Exercise Physiology | Respiratory System (Part 9)
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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, joined by my co-host, an extinct 65 million year old Tyrannosaurus Rex. Welcome T. I didn't want to believe my dad was stealing from his job as a road worker, but when I got home, all the signs were there. That's one of your better ones. That's one of your better ones.

How are you? Good, good. What's happening? It's cold today. Yeah, I mean for Queensland. We are recording early. My old man called me just before when he goes, first thing he said on the phone was, it's bloody seven degrees. And I go, yes, that's Celsius, yes. Well, I don't think we've ever hit seven degrees Fahrenheit here in Queensland. I don't know what that would even be in Celsius. Is that below zero? Yeah. Okay, like well below zero?

I'm sure. Probably like negative 15 or something. Okay. It's never been that. Matt, we are going through our series, our special edition series focusing on exercise physiology. And we're up to, God, whatever episode it is, on the respiratory system. So respiration during exercise. Yeah, it's something. I think it's nine. Nine.

I've done a fair few. So now we're looking at what does the respiratory system do to help support exercise, but also how does the respiratory system respond to exercise? So to begin, Matt, question for you, my friend, is what is the role of the respiratory system during exercise?

Um, so specifically to deliver oxygen, we'd say to the muscles, exercising muscles. So getting the air from the outside world to the muscles. Okay. What about carbon dioxide? And removing them. Okay. All right. So that's pretty simple. Getting O2 to the muscles, removing it from, removing carbon dioxide from the muscles. Um, so to, to talk about this, there's four stages of what they term respiration. Um,

And, but before I talk about that, I want to define two important terms that people probably mix up all the time. One is ventilation. One is respiration. Colloquially, they mean the same thing, right? So you took somebody down the street, it's the same thing, but in medicine and in exercise physiology, very specific definitions.

So ventilation is the air that enters and leaves the lungs. So basically the air we just bring in and out. And respiration is specifically when gas exchanges across a membrane. Okay. So you need to understand those two. Do you get that, Matt? Yeah. So what happens if you use, say, pulmonary respiration versus ventilation? Okay.

Okay, so pulmonary ventilation for me would be bringing air into and out of the lungs. Pulmonary respiration. Oh, and pulmonary respiration would be exchanging gases at the lungs, between the lungs and the blood. Yeah, I think so. If you were to say pulmonary respiration, that encompasses both ventilation and the gas exchange across the alveoli. Yep. Whereas ventilation is just one part of it. Yeah, yes, exactly. So let's talk about these four stages of respiration.

The first stage is ventilation, bringing that air into and out of the lungs. The second stage is alveolar respiration or alveolar gas exchange, giving the oxygen from the alveoli to the blood and the carbon dioxide for the blood to the alveoli.

The third is circulatory transport. So actually, this isn't the respiratory system at all. This is the cardiovascular system. Not last week, last podcast. That's right, last episode. Using the cardiovascular system to transport these gases.

And then the last one, number four, is systemic respiration or systemic gas exchange, giving the oxygen from the blood to the tissues and from the tissues, carbon dioxide to the blood. And that's in today's context, the systemic is the muscle, the exercising muscle. Ah, good point. Yes. Yes. Great. Frame it. We're talking about what's happening, the interface between the respiratory system, the cardiovascular system and the muscle. So with that, all those four stages then...

That would essentially dictate your VO2 max. Yes, yes, which is going to be how efficient you are at delivering the oxygen to the tissues of the body. So basically it's like your VO2 max, which is the most oxygen you can extract out of the blood into the muscle, is a combination of how good your gas exchange is, how good your transport is, and how good your extraction from the blood into the muscle is and the utilization is.

From a tablism point of view. Yes, that's a great point. It's multiple organ systems working together is VO2, your VO2 max, not just the respiratory system, which I think a lot of people who aren't involved in exercise physiology don't realize. They think it's just, oh, how much can your lungs hold? I think is what a lot of people just think the VO2 max is. We've spoken about VO2 max before. We're going to speak about it more, not just in this episode, but in future episodes, because we've still got a couple episodes left.

But before we jump into any more, we need to talk about the structure of the respiratory system. So a lot of textbooks tend to divide it into whether you're talking about the structural organization or the functional organization. Do you want to talk about the structural organization and I'll talk about the functional? Okay, so structural would be the anatomical respiratory tract. Right. So from the start to the end. Right.

Meaning, how do you first get the air into your body or into the respiratory tract and how do you get it right to the point of gas exchange? Okay. Usually speaking, the respiratory tract is broken into an upper and a lower section. Yep. So sometimes you may have heard this when you refer to an upper respiratory tract infection. So what do you usually think of that when you hear an upper respiratory tract? Head cold. So these structures would be

The nose, the nasal mucosa, the oral cavity, the pharynx. And the pharynx is usually broken into three subsections. So that would be the nasopharynx, oropharynx, laryngopharynx. Yep. And where you would say the upper respiratory tract ends is the larynx, which is kind of your vocal cords. The voice box. The voice box, yeah. And everything below is the lower. That's right. Okay. So...

Do you want to talk about the, so in terms of the upper respiratory tract of these structures, do you want to talk about what they do or you want to bring that more into the functional organization? Yeah, we'll do that after we go through all of it. So then at the point of the vocal cords inferiorly, they're going down now, this would be all lower respiratory tract structures. Right. So you go from your vocal cords now, which is the larynx down to the trachea.

Or the windpipe or in America, trachea. Trachea. Trachea. Do the accent, Matt. Trachea. That's right. So then that goes into the thoracic cavity. Okay.

And then you would bifurcate it, so split it in two parts, and that would go into the bronchi. And they would continue to divide. So you have your primary, secondary, tertiary bronchi. Then you go into your bronchioles, and then you into your lungs. So the lungs is kind of the end point of your lower respiratory tract.

And the site of gas exchange, right? Yeah. Okay. So you've got... So structurally, the organization is upper versus lower respiratory tract. Upper going from the nose to the larynx, the voice box, and lower everything below that. So when we look at the functional organization, you split it not from upper to lower, but from a conducting zone to a respiratory zone. So effectively...

Because we're talking about the functional organization, it's what does the respiratory system and tract do functionally. And so it's either going to carry air or exchange gas. And that's effectively the conducting zone is carrying the air and the respiratory zone is exchanging the gas. So the conducting zone is going to be the majority of the

It's the pipes, the nose, the nasal and oral cavity, the pharynx, the larynx, the trachea, the bronchi, the various bronchi divisions, like you said, even the smaller bronchioles, which are basically...

bronchi that are less than a millimeter in diameter. They tend to have more smooth muscle, less cartilage compared to the bronchi and trachea. But what we find is that when we look at these conducting zones, they go all the way up to what's called terminal bronchioles. And that is the very last portion of the conducting zone. So again, all just pipes that carry air. The

The beginning of the respiratory zone is what we call the respiratory bronchioles and attached to the respiratory bronchioles are alveoli in what we call alveolar sacs. And this is where gas exchange occurs from individual and individual alveolus. So alveoli, plural, alveolus, the singular. Now, if we look at the conducting zones, these pipes,

The trachea is the largest pipe and we've only got one, but then it splits into two smaller bronchi, which split again into four and then again into eight. And then it splits into bronchioles, which we've got, you know, 16 divisions and then 32. And then the terminal bronchioles in which we've got

60,000. Right. So it's divided that many times. That's right. And they're very small, but they're very numerous. So what this tells us is that even though the pipe gets smaller, it gets more numerous. So the surface area actually significantly increases with every division of the pipe. But this is still the conducting zone. Still the conducting zone, but it's allowing us to be able to carry that air through.

Right. But then when we get to the respiratory zone where we've got now respiratory bronchioles and alveoli, we've got 8 million respiratory bronchioles, or more specifically 8 million alveolar sacs. Okay. Now that's not just the individual alveolus associated with each. So the alveolar sacs are like a bunch of grapes. So there's many individual grapes associated with it. So the alveoli, we've got about 300 to 350 million alveoli. Right.

Now, they're very small but numerous. So if we open it up and look at its surface area, how big do you think it is? Well, we spoke about this before. So it generally is –

Kind of tennis court size? Probably half a tennis court. Okay. About 60 to 70 square meters, which I think's- Up to 100 even. Yes, it can be. But yeah, 60 to 70 square meters on average, which is a huge surface area. And that's really important because we're going to talk about soon the size of the surface area can determine how much gas can be transported across, which makes total sense, right? Yeah.

Now, you were talking about before the function, right? So what are some of the things that can happen as the gas moves through these areas? So three main things, right? The first thing that your respiratory tract can do is filter. What's it filtering? So this would be, you know, the upper respiratory tract primarily, let's say, right? Yeah.

And so this is where you've got mucus membranes and they're very watery, so they would be humidifying the air. But they will also... So you've added a second one. So we've got filter and humidify, yep. But they also allow particles that are in the air that it's difficult to get rid of. That could be anything from dust to smoke to pollen, whatever.

To microorganisms. Yes. And that would get stuck on the wall. Because what the upper respiratory tract is trying to do, particularly the nasal mucosa with the turbinates is... What's that? What's a turbinate? It's the conch of your nasal...

Doesn't make it any easier for me. Kind of like seashells, I guess you'd say. So, you know, when you walk on the beach and you find shells that got the spiraling. Yes, I always go collect them.

Your nasal cavity have these as well. Three of them, superior, middle and inferior. And when the air comes into your nasal cavity, it kind of swirls it around in these kind of turbine-like... So they're sort of like grooves and divots in your nasal cavity. So when the air goes in, it spins it. Okay, what's the purpose of the spinning? Just increase the surface area of the air...

meeting the walls of the nasal mucosa. Do you reckon it also works as like a centrifuge in a way that it sort of throws any of the particles to the exterior? Maybe, yeah. And then it sort of allows for the... Okay, so we've got cleaning, we've got filtering. You said humidifying. So when we humidify air, we're adding more water molecules to it. Why would we want to do that?

to the air that we breathe? It's just when you're breathing in cold, dry air, it's an irritant to your respiratory tract and it would make you cough. Right. And it could potentially dry them out and damage them. Which could also change the properties of the gas exchange because you do want a little bit of film of, and we'll get to this with the properties of gas exchange or diffusion of gases. When...

You want a bit of film of water there. Yes. To allow the gas to dissolve, the oxygen to dissolve, but also the carbon dioxide dissolve in the alveoli level. Yes, exactly. Which you'll get to. So it can't dry out. Okay. So why do we want to warm the air? Um...

Yeah, good question. I guess, again, you just want it to be at a temperature that's the same as the inside of you. And it's more efficient for gas exchange. Yeah. So I think that's another really important point is that it makes it just more efficient to be able to exchange that gas once it gets to the alveoli. Okay, so now what we need to do is take a look at how we breathe, right? So how do we do this? What is the mechanism for breathing?

Being able to bring air into and out of the lungs. Can I add one final thing? Yes. With your conducting zone, and you went through from one pipe to 65,000 pipes, which is known as a conducting zone, and they're not going to play any role in gas exchange. What will happen in this region is you're going to have an area of gas that

movement. So the transport of the air that you're bringing into your lungs, but out of your lungs. So almost see it like a column of air that's moving down and back up. Yep.

