Exercise Physiology | Muscle (Part 7)
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Welcome everybody to another episode of Dr. Matt and Dr. Mike's Medical Podcast. I'm your host, Dr. Mike Todorovic, and today I'm joined by child actor, Will Wheaton. Hello, Will.

The other day Zabin told me that at times I can be condescending. All right. That means I talk down on people. Okay. Just so everyone knows, Zabin's Matt's wife. I feel for her. Poor thing. You are condescending. You know that? You know, everyone writes hate mail to me saying that I'm rude and I bully you, but they don't understand. As soon as these things, I might be like that on the show, but as soon as I turn the recording device off, you are cruel and condescending. Everyone knows that's not true. You beat me.

I've got the marks. Beat you in most sports, yes. Oh, sure. Like what? Golf. That's true, actually. Actually, Matt's very good at golf. Hey, can I tell the story of you when you started playing golf that you would play with right-handed clubs? Left-handed. I'm left-handed. Yes, but didn't you have to start playing with right-handed because they were the only ones available? But you're a left-handed golfer. But you're not left-handed in your writing, are you?

Just with your sports? Yeah, just sports. Why? I have no idea. Interesting. Right dominant hand is the top hand. So more guidance and control opposed to lift and uplift. But wouldn't the power have to come from the left in the drive? You'd think so, wouldn't you? And you'd think that your dominant hand would have most power. I remember once because I was –

Like left-handed golf player. Yeah. And that's what I played mostly. But as you said, I learned playing right-handed. I remember once my mum started playing golf with her friend. Okay. And she's like, oh, just come out for a hit with us and just give us some tips. So I went out once and it was difficult to watch. You couldn't give any tips. And then we're on the second hole and it's par three, so over the water.

onto the green and I think both of them probably hit in the water a number of times. Right. And I was like, just give me your club. And then I took the right-handed club onto the green. Wow. Wow. I was actually impressed myself. Were you always good at it? Was it something that you picked the sport up and went, hey, this is suited to me or did you? Oh, it's because I played a lot of cricket, which is –

The tender batsman? Yeah. Right. Just what we did in the afternoons as a boy. Right. See, when I was a boy, I used to play real sports. You used to go around with a Shanghai...

That's right. And just put holes in people's windows. Yeah, yeah. And just beat up the neighbouring kids for their lunch money. No, of course not. I play football, AFL, rugby, soccer. I did a lot of skateboarding when I was young. A lot of skateboarding. But anyway. This is all very relevant to today's topic. It is because we probably will talk about at some point whether you choose the sport or whether the sport chooses you. So it all links together, doesn't it, Matt?

Do you remember, so I called you Will Wheaton. Do you know who Will Wheaton is? Did you ever watch Star Trek? No. Was he in that? See, everyone, this is what I have to deal with. Matt doesn't or has never watched an episode. That's because I was always outside playing sports. Oh, okay, yeah, okay, because Matt was a super popular guy. Sorry, I was out being a jock, playing left-handed cricket and golf with my mum. Sure. Yeah.

All right, the cool dude here. All right, so this episode we're talking about the role of skeletal muscle in exercise physiology. And there's a lot to go through. We're going to talk about the anatomy and physiology of the skeletal muscle. And then we're just going to move through and start talking about things like muscle fatigue. We're going to talk about muscle cramps. We're going to talk about the different muscle fiber types and what makes one a particular fiber type compared to another and the predominance of one fiber type conditionally.

according to sports. And then we'll talk about things like force, power, speed, generation and so forth. Let's begin. The best place to begin is at the very beginning. And I believe that is a quote from Mary Poppins. So... My daughter's watching that at the moment. Really? Yeah. Did you tell her that it's 80 years old and that there's more contemporary things she can watch? There is actually an updated version of Mary Poppins. No, it's probably not worth watching though. Yeah.

Apparently, the new Snow White and the Seven Dwarves is horrendous. Oh, really? I think it cost them $300 million to make and they've made a handful of millions. Wow. Supposedly the biggest Disney flop. Anyway. Thanks for adding that in. That's okay. Skeletal muscle, let's begin with your body, which I know not the most – well, I was going to say – Aesthetically sound. Aesthetically sound.

but it came out as aesthetic, which is also true. So it's not the most athletic or aesthetic. How many skeletal muscles are there in your body? Me personally or just humans? Human beings. Well, it depends. Do you classify yourself as a human being? I'm a sapien.

Yeah. Okay. 600 ballpark. Yeah. Roundabout. Probably more, likely more than 600 muscles of the body. All right. How, if I were to weigh you and then 87 kilograms. Okay. Yeah. 87 kilograms. If I were to pluck just the muscles out of your body and weigh that, what percentage of that 87 would be muscles? Do you think? About half. Okay. And what about for me?

90%? Four-fifths? Yeah, exactly. Thank you very much. Yes, so around about 40% to 50% of your body weight or mass is skeletal muscle, which it's not the most prominent. Abundant. No idea. What is? Blood cells. Which ones? Red. Okay.

You just classify things according to the red blood cell, white blood cell. That's all there is. There's platelets. We were doing a chapter the other day, you and I, hematology for a textbook. And do you remember that section where it was speaking to how many blood cells are made per second? Oh, yes, yes, yes. And in cases of extreme hypoxia where they spoke about, you know, where you've got high levels of EPO,

You can be making upwards. Obviously, this is not going to be able to be sustained for long periods, but you could be making up to 10 million red blood cells a second. Jesus, that's nuts. Yeah. A second, which blows my mind because- Mind you, you're losing a million a second. True. So there is that balance. But just saying how abundant these cells are. In a similar way, 50% of your body cellular activity

is red blood cells. By cell number. Not by mass. But 50% of your body by mass is muscle cells. But by...

not even close in regards to... Like three or four kilos of your body would be red blood cells. Right. Okay, so we're saying that we don't have a lot by number, but we've got a lot by mass. There's a lot of bulk, which tells us we need to talk about what's inside of the muscle cell, right? But before we do that, let's just talk about why we have skeletal muscle. I think it's probably straightforward that it's attached to the skeleton, so it allows for our skeleton to move, conscious movement. Which I call locomotion. You call that locomotion. Yeah.

Wasn't there a song in the 80s called... Call him a nook, Australian. How's it go? Do the locomotion with me. Sway your hips up and down. Come on, baby. Do the locomotion with me. Something else. You really got the knack. Okay. I see Matt attended many blue light discos when he was little. Is that an Australian thing? Blue light disco?

It's an underage disco that we used to have in Australia. Anyway, Matt would dance to the locomotion and the nut bush. And so the functions, yes, locomotion, which means movement, but let's just classify the roller skeletal muscle into three main functions. One, it's for force generation. That's the first thing. Force generation for locomotion and breathing. So movement and breathing. Number two, force generation for postural support. So what does that mean?

Putting your body in positions where you can do the first, which is... So you sitting at the desk right now? Yeah. Keep it back up straight? That's right. Instead of slumping all over this desk? Correct. Like the slob that you are. All right. And then number three is heat production during cold stress. Explain. When you are having that cold ice bath after your workout. Don't do that. Oh, you don't do that? No. Okay.

If you just get cold, an involuntary response that your body utilizes is shivering, which is an involuntary contraction of skeletal muscles, and that generates quite a lot of heat. So the byproduct is heat? Yeah. Okay, so we've got force generation for movement and breathing, force generation for postural support, and heat production during cold stress. These are the major functions of skeletal muscle. Okay, brilliant. Next thing I want to talk about is...

I said it's attached to the skeleton. How is it attached? Is it just attached directly to the skeleton? In what way is it attached? Via connective tissue, which we call tendons. Right. And so they're just extensions of the ends of the muscle? Pretty much. The muscle has an outer covering, which we call the epimycin, epi being upon mycin, I guess, muscle. So this outer, what would you call it, like cling film wrap that kind of just...

encapsulates the whole muscle belly and then at the end tapers off into the tendinous collagen tendon which then incorporates itself equally into the bone. Because I guess embryologically both structures, bone and muscle, originated from the same precursor. Oh, okay. And so they then just differentiated separately. Very nice. Yeah. Okay, so...

In order for us to move the skeleton, the skeleton moves because we've got joints. So that means that in order for the bones or the skeleton to move, the muscle must cross joints. And so it can cross one or more than one. If we take the muscle of the biceps, now obviously there's two heads. Brachii? Yeah, biceps, brachii, two heads to that. But let's ignore that and just say that the muscle crosses the elbow joint. Now obviously part of it does cross the shoulder joint as well. But let's just say crosses the elbow joint.

