Exercise Physiology | Cardiovascular System (Part 8)
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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. I'm joined by my co-host, George Clooney, my favorite Batman. That's not true. But don't tell him. How are you? I went to the GP the other day for a sore foot. I limped in and said, Doc, my foot's been killing me all week. He looked up and said, gout. Jeez, I just got here.

It's a good one. That's a good one. So you're very good at making it medically focused, but also funny. I mean, there were no laughter. There's no laughter. Nobody found it funny, but I think there'll be one or two people that might find that funny. Yeah.

Matty, how are you? Good. Good. I'm good too, thanks. We're talking about the role of the cardiovascular system in exercise physiology. So this continues our series on... Exercise physiology. Yep.

And we have, what did we do last time? We did muscles last episode. Now we're doing cardiovascular. We're talking about how does the cardiovascular system support exercise, but also how does the cardiovascular system respond to exercise?

Have we had a huge uptick in listeners that are doing exercise physiology? Great question. Don't know. If you are studying exercise physiology, physiotherapy... Or you are an exercise physiologist. Yes. Let us know. Send us an email.

at admin at drmattdrmike.com.au. We've received a couple of emails there that I have not got to yet. So if you've sent an email to that and I haven't got back to you, my apologies. Blame Mike. Blame me. I will get back to you very soon. But yes, we've had a big uptick in the listens of these episodes. Oh, that's good. They've been quite successful. We've had well over 100,000 downloads of just the exercise physiology episodes

I think we've done six or seven. Lovely. So that's good. Did you know, this is just for our listeners, did you know this podcast has had more than three million downloads of its episodes over the last couple of years? Yes.

Thank you. Thank you. That's good. Well done. I'm a bit croaky today. Back on you too. Are you sick? I'm not sick. I think I've got reflux issues. Oh, no. Okay. You've been all the alcohol and deep fried chicken you've been eating? What is it? You don't drink, do you? No, I don't drink. Okay. Do you eat deep fried chicken? I drink water. Oh, okay. Deep fried water? None of that?

It just happens to be. I've got mild reflux, which I've been taking PPIs for. But it's given me like a sore throat, a continuous sore throat. And I went off it because I don't, well, I shouldn't say I don't want to be on it, but I'd prefer not to be on it. But yeah, I can understand not wanting to be on it. But if you've got the problem. And the sore throat's come back. And so just a bit.

in my throat. But you're not sick? Not sick. So you've got the energy for this podcast? I hope so. You've got the vim and vigor. Okay. So this episode will be in our series of exercise physiology, looking at specifically the cardiovascular response to exercise. That's Matt saying let's get on with it. All right. So...

The reason why we need to talk, so firstly, when we say cardiovascular system, we're talking about the heart, the blood vessels and the blood, right? And its role in exercise. Importantly, I want to ask you the question, Matt, what is it about, broadly speaking, why do we really need to focus on the cardiovascular system when it comes to exercise? It's obvious, but let's just put it out there. Well, when you exercise, I'll say you, not me, because if I talk about me exercising, you'll criticize it. And I'll get emails saying I'm bullying you.

So when you exercise, moving from a resting state to a full-blown VO2 maxing exercise, which you do at times, you know, time to time, right? Yeah. Why? Why do you say it like that? Your muscles need significantly more oxygen than they would at rest. That's true. So much so, 25 times more oxygen demand. Right.

at high intensity exercise than they would at rest. So to get that oxygen, we know that oxygen is carried in the red blood cells of your blood, but it doesn't just get there on its own. It needs to get pushed there, which is the cardiovascular system. So the heart is the pump, the vasculature is the vessels, and the blood is the medium. Right. So to get all that oxygen...

you need a functioning cardiovascular system to deliver that. But on top of the oxygen, it also needs the fluid, the plasma, to hydrate and it also needs to – with the nutrients, with the energy, but it also needs to remove all the wastes. So to put it as a soundbite, when you exercise, the oxygen demand goes up. We need the cardiovascular system to meet that oxygen demand so that the muscle has the energy needed to work.

to contract. If you're one cell organism, you wouldn't, but we're got 30 trillion cells. So we need a system to do that. Very true. Okay. So in order to do that, however, the cardiovascular system broadly does two specific things compared to at rest, what it does to meet that oxygen demand. Two things, two things. What are those? Did you come up with these two things? No. Well, is this your category? This is just, you know, the way that myself and my colleagues within the exercise physiology realm, uh,

This is how we think about it. So what are the two things broadly that the cardiovascular system does to meet those oxygen demands due to exercise? It would need to increase the activity of the pump. Which is the heart. Yeah, which is cardiac output.

And it would need to direct more blood to the muscle and away from areas that's not important at that point in time. Yeah. It needs to increase the amount of blood it pumps out every minute. And it also needs to redistribute the blood flow to the muscle away from areas that probably don't require it in that time of exercise. And that's what we're going to focus on, how the body does that plus other things.

But to begin, we need to talk about the anatomy of the heart and the cardiovascular system. So Matt, if I were to say to you, we've got a heart, what's it look like? Very broadly... It's questionable that you do. Okay, thank you. I mean, I did run a whole bunch of anatomy and physiology sessions to my medical students this week, Matthew. I mean, a spiritual heart. Oh, okay. Sorry. You know, that's true. I'm like the Grinch. It's fine.

