit here, right? We're going to have these guys coming down into it. What were those called?
The T2 field, right? So my positive charge again, it would basically just be traveling. It's going to kind of jump and it's going to keep going across.
I'm not drawing in the receptors or my little, my channels at this point, but again, they would also move down through my T-tubule down around that sarcoplasmic, again, reticulum. And what ends up happening is then inside here, let's see, they did blue. So let's do a blue color.
So this is my sarcoplasmic reticulum. which is basically packed full of more calcium, these positive charges again, they basically open up my calcium channels that I now have in the sarcoplasmic reticulum and calcium will start moving out. Everybody following along okay so far as we're moving through?
All right. So then my drawing skills are not going to allow me to kind of do this, but basically now this is again, kind of sitting around those myofibrils that we were looking at. So again, if you have your whole muscle fibers, you have those smaller tubes inside of it.
And basically what's going to happen now is all that calcium is going to diffuse down into those smaller tubes. That's what we're going for now. So basically If we zoom in more, what we would then have again is that now, if we zoom in real deep, just on one of those little myofibrils again, this is where we would have the sarcomere.
Remember, you have to do it like opposite of each other. So that would give us, oh, wait, no, I literally just did that. parallel opposites go so you know we need a red one i mean don't mind me with my not very you know not supposed to be the soccer mirror looks almost as good as the you know the book right but if we were to um excuse me if we were to like zoom in just in a single one of these right what would be happening now is kind of looking at it you know way more zoomed in if this is my actually i think there's purple now that i think about it we'll switch to purple on my actin again Actually, I'm just going to have to do this.
Something kind of like that. Basically, again, once my calcium binds to the little troponin, it's now going to sort of pull my bands kind of around so that they are again away from those myosin binding sites. And that gets us into that whole cross-bridge cycling, right? So in this case here, now if this is my... actin and I'm just going to draw it again out kind of like a single one with my myosin kind of ready to go once my triple myosin is pulled away so it's no longer on the binding site and my myosin will bind to the actin.
I'm actually just going to do this real fast here. And with our little ADP and our inorganic phosphate, once those are released, Actually, I should just kind of draw that all together again, just a little bit. Now, I will hold my actin closer towards the midline of my, towards the M line, which would again be somewhere like inside of here. So we're kind of going down this way.
And then because, of course, I did this to where I'm going to run out of room. what will then happen again is once we add let's raise a little bit here oh okay so once i add my atp i let go and then next thing i would do is then basically Okay, I'll just work with this is the one I want. Once I hydrolyze that ATP again back into ADP and inorganic phosphate, it will now be sort of reset. And then I'm basically ready to go again, whether now, let's get rid of this here or not.
I would basically just kind of re-go back up that way, except of course now I'm not binding to the first one, I'm binding to the second one. Does that kind of make sense? And that's, again, that's our, this is the cross-bridge cycling that we do.
And we're going to do that enough times to where that our muscle will finally fully contract to the point that we need it to. And again, that's basically all dependent on if we move all the way back out and we go up to here. So if I come up here and I basically shut this down, now I've cut my signal.
And if I cut my signal, I cut this part, no longer releasing acetylcholine. And if I'm not releasing acetylcholine. I block this part.
And whenever I block that part, this is now negative, meaning that over here, again, now becomes negative. And again, we'll kind of go through and talk about how these negative charges occur. Again, when we start talking about the way that neurons work.
Same thing down through here again. Everything here basically would now be a negative charge, and that means this process does not happen. But through a different kind of channel, we're now basically telling all that extra calcium to move back in. And because all the extra calcium is moving back in, that means that now we're going to strip it off of here. and now everything would bind the way that it normally would again on our actin.
And because everything is bound normally on the actin now, that basically means that all of this is now shut down. Now we're kind of feeling about that. Does that make a little bit of sense, hopefully?
And then of course the last step is that we have that connectin in here that would basically like push everything back into the right shape. Okay, how are we kind of feeling about the flow? Better?
Okay, that's what we're going for. It's better. So, all right.
So, it's a mass and binding to the actin. I'm just kind of thinking of it as like a ratchet strap. Yes. When you're done, the connect is releasing it.
Okay, yeah, you can think about that. Yeah, so again, just yelling. Just kind of click it in little by little.
It gets tighter and tighter and tighter. And then whenever you actually let go of it, it just pushes it back up. That's a good way to think about it. Okay.
How are we feeling about the way that a muscle contracts and then relaxes? Good deal. See here.
So another, you know, cheery topic. Let's talk about rigor mortis and the way that rigor mortis works. Basically, rigor mortis is this progressive stiffening of the body after an individual has died.