When muscle contracts, which is the job of muscle, it shortens. And when it shortens, hopefully as it crosses the joint, it changes the angle of the joint. So if I were to contract my biceps and I was to reduce...

the angle of the joint. What's that called? Flexion. And if I were to increase the angle of the joint through relaxation of the biceps? Extension. Okay. So the biceps is an elbow flexor and an elbow extensor according to how it changes the angle of the joint. You'd say flexor through its primary shortening contraction, but... Perfect. Yeah. Yes. Yes. So yes, you're totally right. Okay.

So for elbow extension, you could say the triceps because it crosses the joint as well. But when it contracts or shortens, it increases the angle of the joint. However, we will get to this. But in terms of the dynamic contraction of the muscle, you could make an argument that if you're lifting a dumbbell... Is that one of yours? When you're bringing the dumbbell closer to your arm, that the bicep is...

concentrically contracting. So it's contracting as it's shortening, but as you're letting it back down, even though you are extending, it would be contracting eccentrically. Okay. Yeah. We didn't need to make Paul. I'm trying to get you out of jail here. I'm sorry. No, but okay. That's true. Thank you. But all right. We will get to that. So good point. All right. Now when a muscle, so we're just going through some basics here. A muscle obviously needs to attach to the skeleton. So if it's

It needs to have what's called an origin and an insertion. Can you just clarify the difference between those two? So these are both attachments. Sometimes I think these are reworded now to proximal distal attachments, right? Probably. Opposed to origin and insertion because they can get a bit confusing depending on what joint's doing what at one particular time. But origin generally means the –

The insertion, the attachment of the muscle that's not moving, that portion that's not moving. That's the origin. That's the origin. Okay. And then the insertion is the part that moves. That's right. So it's sort of like pulling on it. So for the bicep, that would be in your forearm. Like a drawbridge. Right. So the part of the drawbridge that is anchored, that's the origin. And then the part that's attached to the bridge that brings the bridge up, that's the insertion.

Correct. Okay. Let's look at the muscle itself as an entire muscle group and then let's just keep zooming in until we get to the muscle fiber itself. So if I were to take your, let's say, biceps again and just look at, like, I peel away the skin. What do I, you know, skin and all that, but I've just peeled the skin away and I see the muscle. What am I actually looking at? You probably see fascia.

which is the outer covering. Yeah. And then it would have the connective tissue that's more intimately surrounding the whole entire muscle. That would be the epimycin. So that's connective tissue, the cling wrap, glad wrap that covers the muscle group. That's right. Yeah. And then that, if you continue that down to the attachment ends, that would then blend into the tendon. Right. But then if you wanted to have a look at the internal structure, you'd have to do a slice through the muscle, so a cross-sectional cut. Yes.

And then from that, you would then see...

Almost like a power cord where it has these kind of grouped cables. Like bundles? Bundles, yeah. So what are they bundles of? They're bundle of muscle cells, which we term fibers. Right. Okay. And the bundles would be bundled up around further connected tissue we call perimycin. So that wraps the bundle. Yeah, that's right. Okay. And there's multiple bundles within a muscle, big muscle group. That's right. Okay. And then...

If you were to focus on just one of those muscle cells, which are now termed muscle fiber. Synonymous. That's right. That would be further wrapped up individually by the endomycin, which is connected tissue. So there's a lot of connected tissue as we move through. And that's probably important because when we think about things like –

not just contraction and relaxation, but also skeletal muscle hypertrophy, connective tissue can't be discounted. Yeah. Right? So when your muscle grows, your connective tissue must also grow. Connective tissue is dynamic. So skeletal muscle hypertrophy isn't just the muscle cell. You can have connective tissue hypertrophy. Oh, so that would be...

Kind of extracellular, intracellular. Exactly. Hypotrophy. Exactly. But also when it comes to contraction and relaxation, your connective tissue must play a role as well. All right. So we're now at the muscle fiber, aka muscle cell. What does it look like microscopically? Yeah. And how big are they? Like how long would these? The length would be dictated by the actual length of the whole entire muscle. So if you're looking at the bicep.

Sorry, what was that word again? Bicep. Was there a T on the end there? Whatever length is from your forearm insertion all the way up to your scapula or, yeah, scapula, that would be...

the length of the individual fibers. So those with longer arms would have longer muscle fibers. Interesting. I don't think a lot of people realize that. They'll think that, oh, there's a bunch of muscle cells that are sort of lined up in series. But no, each muscle cell will go the entire length of that entire muscle. That's right. And what shape is it? A cylinder. A cylinder? Yeah, cylindrical. Okay. Can you compare that? Because skeletal muscle is not the only type of muscle.

What are the others? Cardiac muscle, which is branched, not cylindrical. I don't know how you describe it. Branched. Yeah, it's got multiple sort of ends to it to articulate with other branched cardiac muscle. So it all contracts together.

And the other is smooth muscle, which you find in, say, blood vessels or hollow tubes. Yep, like your brain cavity. That would be – what's the – Spindle shape. Spindle. What's that technical term for it? Spindle. I thought it was spindle. No, that was something else. The eye shape. Yeah, the eye shape. Tapered.

I say spindle. That's okay. Okay. Yeah, it looks like an eye. Yeah. All right. So we've got this cylindrical skeletal muscle cell slash fiber. So what is it just jam-packed with? Myofibrils, which are just contractile units. Now, they would also be –

long bits, like almost like they're another, I guess this is becoming, what did you call it? Babushka doll, which is just. No, try it for the third time. So just smaller and smaller and smaller and smaller units that fit within the one proceeding. Do people know what a babushka doll is? Russian grandma doll?

Where sort of you get the doll and you pull it apart and there's a smaller doll inside. You pull that apart, smaller doll inside. So inside the muscle fiber, you've got myofibrils. And inside the myofibrils, you've got contractile proteins. And what are the two contractile proteins? Well, there's lots. Yeah. Two major. But the main two is actin myosin. All right. All right. Now, another thing I want to add here are satellite cells. Okay. So if we have a look at the muscle cell itself –

because in biology we like to make things difficult for students, we just change the names of things just on a whim. On purpose, yeah. So in a muscle cell, so in a normal cell, right, we've got the cytoplasm, which is like the fluid filled inside. But what do we call the cytoplasm in muscle, Matt? Sarcoplasm. What's sarco mean? Flesh. Okay. Instead of having the cell membrane, which is the outer wrapping of the cell, what do we call that? Sarcolemma. Sarcolemma. All right. So...

The sarcolemma, the cell membrane for the muscle cell, just above it and just below the connective tissue. Basal lamina. Yeah. Which is also the endomycin. It probably is separate but-

Let's for simplicity say they're the same. So underneath the basal lamina, but above the sarcolemma, the cell membrane, you have these quiescent sleeping satellite cells that are sitting there waiting. Would you say that they're stem cells or stem cells? They're progenitor cells. Progenitor cells, yep. And they've got the capacity to turn into myoblasts. So what's the prefix myo mean? Muscle. And blasts?

Like immature cell has the capacity to turn into something. So basically it's an immature muscle cell that it can turn into. And if you stimulate these satellite cells, they can turn into myoblasts and effectively incorporate itself into the existing muscle cell and donate a nucleus to it. Now, two questions to you.

One, what triggers the satellite cell to undergo this differentiation into the myoblast? And two, what is the importance of it donating a nucleus? Okay, so a stimulus like an injurious stimulus. So let's say the muscle has been injured or is wanting to repair itself. Examples? Yeah, it could be through microtrauma of doing resistance training. Okay. So there has been...

Small degrees of injury in the muscle fibers. There's inflammation. And as we know, when we have inflammation, we want to signal to cells. We send out cytokines and those sorts of things. Fix me. That's right. And so that would be then sent to the satellite cell, which then gets that signal to, hey, we need your help here. Now, typically...

Again, a unique aspect to an acetyl muscle cell is that it doesn't have a singular nucleus. It's got many nuclei. Oh, good use of singular and plural. There we go. So why would we need to have many nuclei in a cell? That was the question I asked you. Okay. Specifically a muscle cell. It just needs, as we know, to express genes in a cell,

from a nucleus, generally expressing genes means you'll make a protein. So you transcribe to translate into a protein. Now we know that muscles are full of proteins. That means we need to constantly make new proteins. And so we need lots of

Perfect. And so in the case, and we also know that within discrete regions of a muscle cell is something called a myonuclear domain, which is a region like a neighborhood that a nucleus can make proteins for.