It's very tiny. It's itty bitty. It's like a little black bit of coal in my chest. But anyway. Keep going. People like you, you know, who have large hearts, I would say cardiomegaly.

What does it look like? If I were to pull your heart out of your chest and to slice it up on this table, what would it look like internally? Oh, look, it's so hard to explain simply. Oh, is it? It's just like a – well, it's a combination of – Oh, allow me. Four chambers. Oh, there you go. That's – yeah, okay. I was going to try and come up with some elaborate kind of pyramidal shape thing. Don't bother.

Yeah, okay, so the internal structure, four chambers, the two top chambers are the atria, which are the receiving chambers, and the two bottom chambers are the ventricles, which are the pushing chambers. Right. So the heart, even though we said it has an overall whole loop system. We didn't. What do you mean?

So it pushes blood around the whole entire body in a circuit. Okay. We haven't said that. It's kind of two... Didn't we say that? No. Okay. We will. All right. There's two parallel circuits that we need to focus on at this point. We have a circuit that is carried to the whole body and there's a circuit that's carried to the lungs. So if we look at those two chambers, two at the top, atria, two at the bottom, ventricle. So four chambers, yeah. Yeah. I mean parallel chambers. Oh, yeah. So do we want to just...

Work in sequence or is that how you want to do it? Yeah, I would say firstly that the two atria at the top, they receive blood. The atria then give the blood to the ventricles below them and then the ventricles will deliver the blood out to the body. To those circuits. Now, one side will go to the lungs and the other side will go to the rest of the body. Do you want to just...

Further elaborate that, not in a great detail because it's not super relevant to what we're going to talk about today. Yeah, okay. So if you look at the right atria, that's receiving blood from the body and that's going to be considered lower in oxygen. From there, the blood drops down to the right ventricle and then that gets pushed out to the pulmonary circuit, which is drop carbon dioxide into your lungs, pick up oxygen, and then that blood returns to the left atria and

And that would be considered oxygenated. And that blood then drops straight down into the left ventricle, which is then pushed out to the entire body to deliver the oxygen to the needed area. And in today's context, the exercising muscle. And then the whole thing starts all over again. Perfect. And so when we take a look, and so the heart is just a big muscle, right? Yeah.

And if we think about the heart muscle compared to other muscles of the body, you know, you've got skeletal muscle, smooth muscle and cardiac muscle.

So skeletal muscle, as we probably know, it's attached to the skeleton. It crosses joints so that when it contracts, it shortens the joint angle. Moves bones. Yeah, body moves. You've got smooth muscle which lines our hollow organs like our digestive tract, our urinary tract, reproductive tract and our blood vessels. When this muscle contracts, it narrows the diameter of the lumen, so the hollow inside, and also shortens it and allows for us to move muscles

through those tubes. That's smooth muscle. Now I've got cardiac muscle, which is a branch shaped cells that are all connected to one another through little, um, uh, basically, uh, discs. Yes. So, uh,

You've effectively got little areas of conversation that can be had from one cardiac muscle cell to another. They're all connected so that when you depolarize or trigger one muscle cell of the heart to contract, it sends that signal to the next to contract and then to the next to contract and so on. So effectively, this is very different. So that's just through ion movement.

Yeah, that's right. It's very different to skeletal muscle where every individual muscle fiber, which is called a muscle cell, needs its own synapse with a motor neuron to tell it to contract, but not a heart muscle. So it's kind of like your neighborhood and my neighborhood. My neighborhood...

all very working together, very harmonious. You're unable to separate, don't talk to your neighbour, keep separated. It's not my fault that that's how my neighbours are. For some reason they don't like talking to me. So when we look at, so if I were to do a, you know, Indiana Jones Temple of Doom on you, put my hand into your chest and pull out your heart, put it on the table, it would beat for a little while. So what's that called when the heart has its own rhythm?

Okay. Autorhythmicity? Yeah. Yeah. Or automaticity or autorhythmicity. Yeah, it's the same thing. So it's got its own rhythm. It sets its own rhythm. The rhythm of the night. In the rhythm of the night, I'm looking at your heartbeat. So as it's beating, right, nothing's telling it to beat apart from itself, right? So it spontaneously depolarizes the cells. But saying that, it does have a pacemaker effect.

group of neurons, I guess you could say, in the heart that kind of dictates speed there, right? That's right. But it dictates only basically one speed. So as we know, sometimes we want our heart to slow down, sometimes we want it to speed up. So thankfully, we've got innovation to the heart. So outside control as well. Yeah, that comes from the sympathetic nervous system, which is the fight or flight, and the parasympathetic nervous system, which is the rest and digest. And also...

hormones as well, right? Yeah. Through the bloodstream. So effectively, you know, you want to speed it up. You tell the sympathetic nervous system, increase heart rate. You want to slow it down. You tell this parasympathetic nervous system, particularly via the vagus nerve to slow it down. And so that's the way that we can regulate that heart rate. We're going to talk more about heart rate in a second though, but that's just to highlight a bit of the structure and a bit of the function of the heart. What about valves quickly?