About a third of that won't ever reach the alveoli, which means it's dead space. It's space that will never partake in gas exchange. So it's almost like useless air. So could an analogy be if I were to take a big, long two-metre pipe and...

and suck air in through it, that obviously I need to bring air all the way through that three metres of pipe. And so the air that's in the pipe itself, that's not being used for gas exchange. Like you said, that's dead air. So that's called dead space. Anatomical dead space, yeah. So anything in the conducting zone is dead space. Anything that doesn't reach the alveoli is dead space. And that's important, right? Because it can affect the way that we breathe and our...

When we start to do exercise, we need to take into consideration this dead space because it can affect the rate and depth of breath. Yeah. We'll talk about that. It's about one third of your tidal volume, which we'll get to in a second. Tidal volume just means the air that you, at rest, you're moving in and out of your lungs. So about a third of that. If you were to say your tidal volume is 500 mils of air,

About a third, so what's that, 150 mils is never going to reach your alveolar. Dead space. Yeah. Okay, let's talk about the mechanics of breathing. So how do we, so I always find this interesting because when I talk to my students, I say, listen, no one's pushing air into your mouth.

When you take a breath in, you take for granted the fact that you're sucking this air in. How do we generate the force to suck air in and then blow it back out again? And it all has to obviously do with changing pressures. So we need to talk about what does the respiratory system do to alter pressures inside the body versus outside to bring air in versus out. So firstly, if we talk about inspiration, right? And I'm not talking about the inspiration that you get when you listen to

Celine Dion on the way to work. I'm talking about the inspiration of bringing air into the thoracic cavity. We have what you could potentially call a closed box with one exit pipe, which is the trachea.

Now interestingly, if there's something called Boyle's Law, that if you increase the volume of a box, the pressure inside that box goes down. And the reason why is because if you've got, again, a closed box, there's going to be a certain amount of gas particles inside that box and they bounce off each other, they bounce off the walls, that gives the pressure inside that box. Okay. Then bouncing off each other. But if I were to just magically enlarge that box, okay,

I've got the same gas particles bouncing around in a larger box. So it means they're less likely to bounce off each other on the walls, which means the pressure goes down. That's pressure. Right? So when you increase the volume of a container, the pressure inside goes down and vice versa. That's called Boyle's Law. That's a...

Now that's an important concept to understand to get air in and out because our lungs and our thoracic cavity is like that container. So what we need to do to bring air in is we need to make the pressure inside that container lower than outside because as you know, you watch the weather every night.

when a high pressure system moves in, it always moves from a high to a low. So gas has always moved from whether it's a high gas area to a low gas area. So we need to make the gas inside lower compared to outside. We do that by increasing the volume of our lungs. And we do that if I want to take what's called a quiet breath in...

by contracting one really important muscle. What's that muscle? Diaphragm. That's it, baby. And is the diaphragm, and this is an important point to highlight to everybody, is the diaphragm a smooth muscle like what would line our digestive system and our blood vessels and reproductive tracts and so forth, or is it a skeletal muscle like the type of muscle that's attached to a skeleton to allow for conscious movement? Yeah, the latter. So it's skeletal in nature. Yeah.

So technically you could say it should be voluntary. Yeah. But it probably isn't. It's both. Yeah. Right? I mean, I think that we could probably argue that when we walk, even though it's volitional, there's some degree of subconscious movement that occurs. Yeah, reflex. Right? Like emotion control. And I think that it's probably...

it's probably similar for the diaphragm in many ways is that there's going, you can override it with conscious control of the diaphragm, but for the majority of the time you're not controlling it, which is probably a good thing. You don't want to. Yeah. I mean, even splitter muscles do this where if you shiver, you don't really have voluntary control over that. Yes. That's contracting. Again, when you listen to Celine Dion in the car and she hits that high note, it just makes you shiver. Yeah.

So the diaphragm contracts. Now the diaphragm is like this dome-shaped muscle that sits underneath the lungs. When it contracts, it pulls downwards to flatten out. And because it's attached to the lung tissue... Okay, so when you say attached, what do you mean by that? Well, one second. When it's attached, I will get back to that. Because it's attached...

It pulls the lungs down, which increases its volume, decreasing the pressure and air rushes in. Particularly the bases of the lungs, yeah. Now, to your point. So it's got tendons like skeletal muscles? Well, it's got connective tissue attachments. Okay. And there are tendons, but I think what we need to – and I'm going to ask you this question –

The diaphragm is attached to the lungs, but it's not attached to what we call the parenchyma. It's not attached to the alveolar sacs. It's not attached to the actual area of gas exchange. It's attached to sort of like an outer coating. So what is this outer coating that the diaphragm is attached to? Turned pleural.

And this would be, so there's a plural covering around the lung itself. So if you were to go into an anatomical cadaver lab. Yes. And saw, they sometimes term it the pluck, which is the lungs and the heart. Yes. So you can kind of see the lungs as these. Why do they call it the pluck? I don't know.

I think it's more to do with butchering. Yeah, probably something like that. When you pluck it out, it sort of all comes together. Yeah, yeah. That would be my guess. Yeah, that makes sense. If we're wrong, listeners do write in and tell us the real meaning of the pluck. So...

The lungs kind of just look like these floppy bags, depending on if they've been... Which again was the original name of Dr. Maddox. Yeah, that's right. So the lungs, depending if they've been fixed or not. So in a cadaver lab, they're usually being fixed with formalin, formaldehyde. So they're a lot more rigid than they normally would be. If you saw them in a live specimen or in a specimen that's just...

recently passed away, it would be squishy, squishy, still very much like sponge. Yeah, that's right. Yeah. And, and we do this in, in the prac labs in anatomy, anatomy physiology. We do it with lamb, lamb lungs. Yeah. Maybe not necessarily lamb. So they're fresh and we actually blow them up. We don't do the butchering. No, no.

So they blow them up and you can see them expand and then go back down. Yes. Plural, Matt. That's right. So plural. So this lung tissue wrapped around the outside of it is this film of tissue that looks a bit like glad wrap or cling film. Just this really thin layer. Transparent. Transparent. That makes it nice and smooth. Yes.

Now, if you were to look on the inside where the lungs usually would have sat, where the ribs are, but on the inside, it would also have that nice smooth covering. Wait, so you're saying there's two pleura? Yeah, two pleura. One attached to the lungs and one attached to the... Tracet cavity. The cavity. So you're sort of the chest wall. That's right.

Now, in the chest wall, you'd also have it on the- Are those two pleura attached? There's going to be a film of water between the two. Okay. And that allows for them to remain attached? Well, with the surface tension of water, it kind of makes them intimately connected.

But you could make an argument they're probably not attached. They're probably molecules of water between them. And it's a negative pressure inside. That's right. Always. So it always should be negative. But if for some reason there was an injury or some kind of...

that was put into the chest cavity like a knife or a bullet, that would then put a positive pressure between the pleural space and that would be a problem for breathing mechanics. Well, it means the lungs will no longer stick to the thoracic wall. That's right. So the only thing that's allowing the lungs to stick to the thoracic wall is the two pleural membranes and the fact that the two pleural membranes...

stuck together, not structurally, but functionally stuck together through fluid, but also a negative pressure. That's right. And also the inside of the diaphragm has that pleura as well. So hence why when the diaphragm pulls downward, it pulls the pleura and it's the pleura that pulls the lungs. So when we change the volume, we're effectively pulling the pleura. Yep.

That's right. Pulling the pleura and pulling the lung tissue with it. And the lung tissue is very elastic in nature. So when you breathe through your diaphragm or maybe some of the... Via your diaphragm, not through your diaphragm. Yeah, via the diaphragm or sometimes with the intercostal muscles. And so you're trying to pull your chest out.

it's almost like a tug of war between your respiratory muscles versus your lung tissue. And they're having this pulling versus an inward pull. That's right. They're having this battle, but usually when you inspire the battle is won by the respiratory muscles. Right. Right. Uh,

So we contract the diaphragm, pulls down. So this is what we call a passive inspiration. So if we take a breath in, a quiet breath in, that's what we call it, or a passive breath in, it's just the diaphragm contracting, pulling downward. And that's important because as that volume increases, the pressure inside goes down, air rushes in. How much volume-wise is a quiet breath in?

Both in and out, it's 500 mils. And what's the term used for that? Tidal volume. Okay. So we've got our tidal volume. So that would be a volume. So sometimes in pulmonology or respiratory medicine, they would measure a whole lot of different volumes and capacities in your lungs. That would be the one that you do at rest, which generally speaking is about 500 mils. Okay.

Okay, about half a litre. All right, so we know that sometimes we need to bring in – so half a litre is enough to bring in for what we're doing right now. Yeah. But if we want to – because today's topic is exercise and people are probably going, when are you talking about exercise, you idiots? Well, hold your horses. Don't be so rude. When we want to take a breath in deeper than 500 mils,

We have to recruit accessory muscles and you alluded to an important set of them, which is the external intercostals. So these muscles are attached between the ribs on the outside of them. When they contract, they basically flare the rib cage up and outward. Like you said, because there's a pleura attached inside the rib cage and that pleura is attached to the lungs, the lungs are pulled outwards.

you know, outward. And so again, further increasing the thoracic volume, further decreasing the pressure in the lungs, pulling more air in. Now you can just keep recruiting more and more muscles like the sternocleidomastoid attached to the sternum and the clavicle, which is then attached to basically your jaw. And then you contract that, you lift

the rib cage further up. You can have the scalenes attached to what? First rib. And then you've got your pec minor. Pec minor as well, attached to the top ribs. Again, further flaring the rib cage out. So these important accessory muscles allow for us to breathe more air in. So multiple litres of air able to come in on top of that half a litre. All right. So when we want to just expire or breathe out or exhale,

If we want a quiet or passive exhalation, we just relax, right? Yeah, and so it's that elastic recoil of the lung tissue that allows it to do so. So you just turn off the diaphragm and that tug-of-war battle...

then goes to the lung and the lung does all the recalling and all the air. Well, the volume decreases, therefore the pressure increases, therefore the air wants to go from the lung back out to the atmosphere. So this elastic tissue is obviously important. So when you take a breath in, you're stretching this rubber band. And then when you want to breathe out, you just relax the rubber band for it to snap back. That's right. And there's conditions, however, which is important for exercise, which can affect this elastic recoil, right? Yes.