Right. It's sort of like you've got the police that police a neighbourhood. If you've got one police station, it polices a neighbourhood of a particular district or area. But just outside of that area, they can't be serviced. So you need to put more police stations in to service wider areas. That's right. So the nucleus is like the police station. It can only service the proteins of that area, making new ones. That's right. But if you embed more nuclei, then you can create more –

Contractile proteins. That's right. Especially if the population changes or increases. So if the population of the neighborhood increases, you need more COPs. Hypertrophy. That's right. Ah, very good. So that therefore means you've got injury, you bring in the satellite cells, they apply or create more nuclei, therefore more proteins. Cool. Okay. Um,

Shall we move on and talk about how we can – well, actually, no, let's – I think we should – oh, no, we can do that in a sec. Talk about contraction. Before we get to that. Oh, I knew it. What? Just in terms of why it's called a striated cell, a striated muscle. Yeah.

Striped? Stripped? Yeah. I guess. If you were to look at it. I think striped. Stripped means to pull something away. If you were to look at it under a microscope, the fibers of the muscle would appear to have stripes on it. Like a tiger. That's right. So the reason for that are the segments, the repeatable segments of the muscle fiber, which we call a sarcomere. So the sarcomere is the smallest unit in the body.

in the muscle cell that can contract and shorten. Okay, Bill Shorten. Now, what is... So, okay, let's take a sarcomere because this is where I was going anyway. Okay, good. Let's take a sarcomere. This is the smallest unit of contraction in a muscle cell. Now, as far as I'm aware, and I know this is correct, but I'm asking anyway, you're going to have...

One muscle fiber slash cell will have many sarcomere in it, both in series. So that means next to each other. It's almost like train carriages. Yes, but also in parallel. So train carriages that aren't just next to each other, aren't just behind each other, but also next to each other. So multiple train lines next to each other. So, and when you contract sarcomere,

The sarcomere, the whole thing, that sarcomere shortens. But all the sarcomeres next to it must shorten as well because they undergo the contraction too. And then all the sarcomeres in parallel need to contract as well. The question is what causes the contraction and it has to do with the actin and myosin that's present. And they basically have to bind to each other, walk across each other to shorten. Okay.

Can we talk about the neuromuscular junction and how we send that signal or is there a little bit more you wanted to say? No, I think that's fine. We can do that. All right. So...

The neuromuscular junction is effectively the interface of the nervous system with the muscle. And we have spoken in our last episode when we talked about the nervous system's role in exercise physiology, that in order to tell a muscle to contract, it must begin at the brain. We spoke about the motor cortex. We spoke about some of the deeper nuclei within the brain, basal ganglia and so forth. But effectively, it starts at the brain.

It then needs to send that signal to an upper motor neuron, which needs to send that signal to a lower motor neuron, which then needs to send that signal to the muscle itself via a neurotransmitter called acetylcholine. And then through a series of reactions, that muscle will contract. So let's talk about this series of reactions. But I've got a number of questions for you. The lower motor neuron will be talking to the muscle itself, the muscle cell.

Does the lower motor neuron actually touch the muscle cell? No. So there's a gap, just like there's a gap between one neuron and a second neuron. That's right. So that's called a synapse from one neuron to a second neuron. Is this called a synapse? Yes. Oh, it's not called a synaptic cleft or is it the same thing? Same thing I would call it. Okay, perfect. But we can call it a cleft.

So this is, I remember from our last episode, we did talk about that one motor neuron, alpha motor neuron, will speak to multiple muscle fibers. So they're the muscle units. Through multiple projections. That's right. But each muscle fiber must have an individual neuronal projection or axon. That's right. That speaks to it. Yeah. Okay. So that means each one must release its neurotransmitter acetylcholine.

All right, so you've got an action potential. Do we need to recap an action potential? No, I don't think so. Okay, so... We just get to the end of the alpha motor neuron and we have the release of acetylcholine. Because of calcium influx, acetylcholine released. The acetylcholine is released from the terminal of the motor neuron. It just diffuses across the synaptic cleft. Yep, yep.

binds to- Receptors on the sarcolemma. Okay, yeah. And what are these receptors? These would be called nicotinic receptors. So they're acetylcholine specific receptors. That's right. And they're basically connected with a channel, a sodium channel. That's right. So when the acetylcholine binds, sodium channels open up.

This, again, is like an action potential. The sodium enters the muscle membrane, the sarcolemma, depolarizes the sarcolemma, the membrane, leading to more sodium channels opening up, leading to more depolarization. But here's an important distinction here.

When we think about that cylindrical skeletal muscle cell, you said earlier it's jam-packed with contractile proteins. All of them need to contract. Yes. Not just the ones next to the membrane. That's right. Which are going to be most sensitive to this depolarization, but even the ones deepest too. So how does the depolarization of the sodium, because that only happens at the membrane, how does it trigger the deeper ones to contract? The deeper contractile proteins. Yeah, there's...

or tunnels that run the whole length of that muscle fibre. And depth. And depth, yep. And so that would be termed the T-tubule and they kind of are just... Invaginations? Yeah, yeah, that's right, to just give more surface area along the muscle fibres. So that allows for the sodium influx to happen not just on what seems to be the surface of the myocyte or the muscle cell but deep within the muscle cell. And then...

At the terminals of these T-tubules, there's like little... Cisterns. Cisterns. Which are like storage sites. Okay, so you've got these storage units. Also tanks, dams, lakes. Okay, let's just call it a storage site. What's its actual name?

In the context of muscle, sarcoplasmic reticulum. What's that? In terms of biology, that would be the endoplasmic reticulum, probably the smooth endoplasmic reticulum, which is a site for storing calcium. So there's the same thing but in the different cells. Different names. Okay, so you just said it's a storage site for calcium. Yeah. So once the depolarization event has reached these storage sites, the sarcoplasmic reticulum triggers calcium release.

So out of these storage pits but into the sarcoplasm. Correct. Flooding the inside of this muscle cell with calcium. That's right. And that triggers the beginning of contraction. That's right. Now we get into the actin-myosin relationship. But you don't just need calcium, right? You need calcium and one other important molecule. Yeah, ATP. Beautiful. So those two molecules often you get this as a question in an exam. Calcium and ATP are required for contraction. Okay.

What's the name of the theory? Now, in science when we say theory, we basically mean fact, right? Right. We've got enough evidence, but we call it a theory, but effectively it's the, like we say, evolutionary theory. It doesn't mean we don't know whether it's true or not. We know it's true. That's the term we use. So it's not the colloquial term for a theory. It's the scientific use of theory. Michael Dodorowicz has a theory on why ducks –

That's a bad example. What's it called? It's called the sliding filament theory. Okay. I was trying to think the other one, which is the lever arm one. Swinging lever arm model. Which I never learned that one. I never learned that one either. I don't think it rolls off the tongue very well. So we've got the sliding filament theory. Can I explain the way I explain it with students? Please do.

You've got actinomycin. So the mycin is also known as the thick filaments. The mycin is known as the thin filaments. And the mycin will have these extensions off the thick filament that look like little golf clubs, right? Yeah. So these arms with little heads. Oh, so they bring you back to golf, I can see. Okay, but they're not left-handed. Drivers. Yeah, little drivers. Callaway. Little Adam drivers. And the mycin head...

of that these extensions of the thick myosin filament need to bind to the actin and effectively they need to walk across and pull it inward to cause the contraction and

But the problem is that the actin filament, the thin filament, has a bike chain wrapped around it and a padlock clicked around that bike chain. So you can't use it. So if the actin is a bike, you can't steal this bike, Matt. You can't use it. So what we need to do is get the bike chain off and to do that we need to unlock the padlock. So we need a key to the padlock. What do you think that key is? I'm guessing a calcium. Oh, winner. Hot dog. We have a wiener.

It is calcium and calcium unlocks the troponin. That's the chain. Sorry, that is the padlock. The padlock opens up. The chain- Unravels. Which is called tropomyosin unravels away and reveals the binding spots. Okay. On the actin. On the actin for the myosin. So the myosin now can bind to the actin, but it also needs ATP to give it the energy to cock into position and

and then perform what's called the power stroke, which sort of drags the actin in together, contracting the muscle cell itself. So would you assume at this point, I know once we get the myosin binding to the actin, the head of the myosin is already cocked, ready to go for a power stroke? Yeah.

Yes, because there is... It's already propped, ready to go. Because there's ATP available at the spot. So effectively, I always explain it as though one cycle of contraction has already occurred because it just makes it easier. So let's just say that the... And this is hard without images. Yeah. I did a short on our YouTube... I saw that with the... Channel. The bike? I think it's very... I mean, it's got some very good views. It's 60 seconds...