Okay, so any time blood needs to move from one area to another area, so from an atrium to a ventricle, it needs to go through a valve, or from a ventricle into a vessel, it needs to go through a valve because they're one way. So effectively, you're going to have the mitral valves, which go from the atria to the ventricles, and then you're going to have the single... There's only one of those, right?

Well, there's a mitral. Sorry, sorry, sorry. You've got the atrioventricular valves, which go from the atria to the ventricles. One's a mitral, one's a trachea. So mitral, you might have seen the new Pope. Oh, yes. I'm all on that. So we've got the new Pope now. We? Pope Leo. We do. No, but you, well, the world. And you might have seen a hat he wore. Yeah. That's a mitre. It's a mitre. Like mitre 10. So the mitral valve is named after that cat.

cap or that headpiece. Anyway, moving on. I just wanted to give you the reason why it's called that. Technically it should just be called the atrioventricular valve but we can call it more commonly referred to as mitral valve, isn't it? And then you've got the semilunar valves and these are the ones that stop the blood. Half moon.

Yep, semilunar. Very good. Very good. And they stop the blood from falling backwards into the ventricles. So regurgitation. Yeah, yeah. So it's important that – so for example, one of the semilunar valves called the aortic semilunar valve. You've only got two. Yes. There should be three flaps so that when the blood leaves the left ventricle –

When it falls back down when the heart... In dice songs. Yeah, thank you. It doesn't fall back into the left ventricle. I've only got two of those, which means it increases... So in your parachute, you've only got two...

Parts of your parachute. That's right. Increases my risk of regurgitation, of the blood falling back in. I might need a valve replacement at some point in the future. Whether that's near or far, that's up to my heart. All right. So we've got those valves. That's good to know. What we need to talk about now, however, is something I want to highlight here.

is the heart muscle, which we call myocardium, right? It's like type one skeletal muscle. Now, do you remember we spoke about the muscle tissue in the context of exercise phys as the last episode? Do you remember type one versus type two muscle fibers? Yeah. Also known as Matt Barton ones. Which ones? Type one. Slow and steady wins the race sort of thing. Slow. Yeah. But reliable.

Maybe. Let's just stay with slow. Slow twitch. Type 1 fibres, slow twitch, aerobic respiration, uses oxygen, they're fatigue resistant. That's the heart. It is fatigue resistant. So they're like the type 1 in the skeletal muscles but they've got even more mitochondria. Exactly right. So it's something like 20% of cell volume in heart muscle cell, cardiomyocytes, are mitochondria. So really important. So that's an important thing to highlight because...

But one big difference is, unlike the skeletal muscle that we spoke about last week, with the satellite cells that can kind of provide more nuclei and protection after injury, cardiac muscle don't have these. So if you injure cardiomyocytes, they're generally dead. Yes. Very important point. Or I should say when they die, not injured. Yeah.

Yeah, yeah, but they don't regenerate, right? So scars are formed and then the heart's contractile capacity is reduced. So we know that the job of the heart is to fill with blood, contract, eject that blood and do it as efficiently and as rhythmic as possible to meet the demands of the body. In this context, the demands of the muscle tissue. So we need to talk about this relaxation and filling, right? And contraction. So when the heart relaxes,

That's called diastole or diastole or the diastolic phase. And that's when the heart fills with blood. Then once it's filled, it will contract and that's called systole or systole or the systolic phase. And that's when blood gets ejected. And both of these are important parts of what we call the cardiac cycle.

So the cardiac cycle is effectively one relaxation, filling and ejection round, which is equivalent to a heartbeat. So let's talk a little bit about if we take one cardiac cycle,

Let's have a look at the systolic and diastolic phases and how they contribute time-wise to what's going on. What do you reckon? Yeah. The only caveat I'll put here is you can have systole and diastole in the atria as well. True. Because they will still do the same. So they'll still have their contracting phase and their filling phase.

But when we generally refer to systole diastole, we're referring to the ventricles. And that's important because they're delivering the blood to the body, i.e. the muscles in this instance. But I want to ask you, you know, yes, the atria have their own systolic phase, so contraction, but why is it less relevant? Well, I guess the atria feel pretty easily on their own. And then when...

they empty most of, what is it like 60 to 70% of atria emptying is just done by gravity or it just opens the atrioventricular valves and just falls into the ventricles. Yeah, exactly. So they don't have to necessarily...

push powerfully to get all the blood into the ventricles. A lot of it just falls into it. Yeah, so meeting the body's oxygen demands, atrial contraction isn't as important as ventricular contraction. So if we take – so now we're going to start looking at rest versus exercise and have a look at contraction versus relaxation. So somebody's at rest. Their resting heart rate, 75 beats per minute per

How long does a cardiac cycle tend to last for? 75 beats per minute. Yeah. That would then mean you need about 0.8 of a second per beat. Okay. Yeah. Times by 60 would give you a heart rate of 75 beats per minute.

Does that make sense? It does. I just don't think that math works out. So if you had a resting heart rate of 60, a cardiac cycle would be one cycle per second. Yes. But if you've got a heart rate of 75, you'd need a cardiac cycle every 0.8 of a second.