What conditions can do this? One of the big one is emphysema and that's generally through a long period of smoking tobacco, tobacco smoke, and that kind of destructs the elastic properties of the alveoli because the alveoli, even though they look like, you know, like strawberries or raspberries where they kind of got...

multiple bumps to it. You didn't like my grape analogy. Well, grapes are smooth end, whereas these avioli sacks with their multiple avioli to it, they kind of got multiple bumps on it. Yeah, they're all stuck together as well. And that's bumps.

are kind of intertwined with a whole lot of elastic tissue. And in emphysema, all that elastic tissue is taken away and then it actually comes to look a little bit more like a grape. So instead of these multiple little bumps that could be 300 million in total, it's now just a single one, which you now lose a lot of surface area with, but you also lose recoil. So it's the difference between...

blowing up a balloon and then letting it go and all the air will disappear as it flies around the room. You do the same thing, but do it with a paper bag. Yeah. And does it empty? No. It just stays big. And that's what essentially happens in emphysema. Yeah. They,

A whole lot of air remains in the lung. I use the analogy that, you know, when you have like an elastic or rubber band, right? You've got a brand new one where you stretch it and it snaps back really well. And then you've got one where it's been stretched so many times that the elastic is sort of worn that it's really easy to stretch, but it,

snap back very well. Like your underpants. Yes, like my underpants. That's right. And my wife would agree. They've got holes in them as well. Okay, that's very different to emphysema.

but it stretches really well, but doesn't snap back well. And that's actually important because it means that they can breathe in, but breathing out is probably a little bit more difficult. That's an aside though, because it's exercise physiology. Yeah, but this is important because exercise physiologists are going to be working with people with chronic obstructive pulmonary disease or CPD. Yes, you're right. And then you have to tailor their exercise program for this. Yes.

Okay, we'll get back to that when we talk about gas exchange because I think emphysema is good to highlight that the smoke does help destroy the elastic tissue but it also...

damages the surface area, which we'll talk about for gas exchange. But let's talk about breathing out. So the elastic recall and just the relaxation of the inspiratory muscles allows for the exhalation. But sometimes we want to forcefully exhale because during exercise, we accumulate carbon dioxide. So sometimes we need to really breathe out to get that CO2 out of the body.

And we recruit, again, accessory muscles to do so. So primary or even secondary exhalation muscles. So these include the abdominal muscles. So the obliques, for example. Rectus abdominis. Rectus abdominis, external obliques. The internal intercostals.

They sit deeper within the ribcage compared to the externals and they do the opposite. They basically drop the ribcage inward. But then you've got –

Well, they're pretty much the major muscles associated with it. And they just reduce the volume because when you contract your abdomen, you do that crunch, right? And your thoracic cavity drops. The volume, the size reduces. Okay. So all this is important because in exercise, like we saw with the cardiovascular system, what makes an athlete more efficient in cardiovascular output is their stroke volume.

At least a big part, right? So redefine, just in case our dear listener didn't listen to the cardiovascular one and they just want to do this one. So just very quickly, soundbite,

What is stroke volume and tell the difference between the stroke volume for an athlete compared to a non-athlete? So essentially we're talking about cardiac output here. This is the amount of blood that the heart can pump out per minute. Right. Now, cardiac output is a combination of heart rate. So how fast your heart's beating versus how much blood can come out per beat. And that's the stroke volume. That's the stroke volume. Now, generally speaking, athletes or trained athletes,

trained individuals, they can... Matt's pointing at me, by the way. You don't have to do that, Matt. We have a video record of this, but that's kind. Put your hand down. So the stroke volume in trained athletes, they can just get more blood out per beat.

Which means they are more efficient at each heartbeat to get an amount of blood out the body, particularly in exercise. And that's why they're resting heart rates lower because they don't need to. So for an untrained person, when they exercise, they need to get more blood out and around the body. But because they haven't trained the heart muscle, they're not able to do that.

the only way they can really do it is by increasing the heart rate, right? They can't change the stroke volume. So effectively their heart's working harder, which is then subject to fatigue. Yes, but when you're an athlete, every contraction, because the muscle is bigger and stronger, it ejects more out. So you basically have that. And then when you really need to increase heart rate for exercise, you can. So you've just got a greater capacity. All right, so why were you bringing this up relevant to breathing? So when you're breathing in exercise, one,

One of the first shifts that you start to see is... So in breathing, we've got just like the heart, we've got the rate of breathing. So how many breaths we take, but also the volume with each breath. So very similar to cardiac output. And that's termed tidal volume, which is equivalent to kind of stroke volume. Okay. So...

So how many breaths should we, so we generally take 15 breaths a minute? Yeah, say ballpark 15, 12 to 18, but 15 is a good middle one. And half a liter with each of those breaths. Okay. And that's given us our ventilation, our expiratory ventilation number, which is like our cardiac output. Yeah. So let's just say seven and a half liters per minute.

is our lung equivalent of cardiac output. Yeah, that's right. Yeah. What we call it, I think we call it our ventilatory expiration. Right. Okay. So, sorry, go on. What were you saying with the exercise? So when you start exercising, at least in the moderate sense, what you'll be increasing...

in the immediate term, is the tidal volume. Now, the way you can do that is recruiting all these additional muscles. So it's not just the diaphragm now, it's the additional ones like the external intercostals plus the ones higher up that you spoke about. And then you also have to force the air out, so you're using your abs and those associated muscles. And that allows for more volume of air to be moved in and out of your lungs. So when I start exercising from rest...

My rate isn't necessarily changing, first of all. So I'm not... Not as much, no. I'm not doing necessarily more than 15 breaths a minute, but I'm doing deeper breaths. That's right. Right. Okay. And you're kind of utilizing more lung tissue or lung volume to be inspiring and expiring. Now, important point here. If we were to...

Because you could make an argument that, oh, okay, so what if we were to keep the depth of the breath at half a litre but increase the frequency? How many breaths? That wouldn't be as efficient for us during exercise than the depth of breath. Why? A couple of reasons. Because you're breathing at a higher frequency, you've still got that same amount of dead space air, so you're not getting a percentage increase of breath.

gas exchange you're just moving it quicker through the dead space you're basically just exchanging dead space air quicker yeah and you're getting the same amount of gas exchanged at the alveoli yeah that's right yeah and another drawback here is because you're you're making your respiratory muscles work harder they're now subject to fatigue as

And that's going to be a limiting factor on performance and how long you can continue in duration and intensity. Wait, so you're saying my diaphragm, because you don't think about this. Your diaphragm is a skeletal muscle. And as we know, like I've seen you in the gym before.

Albeit once, but when you were weight training, your muscles fatigued relatively quickly. But if the respiratory muscles, such as the diaphragm, if that's a skeletal muscle, that's subject to fatigue as well. Correct. Right. So it is, I assume it's very much like a type one oxidative fiber. Yeah. But this can be trained and this is probably the one area where you

Let's say more endurance aerobic training can make your respiratory system more efficient. Generally speaking, unlike the heart, when you become more...

Yeah. As we spoke about a few minutes ago, where you get a more efficient heartbeat, more stroke volume. You get structural changes. You get structural. The lung tissue doesn't change structurally. It's generally what you're born with is what you'll be with even if you train. That's interesting. Because anatomically, it's not going to change. I mean, if you get lung disease, it will change. Sure. But generally, athletes won't get a bigger lung tissue, like more pipes or...

Or larger viola sax. Wider pipes, yeah. Yes. I think that's an important point. And people might sit there and go, but isn't the respiratory system an important rate limiter for exercise? Because a lot of people say they'll do exercise and they're gassed, right? You go, oh, yeah, I'm gassed. My respiratory system couldn't keep up. That's probably, if we're talking about submaximal exercise, right?

So mostly the respiratory system is not your rate limiter. No, no. There's a lot of redundancy in it. Well, that's exactly right. And I think that was the point I was going to make is that effectively your, your respiratory system is overbuilt for its function. So it's,

a young, healthy, fit athlete, their lung tissue, the parenchyma, the pulmonary system itself, it's absolutely fine to match the performance that they require. The only probably notable exception to that is probably 10% of even athletes have a degree of asthma or exercise-induced asthma.

And that's just a kind of hyper responsive airway, particularly to exercise or to other stimuli, which then narrows it, which then would impact it. But you can kind of negate that or manage that with bronchodilators like salbutamol.

Can we just talk about that airway resistance a little bit, right? So we spoke about the functional organization of the conducting zone and then the respiratory zone. Even though you start with big pipes, but few of them, and we go to smaller pipes with many of them, those smaller pipes are covered with smooth muscle, right? The bronchioles, they've got a lot of smooth muscle. So they are...

They have the ability to change diameter. And so if somebody has asthma, and let's just say it's exercise-induced asthma, in which whatever the stimulus... Do we know what the stimulus is? I mean, we know that there's... Well, it can be activity, but it can also just be the irritation associated with the air movement. Yes. But also temperature changes. Yes. But it's usually... I don't think it's a topic like...

Other kind of allergy-induced asthmas, I think it's just the stimuli behind exercise can cause kind of a reactivity in the airways. It could have an association with kind of the same inflammatory mediators like what mast cells release and leukotrienes and stuff like that, and exercise can be an inducer of that.

But my guess would be it would be a different kind of background mechanism as what you would see in an allergy-induced asthma or atopic asthma. And so when you get that asthma attack and you get the narrowing of the airways, like we spoke about in the cardiovascular system, that law, which I always have difficulty pronouncing, Porcelli's law, Porcell's law, effectively says if you have the diameter of a pipe

you're actually increasing the resistance by 16 times. Now with the respiratory system, you've got all of these little pipes that will drastically affect gas exchange. So when we think about what is needed for the respiratory system to match exercise performance, we need patent or open airways, right?

an efficient gas exchange. We're going to talk about gas exchange in a second. But one part here is that the movement of the gases need to occur. So any blockages which could happen pathologically, so chronic obstructive pulmonary diseases, COPDs, emphysema, chronic bronchitis, they can narrow the airways. But also asthma can narrow the airways even though it's a reversible condition.

But in a second, we're going to talk about gas exchange because that's the second important thing that can limit exercise performance. And the last thing I'll just say with respiratory muscle fatigue, like we saw with muscle fatigue when you're performing an exercise as the metabolic response,

increases in the muscle because remember a few episodes ago when we spoke about how does an exercise in muscle get its blood or change the proportional blood to that area and it's a combination of autonomic nervous system with hormones and

plus all the metabolic products that the muscle is spitting out changes the flow to the muscle, which hopefully matches more blood flow, therefore more oxygen and energy, molecules, et cetera. And then at the same way, taking all the byproducts away because they can become toxic, right? Yeah.

The same thing happens with respiratory muscles. As they're fatiguing, their metabolism is going up and probably coming more anaerobic, right? And therefore, they are getting more proportional blood flow to them. Yes. Now, why that's important, well, if you're performing an exercise, then you're taking blood away from the exercising muscle. Yes. To the respiratory muscles. So now your efficiency is dropping. Yes.

That's a good point. So you've only got a certain amount of blood in the body that you've got to divvy up. And if you're sending it all to, you know, the quadriceps for running, but then you start to tax the respiratory system. So the diaphragm and the intercostals are going, Oh, I myself need more blood. Yes. You're taking. It's the divert. Right. That's a good point. And then, and then efficiencies drop in. So therefore, if you become more efficient, so you train, then you're,

respiratory muscles become more oxidative, meaning they're better with using oxygen more efficiently. Exactly right. All right, let's talk a little bit about pulmonary volumes and capacity. So we can talk very briefly about pulmonary function tests, and then we can talk about gas exchange. So this is important for exercise physiologists to understand is that

Matt spoke about tidal volume being half a litre in, half a litre out. So I'm sure that if you're a student listening to us, that you've seen this graph of squiggly lines that is called the spirograph or the

What would you call it? Spirogram. Yeah, spirogram. Effectively, it shows the half a litre in, half a litre out. That's tidal volume. Now, Matt, if I asked you to breathe in a normal quiet breath in the tidal volume, do that for me. Okay. Now, I want you to breathe on top of that as much air in on top of that quiet breath in. Very good. Very good. So what Matt's done is he's just...

breathed in what we call the inspiratory reserve. Sounded like a jet fighter taking off, didn't it? Yeah. Yeah, Matt, it did. It did, buddy. So that's called the inspiratory reserve volume. That's the amount of air you can breathe in on top of the title volume. Do we know how much that is generally speaking volume-wise?