And kind of the reason why the rigor mortis works is because those little pumps that take all that calcium, whenever we're done contracting and putting it back into the sarcoplasmic reticulum, they run out of energy. And when they run out of energy, there's nothing from keeping the calcium from moving out. And whenever that calcium then all starts moving out, well, causes your muscles to contract. And basically, again, you get these full body contractions throughout the individual. And normally, again, without a lot of that ATP there to basically release those myosin heads, they're just going to keep contracting.
And then eventually they're going to hold still because we can't release them. So this can happen. and it can remain for about 48 hours to 72 hours after death, where that an individual, again, is just sort of locked up really, really tightly at that point. And basically, the thing that ends up happening is that the continual contractions of the muscle fibers will eventually break them.
And that's when they start releasing all those contractions. what happens after that then they become very flaccid so it's worse oh you've seen it or it gets mushy yeah so i guess you did say you worked in uh we did some work in a morgue or something like that yeah and ems you just never know never know when you're gonna find something yeah so That's, you know, rigor mortis. Okay, so let's talk a little bit about the energy sources that we have for our muscles. Probably the main type of energy source that we use, a lot of times, again, we think of ATP as the energy currency for the cell, and it is the one that we tend to use, you know, to perform a lot of these different functions. The biggest problem, though, with ATP is that it is incredibly volatile, basically.
It does not like to hold all that energy for a very long time. We're talking like seconds when it comes to storing ATP. So it makes it kind of bad. for trying to store energy if you can only hold it for a couple seconds and then it's gone.
So instead, we have to do it alternate ways. One of those is creatine phosphate. Basically, the way that creatine phosphate works out is that, again, ATP, very volatile, wants to get rid of its third phosphate. However, ADP, much less so. So what we can do is if we just have that creatine phosphate, which holds an extra phosphate molecule, it can just kind of associate with phosphate real fast or ADP, donate its phosphate, and then bam, we now have ATP.
So we generally have about five to six times as much creatine phosphate in our cells compared to ATP itself. And if you're performing small little functions, so a lot of times, again, you know, like I'm up here talking with my hands and stuff like that, I'm likely to be using, again, this creatine phosphate to perform these small sort of movements. and that's kind of what that one is for there so just kind of these first little things that your muscles are doing just kind of small little movements like that generally can sustain muscle contractions for about 10 seconds or so and then after that again you kind of have to switch to some of these other ones so is that why weightlifters eat creatine oh we're gonna we're gonna hate on that here in a minute so yeah that's hear a lot about it but i've never understood yeah um when it comes to a lot of those remedies we're really not going to like those in this class so it's like that it wouldn't be very helpful for lifting so yeah it's more like when it comes to stuff like that it's very burst and that's where this idea comes into play but we'll look at some of the stuff we just did so Another type of energy source that we have is glycolysis.
So this is basically like an anaerobic version of performing energy conversions. So this is generally like you're out of oxygen and I need energy fast, a type of reaction that we got going on here. So basically the way that this one works is that you just do glycolysis. And kind of the reason why we like glycolysis is that it's incredibly fast compared to cellular respiration.
meaning that you're going to get energy very, very quickly. The downside, too, is you only get 2 ATP per glucose molecule. I don't know if anybody remembers from one of their other biology classes how much ATP you get from cellular respiration per glucose molecule.
accurate data, but that's, yeah. But anyways, the big thing here is 2 ATP, 36 ATP. Huge difference in the amount of ATP that you get. It's just that glycolysis is way faster.
The problem here again is that this is normally an anaerobic process. So we make a lot of byproducts, specifically lactic acid. So if you've ever been in the gym and you're feeling the burn, so lactic acid building up basically knowing the pH of your cells, making them feel as if they're burning.
telling you that you need to slow down, got to breathe more basically. So one of the nice things about this process though, again, it is good for about 30 to 40 seconds, upwards to like a minute. You can generally sustain yourself on this type of activity. But then after that, the body's going to be like, yeah, you got to stop. Right.
And that's where a lot of that burning sensation and just fatigue is going to come into play. All right. Oxidative catabolism, aerobic catabolism.
glucose, catabolism, cellular respiration, aerobic respiration, they're all kind of the same names for the same process. Basically what we're saying here is I'm going to take glucose, I'm going to put it in the mitochondria, and again I'm going to get about 36 ATP from that. The downside to this process again, it takes a long time.