Yes, true. Yeah. Okay. Does that make sense? Yeah, that makes sense. So then... That's exactly right. Sorry, my math is ridiculous. So if you multiply... So you've got 75 beats in a minute and you've got 60 seconds in a minute. Yeah, yeah. You just do the math and divide one by the other and you've got 0.8. So one cardiac cycle is 0.8 seconds. I'm sorry. So...

Of that, that cardiac cycle needs to be made up of one diastolic phase and one systolic phase. If we just refer to the ventricles, that's right. So how long, if we were to, let's say the systolic phase, the contraction. Let's start with the diastolic, the filling. So you'd think, I would have thought logically more of the phase would be systole. Why would you think that? You just think that more...

Both are obviously important, but more of a dominant part of it would be just getting all that blood out to get throughout the whole body. Because the body needs the blood, so it's reliant mostly on contraction. And it...

would take more time to really force it out and empty the ventricles in the systolic phase. Therefore, it needs more time. So it's interesting you say that because in a way, the systolic phase is very important and we'll see why in a second. So to the point that you were saying, of that 0.8 seconds, the systolic phase is only 0.3 of a second, right, of that 0.8. Right.

And the diastolic phase is 0.5 of a second. So of the total cardiac output percentage-wise, 63% of the whole phase is in diastole.

On the cardiac cycle. Yeah, yeah. So two thirds is diastole, one third is systole. That's right. Ballpark, yeah. Yes, yeah. For that one cardiac cycle. At rest. All right. So this is important. This is at rest. So again, systolic, 0.3 second, diastolic, 0.5 second. So more filling time and then a shorter contraction time. Two thirds filling, one third contraction. But then I'm telling somebody to, I'm telling Matt to do exercise. You're going to

Max yourself out. Let's say you get 180 beats per minute, right? At 180 beats per minute, your cardiac cycle is obviously changing. Yeah. So you're having one cardiac cycle every 0.3 of a second. Okay. Every point. Okay. Every 0.3 of a second. So of that 0.3 second, there's not much. You're doing two phases. You're filling and ejecting. That's amazing, isn't it? All right. Let's have a think about which one. So

The systolic, I said at rest, was 0.3 of a second, but that's for 0.8 second cycle. The systolic goes from 0.3 to 0.2, but it's only a 0.3 odd second cycle. So now it switches and now two-thirds of the cardiac cycle is now in systole and only a third is diastole. So it's…

Yes, so the diastolic is 0.13 of a second. So what we're saying here is that when we go from rest to exertion or exercise, that your diastolic goes from being the prominent part, filling, to being the least prominent part...

Because we need to just get that blood out. So it obviously also means that when we exercise, less blood is filling the heart, which will also mean less blood is getting ejected. But the thought is that if we're contracting more times in the minute, over that time, more blood will hopefully get out. Even less is...

even though less is filling, more blood will hopefully get out over that time period. Does that make sense? It does. So that goes back to your original point about thinking the systolic phase is most important. It obviously is because it's the one that's least affected going from rest to exertion. It's the diastolic phase that significantly drops down. Now, we need to talk a bit about

when this blood exits the heart, do you want to talk about cardiac output now or would you like to talk about anything else? Let's just do blood pressure quickly because the systole and diastole is also pretty much the same in blood pressure as well. Yes. So when we take a person's blood pressure, we have this high value and low value and that correlates similarly to the left ventricle which is generating these forces. So...

Blood pressure is generally taken on a person's arm, upper arm. And what's the physiology? What's actually happening when we take blood pressure? So you put a cuff around your arm and you start to pump up the pressure within the cuff so it gets tighter and tighter around your arm. Now...

We've got arteries and veins in our arm. So I want you to tell us, I know you asked me the question, but as I pump up the pressure of that cuff, over time, will that cuff start to close off veins first or arteries first? Yeah, veins will go first because they're superficial and they have less pressure in them. So they would get closed off sooner. And you'd probably see this if you were ever to give blood

The person who's taking your blood generally puts a lighter tourniquet around your arm just to make your veins stick out because that's just occluded them so the blood's not returning well and they become more prominent so then you can stick a needle in there and extract the blood out. But that tourniquet, that light tourniquet wouldn't stop the arterial blood. Yes. But when you do a blood pressure cuff...

and you pump it up, it would stop both. Okay. So once you've hit that point where it stops both, that means you no longer have a pulse in that artery of your arm, that brachial artery, for example, because blood can't get through it.

So what then happens? You get a stethoscope and you have a listen to that brachial pulse. Yeah. And you shouldn't hear anything once it's all pumped up, right? That's right. I mean, it's pumped up beyond the flow in your artery. Yes. So if you think about this, right, if the pressure in that artery of your arm –

is let's say 120 millimeters of mercury. All blood pressure is, is the force that the blood places on the walls of the vessel. So it's trying to, trying to basically leave the vessel, right? It's trying to push its way out.