For which one? Inspiratory reserve as well? Yeah. 3,000 mils? So about three litres on top of that half a litre. Okay. So then I say, Matt, just breathe out normally and you exhale. So you will exhale that tidal volume and that inspiratory reserve volume. But then I say, okay, I want you to now breathe out every drop of gas that you have in your lungs. Go. Okay.

Wow. That's SpaceX taking off. I feel sorry. I should have warned the listeners, turn the volume down before Matt did that. That's called the expiratory reserve volume. How much can we breathe out for the expiratory reserve volume? Liter to liter and a half. Okay. Now, is that all the... So if we add it up, right, the...

uh, expiratory reserve volume, the tidal volume and the inspiratory reserve volume. So that's basically vital capacity. All right. So that's everything that you can forcefully blow in and out. Yeah. So a vital capacity is the maximum amount of air that can be expelled from

After maximal inspiration. So everything you did? Yes. Breathe in as much as you can, breathe out as much as you can. That's vital capacity. When you breathed out as much as you can, did you actually breathe all the air out of your lungs? No, there's going to be some that remains. Why?

Why? Why? Tell us. Hurry up. Well, you've got tubes and pipes that are rigid and you just can't- Oh, speak for yourself. Mine are floppy. You just can't collapse them all in. So there's going to be air remaining. Explain, explain, explain. No, say that further. So I take a breath out. It doesn't matter how many muscles I recruit. I can't decrease the volume of my thoracic cavity enough to increase the pressure enough to get all that air out. That's right. But that's important. We don't ever want to do that.

No, because then you deflate the lungs. Yep. And then you probably wouldn't be able to reinflate them in the next breath. And you also probably need some gas remaining in there for some degree of gas exchange to occur. Let's just talk about that point that you made about lung collapse from exhalation.

When we look at the 300 to 350 million alveoli, they're very small balls, right? I won't make a joke. Now, these, if you have a look inside because- I was in the pool. Yes, it's winter. God. All right, George Costanza. If you have a look inside each of these alveoli, they're lined with water.

And the thing about water is it's actually on a molecular basis. It's very sticky. Now we might think it's not sticky. I drink it all the time. Honey's sticky, glue's sticky. But if you look at water microscopically,

Water molecules love sticking to other water molecules. I mean, this is how trees, very tall trees, get water from their roots all the way up the top through what's called capillary action, allowing the water to drag more water above. And we see that when we fill a cup up, it forms a meniscus. That's sort of the water. Looks like it bubbles up the top without it falling down the side. You see those games on TikTok where they...

Have a big line of people and have to add a couple more drops to the glass before it overflows. Yeah, whoever breaks the meniscus gets a slap in the face with a bit of pita bread or something. So, because that's how TikTok works. Um...

My point is water's sticky. So if you were to breathe out all that air, the alveoli, they do start to collapse. And they would collapse. And they would collapse. Now, because there's the water lining the inside, the water would stick to each other and it would be, you do not have enough muscles in your body to reinflate those alveoli. Effectively, it's like trying to

crush a ball bearing in your hand. Like it's, it's, it's that tough. Oh wow. I don't know if any of our listeners have ever performed any research, let's say, uh, micro use microscopes, but I don't know about you, Matt, but I remember this one day in the lab when I was doing my PhD, uh,

I had a microscope slide and often you need to put some fluid on it, some oil or whatever it might be. But I remember that I was cleaning the microscope slides because we had to reuse them. We didn't have the money to buy new microphones. So, you know, I'm cleaning it with ethanol and water, but I was cleaning it with water and I dropped it on the smooth lab bench and it had water on it. I could not for the life of me,

peel it up off the bench. I had to slide it to the edge of the bench before I could lift it up. Get air into it. Because yes, because the water, the sticking of that, and that's how the pleura basically works, right? So the point I'm trying to make is the alveoli would collapse. Now, luckily the body produces all the alveoli, there's cells in them, which I think are called type two pneumocytes. What do they produce?

A detergent or a surfactant? Surfactant. And what does the surfactant do? It just breaks that water tension. Yeah. And okay. Again, I know this is exercise physiology, but a bit of clinical, why is this important for people to understand? Well, clinically it's important because, um, babies that are born premature, their type two pneumocytes haven't matured yet. Generally pre six months. So they haven't. Yeah. So kind of in the early 30 weeks, this could be a problem. Um,

And so they haven't matured these cells, so they're not producing surfactants. So when the baby's born...

their alveolos stick together and they go into a distress syndrome. Yeah, they take their first breath in and then their first breath out and they can't reinflate. And the poor bubs don't have enough muscles and they haven't used those muscles either really. Maybe practicing using those muscles through hiccuping. Yeah, apparently that's a theory of why we hiccup. Matt and I may be writing a book that might just allude to a little bit about what a hiccup is.

But, okay, so where were we at? Okay. So the treatment of that would be mechanical ventilation. Oh, yes. But also I think they have artificial surfactant spray now that they put into the premature baby. Yes. And it doesn't take long for them to produce that surfactant after the fact. Okay. So we spoke about vital capacity. So-

Because you said there's still gas left over in our lungs. It's called residual volume. Okay. So everything, so the vital capacity plus the residual volume is effectively everything that the lungs can manage. What do we call that? The total lung capacity. Beautiful. What's the volume potentially for the total lung capacity? Is it like six liters? I think it's something around that.

But it's important to note here that this is all relative to age, body size. Yeah. There's a bit of racial difference in it as well. So I think certain ethnicities have just a bigger thoracic volume, so they're going to be different. Yeah. So this is important to, when you do a spirometry, that's why they ask you for these kind of democratic definitions.

These questions about age, gender, background, height, because that's going to be different. Or communistic, I suppose. That's right. So you're comparing yourself to someone more like you, opposed to, you know, my capacity is going to be different to your capacities because I'm taller than you. Oh, because you're going to say you're a redhead. So have you done your... Were you a respiratory... You weren't a respiratory scientist, were you? You were a sleep scientist for a little bit. I worked in sleep science, which is...

Closely tied to respiratory medicine. Okay. So did you do a number of these? No, no. Okay. But we did these a lot in physiology. Yeah. Okay. So let's talk a little bit about the spirometry testing, right? You said the vital capacity is the amount of air that you can forcefully inhale and exhale. Yes.

Kind of not forcefully necessarily. It's just you can do it over time when you do it forcefully. So these capacities that you spoke on the spirogram is not subject to time. Yeah. You can just do it as long as you can do it. Okay. Right. But when you put time into it, that then becomes forced. Yeah. Okay. So then as soon as you say, do a vital capacity maneuver, okay.

So breathe in as quickly as you can and get rid of it as quick as you can. But in the quickest period of time, then it's forced vital capacity. Okay. So let's say...

You were to do a forced... So I attach you to a spirograph. Yeah. I say breathe in as much as you possibly can. You take in your maximal breath in. And then I say I want you to breathe this out as fast as you can and get as much of it out as you can. So all the air that you breathed out...

forcefully was your force vital capacity. Let's say it's five liters, right? And then I measured how much you breathe that in the first second, which we call the forced expiratory volume in the first second, right? And let's say that that was four liters. So you were able to get out four of the five liters in the first second and

Then I do the ratio of that four divided by five times a hundred gives me 80%. So I've just got a value, which we call the forced expiratory volume 1% or the FEV 1% of 80%. What does that tell us? What does that mean? This is usually it.

done for an obstructive, checking obstructive changes in the lung. Because if you were to have narrowed airways, like you spoke about earlier with asthma, if they were narrowed down, you can't move the flow. The flow of the air can't be moved as quickly. Right. So therefore more will remain at the lower parts of your lung. So therefore, yeah, just that your ability to move the air is diminished and that's telling...

The physician that there's obstruction. So above 80% is normal. And so, okay, let's do the example of you. Let's say you have been a five pack a day smoker for the last 30 years. And Matt doesn't smoke by the way, even though he's got that nice gravelly sort of ASMR voice. No, he doesn't. So let's say you did your, but you do have emphysema.

your vital capacity, your force vital capacity, when you breathe as much in and as much out was three liters. It's not five, it's three liters, right? But then, so that's reduced. That makes sense because your airways are sort of diminished capacity.

But the amount that you breathed out in the first second was one liter. Now, previously it was four, but now it's one. So we do the ratio, one divided by three times 100, that gives us 33%. So that is a lot lower than 80%. So that would tell us, that's an indication that this person has an obstructive respiratory disease, right? Correct. Okay. So anything below 70% is obstructive in nature. Yeah.

Okay. And that could be emphysema. It could be asthma. It could be chronic bronchitis. But you could also have what, because we tend to say we've got obstructive respiratory diseases and restrictive diseases.

And restrictives tends to be anything that restricts the lungs ability to inflate. Inflate, yeah. Right? So if you've got some sort of scar tissue around the lungs, for example, we might find that your vital capacity is low. Yeah. But your forced expiratory volume in the first second might be normal. Normal. Right? So again, you do this test and it might look normal, right?

Because the percentage is high, but then you have a look and go, oh, the forced vital capacity, it should be around five liters, but it's like two and a half. Yeah, that's right. Okay. All right. Let's move on to the diffusion of gases because this is important for exercise physiology. We need to understand the fact that oxygen needs to go from the lungs to the blood and from the blood to the lungs.

As we know, we spoke about getting air into and out of the lungs. That works by going down a pressure gradient. Now, importantly, on the molecular level, when we have gas exchanging, the gases will only go down their own pressure gradient, right? Yep. Which we call the partial pressure. So there's something called Dalton's Law.

Which basically... There's a lot of laws here. There's a lot of laws. A lot of laws to break. Exactly. You know, we're rebels. You and I, we're physiological rebels. What... Okay, so we live in Queensland. It's mostly sea level, right? Because we live at beautiful Gold Coast. What is the... If I were to put a...

Life pressure monitor. No, no, no. Let's say that I were to get a tube, a one meter in diameter tube and put it over you. And that tube goes all the way up into the sky. And we were to measure all the gases above you, placing a pressure down onto you. What would be that pressure?

At sea level? At sea level. 760 millimeters of mercury pressure. Now that's interesting. I always say this to my students. I go, remember when we talk about blood pressure, that the pressure in the aorta is how much? 120. Right. And that's enough to squirt blood out a meter or two. Yeah. Right. But the pressure above us is six times that.