So normally we tend to see this more in like postural muscles because they're going to be working all day long. So they tend to just be packed full of mitochondria so they can keep pumping out lots of ATP all day long. So legs, the back, where we tend to see a lot of that kind of stuff. Of course, the biggest requirement for this type of process is oxygen. It's basically, again, the last electronic sector in this whole model.
process that we have so if oxygen is not present that's where you you have to switch to one of those other processes all right but i've been feeling about the three basic energy sources that we have so again one is more for burst stuff one is if you run out of oxygen and then this one is like your standard everyday type stuff that we do So basically, one of the big things about, you know, exercising and performing strenuous activities is that you're eventually going to get oxygen debt. And this is one of those kind of silly concepts that are fairly self-explanatory. Oxygen debt means you do not have enough oxygen in your body. Probably makes sense. Whenever you do not have enough oxygen in your body, you start getting some of those, you know, anaerobic processes.
So you're going to run out of glycogen. You're going to run out of ATP. You're going to run out of creatine phosphate because you're using up all these items to keep your body going.
You have to replace. So whenever it comes to oxygen debt, your body's going to tell you to slow down so that you can get more oxygen in your body, get some of this lactic acid out of your body because it's going to start hurting after a while. But I'm assuming everybody's probably fairly okay with this concept here.
If you work out too hard, you're going to get tired. That's because you're losing these parts inside of yourselves, basically. There it is, our creatine supplements. So basically, again, the whole thing with taking creatine, the thought behind it is, again, the more creatine you have, the more creatine phosphate you should have, which means you can sustain your ATP supplies longer.
Makes sense kind of with the way that the first pathway works out. So it mildly improves performance for certain like burst activities, again, like heavy weightlifting and stuff like that. Research suggests that any type of endurance activity, which doesn't really use that pathway at all, it has basically no effect because it's not used. The downside to a lot of this kind of stuff, though, is like weight gain. Basically, creatine will get stuck.
kind of inside of your body. And because of that, you need to pull in more water to counteract that cellular level. The other one is like kidney damage, again, because of this extra regulation that your kidneys have to do.
So most of the time, it doesn't really have like any type of noticeable effect, just, you know, lots of downsides. The big thing here is, again, your muscles can only store so much, meaning that if you take a whole bunch of it, you just put extra strain on the kidneys instead, because they now have to try to filter it out. So another fun thing too is quality control for a lot of creatine supplementation is not FDA approved or like it's not FDA required, meaning that you don't even have to put creatine in it. And you can still sell it as a creatine supplement.
So the whole thing was being energy drinks for a while. I was really upset because they didn't actually have creatine in them. They haven't tested it yet.
Oh, I have no clue. I try to stay away from. I try to stay away from energy drinks.
I've actually been caffeine-free since Thanksgiving. That's impressive. Yeah. What?
It couldn't be me. I don't drink coffee or energy drinks, but I definitely drink a lot of coffee. Sonic drinks?
Yeah. I don't want to say your name. It's not a name. I'll still drink pop, just non-caffeinated pop.
I wonder how much caffeine in a large bottle of Lush we're talking about, because I have those at least once a day. Probably two months. Isn't that like 32 ounces?
I think so. Okay, maybe not a lot today, but I have like a lot. So with the creatine, especially in correlation with kidney damage, one thing that I've seen quite a bit of, which is why we asked a lot of like younger, very active, fit animals who are complaining of like, you know, kidney stone type symptoms, is we asked them, like, do you use a creatine supplement? So is there a correlation to the kidneys being unable to filter out that much creatine that starts to develop kidney stones?
It could be. Basically, the way that like kidney stones kind of work out is. the like anatomy of the kidney isn't quite perfect so whenever you like make your filtrate and it comes out uh into the kidney there's like a portion of it like you have stuff that can settle at the bottom basically and if you keep getting you know a lot of that water out of it but like the salts and stuff i would assume that one might happen with the creatine years and just kind of gets into part of that and the more that you have the more likely they just start to like settle and make those little kidney stones because yeah it's pretty much the more you make your kidneys work the more likely you are to get a kidney stone because it's constantly adding right it's like and if you're adding more stuff to filter there's a high chance that's going to get stuck somewhere and kidney stones are just no fun they are no fun so all right um Do we need to take a little break? We're still, we still got some stuff to talk about and I've kind of talked a lot already.
Do we need to take a little break before we continue? Seeing a thumbs up. All right, let's take like a 10 minute break and then we will, we'll come back to this.
All right. So jumping back into our talk here about muscles, kind of the next thing we'll talk about is the, uh, basically if you study muscle contractions and the way the muscle contractions kind of work out from an electrical standpoint. So when we're looking at a muscle twitch, a muscle twitch is basically the smallest amount of muscle contraction that you can measure and smallest amount of muscle contraction you can have. We generally don't see this like in an actual muscle.