Go to our YouTube channel. Look at muscle contraction. This is a video of Michael stealing a bike from a train station. That's right. But I've also done a – it's a good bike too. I got a lot of money from it, from cash converters.

You can watch the full length video that I did on sliding filament theory and skeletal muscle contraction so you can see me doing these actions that I'm just about to talk about. But effectively, let's say that we've had one cycle of contraction and the myosin head is bound to the actin.

In order for the myosin head to pop off the actin, ATP needs to... Has to be present. Yep, has to bind to the myosin head. When ATP is bound to the myosin head, it'll pop off the actin. Now it's free. Then the ATP needs to hydrolyze or disassociate into ADP and inorganic phosphate. Both of those molecules are still bound to the myosin head, both ADP and phosphate. But that hydrolyzation gives it the energy to cock the myosin head into position...

and then bind back to the actin. So if the binding site's not available, this was my point. So let's just say you got to an end point of contraction, everything stopped. Is the myosin cocked ready to go for the next contraction?

But it's just not attached? Does that make sense? So then when the next depolarisation event comes into play and calcium is released and the myosin binding site is now available, is that then locked on? I think it's too hard to know. Okay. I think it's too difficult to know because effectively...

It's all happening simultaneously. That's why it's a cycle. There's no stage one necessarily that's happening. You could argue that the stage one is that the stage one would be the myosin binding to the actin and then you need ATP to pop it off and then it begins. Okay. But now it's all confused because you didn't let me finish the cycle. So let's just say that you've got – let me start from the beginning because I don't know where I was. So you've got –

The myosin is bound to the actin, right? So one cycle has begun. ATP comes along, binds to the myosin, and the myosin head pops off. Then the ATP hydrolyzes into ADP and phosphate. They're still bound to the myosin head, but that gives it the energy to cock into position and bind back to the actin. Then the phosphate, which is called inorganic phosphate, that needs to pop off the myosin head. And when it does, it gives it the energy to perform the power stroke, which is dragging the actin, causing the contraction.

Then the ADP pops off, but the myosin head is still stuck and bound to the actin. So we need something to pop the myosin head off, and we said that that's ATP. Then ATP binds back to the myosin head, and the myosin head pops off. ATP hydrolyzes into ADP and phosphate, cocks into position, binds to actin. The phosphate pops off, performs the power stroke. ADP pops off, neutralizes.

New ATP binds, it pops off and the whole thing just continues on and on. So that's called a cross-bridge cycle. Yes. Now, if you wanted to do a full range contraction of your bicep curl, then is this only happening once or to go from a full straight arm to bring it as close as you can to your arm, then forearm to arm inflection? A full bicep curl. How many cycles would we have to do?

that you just spoke about? Well, I don't know how many cycles. I don't know if we know how many cycles, but effectively, if you only did one cycle of that, you'd probably shorten the muscle by 1%. So obviously many cycles. And you can't shorten the muscle by 100%, right? So some muscles you can shorten by 60%. Well,

Anyway, I'll leave that one. But you probably only want to shorten it by 60% or something. It depends on the muscle. So it might be hundreds of cycles, dozens of cycles. And we'll get to certain muscle fiber types that can do the speed of contraction more efficiently. Yes.

So does that make sense? Yeah, it does. Because this is an important concept to understand because when we talk about muscle fatigue, which we're going to talk about in a sec, you need to understand this cross-bridge cycle and sliding filament theory. Does this also explain rigor mortis? Yes, it absolutely does. Can you explain that for us? Well, first, what is rigor mortis? Rigor...

means stiff and mortis means death. Okay, stiff death. So this is when after somebody has died, all their muscles contract and remain technic, so fully contracted for an extended period of time. Yeah. 12 to 24 hours-ish and then it slowly relaxes. So if you think about the two things that we need, calcium and ATP for contraction, when somebody's dead, okay, here's an interesting question.

What is – and I think we may have spoken about it before. How do we know when somebody's dead cellularly? So when somebody's dead – Neurologically? Well, you can say somebody's dead neurologically. You can say somebody's dead according – like heart – Oh, right. So heart stopped. There's many different ways. Like you could be neurologically. You could be cardiac-wise. You could be – so –

But cardiac would be still neurologically. Sure. But people's heart stop and their brains keeps going, obviously for a certain period of time. But anyway, that's not the point I'm trying to make here. The point I'm trying to make here is that- When is everything death? Like when is death? And there's no sort of hard delineation point for what's death because you could argue that after your brain's dead and your heart stopped beating, that cells keep going for a certain period of time. Some would last days. Exactly. So-

So what's dead, right? But here's the thing. When in biology we often term cell death as

By what? One of the things that we sort of use to determine when a cell is dead is when it… Yeah, either necrosis or apoptosis. But it releases huge amounts of calcium. Particularly, yeah, yeah, I guess so, yeah. So often we'd say that a huge amount of calcium efflux or release of calcium…

tends to be a trigger for cell death. Because it's a calcium-dependent process. That's right. So that's one way. And this is important in this context because when these cells are dying, lots of calcium is released. Now, if lots of calcium is released, that means the troponin, the bike lock, and the tropomycin, the bike chain, fall away. Now you've got all these active binding sites on actin. So the mycin heads can bind.

And because there's ATP available, just because someone's dead doesn't mean their ATP goes straight away. There's ATP. So the muscle goes, cool, I'm available. Let's contract. So it contracts. But then the problem is...

In order for the myosin head to pop back off again, what do we need? ATP. To make ATP, but we're dead. We can't make more ATP. So the myosin remains bound to the actin for an extended period of time until degeneration occurs. And then simply just due to the chemical milieu of death-

the myosin heads will pop off over time. So you get a contraction called a rigor mortis and then over 12 to 24 hours that will start to subside. Yes, depending on the environment and there sometimes is a post-mortem analysis that the, what's the term of the medical doctor that does? The coroner. Yep, forensic pathologist or coroner would look at.

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Did we talk about this in our book? Yeah, we did in the book. Yeah, I think you wrote a chapter in our book, which will be released at the end of this year, but we'll talk more about that in the near future. But that also brings an important point here, that calcium for its efficiency of contraction needs to be released in a very synchronised pattern of

So it's not just about having calcium flood the cell. It needs to flood the cell at a point of coordination with the neural stimulation. And at the same time, it needs to be re-uptaken. Taken back up is the term that we use. Back into the psychopathic reticulum to then be released again. So this process needs to be done. So if that's not done in a coordinated fashion...

Just having calcium flooded in the cell won't necessarily make an efficient muscle contraction. Yeah, I wouldn't say calcium flooding the cell. I'll just say having calcium available...

doesn't make for an efficient contraction. And this actually leads to... You need calcium to flood the cell at the right time for an efficient contraction. And this leads us to potentially a cause of muscle fatigue. So this is where muscle fatigue being a reversible decline in muscle power or output or efficiency that sometimes comes about, will come about with either very high intensity muscle

of activity or longer duration, you know, hour plus of it. Yeah, exactly. So this is where you start to lose the efficiency of contracting a muscle. Can you start speaking to that a bit more? Yeah, sure. So you're talking about exercise-induced muscle fatigue. Yeah.

Because you can have muscle fatigue off the back end of a pathology, for example. And that's a different mechanism. So exercise-induced muscle fatigue, yeah, Matt highlighted perfectly exactly what it is, you know, the decline in the muscle's ability to produce power or generate force.

Effectively, you know, we spoke about in order for a muscle contract, all the things that need to happen. The brain, upper motor neuron, lower motor neuron, neurotransmitters, action potentials, calcium released, ATP availability, all those things.

All of those factors contribute to effective muscular contraction and therefore force generation. So the argument that can be made or the argument that is made is that alterations in any of these things will alter your force of – can alter your force of contraction and can contribute to fatigue. And so if you have a look at all the causes of skeletal muscle fatigue from exercise –

They're all of those things. It can be the nervous system, which is called central fatigue, or it could be all those other factors in the muscle, which we call peripheral fatigue.

Now, instead of going through every single one of them, because it is multifactorial and complex, we do know that there are some factors that contribute more strongly under certain conditions than others. So the first thing that we all need to understand is that there are background influences or factors that influence our fatigability. Right. So, for example, if we were to compare each other, right, and we were to do the same exercise...