Right. Seven times that I should say, sorry. That's, but we don't feel that pressure. Why? Because I guess we're in that frame of reference. Is that the reason? Like if we were in a blood vessel living in the aorta, we probably wouldn't notice the pressure maybe. Yeah. It's like that. I don't know who said it, but it's like that, that story of the fish swimming through the ocean and meets another fish and the other fish says, Hey, how you doing?

And the fish goes, good. He goes, man, how's the ocean today? And that first fish goes, what's the ocean?

Because he's in it. It is everything. So you don't know what pressure you're experiencing because you're born into that pressure. Now the point of this is that that tube of gas above you and around you is putting 760 millimetres of mercury worth of gas pressure onto you. And Dalton's Law states that that 760 is simply the sum of all the gases. That makes total sense. So for example, 20.93% mercury

of that gas is oxygen. So you could take 20.93% of 760, which, and that gives you 150. The partial pressure of oxygen in the atmosphere. Yeah. At sea level. Which is 159 millimeters of mercury worth of pressure. And it's important because when you take a breath in, Matt, while you're breathing in 760 millimeters mercury worth of air, the oxygen that you now bring into your lungs is

The oxygen pressure, the partial pressure of oxygen is 159 millimeters of mercury. Now, by the time it gets from the atmosphere, which is 159 millimeters of mercury into the alveoli, it's actually dropped. Right. Do we know why? I would say it's the mixing with the dead space air and the air coming back out.

Yeah, that's right. We lose some of the oxygen as we bring it into the alveoli. So yes, that's one reason. Another reason is because some of that oxygen will get dragged into the bloodstream, reducing it, which is exactly the point that we're trying to make here is that in the alveoli, it's about 105 millimeters of mercury worth of pressure.

In the alveoli of oxygen? Yeah, about 104, yeah. Okay, 104 millimeters. On the alveoli side. Yep, in the alveoli itself. Then in the blood that's coming past in the pulmonary circuit, the oxygen's only, what, 40 millimeters of mercury? So there's a big pressure gradient. So the slide that it wants to go down is steep. Yeah. So the oxygen, whee, goes down that slide. So that's great.

If we look at the carbon dioxide, however, the carbon dioxide that we breathe in is minimal. It's a point of a percentage, right? Yeah. So the carbon dioxide we breathe in, it's actually, by the time it gets into the alveoli, it's about 40 millimeters of mercury worth of pressure. But the blood going past is what?

46. 46. So there is a slide here going from the downhill part of the slide is going from the blood into the alveoli. It's not a very steep slide. Very modest. Okay. So a couple of points we need to talk about. I'm going to ask you some questions. The gases we see here, they're diffusing in the direction that their partial pressure gradients are going down. Right? Yeah.

That makes sense. The oxygen one is very steep, going from 104 millimeters down to 40, and the carbon dioxide is less steep, going from 45 to 40 in the opposite direction. Importantly, gases only move down their own concentration gradient. All right. So one thing that determines gas diffusion is the partial pressure. We've got that. I'm going to get back to that in a sec because I've got a question to ask you. The second thing I want to ask you is the surface area.

In what way would the surface area play a role in gas diffusion? So we said it's 60 to 70 square meters in a healthy. Yeah, up to 100 even. Okay, up to 100. So let's talk about if that was halved. Yeah. What could you assume?

There's just less space for that transfer to occur because it has to cross a membrane and that membrane we're talking here, there's kind of three parts of that exchange that has to go across is the cell of the alveoli, which is the type one pneumocyte. So it has to go across the cell membrane through the cytoplasm

through the other side of the cell membrane. So it has to go through a very squashed cell. Yeah. Now on the underside of that squash cell is a basement membrane, which is just a bit of connective tissue. And then that's connected to the blood vessel wall, which is the capillary endothelium, also very flat. So that diffusion has to go across those three structures, a type one pneumocyte, a basement membrane and the endothelium. Yeah. So that's the surface area. So,

the space for this to happen, the more oxygen you can transfer. Yeah. Think about this. I think this is a good analogy. When I know you don't drink soft drink, Matt is quite the pie. I do a little bit. Do you? Okay. So let's just say, let's say soda water. You like spring, you like mineral water, right? Matt's a mineral water man. So if you open a bottle of mineral water and you leave the lid off,

The surface area for the gas to exchange from the bottle to the atmosphere is small. It's just the size of that open lid. So it takes a while for it to go flat because it's diffusion. But if you were to do the same thing, open that bottle up and pour it onto this table, you've now increased the surface area for that gas to diffuse from the liquid into the atmosphere and it diffuses faster and easier. And it's the same thing, surface area. Yeah.

Okay, so we've got- Good analogy. Thank you. You've redeemed yourself. Oh, I appreciate it. I didn't know that I was in bad stead. So we've got partial pressure. We've got the surface area. We've also got something called the diffusion coefficient, right? Which is basically how easy is it for the gas to diffuse? Now-

It's basically solubility, right? How soluble is this? Whose law is this? Well, this is part of Henry's law. Is this Henry's law now? Yeah. So we've spoken about Dalton. We've spoken about Boyle. We're about to talk about poor Henry. Henry's cat. She was spectacular, wasn't she? Singing-wise. She had a killer voice. Was she the first one? First what? The first... Was it like UK Got Talent or something? It might have been...

Was it UK Idol? Something like that. Britain's Got Talent, Britain Night, something like that. Anyway, hope you're doing well, Susan. So we've got the diffusion coefficient. How soluble is that gas, right? Okay. Oxygen compared to carbon dioxide. Which one is more soluble? Carbon dioxide. Carbon dioxide.

Compared to oxygen? Yeah. How much more soluble, do we know? I haven't got the percentage. I think it's like- Quite significant, right? 20 times more soluble? And that's hence why you don't have the same partial pressure of carbon dioxide to oxygen. So say that again. So when we look at that partial pressure difference, as we saw with oxygen at the alveolar level, the partial pressure between the alveolus and the blood is 104%.

to 40 respectively. So steep slope. Very steep. Whereas carbon dioxide is 46 to 40.

So not as steep. Not as steep. But because carbon dioxide is 20 times more soluble, it doesn't need to have a steep slide. So it doesn't need that push to get across the membrane. But the oxygen needs a bit more of a push, hence why the partial pressure difference needs to be greater. Greater, yep. Okay. So we've got three things. Now, the fourth thing is the thickness of the membrane. You were talking about that before. So talk a little bit more about that respiratory membrane it needs to travel through, but what could thicken it? Yeah, so I'm not sure. I'm guessing it would be microns, probably microns.

under 10 maybe. So not very thick. All the tissue is very flat. But if anything was to increase that thickness, that then would impact the ability of a gas to exchange. So the most probably common example of a lung issue that could do this would be just getting fluid down in the lungs. Right. So this could come about from an infection or pulmonary effusion, which is just exudate

Filling up the base of the, not the base of the lungs, but the alveoli sacs. And anytime you get inflammation, you get fluid accumulation. So COVID-19, this can happen. So it basically means that there's just a thicker tissue

Like a consolidation, yeah. You'd see that with pneumonia, which basically means lung inflammation. But like you said, with COVID, when COVID infects you or infects us, it's usually upper respiratory. So that's why you get the symptoms initially with a cough, runny nose, sore throat. And then if it's unfortunate to drop down into the lower respiratory tract, it then involves lung tissue.

it will start to cause consolidation or extradite in the alveoli. So now all of a sudden you've got fluid in there. That's a bigger distance for the gas exchange to take place. Yes. But also you get scarring around that basement membrane. The connective tissue. And that's going to thicken it as well. Yes. Now all of a sudden you're making the diffusion capacity drop.

And so you're going to have problems oxygenating. And this is the big issue that people encountered with COVID, particularly in the early few years before we developed the vaccine to prevent the complications. Yes. And the way that these individuals were treated was,

If they got to that bad point where they're really deoxygenating, they have to go into ICU and they go in very high flow oxygen. To increase the partial pressure. Yeah. So a lot of liters of oxygen per minute and then also mechanical ventilation.

So they're really increasing their tidal volume massively. So instead of that 500 mils of movement, they're now inflating the lungs and keeping them really open up to enhance that movement.

You need to push that oxygen. Like we said, we've got to increase that partial pressure to increase it. So the four things you need, the tissue surface area, the diffusion coefficient. So how soluble it is, the partial pressure of each individual gas and the thickness of the tissue. All of those things affect the diffusion of the gases. Now we're just going to stop for a quick ad break. Listen, uh,

have a little bit of a listen from our sponsors and we'll be back to talk about what's called ventilation perfusion coupling and how exercise can affect this.

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And we're back. Now, an important thing that we need to understand here before we move on is exercise. When we perform exercise, we are using oxygen.

So we need to deliver this oxygen from the alveoli to the blood and the blood needs to carry that oxygen to the tissues and the tissues use the oxygen. So the way that the oxygen moves from the lungs to the blood, from the blood to the tissues is by going down its own partial pressure gradient, right?

Now, when we start to use up oxygen in the tissues, the partial pressure of the oxygen goes down in the tissues, which facilitates the movement of the oxygen from the blood to the tissues, which means the partial pressure of the oxygen in the blood goes down, which facilitates the movement of the oxygen from the lungs to the blood.

And the same thing happens with the carbon dioxide in the opposite direction. Now, we're going to talk more about the oxygen and its transport in the blood in a second because that's really important. But let's talk about something called the VQ relationship, the ventilation perfusion relationship, because it's not just about those, you know, the tissue surface area, the diffusion coefficient, the partial pressure and the thickness of the tissue. If you don't have the buses driving past the stadium to pick the people up,

then the people are stuck there. At the stadium, after a football game. Exactly. So we need the blood to move past to match the people coming through. So just like that analogy we alluded to, a football game's just finished. You've got tens of thousands of people leaving the stadium and they all need to go home via buses. You need just the right amount of buses to take those people home. Not enough buses, people are left over. Too many buses, you've wasted the buses.

So the buses are the bloodstream coming past the pulmonary circulation and the people are the gas molecules, specifically oxygen in this instance. So this would be the VQ matching. Yes. And what's the V, what's the Q? Yes. So V is ventilation. Q, I think it's either, it either stands for

or it's in another language. But the Q is the perfusion, effectively the amount of blood going past. So you want to match the amount of... So the Q is the buses...

Yeah. And the V is the people coming out of the stadium. That's right. And obviously you want it to match as close to one to one. Yeah. Now the thing with the lungs is that it doesn't really match one to one in most tissues. On average, it's close-ish to one to one if you take all the areas, but it's quite different from like the top of the lungs to the bottom, right? Yeah. So,

Matt, if I were to be a scientist right now and I were to measure the ventilation at the apex, the top of the lungs, what – now, ventilation being, you know, litres per minute, right? It's like our cardiac output. So what would the ventilation be-ish at the apex, the top of our lungs? It's about – so at rest, it's about 0.24 –

Litres per minute. Okay. So about 250 mils-ish. Okay. What about the blood flow, the perfusion at the apex of the lung? It's also very underperfused at rest. So the apex would be getting... So if you were to measure the blood flow proportionally through the lung and go via rib number...

Rib 2, which is kind of towards the top of your apex of your lung, would be receiving the least blood. How much? I haven't got a number. No, I do. 0.07 litres per minute. Per minute. So we've got at the very apex, the ventilation is low and the perfusion is really low. Okay, so...