This is more like in a laboratory setting where they hook up, you know, muscles to like different probes and things like that. And then, you know, measure that kind of stuff out basically. But overall, what this kind of research have shown is that there is a basic like three step. process to a muscle contraction. There's a latent period that's defined between stimuli until you start to contract, there's the contraction period where the muscle is contracting, and then there is the relaxation period.
where the muscle is relaxing. Hopefully that seems to make enough sense, right? So it takes a little bit of time to get all those chemicals and all that, all those positive charges down in there to release the calcium.
That's basically the latent period. Then we contract, then we relax. And one of the things about muscles is that they have what we call a refractory period.
And this refractory period, it basically starts from your heart. onset of the latent period, and then it ends kind of at the beginning of the contraction period. So all we're saying here is that you can't like double contract your muscle within that short time frame.
Now that doesn't mean we can't tell our muscle that's already contracting to keep contracting or contract more. We'll kind of talk about some cases where this happens here on the next slide. All right.
Okay. So basically, again, the normal way that our body is supposed to stimulate a contraction, it is stimulus, contract, relax. And then we do it again, stimuli, contract, relax.
However, sometimes our body decides that it's not quite going to follow that pattern. And that is where then we can get what we call wave summation. So wave summation is basically an increase in tension caused by repetitive stimulation of a muscle fiber.
And basically what we're saying here is that you have a stimulus, you start contracting, and then whenever you're trying to relax, before you're fully relaxed, then you start contracting again. And there's two basic ways that we can get this. We can either get unfused tetanus again, that's where we basically start relaxing, and then we contract and we start relaxing.
contract and eventually our muscle will tense up fused tetanus is basically where that you have so many stimuli so quickly you never actually get to the relaxation part of the muscle contraction and like unfused tetanus is generally what we get when we start getting a cramp fused tetanus is you know you're laying at home kids are in bed it's time to relax and the mic is like john horse you like senses are real bad right that's that kind of stuff so you uh because no relaxing right it's not allowed so um but basically all we're saying here is that if for some reason we send too many signals from our brain to a muscle it's going to cramp to some degree right and all that is is you just do not allow your muscle to fully relax and that is then just what we call tetany so tetanus i don't know if you guys know what happens if somebody actually gets tetanus like the disease they ends up real tight right and they die from that so um that's why you got to get your tetanus shot right super easy to treat or super easy to prevent very problematic if it has a long onset so all right another thing which hopefully should make a lot of sense too is that if we're looking at if i have a muscle at what point can my muscle generate the most tension you So I can either look at that in a state where my muscle is fully contracted, it is in its relaxed state, or it is fully basically extended. The point where my muscle can generate the most tension is when it's relaxed. Because if it's fully contracted, I have nowhere to go. And if it's fully extended, I have very little overlap to grab with.
So I can't pull as much because I don't have as many myosin heads that can grab onto the active. how we're kind of feeling about that does that kind of make sense yeah so i don't know if you guys ever you know in the gym when you've been doing curls and stuff like that it's always like a little bit tougher to get that first part of it up because again you're fully extended at that point and then it gets a little bit easier and then of course you can only go so far basically so Whenever our muscle is relaxed, that is the optimal length that we have basically for contracting. All right.
That gets us into talking about basically the opposite of tetany, which is botulism. So Clostridium botulinum. I just realized this now.
My micro senses are hurting. Always italicized, right? Species names. Anyways, Clostridium botulinum, it is a bacterium. It is in the same family as Clostridium tetany, which causes tetanus.
But Clostridium botulinum, it causes botulism. And basically, It is in the top three, like the toxin, the botulinum toxin that it makes is in the top three most deadly toxins on earth. It's basically proposed that if you could effectively administer the toxin to everybody on earth, you would need about, yay much, vile about that big, and that would kill everybody on earth. And of course, we use it for Botox, right?
So we're like, yeah, let's shoot that straight into our face. Cause you know, that's, that's good stuff. Makes sense, right? One of the things about the way that the botulinum toxin works is that it blocks the neuromuscular junction, basically meaning that you can't do that acetylcholine deal. And if you can't do that, again, you can't contract your muscle.
So the way that people die from botulism is what we call flaccid paralysis. Basically, all their muscles stop moving. And then once either the heart or the respiratory muscles stop moving, you're having a bad day.
Now, as long as our Botox stays within a specific muscle, it's fairly safe. So if you put it again in the facial muscles, and as long as it stays in those muscles, it's all good. It's just going to paralyze those muscles. If it gets into the blood, though, then it's going to go to other muscles, and then you have a problem. So that's why, again, like Botox, if you're going to get Botox, I'm not trying to hate on it too much, make sure you get it from, you know, an actual doctor, not some back alley doctor.