But luckily vessels don't let that blood out unless hopefully we're at capillary beds. So if it's 120 millimeters of mercury, you've got 120 millimeters of mercury worth of pressure pushing that artery outward, right? Which is the head of force that your left ventricle has created at the systole, at the heart in the cardiac cycle. Exactly. And so when you put that cuff around your arm and you pump it up,

If you pump that cuff up to 120 millimeters of mercury, it should equal the outward force of the blood because now you're squeezing the vessel. It should equal the force of the pressure in the vessel and then close it. So anything above 120 millimeters of mercury pressure on the cuff should close that vessel. That's right. And so you then can put a stethoscope onto the –

and you shouldn't hear anything, right? Correct. So then what do you do to find out what the blood pressure value is? The person taking your blood pressure would slowly release the pressure in the cuff and then to the point where the lumen in the artery...

or just the side, the diameter of the artery would start to open and blood is starting to move through it again. Okay, so it's opening up a little bit, little bit, little bit at a time and it'll hit a point where blood can now start going through. And you'll hear that whoosh through that occlusion and that's what you can hear on your stethoscope and that's the first...

highest number that's telling you the pressure in your artery at the highest level of system it's pretty smart because it's basically saying well we've released the pressure enough on the cuff that we now know that this is the pressure of the blood vessel this is the pressure of the blood in the vessel because it's enough to overcome the opposing force of the cuff yep

So let's just say you release it at 120 millimeters of mercury and you start to hear the whooshing sound. Ah, okay. I've got the highest pressure.

possible in this brachial artery, and that's 120 millimeters of mercury, that's going to be equivalent to, like you said earlier, the force generated by the heart contracting, which is the highest force. So that's the systolic value. So you've got 120 millimeters of mercury for your systolic value. But how do you find the next value, the diastolic value? You just keep releasing it. And because you're taking the pressure off the cuff, the blood vessel gets bigger.

So it's still got resistance as you're decreasing the pressure. So there's still some resistance against the flow. But as soon as that resistance has completely been relieved, then you shouldn't hear any turbulence. And that's telling you that that's the complete relaxation process.

of the heart at that point. Oh, sorry, the blood vessel at that point, which is also the relaxation phase at the heart or the diastole phase, the filling phase. So that's then telling you that there's no further resistance. So that would be...

When the sound disappears. So to further explain that, when your heart contracts the systole, blood will get ejected at its highest pressure, 120 millimeters of mercury, right? And that will stretch the aorta, which is a large artery, very stretchy. And that pressure, like we said, 120 millimeters of mercury, the systolic value. But...

But once it's stretched, the heart will then relax and be in its diastolic phase. And that stretchy artery snaps back. And as it recoils and snaps back, it continues to push that blood through, generating a second pressure, which is the pressure that's now been generated from the elastic recall of the artery. The heart's relaxed, and that's why we call it the diastolic phase. So when you've got that cuff on and you're slowly releasing it,

It's still too tight for the diastolic blood phase to move through, but not for the systolic. So you hear whooshing coming through because the diastolic isn't enough to get through. It's not strong enough. And like you said, then once it's fully open, then you stop hearing whooshing because now you've found that point where the diastolic can get through, which is about 80 millimeters of mercury. Because I always used to think, how come the diastolic phase isn't zero? Because if the heart's

fully relaxed, no pressure should be generated. But the diastolic value is reflective of the elastic recall of your arteries, not the pumping power of your heart. The systolic value is representative of the pumping power of your heart. But saying that, if you were to take a blood pressure of the last blood vessel returning back to the heart, it would be zero. True. Or almost zero. Because the pressure drops as you move through, right? Yeah.

Just quickly explain why that's an important concept to understand, that it goes from high pressure to low pressure. Because blood flow is determined by the difference in pressure within the system. So you generally want to have the highest pressure at the front end of the loop.

and the lowest pressure at the last point of the loop. And that then creates a gradient from high to low, and therefore blood will flow in that direction always. Perfect. And that's important for determining how blood will move through the body. Now, if we look at blood pressure, there's an equation that represents blood pressure, which helps us move on to the next part, which is talking about the muscles and exercise specifically. So the blood pressure equation...

is that your blood pressure equals the amount of blood being ejected from your heart every minute, which we call the cardiac output,

multiplied by what we call the total peripheral resistance, sometimes termed the systemic vascular resistance. Sounds complex, but effectively it's just saying how much resistance the blood is facing in the vessels, which generally speaking is just the diameter of the vessel. So if your blood vessel is constricted and the diameter of the hollow lumen of your blood vessel is narrowed,

...the resistance goes up. And if the resistance goes up... ...your blood pressure goes up... ...because blood's finding it harder to move through... ...and the blood backs up into the heart. And then when the heart has more blood in it... ...it ejects more blood, right? So we just have to multiply those two things... ...cardiac output times the resistance in the vessel...

And it gives us our blood pressure. So if you increase your cardiac output, you increase blood pressure. If you increase the resistance in your vessels, so by narrowing them, you increase blood pressure. But the cardiac output itself has some values that contribute to it. What are the values that contribute to our cardiac output? What are the two major values? So cardiac output is the amount of blood that comes out of the heart per minute. So there's going to be...

And this is going to be measured in mils per minute. Sometimes cardiac output is termed Q. Really? Yeah. Do we know why? Quotient, possibly. Yeah, I think it's just in terms of flow. It might be an engineering term. Okay. Q, measurement of flow. Yeah. I think it's quotient because it's like the PQ ratio of –

when we talk about alveolar ventilation, right? Anyway, go on. So the cardiac output is measured in mils per minute. The minute part is to do with heart rate. So this is how many times the heart's beating per minute. And then you've got mils, which is the stroke volume, how much blood's coming out of the heart per beat.