Why? Why is the ventilation low? Why is the perfusion really low? Well, at rest, the most efficient way of inflating lungs is just by using your diaphragm. And as the diaphragm flattens out, it's really just increasing the volume at the base of your lungs. Of course, it's stretching the bottom. Yeah. So the apex isn't really getting stretched at all. So it's not really getting any load differential. So that means there's no real airflow in the apex area.

To much degree at rest, but most of it's happening in the base of the lungs. Okay. So that explains the reduced ventilation, but blood flow perfusion isn't dependent on the diaphragm. So why is the perfusion really low?

I think probably a lot of it's to do with gravity. So more blood is just going to the bottom parts of the lung. But I would probably imagine there's probably also just because of the pressure change and the volume change, there's probably, as we saw in the cardiovascular system, you do have the, remember the muscle pump kind of activity in the thorax? Yeah.

That's probably, I'm guessing would have some kind of plane. The respiratory pump. Yeah. Yeah. Okay. So if we just take that apex, you said the ventilation is about 0.5%.

0.24 and the perfusion is about 0.07 because it's, we look at the VQ ratio, the V over the Q that ends up being a ratio of 3.43. Right. Now we said we want it, you know, you want the V to be one and the Q to be one, right? So that the ratio is one. So it's a perfect matching here. You're getting,

because it's 3.41 it means you're getting over ventilation and under perfusion in that area yes that's right okay so let's just bench that let's just shelve that let's now go to the base the bottom of the lungs what's the ventilation at the bottom of the lungs about 0.8 liters per minute okay so it's higher than the the apex what's the perfusion at the base of the lungs

liters per minute? No, I think it's 1.29. I read the ratio, sorry. Okay, so it's 1.29. So the perfusion is... So...

And that, again, I think has to do with mostly gravity. So you've got at the base, the ventilation's higher, but the perfusion's way higher. So now the ratio is more in the perfusion favour as opposed to the ventilation like we saw at the apex. And the VQ is 0.64. So in the base, there's more buses than people coming out. Yes, and in the apex, there's more people coming out than buses. That's right, relative to their area.

But if you were to average from between the apex and the base, and like you said, go down via the ribs and sort of meet in the middle, the average is going to be close to a one-to-one ratio. Yeah. Now it's important to note here at rest, you don't really, because there's so much redundancy again in the respiratory system, we don't really need to get a close match in a one-to-one.

So we want to start to get closer to matching. Why is that though? When we're at an exercising state, but at rest, there's still a lot of redundancy we can get by by not being overly efficient.

Yeah, I think as long as it's above 0.5, we will get our red blood cells fully saturated and deliver it and get enough oxygen in the bloodstream to meet the demands of the tissues. But when we start exercising, we don't want this very strange VQ matching from the apex to the base to be so different.

So it changes, right? Yeah. So what happens when we start to perform exercise? Well, when we start to perform exercise, we usually, so this would be a moderate exercise. So I guess you'd say 40-ish VO2 max. 40%. 40%. Yeah. The first main things that are going to be changing is more inflation proportionally to the base. And so as we saw with that VQ match-in or lack of match-in,

the base is getting way more muscles. So it's normally getting over perfused with blood. Yeah. So when you go into an early stage of exercise, you're just bringing the ventilation closer to the blood. Yes. So that means it's closer matching that VQ, which probably is enough in

in the first stages to provide all the additional oxygen requirements at that point. And that's just because we're now increasing the volume of the thoracic cavity. We're recruiting more muscles, stronger inspiration, more gas getting in.

And then as we start to progress in our intensity. Yeah, as you're working really hard, then that's when you're bringing all those additional inspiratory muscles in where you're using all the neck, the top part of the neck. All right, so it sits at the top. So it's increasing the volume at the high end. So now the apex will start to go up, yeah.

Right. And because we're increasing blood flow more broadly, we're going to get our perfusion matching at the apex as well, because we know that during exercise, the blood pressure in the pulmonary circuit, so when the heart contracts,

it pumps out five liters per minute through the systemic circulation. So the left side of the heart, but also five liters per minute from the pulmonary circulation, which is the right side of the heart. But the pressure is really low on that side. But when you exercise, the pressure goes even lower, uh,

Because the blood vessels dilate and capillaries open up, but that means it's easier for perfusion to happen at the lungs. And so that's why we get also an increase in the Q, in the perfusion, in all those parts. So it all starts to match. When we start to perform exercise, the matching gets closer to one-to-one throughout the lungs. Particularly athletes. Athletes would do it even better. They would really match it as close as you can be.

All right. Can we move on to, we've now exchanged that gas. It's in the bloodstream. How do we move this gas around and how does exercise alter this movement? Yeah. So if we're talking about oxygen, there's two forms that oxygen is carried in the blood by far. So what is it like 99% of all oxygen is carried on the hemoglobin?

In the red blood cell? Yep. So in each red blood cell, there are 250 million molecules of hemoglobin. That sounds like red blood cells are packed with hemoglobin. That's right. It sounds like they almost have nothing else but hemoglobin. That's right. They've lost all their organelles. They're pretty much just a cytoplasm full of hemoglobin. So 250 million hemoglobin molecules. All right. And then in each molecule of hemoglobin, there are...

Four chunks of iron and that's where the- Chunks, really? That's right. Chunks. Like, you know, like- Not just an iron ion, but a chunk of iron. That's right. Like the size that you would require to make a sword or- Right, yeah, exactly. Okay. So as you'd see like in the Pilbara of Western Australia-

That red oxidized soil. That's right. So you've got four per hemoglobin. That's right. So if you do the math, that's a billion spaces for oxygen to bind per red blood cell. Right. And red blood cells, what is it? Four to five million per microliter. Is that right? Yes. Yes. So we're talking...

So let's do some maths here. Sounds like trillions of oxygen molecules. When one gram of hemoglobin is fully saturated with oxygen, it will carry about close to one and a half mils of oxygen. Now, if you put that to a...

Yes. Males have about 150 grams of hemoglobin per liter of blood. Right. And females a bit less, 130 grams per liter. So when you saturate all those, a male...

Adult would have a capacity of carrying 200 mils of oxygen per litre. And we have about five to six litres. That's right. So we've got about a litre of oxygen in our blood. That's right. A litre. And think about that. So a quiet breath in is half a litre. You've got twice that.

of oxygen, bantam hemoglobin in your blood. Yeah. That's amazing. Phenomenal. So what that tells us is that, again, we said earlier that the respiratory system's overbuilt and that we really can, it's very easy to saturate our red blood cells, um, at rest. So, I mean, even during early stages of exercise, our red blood cells are saturated. That's right. Right. So this is why I always found it funny when you'd watch, uh,

professional football and sometimes you'd have like football players with oxygen masks on on the sidelines to try and get that oxygen in. It's, no, you can't oversaturate by definition. They're already saturated. Your red blood cells are saturated. That's not where the issue is. The issue is the muscle fatigue likely. Yeah, yeah, that's right. Okay, so. And the other 1% is carried, dissolved in the plasma.

Oh, so just directly dissolved. And that would be called the partial pressure of oxygen in your blood. So if you were to do a blood gas, you would get the saturation, which should be 97% to 100%. That means of all your hemoglobin molecules, 97% of them are saturated with oxygen. Yeah. But the partial pressure of oxygen in your plasma should be 80 to 100 millimeters of mercury.

80 to 100 millimeters of mercury. 80 to 100, yep. Okay, so let me just, because we're going to talk about something in a sec and students find it difficult to understand. If you think about your blood and the oxygen in your blood, you've got the oxygen bound to the hemoglobin. Imagine that as, you know, they're stuck there to that hemoglobin, right? But they're surrounded by oxygen dissolved in the blood

And that puts a degree of pressure, because it's a partial pressure, on that hemoglobin. Yeah, the affinity for it. The affinity for it. So if you've got more oxygen dissolved in the blood, the partial pressure of oxygen will go up, understandably, which then means...

because let's say I'm a red blood cell and I'm holding onto, let's say I'm one hemoglobin and I'm holding onto four oxygen molecules, but I see that surrounding me, the pressure of oxygen is really high because there's heaps of more oxygen dissolved. I'm less likely to let go of an oxygen, right? Which is called dissociation. Yes. But if the partial pressure of the oxygen around me drops, I'm more likely to let go of the oxygen, disassociation, right? Yeah.

To hand it off to the tissues. Yeah. And so this is what we call the oxygen hemoglobin disassociation curve in which when the partial pressure of oxygen in the blood is zero...

basically none of the hemoglobin are going to be saturated. Yeah, they're all off as well. Yeah, because they're like, oh, there's no oxygen around me. I better let go of all my oxygen because the tissues obviously need it. Does that make sense? Yeah. But when you look at 100, 100% oxygen, 100 millimeters of mercury, which you said is around about the partial pressure in the blood, the arterial system,

you're going to get 100% saturation because it says, oh, look at that. There's heaps of oxygen dissolved around me. I'm going to hold on to the oxygen. I don't need to let go of it because it's fine. And this disassociation curve, an important point to highlight is that at around about 40 millimetres of mercury of partial pressure is where we get the steep slope of the curve where we now go from – so basically going from 100 millimetres of mercury to 40 in that arterial system –

we'll lose one of the four oxygen molecules from hemoglobin. That's right. So about 75% saturated. Yes. So we've still got three attached, but then going from 40 millimetres of mercury down to zero is where we steeply start to release the oxygen from the hemoglobin. Exactly right. And that's important because what it says is that, okay, with the red blood cells, the hemoglobin has a high affinity for oxygen under great pressure.

partial pressure conditions. But when the partial pressure drops in the blood and now you've got to think, why would the partial pressure drop in the blood? Well, when the muscle tissues need oxygen, it's partial pressure drops and the gas will diffuse from the blood into the muscle and

And the blood partial pressure will drop, which then signals the hemoglobin to release its hemoglobin. So it's using sort of like the signal around it of partial pressure as to whether it's going to release the oxygen. Exactly right. But there's other things that can affect how it lets go, which is important during exercise. So what are some of the factors that I'm exercising? Not only does the partial pressure of oxygen drop in the muscle to signal the hemoglobin to release more oxygen, what else can happen?

Well, remember the hemoglobin is a protein and we know what are the two big things that change the shape of a protein? The pH and the temperature. Yeah. Now, would you expect those to... I was trying to think of something funny and I couldn't. Would you expect those two to change...

in a state of exercise? Matthew, I think I would because when muscles contract and relax, they release heat. So that's going to change the temperature and the blood is our conduit for temperature transfer. So the blood will change temperature, hence hemoglobin. Particularly when you get down to the muscle point.

And I think that the pH will change because a byproduct of metabolism is hydrogen ion production. Yeah, exactly. So both will change. So as the blood leaving the aorta is moving through the smaller and smaller arterioles as you get to a capillary bed, particularly as you get into the exercise in muscle capillary bed, what the blood will start to realize as it's getting to this, it's like...