I might fatigue before you. And then the question is, why is that the case? And the answer would have to do with, well, the state of fitness between us, our fiber type composition, which we'll talk about later, type one versus type two fiber predominance, nutritional status. So maybe you're just fueled better and the intensity and duration of the exercise. So all these things contribute. So there's more background factors we need to think about. Now, if you,

If we were to break it up according to heavy, very heavy and severe exercise, which is what exercise you can't really do for longer than 10 minutes. So you're trying to generate a lot of force very quickly, but you can't maintain it for a long period of time. And then compare that to moderate intensity exercise, which you can maintain for a long period of time. The exercise-induced fatigue you get...

from one versus the other... Is different. Yeah, the factors that contribute are different. So let's look at the heavy, very heavy, severe fatigue. Generally speaking, the major factors here is an increase in the hydrogen ion concentration. So what would cause, in this instance, what would cause hydrogen ion increase? Yeah, anaerobic respiration.

The production of ATP without going through the full length of going into the Krebs cycle and the oxidative phosphorylation. So it ends up going where? What's the pathway? Either just relying on phosphocreatine or glycolysis only. Yes. And so one of the factors it produces is lactate.

And lactate probably isn't a major contributor to skeletal muscle fatigue. It might even be protective. But one of the things that it does produce when it goes through this anaerobic respiration is hydrogen ions.

And so as the hydrogen ions increase, so does the acidity of that microenvironment. And what do we know happens to proteins when acids are bathing them? Yeah, changing the pH environment of a protein changes its conformation or changes its shape, therefore its function. Yeah, so it makes sense that if it becomes more acidic in that microenvironment, the contractile proteins just won't contract properly. Or it might just be things like when you spoke about the troponin, tropomycin, that

they're also proteins. And if you're changing their conformation, the way that they will allow calcium to bind to them may be less efficient. Yeah. And it could also be that the hydrogen ion concentration alters the channel for the calcium to leave the sarcoplasmic reticulum, making the calcium leak out over time. And to your point before, so you don't get a nice big release of calcium flooding the system. So you don't get a nice strong contraction.

So basically an increase in hydrogen ions affects the whole environment. So that's one important factor here for the heavy, very heavy, severe exercise intensity. The other one is an increase in the inorganic phosphate. So this is the phosphate that's produced from the ATP when it hydrolyzes into ADP and phosphate, right? That's the phosphate. On the myosin head. So if you're obviously using heaps of ATP because you're doing heaps of contractions,

you end up releasing a whole bunch of phosphate into the solution. But if you've got a lot of phosphate in the solution, there's now a high concentration and the phosphate that's attached to the myosin, remember I said that in order for the myosin head to perform the power stroke, i.e. the contraction or at least one cycle of it, the phosphate needs to pop off.

But if the environment has heaps of phosphate, it's less likely to pop off because of concentration changes. That makes sense. And so it stays on, less likely to contract. And so that's another – so both of those two things, important factors, and again, both of them can affect the calcium availability. Yep.

Then for moderate intensity exercise, the factors are different. So predominantly here, because you're doing exercise over a longer period of time, over an hour, you're relying on oxidative phosphorylation, the mitochondria. So these are the less fatigable fiber types. That's right. They rely on oxygen, the mitochondria, the electron transport chain. And one of the things we know that this spits out is reactive oxygen species.

which are fine generally, but they can cause damage. So reactive oxygen species, again, similar to like an acidic environment, can affect proteins. Okay. And it can affect, again, that channel that allows for the calcium to leave the sarcoplasmic reticulum, causing constant calcium efflux. So it's sort of calcium is just leaving, trickling out, and you don't get that nice strong calcium efflux.

you know, big bolus or, you know, big pump out of calcium for a nice strong contraction. And there's also a pump that does the opposite of sucking the calcium back up into the endoplasmic reticulum that also starts a dysfunction as well. So ultimately you're having more calcium just in puddles around the cell. Yeah, I'll just say that...

you're not getting a nice coordinated release of calcium. It's sort of trickling everywhere. Did you come across with calcium puddles, did you come across that – Not a technical term by the way. This is my technical term. That having more calcium that's just –

remain in, in the psychoplasm with all this phosphate can actually then cause precipitation. Yeah. Yeah. So the way I think about this, and it's not entirely accurate, but we know that calcium and phosphate are

...in the bone... ...come together and mineralize... ...to form the inorganic bone matter. Basically what makes the bone hard. It forms something called hydroxyapatite. And that is bone mineralization. Now that phosphate is a hydrogen phosphate...

HPO4 3- or HPO3 2-. Anyway, one of those. When calcium and that comes together, crystals. But here, calcium and inorganic phosphate can also come together. It doesn't form crystals, but they basically bind each other up. So effectively making the calcium less available for the contraction as well. So yes, that can absolutely happen.

The other major reason, so one reactive oxygen species for moderate intensity exercise. The other one is basically because you're exercising for such a long period of time, your energy stores are dropping down. So your glycogen is disappearing. Less glycogen, less ATP, less ATP, less contraction. Particularly in the intense bouts, right? Because we know that...

utilizing fast energy? Well, no, this is in the moderate intensity exercise. So the major contributing fact, because you're going to have enough glycogen for 10 minutes of exercise, right? So it's the glycogen stores are diminishing and depleting for the moderate intensity exercise over time. And that reduces the available ATP. And so as you can see, now we didn't- It's quite interesting though, isn't it? We did. It is. But we didn't talk about the-

central nervous system contribution. So just so people are aware and we're not going to focus on it because we... It's complicated and it's not completely known precisely what... It could even just come down to losing motivation. That's a great point. Exactly. So that's probably a huge part of it is as you get more tired, your motivation and sort of psychological desire for motor output will diminish as well. Do you think this is where some of the pre-trainer...

supplements work, you know, like some of the really stimulant-based ones where you just get in more psychologically activated for the exercise? Look, I'm sure that that's part of it. I don't think it's the predominant. I think that's got to do with the caffeine, the availability of adenosine, the fact that there's, you know, a link between that and ATP availability and things like that. But, yeah, I'd say there's a – I mean –

You always hear, you know, like special forces, you know, ex-soldiers. I hear it all the time. Oh, I know. You hang out with them all the time. But I've heard a number of them say that, you know, when you say that you can't do any more exercise, you know, you probably tapped into 10% or something like that. My neighbour, my ex-neighbour, he has broken the –

the world records, like I should say, of running and cycling around Australia. Right. Okay. And he said the same thing. Yeah. It,

Your body, when you feel like you just want to give up, that's only a part of it. Yeah. It's all mental now. Yes. Yes. And so there's – so that fatigue, quote unquote, fatigability, a huge part of it is mental, which is hard because that's psychological and that's not our area of expertise. Right. But then you're also going to have alterations in action potentials and ions because – Neurotransmitters. Neurotransmitters. So all those things will play a role. All right.

That's interesting. But just to add one final story, I went indoor rock climbing the other day. Oh, good on you. And I hadn't done that for a long time. How did you feel? But it got to the point where there's no way I could have got any longer with holding force in my forearm. Right. You know, when I first started, I could do all the maneuvers quite okay. Oh, sure. Every single one. Not like Tom Cruise-ish, but, you know, holding yourself up with a few fingers, right? Yeah.

But then it got to the point where no longer that's possible. Yeah. You wouldn't be able to do it even for a second. So all the strength in your forearm is gone. Yeah. So I'm guessing that is more to do with the local opposed to the central. Yes. Yeah, exactly right. Peripheral, yeah. All right. So have you ever – did you get any cramps while you were rock climbing? No. Have you ever had a muscle cramp?

I used to get them a lot when I would ski because I have the ski boots that I used to tighten them up quite a lot. Sure. And just where it'd come up to in the calf. Are they knee-high boots? They're not knee-high leather boots that you used to go? Halfway in your, you know, calf. All right. But because you'd wear them for six hours in a tight position. All right.

By the end of the day, some nights I'd get cramps in my calves. Okay. They're not fun. No. I don't get many cramps, but the ones that I've had have been extremely painful. Now, what causes a cramp? This is interesting. What is a cramp? Tell us. Well, it's a painful involuntary spasmodic muscle contraction. Okay. That makes sense.

It's the, what causes muscle cramps has sort of been up in the air for a while. I remember learning that it was due to an imbalance of ions and dehydration. Electrolytes. Yeah. So you got, you're dehydrated, you're electrolytes like sodium and magnesium, for example. You need to eat more bananas. That doesn't make sense, right? Like why wouldn't that make sense?

I guess if you were dehydrated slash deficient in electrolytes, you would be then expecting to get these muscle cramps in other muscle groups, not just that one that's been exercised. You're not dehydrated at that one muscle that you're using or the ions aren't just out of whack in that one muscle, right? It's global. It's systemic because your blood circulation carries the water and carries the ions.