They'll do it for cheap. There was a case with a lady that, you know, she got some cheap Botox and basically the guy that, you know, gave her the Botox ended up getting it inside of her blood. And she was starting to feel the effects of it.
Got, you know, like not feeling super great. She's like, all right, I'm going to get in the jacuzzi, just hang out in there for a little bit. No water.
I told you about that already. Okay. All right, well, so yeah, so she gets in the jacuzzi, paralyzes her body, she slips down into the water and drowns. I'm trying to remember in what way I told this one.
Wow. I really think there was another A&B in the real world talking about Botox. Oh, yeah, we were. Trying to think about which one that was.
I don't know. One of them. That was so stupid.
Imagine just sitting there and you just start. going down and you literally cannot do it yeah you're just would that like hurt like you know how like you think drowning would like hurt do you think that was like like paralyzed i'm sure it would feel great you can hold your own airway yeah can you like hold your eyes like hold your breath you know like can you breathe for yourself because your diagram would come paralyzed too wouldn't it well you would eventually start i mean I would assume the drowning gets you before the respiratory failure, but it's not a good prognosis if you're already becoming paralyzed like that. Especially, you know, at home in water, not looking good.
So anyways, that's Botox. Safe-ish, as long as it's done right, you know. All right. Let's talk a bit about...
the different kinds of muscle fibers we then have inside of the body. So we can basically break muscle fibers down into type 1 and type 2. And you can think of these as slow twitch fibers and fast twitch fibers. Slow twitch fibers are for endurance. They're basically packed full of mitochondria, and they like to basically last for a long time.
When it comes to our fast twitch fibers, they're burst. So they're used more again for explosive type contractions, basically. Well, let's see. Normally, when we're looking at muscle that has a lot of mitochondria in it, it tends to be a lot darker because it has all that mitochondria in it.
So kind of again, thinking back to Turkey Day, right? When there's dark meat and there's the light meat, the dark meat is basically the stuff that is the slow twitch fibers that are. our turkeys that we eat and then the light meat are some of those type 2 fibers that we have. Again, when it comes to type 1 fibers in humans, it's primarily again in the postural muscles because those are the ones that are kind of needing a lot of that oxidative catabolism throughout the day basically. When it comes to the type 2 fibers again, they tend to have a lot less mitochondria in them, they do not have as much myoglobin, they do not have as much of a blood supply.
Again they're more just for burst type actions that we see. So there's two types. There's basically the fast oxidative glycolytic ones and then fast glycolytics.
Your fast oxidative glycolytics are like an intermediate between your type one and then the fast glycolytic. So the fast oxidative ones, they have an immediate strength, but they can also last for a bit longer because they have some mitochondria in them. OK, so that would be the middle colored one? Middle colored one, yes. And then the very lightly colored ones, that's going to be your fast glycolytic ones, because they're basically like all anaerobic.
Very few mitochondria inside of those. And again, they basically just, they're like, all right, we're going to make a whole bunch of ATP right away so we can have a huge, like explosive contraction within that type of muscle fiber. And then from there, you kind of, you know, fatigue very, very quickly because you can't sustain that for very long.
So this is one of those fun things where that genetically individuals are going to have like different proportions of these inside of their bodies. That's one of the things that we see where like depending on specific individuals, they'll just be genetically more adapted at like burst type sports or things like that compared to like endurance. So that doesn't mean that again, if you have somebody who's genetically like more adept at burst type, they can't become a marathon runner. It's just that if you happen to have a higher proportion of type one fibers in your body, it's just easier for you to condition your body to like run marathons.
And then the other way around as well, if you're like, you know, a lot of those type one fibers, well, then it doesn't mean you can't do heavy lifting. You're just going to have to work harder because you have a smaller percentage of those fibers in your body. Yeah.
That's kind of where genetics can play into a little bit with what we're more. not necessarily predisposed, but just more adapted at being able to, what type of sports and things like that to be able to do. All right, the next concept that we're then going to discuss is muscle tone. So one of the things about our muscles is that they always have to be excited to some degree and the main thing here is that especially again the muscles that we use for posture and things like that if they were to just stop being excited then we would fall over and land on the ground yes what about like when we're sleeping like do they still be like excited like that they're always somewhat contracted they all have some degree of tone basically um basically all it is again is that you know if we want to break it down again just as like a silly kind of you know just theoretical example again if we talk about just like the biceps and we say it's divided by five units the way the muscle tone would work out is that then like in the first second unit number one is excited then we let that one relax and then in second number two we excite the second unit and then the third and the fourth and it basically ensures that our muscles are always a little bit constricted a little bit ready to go and it is kind of important for a lot of vital processes within the body Some of those big ones could be like blood pressure. We always constrict our blood vessels a little bit because what's going to happen if we don't?