Coming into Florida after... Are you saying turn around, go back? Or are you saying that it's getting hot and humid? Hot and humid, that's right. So, you know, like the... I've never been to Florida. I'm not making a judgment. You know I don't know anything about geography. I'm sure it's a beautiful place. So, you know, as the blood's coming into that region, it's going, oh my God, it's hot here.

And it starts singing Nelly. It's getting hard in here. Now, it's also getting acidic in here. Oh, no. So what happens, so lactate or hydrogen ions being produced from the metabolism of the exercising muscle, but also all that heat that's generated from all those cross-bridge cycling.

that's going to change the properties of the hemoglobin. Oh, no. But at the same time, it's extracting all the oxygen out of the dissolved plasma. So the partial pressure has now dropped from, what did we say, 80 to 100, which is in arterial blood, now to 18, 20. In the arterial blood. In the capillary muscle. At that area. So huge partial pressure drop.

It's getting hot and it's getting acidic. So it says, let's take off all our oxygen. That's right. So all of a sudden now you're offloading. This is the dissociation. It's shifting the curve to the right. So heaps are coming off. So it's unloading, which is what you want to happen at the muscle when you're exercising that muscle.

Yes. Either in duration or intensity. And another thing that can affect it is the carbon dioxide. So the carbon dioxide that's going from the muscle into the blood. Oh yeah, that's a good point. It's transported in three ways, not just two. So one, yeah, it can be dissolved like the oxygen, but the oxygen, remember we said the solubility is different, 20 times different. So the oxygen, while 1% is dissolved, what is it for carbon dioxide? It's 5%.

35 to 45? Yeah, roundish. Millimeters of mercury? Because it's just more soluble. Then it also can bind to hemoglobin, but not the heme part like the oxygen, but the globin part. But when it binds to the globin, it changes the structure of the hemoglobin, making it more likely to release oxygen, which makes sense because when the carbon dioxide leaves the muscle, you want to exchange it for oxygen. Yeah, exactly. So that's perfect. And then the final way, which is the most prominent way, which is what, 70 something percent? Yeah, 30%.

The carbon dioxide will actually mix with the water. In the red blood cell? Well, it can happen in the red blood cell and it can happen in the plasma. But effectively, regardless, let's say it's happening in the red blood cell. The carbon dioxide mixes with the water inside there. It forms something called carbonic acid and that splits itself apart to release hydrogen ions, which makes something acidic.

which is good for releasing more oxygen, right? But also bicarbonate ions. So the hydrogen is buffered by the hemoglobin? Yes. And then you're left with a bicarbonate? Yep. And now you've got a... What's a bicarbonate? I don't know what to do here. But it's also making a charge difference, right?

Only when it leaves. Oh, so it leaves. Okay. So it goes down its gradient and goes into the blood plasma. And now you've got a charge difference. So you've got to bring something negative back in and that's the chloride. You bring the chloride into the red blood cell and that's a chloride shift. That's called the chloride shift. Yes. So effectively it...

the chloride enters the red blood cell to buffer it out, which means effectively the chloride concentration in the blood plasma reduces just because it's hidden in the red blood cell transiently. So now what you've done is you've offloaded your oxygen...

You've loaded up your carbon dioxide and now you're ready for a return trip back to the lungs. That's right. So as we said, what can affect this is temperature, hydrogen ions, carbon dioxide levels, all things that are important for exercise and the partial pressure. So all those things are really important. Now an interesting side point here is that there's something called exercise-induced hypoxemia in the athlete.

So for whatever reason, so, okay. You take an untrained person, right? When they exercise, they have a drop of arterial partial pressure of oxygen. It drops by like 10 to 12 millimeters of mercury. So it goes from, let's say a hundred millimeters of mercury down to 80 ish, right? Yep. 88. 88 ish. Okay. Now that's,

And this is during heavy, severe exercise. So a great point here is that, oh, your partial pressure of oxygen actually doesn't change much in your blood.

during like the hardest exercise. Hence why wearing the oxygen masks aren't really going to help somebody. And this is even in an untrained person, right? So it drops. Okay. That's fine. It's dropping because it's the oxygen is diffusing from the blood into the muscle tissue and it triggers the decoupling or disassociation of the oxygen from the hemoglobin. Okay. No problem. That's fine. You look at an athlete now in around about 40 to 50% of athletes, right?

you get a drop as well in the partial pressure of oxygen in the arterial system, but it drops by like 30 to 40 millimeters of mercury. So it goes from a hundred. It falls off the cliff. So it goes from a hundred to 60 millimeters of mercury. Now you would think that this drop would, athletes will have, would have developed some degree of buffering or,

built in a capacity to be better at maintaining the partial pressure of oxygen, but we see this phenomena happening. And so this... So this would be endurance athletes, right? Like marathon runners or something. Yes. Yes. And so this, well, I mean, yes, but it can happen due to heavy and very severe exercise, which you can't maintain for a long, long period of time. But this could happen

Okay, why is this happening? Well, it could be that there's, you know, the increase in CO2 in the athletes mean that maybe they're training harder, producing more CO2 in the muscle tissue, which is just telling the hemoglobin to unload more and it just, the diffusion, you've got better diffusion occurring from the blood to the tissue, but probably more

But this would be still arterial blood, so you're not really measuring at the capillary level. No, that's true. So what could be potentially happening here is that, as you said earlier, that an athlete's heart, their cardiac output is greater, right? Yeah.

And that's a great thing because that means they can deliver more oxygen to the tissues. But when you've got an athlete whose heart is throwing out 30 liters of blood a minute, right? Compared to an untrained person who's throwing out 15 liters of blood a minute, the blood is moving faster, right?

Yeah, yeah. Through the circulatory system. So the pulmonary- So the buses are going 100 k's an hour instead of 40? It's speed, right? It's the movie speed. Got to jump on the movie bus. Can't go below 100 kilometers an hour, right?

So the blood's moving through so fast that the oxygen transfer from the alveoli to the blood is not efficient enough. And that's probably the main reason why we get this, is it's a byproduct of such an efficient heart. It's not letting the oxygen diffuse down its concentration gradient sufficiently. It's interesting. It's interesting. Yeah.

What about, just quickly, the myoglobin in the muscle? Oh, right. Yes, myoglobin. So how does that play a role with...

kind of oxygen storage and then utilization in an exercising situation. Well, myoglobin sounds like hemoglobin and myo means muscle. So it's the hemoglobin version for muscle. And effectively it's the same. It's a lot smaller though, isn't it? It's a lot smaller and it binds with stronger affinity. So what that means with the disassociation curve is that we said that with the disassociation curve,

Between arterial partial pressure of oxygen, between 40 and 100, you've effectively got... It's very strongly attached. Yeah, so you've got three oxygen molecules still attached to one hemoglobin between 40 to 100. Once you hit 100, it's still holding onto it. But for myoglobin, it has to get all the way down to 20 millimeters of mercury. Even less. Like when you're at 20...

When you're at 20 partial pressure millimeters of oxygen, you've still got 85% saturated. Yeah. So what it says to us is that, okay, think of this is in the muscle itself. In the muscle, yeah. Right? So this is in the muscle. It is there as a last resort to provide like a reservoir of oxygen. The muscle is going to rely predominantly on the capillaries going past, so the circulatory system. Right.

This myoglobin is like, okay, I can see that, you know, around me, the partial pressure of oxygen is still, you know, still 20. That's fine. I'm holding on. I'm holding on. I'm only going to give it to you if you show me that you really need this oxygen. So that's the drop below 20 millimeters. Do you think that's the reason why they're using oxygen on the sidelines of a football game is to refill their myoglobin? So when they go back on the field, this myoglobin stores are topped back up. I don't think so. Because again,

The partial pressure needs to get really low for the myoglobin to release it. And because myoglobin has such a strong affinity for oxygen, it would resaturate pretty quickly.

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So I would say that all the athlete would need to do is rest, not even need to go and just rest. And the myoglobin will become resaturated again.

Just a point to highlight before, when you said that, you know, increased hydrogen ions and carbon dioxide and increased temperature tells the oxygen to jump off the hemoglobin. It just makes it easier, that's all. Well, it's called the Bohr effect. I just wanted to let everyone know. Boron. Not Boron, not our favorite textbook, Boron, but it's called the Bohr effect, just so for completion's sake. All right, let's now talk about

in the sense of, no, okay, before we do that, let's talk about the control of breathing. Okay. Just quickly, all right? When we, we need to signal the diaphragm and the muscles to tell us to take a breath in, take a breath out. And as we know, that signaling needs to alter for exercise, in response to exercise. So we've got basically an area of the brain called the medulla, which is our respiratory center. And then we've got like a,

a tweaking center above it at the pons, which can sort of tweak the medullary center. So the medulla is going to be there to control our rate and our depth of breathing. And this pons will fine tune that rate and pattern of breathing. Okay. Now to trigger the medulla, we need a couple of things. One, you can either have neural input to it.

and this neural input can come from the muscles themselves. It could come from the lungs stretching. So basically it's just nerves going and saying, hey, the lungs have stretched.

we need to change our breathing or, hey, the muscles are really contracting. We need to change our breathing. Or you can have a humoral stimulus, chemical. Solved in blood. This could be carbon dioxide levels, hydrogen ion levels, potassium levels, even oxygen levels, temperature, noradrenaline. These types of things can trigger it. So either you can trigger it directly at the medulla, which is called central chemoreception,

Or you can trigger it peripherally. So there's actually other areas that detect these chemical changes in the body. So where are these peripheral chemoreceptors? Okay, so going from your... So you've got your respiratory center, which as you said is the rhythm and rate and depth and all that dictated. But then you also need to get feedback from the body to go, well...

This is the state that we're in. Now, you asked about the humeral. Specifically, I guess you could say the chemicals that may be surrogate to how much performance, how much exercise you're currently doing. Yeah, and I said there's hydrogen. I said there's potassium. I said there's carbon dioxide. I said there's low oxygen. I said there's noradrenaline as well. So with some of those gases, oxygen, oxygen,

Sorry, carbon dioxide and hydrogen. They would be centrally modulated or sensed, and that would be in... So directly at the medulla. Yeah, in the CSF. So what's dissolved straight into the CSF would be what the medulla is bathed in, therefore what the respiratory centre is bathed in. And we also said that carbon dioxide levels and hydrogen ion levels...

are directly related because the carbon dioxide turns to hydrogen ions. So either it's measuring the carbon dioxide directly in the blood or it's measuring it indirectly via hydrogen ions. That's right. But then we can go peripherally, which means away from the central nervous system, and these would be in two primary structures, your aorta...

So the big blood vessel leaving your left ventricle and also the carotid sinus or the carotid bodies, which is going up towards your neck, where the external and internal carotids separate apart. There's kind of a cluster of cells around there that can be both for stretch for blood pressure, but also chemical in this case for breathing control. And

And where's the receptors for the – because the aorta is big. It goes all the way from the heart all the way down to the abdomen with multiple branches. So where are these – I guess you'd say in the arch, right? So where it curves straight out of the heart. Yeah. And there's bodies there as well. So you've got aortic bodies and you've got carotid bodies and they both detect chemical changes. That's right. Do they detect the same chemical changes or different chemical changes? I don't know.