So that doesn't make a lot of sense. And I guess adding to that would be that for most individuals who get cramps, the treatment for it, at least in the immediate term, is to passively stretch it. And if you were to passively stretch, that doesn't change the hydration or electrolyte status of the muscle. Good point. And this is anecdotal. So, I mean, take this with a pinch of salt. That might help the cramp. Wow.

When I've had cramps before, they tend to be of my hamstring and it's happened when I've over-contracted the hamstring too early in the exercise.

Like if I do a forceful hamstring – You mean without warm-up? Yeah, really without a – yeah, that's what I mean by too early in the exercise. So I haven't warmed up well. I haven't sort of potentiated that muscle yet, which we might talk about later as well. And that's when I tend to get those cramps. But I don't get them too often. So, all right, what's the predominant theory then? I'm going to say what it is. You mean the new theory? Yes. Yeah, well – Or the newish. Newish theory. I'm going to say what it is and I want you to sort of put it into –

easier terms to understand. So it's called the altered neuromuscular control theory. And what it basically says is this. We spoke last episode that in the muscle cell itself, we've got detectors, receptors that can determine stretch, contraction, force, all those types of things. And it sends an afferent signal back to the brain to tell us, oh, that's too stretched or that's too contracted or whatever. We'll say it's the central nervous system.

You're right, central nervous system. But still, it sends that information. Am I too stressed? Am I too contracted? How long is this muscle? And so forth. One of those are called muscle spindles and they are what detectors? Length. Length detectors. And then you've got Golgi tendons which are what? Tension. Yeah, sort of like force detectors, right? Now, if I were to stimulate the muscle spindles,

Tell me what happens. Tell me what stimulates muscle spindles. Tell me what the outcome of stimulating a muscle spindle is. Just to recap. It's basically just lengthening a muscle would activate muscle spindle proprioceptors. Saying, oh, I'm lengthening. I'm lengthening, which then would get sent back into the spinal cord.

and just have a simple sign out, back out, which would activate an alpha motor neuron to that same muscle group to then contract. Okay, so stimulating... So it would be excitatory. Right, stimulating a muscle spindle will ultimately tell the muscle to contract. Okay, what about the Golgi tendons? What stimulates that and then what's the outcome? Putting force into the tendon. So it's getting...

No, essentially pulled apart more so, which is then telling it, hey, we're under a lot of tension here. This could be damaging. We may be going into damage here. So we need to moderate or mitigate the amount of force we're putting into the muscle now because we may rip it off the bone. So it goes, oh, there's too much contraction happening. Yes.

Let's just totally relax. That's right. So also it's proprioception. It goes into the spinal cord but probably works in coordination with an interneuron and that now sends an inhibitory signal which is then going to the muscle to tell it to stop contracting. All right. So now that we have recapped those two, we can understand the altered neuromuscular control theory because what this theory states is that due to whatever reason,

you increase the activity of the muscle spindles and decrease the activity of the Golgi tendons. So you stimulate that contraction stimulator and you inhibit the inhibitor. So you get an overstimulation of contraction, which seems to translate into a cramp. That's right. And if you were then to do the passive stretch to stop the cramp, it seems to recalibrate those two...

Receptors. Poorly coordinated fiber that are kind of sending the muscle out of balance. That makes sense. But if you were to just hypothetically, I mean, they've done this, but if you were to stimulate just the Golgi tendon organ, which is the inhibitory, that would also reduce the cramps or stop the cramp, relieve the cramp. All right. So that's sort of the...

main theory for cramps at the moment. Anything to add before we move forward? No. And I think, yeah, the best evidence now is that passive stretching relieves cramping, not to discount that electrolytes and hydration has no role whatsoever. Stay hydrated. But it's just not as strongly evidenced as the passive. Yeah, I agree. All right, let's talk about the muscle fibre types. So...

What are the two major muscle fibre types? Slow twitch and fast twitch. What are their other names? Is there one? Yeah. Type one is slow twitch and type two is fast twitch. Okay. What do we mean by that? What do we mean by slow twitch and fast twitch? The speed of, like if you were to time, I guess, if you were to stimulate, I guess they, I think they did this on frogs. All right. Where they would...

Always bringing it back to harming animals in your experiments, man. Usually it's dogs between frogs today. So if you were to, and now this sounds worse, but in my area of research, which is peripheral nerve injury repair, we perform nerve conduction tests to see how well the nerve has regenerated. On people, right? No, no. Oh. In my case, they're usually rodents. So the rodents are asleep.

Okay. So you sneak into their bedrooms at night to do this. That's even worse. Under general anesthetic. You drug them as well. We use the sciatic nerve usually. Yeah. Now, you'd artificially stimulate the sciatic nerve. So you put electrical impulses into the nerve and then we can record from the muscle belly. Yeah. Okay. So you can record. So you've got electrodes that wrap around the muscle belly. Okay. And-

what the muscle activity is actually doing. Okay. Yep. So if you artificially stimulate them, you can then record how much power has been put through it. All right. So is this at some point going to answer the question of the difference between... I forget what was your question.

What's the difference between type 1 and type 2 fibres? I said what does fast twitch mean and what does slow twitch mean? Yeah, so it just means the speed at which the twitch, which is the contraction, particularly you can notice when you see the actual muscle respond, which is the twitch. Okay. You can actually see how quick the contraction, the velocity of the contraction speed. Okay. Okay, correct. And also is the force of the contraction of these two fibres different?

Yes, definitely. Now that doesn't come into play with the research that I do. I don't look at the different fiber types. We usually get to the point where you grade it. So you start to increase the strength of the contraction. So either the current or the voltage and you'll start to, and this is where the muscle, the motor unit recruitment would come into play as you get to a full super maximal contraction and

All the muscle has contracted. You won't get any more power out of it. Yeah. So as you start to increase it, you get more power out of it. And then the fiber types would play a role here. So if you are looking at the type two, which is the fast twitch, uh,

you'd get more power, more force, more speed out of these muscle types. Yeah. Okay, so if we have a look and just compare type 1 slow twitch with the type 2 fast twitch, effectively the slow twitch like you alluded to before, these...

recruited first generally when it comes to contraction. And there's a reason for that. There's a reason for that. Well, one is because they generate less force. So you don't want to – you basically – it's that size principle where you recruit the smallest motor unit and you build and build and build until you've recruited all the way up from the slow twitch to the fast twitch and now you've got nice big forceful contractions. But we'll talk about the force of contractions later. I call it the Ilya Todorovitch –

concept or principle. Why is that? That's my son. That's your son. Doing the least possible. Oh, yeah. Well, that's for sure. That's for sure. So the type 1, they're called slow twitch also because they are slow oxidative fibers, meaning they undergo oxidative phosphorylation. They can generate huge amounts of ATP but more slowly. It takes a lot of time. But they tend to be –

fatigue resistant, at least more so. So you find, so they don't generate a lot of force, but they can be used over a long period of time. So these tend to be often either the muscles we use for, you know, postural support, but also the muscles that tend to be more predominant in people who are marathon runners, for example. Endurance. They need to go for a long period of time.

Then you've got the glycolytic. These are the fast fibers. So they don't necessarily undergo oxidative phosphorylation but more glycolysis. So you can produce a lot of ATP quickly or at least you produce less ATP than oxfos but you produce a lot of it quickly. But like we spoke about earlier, you've got those byproducts that accumulate hydrogen ions and inorganic phosphate.

So they're fatigable very, very quickly. So these can be broken into two subtypes. Yes. Based on that, right? The type 2 fiber, sorry. Yes. You've got 2A and 2X. Is that Elon Musk's type?

That's right, the 2Xs. So 2A is an intermediate between the type 1 and type 2X. It is a fast twitch fiber, but it's also oxidative. Can do a bit of both. Do a bit of both, that's right. And then you've got type 2X, which is just fast twitch glycolytic.

Now, if we have a think about, you know, the characteristics that are important to determining these fibre types has to do with its oxidative capacity.

has to do with the type of myosin isoform that's present and it has to do with the abundance of the contractile proteins. So those three things really do contribute to which fibres which. So if we think about the oxidative capacity, that's easy. Slow twitch have a greater oxidative capacity, fast twitch have less.

Talking about the type of myosin isoform, this has to do with the myosin, what's called ATPase, its ability to break ATP down into ADP and phosphate. If it's got a high ATPase activity... Like type 2X. Like type 2X, it does it super quickly, which means it contracts very quickly, hence fast twitch. Fast velocity, yeah.