Yeah, basically, if they all open up real fast, then you just go and you're going to pass out. We'll talk a little bit about that, you know, with like orthostatic hypertension and things like that. The whole thing where people stand up and then they pass out, that kind of stuff.
So that's later on in the cardiovascular unit, I believe. But all around again. our body is always like a little bit contracted for preparedness and then again blood pressure and other things are just naturally maintained by this constant like exciting certain parts of the muscle all right when it comes to a muscle contraction we can basically break it down based on three types of events so one type of muscle contraction that we can have is what we call an isotonic concentric contraction.
And that's basically what we're doing whenever we are generating tension within our cells, but we're also shortening the muscle. So again, if you're like doing a curl, again, the dumbbell is going to be harder and harder to move, but you're shortening the muscle, again, that is performing that curl. So that is an isotonic concentric contraction.
In an isotonic eccentric contraction, this is where the, again, we're still generating tension, but the muscle is now lengthening. So letting, again, the dumbbell kind of go back down, unless you're one of those people in the gym, the basic, you know, just drop them, which don't be that person, right? You know, you got to let them down slowly.
And because of that, again, it still generates tension in the muscle, but now the muscle is becoming longer. So you let it down slowly and then you drop it. Don't drop the weights. I like that. I can't remember if it was Planet Fitness or somewhere else that had a little sign, you know, it's like, if you can't, if you can't put the weights back on the rack yourself, just go ask one of the girls in the front and they'll help you.
Something like that, you know, it's like, yeah. That is the worst though, like when you're at the gym and then somebody has like eight weights just around them and they're only using one of them then getting on their phone and it's like, come on, Mike, you don't need to hog all of them. Like if you're about to change the weight, I understand that.
Just put it up. Anyways, I was talking about concentric versus eccentric. Concentric shortens, eccentric lengthens.
And then whenever we have an isometric contraction, that's basically where that, again, tension is going to keep increasing, but you're not changing the length of the muscle. So that's just holding it out. And again, it's going to get heavier and heavier and heavier over time, but you're not changing the length of the muscle at that point.
Does that actually like build muscle? Yeah, that's more endurance based than it is like strength based. So I guess you have to mention that too, like with the muscle tone. whenever people say that they want to get toned basically what you do with that is you just have more of your body or like the brain naturally exciting your muscles at a given time and that's how toning works all right um delayed onset muscle soreness basically uh to kind of do this one kind of short if you've ever exercised you've probably been sore the next day because that tends to happen, especially if you haven't exercised in a long time. And kind of the idea behind this is that you kind of tear your muscles a little bit, and then you repair them, and that's how your muscles kind of get stronger over time.
So unfortunately, the only way to get rid of muscle soreness is to do more exercise. Basically, you just got to, you know, deal with it. And the stronger you get, the less sore you will be. So that's fun.
Is that like... the less sore is that because like you're not getting like as many small cuts in your muscle or are you just kind of like used to it basically yeah your body becomes adapted to it we'll talk about the way i think it might be on the next slide the way that the body can actually change so the more adapted you come to you know like big thumb to certain types of exercises the less your body just has to work for it and again you're just not going to feel it as much so That basically goes into the concept of myoplasticity. So myoplasticity are all the kind of changes that our body can go through with our muscles if we are exercising or not exercising.
And depending on the type of exercise, we'll have different kinds of changes. So one of the big things about our muscles is that a lot of them are amyotic. So again, they do not undergo mitosis, meaning that we're not really going to get any more muscle. You kind of have the muscles that you're born with, and that's really about it. We do have satellite cells, and satellite cells are these kind of unspecialized cells that can kind of go in and repair our muscles as we need them to.
But it's not one of those things where, again, if you lose like a good chunk of a muscle, you can't really regenerate that fully. It's going to undergo fibrosis and heal as a scar instead. So because of that, again, Whenever we exercise and things like that, we don't gain more muscle. We don't get more muscle cells. We just change the size of those muscle cells or change what is in them.
How's everybody kind of feeling about that concept there? Make sense? All right. So I'm getting ready to write this down and then we'll talk about the different ways that our muscles can change.
So basically when it comes to a muscle there's kind of three ways to change it for a muscle fiber. So if you do a load of endurance training you generally will not increase the overall size of the muscle a whole lot. Instead, what's going to end up happening is that you will put more mitochondria in there.
And the more mitochondria you put in there, the more ATP you can generate per unit time, meaning that you can sustain an activity for a longer time or a longer time period. You will normally also add more vasculature. So you will put more blood vessels around it to supply it with more oxygen. When it comes to resistance training, so like heavyweights and things like that, Now we're more concerned with burst activity.