From my understanding, the Aorta is similar to the central, so carbon dioxide and hydrogen. And that probably makes sense because the one product that plays around with respiration most effectively and most impactful is

Earlier on is CO2. Yeah. So kind of pH changes. That seems to modulate your breathing more profoundly. Why wouldn't we rely on drops in O2? Yeah. Again, I think this speaks to that dissociation curve because once you're developing hypoxia, so you're getting a very low, things are progressing or going downhill pretty quickly. Yeah.

So you don't really want to be relying on that, whereas the fine-tuning of carbon dioxide is probably a better way of regulating breathing rate than oxygen. Now, not to say that oxygen doesn't kick in. You do have kind of a secondary respiratory rate controller, and this is probably going to be more of the carotid bodies. That's where oxygen has probably a little bit more of a stimuli component.

But this is going to be where you have more of a state of hypoxia. So one should get in below 60 millimeters of mercury partial pressure, then that's going to start to drive your...

breathing rate more profoundly. So effectively, the reason why we rely on carbon dioxide, not oxygen is because one, we know that oxygen remains quite saturated within the blood for quite a while. So if we waited for that, we would probably accumulate far too much carbon dioxide. Yeah, that's right. And as we know, carbon dioxide forms an acid. So if we're relying on the drop in oxygen, we're going to be waiting a long time. So we go, well, the rise in CO2 is happening faster.

And its implications are more immediate because of pH changes. That's right. So let's use that as the stimulus. Okay. And in addition to the oxygen drop in the carotid bodies, you've also got high levels of potassium, increase in temperature, and also some of the catecholamines will play around with the carotid body sensitivity. Okay.

Hence, it's sending signals back to the respiratory centre to change breathing rate. And just to highlight how strong carbon dioxide is as a control mechanism, for every one millimetre of mercury increase in the carbon dioxide partial pressure in the blood...

that stimulates ventilation to increase by two litres per minute, an increase of two litres per minute for every one millimetre of mercury increase of carbon dioxide partial pressure. So it's really like we need to get this thing out here, okay? So that's the humoral. Yes. In terms of neural stimuli control of breathing, another one you could talk, we can talk about,

is the motor cortex. Oh, yeah. So in a similar way... The command center. Yeah, the command center. You know how we spoke about some time ago where they've kind of reimagined the primary motor cortex not just being neurons there to dictate somatic motor output? The new homunculus. Yeah. There's also...

visceral control as well so when you imagine a movement that you're going to perform not only is it going to stimulate upper motor neurons to go to lower motor neurons to move say to do a squat or something it also dictates how much cardiovascular output will i need for this but also how much respiratory output will i need for this so by a more kind of exaggerated primary motor

Yeah. Would also go to your, that would also send neurons to your respiratory center, which would also change your rhythm and rate. Right. So just thinking about the movement can. Or initiating, you're about to execute it. It's not only going to your somatic motors, somatic muscles, but also going to your respiratory center. So as the motor, as the motor signal. Yeah.

descends down through the spinal cord. As it goes past the brainstem, it can sort of spill over its information into the medulla and basically go, look, I'm going to tell these muscles to contract. You probably should start preparing to increase your rate and depth of breath. Yeah, that as well. I think it's that on top of designated neurons going to the center to say we're about to perform this kind of exercise, therefore prepare yourself for it. Okay, so you've got the motor cortex. What other neural...

What you spoke about the lung, the lung has to feed back. It's its own proprioception. So the lung is being told to move. It needs to send sensory information back to the respiratory center to say, this is how much I'm performing. And if it's not keeping up, this is where I think you spoke about it earlier, where we have conditions where restrictive lung disease, where your lungs might be scarred. This would be like things like,

where instead of being elastic, now it's collagen-based and your lungs are very dense and rigid and not likely to expand well. This would send information back to say, hey, I know you're telling me to get bigger, but I can't do it. Therefore, I'm telling you I can't do it. And that would give the impression to you that,

I'm out of breath. Yes. And so that's dyspnea. Yes. Okay. So you got that plus you got all your muscles, your muscle spindles, your golgi, tendon, your joint receptors. As they're performing the exercise, they're sending information back to the respiratory center to say this is how much more respiratory output we need because we're working really hard here. So what I hear is that there's quite a significant overlap between

in all the different afferents. So they'll go to the medulla to tweak. So we're going to have what's in the blood. We've got direct stimulus of the medulla. We've got stimulus of the peripheral receptors. We've got neural afferents that are heading in as well. And they're all going to tweak it. And basically, we don't have a lot of evidence about

you know, if we were to start going from rest to moderate intensity to heavy and severe intensity exercises to which of these systems plays a stronger role compared to the other, because there's a lot of overlap. But I think we do know that at least going from rest to moderate intensity exercise, that at least in the initial phase, a lot of it is just due to the motor cortex telling the medulla,

let's get ready for this exercise. We now need to just increase our respiration rate and depth of breathing. But obviously, as you start to exercise, you will produce metabolic byproducts. You will produce carbon dioxide, hydrogen ions, potassium, lactate, and these types of things will stimulate these chemoreceptors to trigger the

breathing to be able to change. And so I think what we end up finding is that, you know, compared to the early stages of exercise, which are probably centrally driven by the motor cortex, that in the really heavy, intense phases of exercise, that's probably mostly due to hydrogen ion

increases, but then also tweaked by the noradrenaline and adrenaline that's released and by the potassium that's accumulating from being dumped out of the cells and from the temperature going up as well. And so all of the, and obviously the stretching within the muscle tissue and the working of the tissue and the expansion of the lungs and so forth.

Importantly, when the lungs expand, there's something called the Henry Brewer reflex. You don't want your lungs to overexpand because you can contract those muscles and really stretch those lungs too much. So the Henry Brewer reflex is basically saying once the lungs have stretched sufficiently, it goes back to the brain and says, hey, stop this. Stop this contraction of these inspiratory muscles.

And then you get the relaxation so that you don't overstretch. Which we saw in the exercise muscle as well with the muscle spindles and the Golgi tendon organs. Yes. All right. To finish, Matt, when we exercise, and you sort of alluded this at the beginning, but do our lungs adapt to exercise? You would generally say unlike the other systems, like unlike the cardiovascular system, unlike the muscles, you would generally say no.

Structurally, no. Yeah. But functionally, yes. Right. So particularly in your endurance capacity of your respiratory muscles, you would say yes, training can help and make them more efficient. And particularly when they're working at a higher intensity or a longer duration, they can just be more efficient at using oxygen efficiently.

and metabolizing more efficiently, therefore not demanding more cardiac output, therefore making the individual more efficient at their particular exercise because they're not needing as much output to go to another area. Yes. But also all those things that you spoke about between the control, so how much feedback is coming and how you're responding to it,

But that could be also at the muscle level as well, that that is all feeding back on the work of breathing and therefore your ability to sustain it in exercise. Yeah, I think most of the adaptations will come from a lot of the organ systems we've already done episodes on. Muscles will adapt.

Your blood stream will adapt. You increase blood volume and circulating red blood cells and things like that. Your nervous system will adapt to change the degree of signals that it sends and how many motor units it recruits and so forth. But the respiratory system is overbuilt in the front end. So it's basically, it's almost like, you know, you buy a car and it's got a 4.5 litre

engine in it. Let's say you bought a car that's got a V8 engine in it, right? But you want to increase that car. You can't really increase that engine much, but you put a spoiler on it or whatever. You do other things to tweak it. So it's sort of the engine is the lungs in this instance. Or the cardiopulmonary system, yeah.

Well, mainly the lungs because you can change the cardio, the heart aspect, right? So you can change the size of the heart and the amount of blood volume it pumps out and the efficiency of its oxygen carrying capacity and so forth, but not...

the lung tissue itself. It's interesting. They did some experiments where they looked at the composition of the air that you breathe. Oh, yeah. So what's the majority of the air atmosphere? Oh, like 70% is nitrogen. Yeah. And they changed the composition. So they kept the oxygen the same, but they exchanged the nitrogen for helium.

Okay, so that's that. I'm doing a great job here. As they're running around the track. Yeah. But because helium is lighter than nitrogen. So both... So nitrogen's inert, meaning we don't... While it jumps into the body and the blood and moves around, we don't do anything with it, right? It doesn't affect anything in the body. So I assume helium's the same. Yeah, that's right. Okay. But it would...

the impact on the respiratory muscles. So because it's a lighter air. All right. So when you're performing an exercise with this composition of air, you're fatiguing less in your respiratory muscles because they're not working as hard because they're...

I guess you'd say a less heavy air to move around. So helium, second element on the periodic table, hydrogen, helium, lithium, beryllium, boron, carbon, nitrogen, seventh on the periodic table. So it's heavier. So you're saying that because 70% of the air is nitrogen-

That's, you know, it's just a heavy gas that we don't use. Let's just replace it with helium. And that resulted in better athletic performance. Or just less respiratory muscle fatigue. Right. So the diaphragm... Less work of breathing. The diaphragm and the respiratory muscles were less likely to... Yeah. At a particular VO2 max. That's interesting. Yeah. I think it was submaximal when they did that. So...

What do you think that tells us then? Like what does that – so does that then tell us that potentially one of the rate limiting – because we said that the lungs, the respiratory system itself isn't the rate limiter to performance. But what this tells us is that maybe the respiratory muscles could be rate limiting. I think they definitely are and there is evidence for that. So if you can make them more efficient, more oxidative –

Therefore, using it more efficiently, it's going to make the whole system more

More efficient. So you can train the respiratory muscles, but the parenchyma, the lung itself, you cannot train and it cannot... It won't structurally change, pretty much it won't structurally change unless you've got some disease set that you can be modifiable, like you spoke about with asthma. That is generally a reversible, obstructive condition. And if you can... And I think they've debunked that if you were to take a beta-2 agonist, which is a sympathetic...

Yeah. That it has any kind of doping effect in elite athletes. Right. Or in performance. So presumably those medications are safe to use in, what's the word, not in performing a...

that is competitive. Yes. But you're not saying that it's okay for an athlete to take because it's not performance enhancing. I think it's been debunked. Yeah, but you also don't know what the WADA restrictions are. So don't listen to Matt if you're an athlete and you're going, oh, well, Dr. Matt said that I can take this because it's not performance enhancing. I think that- Definitely check the regulations. Yeah, definitely don't listen to Matt. But my understanding generically that it hasn't been considered in that regard.

Okay. Matt, what an episode. Long one, wasn't it? It was a marathon. Breathtaking one. Oh, lucky my respiratory muscles were able to cope. I could talk forever. Matt, thank you so much. Listener, thank you so much. You can contact us if you're still listening. Admin at Dr. Matt, Dr. Mike.

You can follow us on social media. I've been talking for too long. You can contact us on social media, at DrMikeTodorovic, D-R-M-I-K-E-T-O-D-O-R-O-V-I-C. Please subscribe to our YouTube channel, Dr. Matt, Dr. Mike, and also subscribe and download. Give us a five-star rating on this podcast. Tell your friends. Tell your family. Let them know that you've got two smart guys talking about how the human body works, and we appreciate it, and we'll speak to you soon.

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