So adding those two together will give you... Multiplying those two together. Will give you the cardiac output. Okay, so let me give you an example. Let's say at rest, my heart rate is 72 beats a minute. That's how many times it contracts, every minute. But with each contraction...

it ejects 70 mils of blood, which is my stroke volume. So heart rate times stroke volume, that should give me my cardiac output, which is, can you do the math, 72 by 70? Five litres? Five litres. Per minute. Per minute, that's right. And I always tell my students, you know, to put this into context,

Fill up a bucket with five litres of water and get a timer and pour that five litres out over 60 seconds. See how much water comes out until that five litres is fully gone. It's a lot of blood. That's at rest. Wait till we start talking about exercise, right? So this is important because...

So let's have a talk about how being an untrained person versus a trained person by exercise compares at rest. And then let's compare the untrained and trained person during exercise. Okay. So I just said untrained, your heart rate is, so let's say you're the untrained person. We'll just do this. Yeah, thanks, random. No, it's all at random. Just let's say you're the untrained ugly person that we do this with and I'm the trained attractive person, right? Yeah.

So your heart rate is 72 beats a minute. Your stroke volume is 70 milliliters. Your cardiac output is 5 liters. Now, my heart rate, you've probably heard athletes like myself, our heart rate is low, right? Me and the rest of my peers. So my heart rate is 50 beats per minute. So that's 20 beats per minute less than mine.

Yeah. So your heart's lazy? 22 beats. Well, let's just wait and see. Just from that, I haven't given you the second piece of information here, but me saying my heart rate's low, you would assume... My cardiac output is less. Yeah, exactly. But...

My stroke volume is 100 mils per contraction. So every time, even though it contracts only 50 times a minute, each contraction will eject 100 mils of blood. So 30 mils more than me. Correct. Per beat. Which makes my cardiac output what? The same. Five liters a minute. So even though both the factors are different...

They are both ejecting the same amount of blood every minute. So it's basically like, let's say you and I want to create, make a concrete path. Oh, thank God. That's what you said. Okay. I was waiting for you to say baby or something. A concrete path. And, and,

We're doing it with wheelbarrows. Okay. Your wheelbarrow size is bigger than mine. Thank you. For me to deliver five – well, it's not much. I love your analogies, Matt. Let's just say five tons of concrete. All right.

If my wheelbarrow is smaller, I have to do more loops up and backs than you do because your wheelbarrow, you can carry more concrete at one given time. You know what? That's actually not a bad analogy. That's exactly right. Yeah. Okay. Before we move forward to talk about what happens to you and I during exercise, why is my, as an athlete, why is my heart rate lower and my stroke volume higher? Well, I guess start with the stroke volume. Yeah.

You're just more efficient in getting the amount of blood out. Why? What is it? What's changed? What's anatomically or physiologically changed? Well, there's a couple of determinants of stroke volume. There's how much blood returns to the heart, which sometimes we call preload. Yep. So this would be, I guess you would say, a measurement of venous return. Yep. So that could be dictated by... How much blood's in your body? Could be, yeah.

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Yep. But also how efficient maybe your...

of returning the blood from that system back to the heart is. So some things that can enhance the venous return could be the muscle pump effect. So this would be if you're moving the muscles a little bit more, you're returning more blood from that. Have you heard of the respiratory pump before? So this is just the changes in the thorax and the abdomen in breathing, right? Yeah, so if I take a breath in...

My diaphragm contracts and pulls down. My external intercostals contract and pull up. So my whole thoracic volume, and remember my heart sits within the thorax, the pressure drops. So the volume increases but the pressure drops. Exactly. And that's why air rushes into the respiratory tract. But at the same – by the same token –

blood will be dragged in from the venous system into the heart. Right. Right? Because it's in the thorax as well. Yes. So you get more venous return through a deep inspiration. Through exhalation, the opposite. It's going to sort of increase the pressure in the thoracic cavity and that's going to push things out. Yep. Does that make sense? It does.

But also just the diameter of your veins would also determine how much can come back. Yes, true, true. Because 60%, approximately 6% of your whole blood volume is in veins. Okay, so me as an athlete, my stroke volume's high-

Because I've got probably more blood volume in my body. I'm probably more efficiently bringing the blood back to the heart. But the venous return isn't the only factor. There's also the effectiveness of contraction.

So how well the heart muscle contracts. That's right. So me as an athlete, I would say that because I've been exercising a lot, my heart muscle is probably bigger and more efficient. Yeah. So it contracts harder. That's right. Okay. Is that the only other factor? And then there's also the pressure pushing against the heart. So if you've got more, this is termed afterload. So if you've got a higher blood pressure, so that's the pressure on the other side of the aorta or in the aorta and beyond. Yeah.

it's harder to push the stroke volume out. So the higher the pressure, the more resistance against the stroke volume. So when that – okay, so the three factors affecting stroke volume is preload, the filling of the heart, contractility of the heart,

and afterload, which is how hard it is for the ventricle to eject the blood into the vessels. Yeah, but keep going. But that afterload is inversely related to the stroke volume. So if the afterload's high, it means, oh man, it's really difficult to eject this blood because maybe the aorta's narrowed or maybe the blood pressure in the systemic circulation's high or something like that. Yes, that's right. And so if that goes up, then the stroke volume goes down. But effectively, these are the factors that affect the stroke volume. Yep.