And then you've got the abundance of the contractile proteins. So to generate more force, you want more contractile proteins and the type 2 fibres tend to have a higher abundance of the contractile proteins. Does that make sense? It does. All right. Now, if we look at the type 1 fibres, I'm going to say a couple – I want you to explain this. I look down a microscope. I say, hey, these type 1, these slow twitch fibres, they've got heaps of mitochondria compared to the type 2. Why? Why?

Well, because you said that they rely on oxidation. Oxfox? Fox. Oxfos. So they want to produce more amounts of ATP per glucose molecule, let's say. So having more mitochondria allows that to be more efficient, I should say. So that's why.

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It has more capillaries. More blood. Feeding to the muscle cell. Bring more oxygen. Take more carbon dioxide away. And more oxygen means more oxidative phosphorylation. Yes, that's right. Okay. Again, this type 1 pharma compared to the type 2, it's got more myoglobin.

What's that mean? This is a protein, myomuscle globin protein. It's a muscle protein similar to cousins of hemoglobin. But hemoglobin just transports oxygen and then offloads it, particularly in environments where... Where do you lose your affinity for oxygen with hemoglobin? Hotter environments, more acidic environments, it drops it off because that's convenient. You want to drop oxygen and...

Yeah, you want to drop oxygen off at tissue where it's lower in oxygen but also where it's got a lower pH and it's hotter because that kind of translates to a tissue that's been used. Sorry, is that myoglobin? No, that's hemoglobin. Okay, so can you – So myoglobin is a kind of a cousin of that but rather than transport it, it's more of a storage site for it.

So how does that benefit for type 1 fibres? It just allows a higher oxygen environment, which then allows it to remain in its ox-phos state. And the other thing that these type 1 fibres have or don't have that's compared to type 2 is they've got less myosin ATPase activity. So it's a speed. Just going back to myoglobin, this is where, for instance, just to underscore the importance of oxygen...

When you look at marine animals like whales that dive deep under the ocean where they can't breathe, they can't. Oh, right. Wow. Breaking news. Because their lungs are all collapsed up but there's no oxygen left.

their myoglobin can hold the oxygen for hours and that allows them to stay underwater for such long periods of time and that kind of underscores the importance of myoglobin in a muscle for this form of contraction. Beautiful. All right.

And so going back to what I said, that was good though. So I'm glad you added that. I'm being serious. I know it sounds like I'm being sarcastic. I thought that was a very cool fact. No, it's kind of silly. It wasn't. I thought it was a great fact. The type 1 fibres compared to type 2 have less... So all those other things were increased. Increased mitochondria, increased capillaries, increased myoglobin. But the type 1 fibres, these slow twitch, have less myosin ATPase activity compared to the type 2. Explain why that's the case. Just...

Why has that? The enzymes are less prevalent, I guess, so therefore its ability to break down ATP is slower. Right, which means the sliding filament theory cross-bridge effects are slower. A slower burn. Yeah, less contraction. Okay, all this means effectively that...

Type 1 fibres are going to be more predominant in those who do endurance activities and type 2 fibres are going to be more predominant in those that do track, sprint activities, right? The question then is, and I get this asked a lot, can you change your fibre type? Well, you'd probably state that the fibres do exist on a continuum. They can not...

completely change into a completely different form, but they can take on qualitative properties that they can become better at that particular activity. So we asked at the beginning, I said, you know, does the sport choose you or do you choose the sport, right? So, for example, when somebody becomes an Olympic gymnast, were they destined to become an Olympic gymnast or was it their training that made their body better?

most compatible with Olympic gym training? Or when somebody becomes an Olympic weightlifter, were they always destined physiologically to be that or could they have been the gymnast? Now obviously the answer is a bit of both but you are born, so your genetics will give you a particular fibre composition. Certain type 1, type 2 fibres distributed in a certain way, that is genetic. Right.

So yes, there's a genetic component to which sport you might necessarily have a product, you know? Yeah, yeah. Predisposed to. That's the word I was looking for. But you can tweak those fibres through your activity. So let's just say you might have huge amounts of type 1 fibres

you know, for endurance, but you go and you go, I'm just going to do resistance training like crazy and go in the gym. I'm just going to do power lifting training. You can tweak those fibers so they become more glycolytic, but they will never be true type two fibers. And so you, it means that your composition isn't determinative and

But it really does... Do you think it could if you were to artificially taken hormones? Like if you were to... Because we know with ageing where there is a reduction in certain hormones that you do shift away from type 2 to more type 1 and that's where it's advised that...

As we get older, we should probably engage a little bit more with resistance training to kind of hold the type, more type two fibres longer. But do you think that if you try to work on a,

higher scale and increase those hormones that they could assist in those. Look, I would never say never because biology is weird. And any time in biology you say an absolute, you'll be proved wrong. So to say that you can never fully change a fiber type, I would never say that.

Well, I think I may have actually said that, but I would say that... You just mean exclusively, like binary. Yeah. It's kind of a continuum where you will have a mixture of. Yes, exactly, in that it's not black and white. Like we said before, it's got to do with...

the abundance of mitochondria and the capillaries and the amount of myoglobin and the myosin ATPase activity, it's not like, oh, the type two fibres have no mitochondria and the type one do and there's no capillaries. So it is a continuum in the sense that which one is it more like, right? Which one does it tend to push towards? Okay. So they're the fibre types.

Let's just finish off here, Matt, talking about just the speed of contraction and the force of contraction. So firstly, if we talk about the speed of contraction, we sort of already highlighted it. The factors that contribute to that have to do with the amount of calcium that gets released. Yep.

You said earlier if you just flood the cell with calcium from the sarcoplasmic reticulum in a well-timed manner, you're going to get a faster contraction and a more forceful contraction. But it also has to do with what we said earlier about that myosin ATPase activity. So the more rapidly you can hydrolyze or split ATP –

the faster the contraction can be. And like we said, the type 2 fibers, the fast twitch, they do both of those things very well, hence why they tend to have a faster speed of contraction. Now, I'm going to ask you a question here. For force of contraction, there's four factors that determine the force of contraction. One, it's the number and types of motor units recruited.

Two, it's the initial length of the muscle contributes to the force of contraction. Three, the nature of the neural stimulus of the motor units contributes to the force of contraction. And four, the contraction history of the muscle contributes. So can I ask you on each of these your interpretation of what this means? I'll contribute. But the first one, force is determined by, number one, the number and types of motor units recruited. What are we referring to here?

So this again goes back to what I was saying with my research. As we increase the stimulus in the nerve, so more of the nerve is now activated under...

causing action potentials within the nerve fiber itself. Because remember, the nerve fiber is a bit like the muscle fiber, that a whole sciatic nerve is made up of bundles of nerve cells. And if not all of those fire, because there's hundreds of thousands of those, right? So not all of them are firing together for an action potential to stimulate the quadriceps, let's say.

Now we'll say the hamstrings, right? So they're not all stimulated. But if you were to maximally stimulate all those nerves in the sciatic nerve...

then you'd get a maximum contraction in the muscle. Does that make sense? So what determines which ones? So if you grade it, so if you... But which ones are going to be stimulated first? Yep, so the slower ones would go first. So the ones that would be innovating the slower fiber types, the type ones. Yep. And again, this is that kind of lazy principle. The size principle. Yeah, just do as much as you need to.

But as you need to get more force out of the contraction, you would start to increase the number of nerve fibers being activated. So again, we would do that. We would grade it up to, we would look for the response in the muscle until we get to what we call a maximum response where we're not getting any more force out of the contraction. And that's telling us now that all the motor units are recruited. We're not going to get any more force.

strength of contraction out of that one burst of stimulation. Yeah. So if I, so if I wanted to, let's say lift this drink bottle up and bring it to my mouth, um, you start by recruiting the, in a way that the smallest fibers, um, or smallest motor units, I should say, um, which tend to be those that generate the least force. And as I need more, I recruit

more numbers of motor units but also different fibre types starting with the slow twitch and moving to the fast twitch. So in a way if you were to put a TENS machine on your biceps, right?