So because of that, we're just going to put more myofibrils in it. More myofibrils means more sarcomeres, means more contraction. So you can basically lift harder. And then if you're on my side of things where you don't work out, that's disused, right? So then you're just going to have less myofibrils, less mitochondria in there.
And things are just going to start becoming smaller and not last as long, basically. How are we feeling about kind of those three basic ways that we can change it? Either more mitochondria, more blood vessels, or more myofibrils, or just kind of less of everything.
Does that change the blood vessels? Like in the top one, there's like three. Yes, exactly. So you increase the amount of like vasculature, so blood vessels to the area as well.
So really what you're doing is you're like, if you just put in more mitochondria, if you don't supply the oxygen to it, it doesn't really matter because they can't run without oxygen. So you also have to supply the oxygen in there to then run the mitochondria. All right, fatigue.
So really, when it comes to muscle fatigue, this is just the inability to maintain a specific level of intensity during a specific activity. And again, the reason why that we get muscle fatigue, we're going to deplete a lot of the key metabolites, whether that is creatine, whether it's glycogen, whether it's glucose, oxygen, those kinds of things that kind of is our next bullet on there, right? So.
If you do not have enough oxygen to your muscle fiber, it's just going to start slowing down over time. Other things too, like if you have a whole bunch of calcium, if you have a lot of ADP, things like that inside of your muscle fibers, that's basically going to be a trigger that you're doing too much and they're going to start slowing down. Certain environmental conditions can also cause muscle fatigue.
So especially things like heat and like... Basically, what happens here is you start sweating. And when you're sweating, you're losing those key metabolites that way.
So for a lot of your like chemicals. There are other things too, like not getting enough magnesium is pretty bad. That doesn't necessarily lead to fatigue.
It leads more to a tetanus type thing. My brother-in-law did that one time. He tried to do the keto diet type thing. Ended up not getting enough magnesium. And I was calling my wife one day and it's like, yeah, I think I need to go to the hospital because he couldn't move his hands.
They had like fully contracted up because magnesium is what holds your calcium inside the sarcoplasmic reticulum. No magnesium means nothing to hold on to. And then they start flooding out. And yeah, so I got to get some magnesium in there, too, basically. I feel like it would be a while.
I think so. I don't remember the exact timeline for that, but he was on it for a bit. Yeah. And then I guess you don't supplement or take a vitamin of some sort. Yeah.
And that's why certain diets can be kind of dangerous if you're not exactly sure what you're missing out on. Yeah. All right.
But that was skeletal muscle. Yay. Right.
Done with that. Only two more types of muscles to go. So.
Luckily, again, this will be just a few slides, basically. So we'll start with smooth muscle and the way the smooth muscle works, then we'll talk cardiac muscle a little fast, and then we'll kind of be done with everything. So smooth muscle, again, is kind of a dense slide, but let's just kind of keep it nice and short, basically. So smooth muscle, it's used to basically propel materials through hollow organs.
Again, is everybody okay with what I mean when I say hollow organ? like stomach, intestines, that kind of stuff, right? So basically peristalsis is the process that we use for that.
It's this kind of squeezing process that we'll discuss a lot more in the GI unit. It also forms a lot of the sphincters that we have around body openings. So again, kind of down to the GI tract and things like that is where we're going to see a lot of those. It helps regulate flow rates, again, through some of these hollow organs, blood vessels, respiratory tract.
just you know gastrointestinal tract and that's all again just by contracting and relaxing you know certain parts to our our vessels smooth muscles does not have sarcomeres again so there are no striations because we don't have those little uh unique contractile units we'll look at a diagram of what their units actually look like here in just a minute basically the actin and The active filaments, again, they're arranged into what we call dense bodies. And they're set up more like a scaffold rather than sort of this nice end-to-end setup that we have. Again, we'll kind of look at what that looks like here in a little bit. And the way that a smooth muscle contracts is also a bit different from the way that our skeletal muscle contracts. Basically...
Whenever calcium moves into a smooth muscle, it binds to a protein called collodulin, and this activates the myosin-amide chain kinases. All around, what basically happens then is that myosin ATPase is then activated, and that causes our cross-bridge cycling at that point. So it's a few, you know, quite a few less steps associated with this one right here.