But just add in one little bit more detail there, a combination of preload, therefore more blood at the end of diastole would kind of stretch the ventricles more, so a bit like a rubber band, but you're pulling it a bit further, stretchy, then it has more capacity to contract harder. And this is called Frank's darling law. So there's a tension-contraction relationship here. And we spoke about that last week with...

How long should your skeletal muscle be to be most efficient in this contraction?

Now, it doesn't want to be completely stretched because it's not as effective or it doesn't want to be kind of all bunched up because it can't contract. It needs to be in that perfect happy medium and that ventricles work in a similar way. If you stretch it a bit, which means it's filling more with blood, it can contract more powerfully. So the Frank Starling mechanism is the more blood that fills the ventricles, the stronger the contraction of the ventricles, the more blood that gets ejected from the ventricles. Okay, so let's just reiterate here,

Me as an athlete. I like how you keep saying that. This is just the scenario. It's got nothing to do with anything but me being an athlete. Attractive athlete. Thank you. I forgot about that. Yes. So me being a very attractive athlete, my stroke volume is high for a multitude of reasons. One, greater blood volume in my body.

Two, I have stronger contractile force of the muscle. Three, I probably have a reduced afterload because the vascular system is probably more dynamic and able to relax better than an untrained individual. So all those things will increase my stroke volume, the amount of blood getting ejected. Now, let's compare all this to when we now do exercise. You as the untrained individual...

And me is the train. Ugly. Sorry? Untrained and ugly. Oh, yes. Thank you for highlighting that. That's right. So you can't write the letters to me. He's saying it about himself. See? So Matt's a beautiful man, by the way. So just in case people think that I'm being, you know, cruel, I love the man. Yes, he's ugly. Yes, he's unfit.

I love the man. All right. So we both exercise. Now we're doing, let's say we're going to our max, right? VO2 max. VO2 max. Your heart rate now goes to 200 beats per minute. That's impressive. Okay. Let's just wait and see. And your stroke volume is 110 milliliters. So it's gone up, right? It's gone up. 40 mils. 40 mils. So 200 times 110 gives you 22 liters per minute of cardiac output.

Good job. You've just increased your cardiac output to try and match the demand of the oxygen required for your muscles. Now, me, let's look at me. So my heart rate goes to 190, which is less than yours, right? So you might think, uh-oh. That's lazy. That's lazy. But my stroke volume jumps up to 180, right?

So that's 70 mils more. Yeah, 70 mils more than you, right? Big wheelbarrow. Which is as much blood that you eject at rest, right? So again, as an athlete, you eject more blood through that stroke volume so your heart rate doesn't have to go as high. Now this can be an issue for the untrained person because there's obviously a sealing effect that can happen with the stroke volume because that's due to...

How much blood's in the body, which is going to be normal. They're not an athlete. They haven't remodeled the myocardium of the heart to make it bigger and stronger. I'm just saying, right? And they probably don't have dynamic vessels to relax, to reduce the afterload. So they have to increase their heart rate in order to try and maintain the oxygen demand. So this is why people who are untrained, when they start to do exercise, their heart rate might go through the roof because they're trying to meet the oxygen supply demand that

because they can't play around with the stroke volume very much. They have to play around with the heart rate. All right, so let's speak this through. So let's say you do it.

an activity and you incrementally increase it in VO2. Yep. So as you start to go into more intensity, your cardiac output wouldn't match that well. So it follows the same linear arrangement. Well, and that's because VO2, talking about the oxygen requirement, and CO2 being the way that you get the oxygen, it's going to be a linear relationship. So if you graph this, it would follow a similar relationship. But then if you...

kind of calculated it, you look a bit deeper, what you'd actually find in the cardiac output is the stroke volumes kind of plateauing or dropping off. At what point? Probably 40, 50% VO2. For who? Untrained or trained? Untrained. Untrained. Yep. And the heart rate is what's compensating. So the heart is just beating faster to maintain that cardiac output for delivery to the muscles. Yes. But in a trained athlete...

What you're actually finding is the stroke volume can still continue to go up. Hasn't hit its ceiling. And the reason for that is it's getting better venous return. So you're more efficient through all those muscle pumps, getting more blood back, probably your veno constricting better. So you're getting all the volume out and your contractility of the heart's more efficient. Mm-hmm.

And you've probably got less afterload. Yeah, yeah. And that's important because that's putting less metabolic demand on your heart. And this also speaks to that when we are talking about individuals who have heart disease, particularly those with ischemic heart disease, which would be narrowing of the coronary vessels, when they are working harder, so they're exerting themselves,

They've got their hearts working harder probably through the heart rate and probably also through the blood pressure afterload.