We all know what a TENS machine is? Yeah. Okay, so I don't explain it? No, I don't think so. Just the patches that have electrical wires going to it. There you go. Explain it. You can turn it up. So if you had your hand on the bottle and I put two patches on your bicep and then I was to turn up the force, how much electricity is going into your muscle, if I had it on a lower force, it

you might just, your hand might just increase a little bit off and the bottle just comes off the table a couple of millimetres. But if I really turned it up and put a lot of current into your muscle, it may be enough for that one twitch to bring it almost to your mouth. Yeah. But I think the point we need to highlight to people is that

As you, you know, because we're talking about how we have the forces determined. One, the number is that is, you know, you start with fewer motor units and those are the ones that innovate the slow twitch fibers that generate least force. And then as you require more force, you generate more motor units and

And those motor units start to shift from the oxidative to then, or the slow to more of the fast twitch. And so that's what we mean by number one, force is regulated by the number and types of motor units recruited. All right. The second point here is it's force is determined by the initial length of the muscle. What does that mean? Well, can we just jump that one for a second and do the third one just because it fits nicely with the first. So the third one is frequency. Force is determined by the nature of the neural stimulation of muscle units. The frequency of it, right? Yeah.

Firstly, explain what you mean there. So instead of the first example I gave you, the TENS machine, which was a one-off twitch where I just put one impulse of electricity into your muscle and you had that one twitch contraction. That was it. If I kept the stimulation coming in frequency, so if I just increased those pulses more frequently instead of just one-off, now I repeat it.

two, three, but then I put them closer together. So now they're happening more frequently. As I'm doing that, that's summating the muscle contraction. So it's going to continue to contract like in the quicker pulses all the way up to the point if I just keep dialing up the frequency to the point where the whole muscle was just kind of locked on. So this is why I didn't like your TENS machine analogy before because you said increasing the current, which is so...

So we need to clarify the fact that when you send a signal, it's all or nothing, right? And we spoke about it, that an action potential, it's not about the amplitude. So how much electrical signal is sent. So the amplitude, so more current, it's about the frequency of each signal that's sent. So when Matt's talking about turning up the TENS machine,

He's not saying I'm sending in more current, meaning it's just more electricity. That's why I didn't like it because it makes it confusing. Do you know what I mean? So effectively when your brain sends a signal out, it's not sending more current. It's just sending more individual action potentials in a shorter period of time. So you send a single action potential, you get a twitch, a small little contraction. But if you send 10 action potentials,

you're going to get more of a forceful contraction. If you send 100 action potentials within the same time period, right? So let's say in one second you send one action potential, you get a twitch. You send 10 action potentials in one second, you get a stronger contraction. Send 100 action potentials in that one second, you're going to get a far more stronger technique contraction. Sorry, I just think that's an important clarification because it's not about the amplitude. Yeah.

So that was number three. And that speaks to the condition we term tetanus, which comes from an exotoxin of a bacteria that then changes the neurological properties and that leads to the muscles being constantly contracted and that is how the person ends up dying is because they go into tetany, which is...

The full muscles contract up and that's probably a horrible way to go out. Sounds pretty bad. Number two, we go back to number two, which is the initial length of the muscle. So how does the initial length of the muscle determine the force that it produces? Yeah, so depending on what the resting state of the muscle, so if you were to think about doing... Can I ask a question to you, right? So...

You go to the gym. So if right now we're in the gym and I said, Matt, we're doing biceps today. I give you, let's say 15 kilos of a dumbbell. And I said, one rep max. Yeah. So I'm saying, okay, I want you to put your arm at full extension. Right. So there's, there's no angle at the elbow, right? Full extension and perform a full bicep curl so that the bar, so that the dumbbells all the way at the shoulder. Right. Okay.

And then I say, now you're starting. And then I get you to rate how difficult that was. And then I say, now I want you to start with the elbow bent 90 degrees, right? And then perform the bicep curl. Which one was easier to perform? Which one was harder to perform? The second one would be easier. Okay. Now use that.

Does that help to explain it or not? Yeah, so if you were to try to contract a muscle and get the most force out of it when it's fully stretched, the way that the actin and the myosin are arranged because it's really stretched out, the amount of binding sites that are available from the myosin heads on the actin is less. There's less overlap. There's less overlap, so the less ability to do those power strokes therefore generate force into that.

But if we were to, if I were to give you the, the dumbbell and say, okay, I just want you to be like 10 degrees off full contraction at your shoulder. Are you going to generate huge amounts of force at that? You know, if, if you had already contracted, let's say 90% of the way,

you wouldn't generate a lot of force from there. No, it wouldn't be similar. So there's sort of like either end of the spectrum, it's not optimal. No, that's right. And in this case, they're acting so close together they start –

butting up against each other and they can't continue the contraction any longer. So that little clicking sound you heard, guys, was Matt butting his fists together. Beautiful, beautiful visual analogies for people. For a podcast, yeah. All right, and then the last one, Matt, is the contractile history of the muscle. What does that mean?

You'd have to talk to me about this one, I think. So the contractile history. So what is the muscle? My muscles lose all the history. Just like your brain. Well, what has the muscle recently done? So if you've just, let's say, I've already done 12 sets of bicep curls with, you know, 20 reps each set. The history for that muscle is fatigue, right?

So I've generated. Yep. I always get fascinated when I watch the level of warm-up that athletes do before an event. So I recently went to the rugby, this is a rugby union, and I watched the warm-up of these guys and I'm thinking to myself, this warm-up is so intense. That's your workout. That I would be buggered before the actual game begins. But what you're saying here, this is the history, that this actually makes their –

their efficiency better in the game. No, I didn't say that. No, I didn't say that at all. What I said was that if you've done, you know, 20 sets of 20 reps of the biceps, your history has been fatigued.

So you've just accumulated a milieu, microenvironment of hydronions, inorganic phosphates, and it makes the muscle less likely to be able to contract and generate force. However, now to your point, there is something called post-activation potential in which you can do a degree of exercise, like a warm-up, for example, which potentiates the muscle to generate more force. So again, just like we were talking before with the length, the optimal length,

You need to find a middle ground, not one end of the spectrum or the other. The same when it comes to the contractile history of the muscle. You don't want to have contracted it too much, but you also don't want to have contracted it not at all. You want to have performed some contraction on that muscle to potentiate it. And that's where you were saying with the footy players, they've done a degree of post activation potentiation and

which is basically just, it's not just warm the muscle up, it's gotten it used to contraction. And so it allows for it to generate more force for each contraction that it undertakes. Does that make sense? It does. I think, have we done? I think we've pretty much covered a lot in this space. Matt, you did a good job. I'm proud of you. Thank you. I mean, not fully proud of you. I mean, probably not proud of you at all, but.

Thanks for turning up. It is a public holiday here today, so you didn't have to be here. You know what today's public holiday is? Labor Day. And you know what happened on Saturday night? What happened? We had an election and Labor won. In your house? Oh. Very convincingly. Can you tell our international listeners who the Labor Party is?

The Labor would be, I guess, the best example is to compare it to the American system just because everyone knows generally the American political situation. I don't know if Americans know the American political system. I'm not going into that. But you would say the Labor Party are more like the Democrats, whereas our Liberal National Party is more like the Republicans. But strangely enough, our Liberal Party aren't... A little bit more conservative. ...are right-wing.

Well, more right wing. Right of centre. Even though they're called the Liberals. Yeah. And our Labor Party is more left wing. Yeah. Of centre. Yeah. Historically. Yeah. I mean, I think now just like every other, you know, Western democracy, it's all blurred and merged. It's changed quite a lot. And who knows where they all sit on that political spectrum. But we did have- A landslide. We had a situation where it was predicted for a long time that Labor would-

Not get decimated, but they would lose their majority. So we had a Labor government leading into this election, but we thought it wasn't going to last. And we had the voting and then what happened? Yeah, it was...

to Labor. But what happened to the Liberal National Party, the LNPs? Well, at least the Liberal component of it, they lost a lot of their seats. A lot? Like decimated? The National's still done relatively well. They're more for the regional rural parts of Australia but the Liberals which were more in urban seats have been...

removed quite significantly. Yeah, which is interesting because no one expected this to happen. No. And usually an existing – I think it's a bit like the Canadian effect, which I think from what's happening in America with Trump, it's kind of reversed in both Canada and Australia. Yeah, I think this possibly is people making an anti-Trumpian statement. Yeah.

Maybe. Maybe. I don't know. It's too hard to know with – I mean, you're listening to this podcast not because – That's why we're biological science, not political science. We don't know what we're talking about, guys. Please know that. Also with history. And the English language. History and geography. History, geography, – you know what? Outside of biology, don't listen to us.

I don't think that's fair, isn't it? To be honest, there's some things in biology you probably shouldn't listen to us talk about. Anyway, Matthew, thank you. Thanks for having us again. In your own house, that's no problem at all. Or car or treadmill. Let yourself out in the way. I want to – Any final updates? Yeah. Thanks. And I'll see you all soon. Bye. Bye. Bye.

♪

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