Again, basically get your calcium in there, bind it to cambodium, activate your MLCKs, which activates your myosin HPAs, and then bam, you're contracting. So just kind of a little chain reaction of events that sort of go along inside of there. So I'll give everybody just a minute to write this stuff down. We'll move on to our next slide and talk about the different kinds of smooth muscle real fast. anybody got any cool plans for the weekend i don't get to get pied in the face all right the humane society is doing like a fundraiser okay it's like i don't know it's like the jordan's way it goes around to like different shelters i think i might have heard about it yet yeah and like we live stream it and so it's like oh see you can buy a pie and say this one's for Nikki and however many people buy me a pie is however many times I have to get pie to the face they're 20 bucks oh wow that's a lot but then it's like um if we reach oh what is it I think it's like 50 dollars or there's one it's like 20 dollars for someone to spend 20 minutes in a cage you Oh, okay.
And then there's, if we reach like $50, the office manager will get an ice bucket dumped on her head, which by the way, the high for Friday is 39 degrees. Good day to do it. I think it's actually supposed to be like 25, but then it's like, oh, I can reach.
5,000, my director will stay the night in a dog cage all night. And then if we reach 10,000, one of our volunteers will shave her head. And all of the chemo managers have to stay the night in a cage all night. So we get to sleep on the dog bed. Probably.
I'll sleep with my favorite dog. That's interesting. Considering we have our exam next week, nobody said study. Oh, it's because it's Friday.
I still got Saturday and Sunday. I still got some time. All right. But yeah, this is basically what smooth muscle looks like.
So a little bit different, again, in the way that it's set up. It has this sort of scaffolding network. And basically, again, whenever a calcium comes in here, it sort of like just contracts it down into a little ball, basically. So it contracts very differently from the way that we see our skeletal muscle. All right.
Now, when it comes to our smooth muscle, there are two types of smooth muscle that we can see. The most common type is what we call a single unit. And basically, this is found in nearly all hollow organs, including places like the uterus.
And these are linked through gap junctions. So, again, you kind of mentioned how it seems inefficient to go electrical, chemical, electrical, right? These guys don't. Basically, if we tell one of them, it sort of diffuses out through a big group of them through these little gap junctions, just electrical currents. The biggest problem though, here again, is distance.
It can't travel as far just because of the way that the signal loses power over time. So a lot of times here again, the ways that we can excite our specific little single unit smooth muscle, they can be through nervous system stimulation, which is a common one. but also things like mechanical, hormonal, or things like local pacemakers can basically cause them to change their shape. And again, the whole thing here is that normally with a single unit, you would have one neuron coming down, excites one cell, and then tells the stuff around it to do something.
In a multi-unit smooth muscle, these are quite a bit less common. We tend to see them in places like the iris or the cilia. ciliated muscles in the eye, walls of our arteries to some degree, and then the erectile pillar muscles within the skin. Does anybody remember what that muscle does? Goosebumps.
Goosebumps, right. That's the one that gives you goosebumps. But basically, the way that this one works out is that now, kind of per little muscle fiber that we have, you just have one little neuron, again, kind of going down there to excite those.
And the big thing here is that it gives you a lot more precision. So rather than exciting one thing and kind of all the stuff around it does something, you're now just kind of pinpointing the specific one that you want. And by doing that, again, you can basically vary the amount of tension that you want by having hundreds of these different little neurons and stuff like that coming out to basically excite a unique type for a unique number of those specific cells. So that gets us to cardiac muscle.
And when it comes to the cardiac muscle, basically, again, they are very structurally similar to our skeletal muscle, except they're shorter, they're branched. But they do still have those striations. And then, again, they have those intercalated discs that kind of serves, again, basically as little gap junctions. We'll talk way more about the way that that works when we start talking about the heart itself. So whenever it comes to the mitochondria we have in these ones, it actually accounts for about 30% of the cytoplasmic volume because your heart is never going to stop working.
If it does, it's not a good day, basically. So got to keep that running, you know, as much as we can. And again, these intercalated discs, they work like little gap junctions.
So again, whenever we send a signal into one part of our heart, it can basically travel kind of all the way out through the other parts of our heart. And we'll talk more about that in the cardiovascular unit. But one of the sort of interesting things about our heart is that it has those pacemaker cells, the sinoatrial node and the atrial ventricular node.
And those basically cause what we call auto-rhythmicity. They're leaky channels, so they constantly have these ions moving in and out of them, but they basically allow you to beat your heart without your brain ever having to tell it to, which is kind of a neat little thing that they can do. Of course, our brain can act on the heart to make it beat faster or slower, but normally again, we don't necessarily need the brain to tell the heart to beat, which is kind of a neat little thing there. but I will talk way more about that when we talk about the like electrophysiology of the heart in our cardiovascular unit.
But that is it. The other parts there is I just wrote out the step step by step for the muscle contraction so but yeah. That is it for our talk today.
So does anybody have any questions?