And therefore the metabolic demand of the heart is greater. Yeah. So it needs more oxygen and therefore it's going to get to its point where it starts to run out of oxygen itself and that causes the chest pain. Yes, yes. And that's really important is that because the heart's pumping more in the untrained individuals to try and compensate and make up for that oxygen that's needed by increasing the cardiac output.

It's putting more demand on itself, right? It's just like, okay, let's take your wheelbarrow example. You're doing way more trips up and back, right? You're exhausted. You're sweating, right? So you need more food to eat. You're breathing more. You need all these things to meet the demands of you just going up and back, up and back, up and back. And so putting that strain on that heart, right?

May potentially lead to an issue. And that's important for, say, the exercise physiologist or the physio that is working with patients with ischemic heart disease. They need to figure out where is the VO2 that they can exercise to without starting to cause too much metabolic demand on the heart and causing potential ischemic events. Yes. But saying that...

How can cardiovascular training, endurance kind of activity be protective to the heart? Well, we know that doing cardiovascular, what would you call it? Training, aerobics. Aerobic, that was what it was. Can actually be protective, cardioprotective, meaning- 60 minutes a day.

That trained athletes who have a heart attack compared to untrained, they fare better post-heart attack. In regards to what?

Well, less myocytes dying. Oh, wow. So two people both having heart attacks, the trained athlete will have less heart cell death. And the reason for that is their aerobic endurance training has made certain metabolic biochemical changes in their heart which may...

make them fare better when they go into that ischemic slash infarction event? Yeah, the cell itself is fitter. It can handle calcium better. The mitochondria has a greater capacity to produce ATP and deal with oxygen. It also has better antioxidant capacity. So there's all these different things that come into play. Another thing I want to add, so we've focused heavily on the stroke volume here, right, those changes.

But let's just talk a little bit about the heart rate and how that can be changed. Because you can...

So it's not just that the heart rate goes down for the athletes simply because the stroke volume has gone up. That is a factor. But the heart rate goes down in the athlete also because they have a better control of their autonomic nervous system that innervates the heart. That's important. So at the start of the episode, we said that the heart, while it has its automaticity, its own intrinsic rhythm from the pacemaker cells...

that we need the sympathetic to speed it up and the parasympathetic to slow it down. Now, athletes have a better control of the sympathetic versus parasympathetic heart rate control mechanism for the heart. They've just got better control of that. And so just so everyone's aware, the parasympathetic nervous system, the thing that slows the heart down,

This is the vagus nerve. It innervates or speaks to the nodes, the nodal cells. So the sinoatrial node and the atrioventricular node. And it basically tells the pacemakers to slow down. Now, the sympathetic nervous system, it innervates the sinoatrial node

And the muscle of the heart. So not only does it tell it to speed up at the side of the atrial node, it can tell the muscle to contract harder by dumping more calcium into the muscles. Makes sense. Right? Okay. So just keeping that in mind. So the reason why I brought that up was because I also want to talk about heart rate variability. Okay.

You've heard of that, obviously. Yes. Before we jump into that. Yeah, just because I think some students would think this, and I probably thought the same when I was a student, is when we look at the effects of, we'll just say the vagus, or should we just call it parasympathetic? Let's just say parasympathetic. Parasympathetic versus sympathetic. And just know that it is the vagus. So in a way, when we are at rest, the parasympathetic is switched on, and in a way, the sympathetic is turned off.

Now, when you start to do a little bit of exercise, so maybe you start walking, you don't necessarily turn the sympathetic on straight away. Rather, you use the dimmer switch on the lights. You start to dial it down for the parasympathetic. So you're almost turning it down.

And in doing so, you're removing the parasympathetic effect on the heart, which is increasing heart rate. But then you get to a point of, say, ballpark 40% VO2. Then you switch to sympathetic on, and now the sympathetic actually becomes outflow dominant. And then that just keeps ramping up. So that's now a dimmer switch, but going the opposite way, turning it up. So now...

So going from rest to your full VO2 max, the change is you're dialing down the parasympathetic effect until it kind of turns off and then you start turning on your sympathetic and then you're dialing that up. And that keeps...

becoming more and more dominant in its overall outflow neurologically. But on top of that, you've got the hormones that are coming from the sympathetic system as well, which is the adrenaline from the adrenal gland, which would also be released as you're getting probably 60% VO2 is becoming more impactful as well. Yep. And so if we talk about something like heart rate variability, because this leads, heart rate variability leads nicely after what you said. So

Basically, this is the variation in time between heartbeats, right? Your heart rate variability. And if I were to perform an ECG on you, so I put the sticky dots on you, the electrodes, and I measure the conduction of your heart, you get that nice ECG trace that probably everyone has broadly seen. And the highest peak of that trace, which is called the R wave, that's representative of the ventricles depolarizing. Effectively, that's what you see just before the ventricles contract.

Now, if you go from one wave or peak of the ECG trace to the next, that's one heartbeat. That's one cycle, right? So you can count how many of those peaks there are in a minute and that tells you what your heart rate is. So the R wave is the ventricles contracting? Yep, effectively. And so if you have a look and measure the time between each R wave...

So for example, maybe the time between the first R wave was 0.5 of a second and then the time between the next was 0.7 and then the time between the third was 0.2, right? Yeah. It's fluctuating quite a lot. Yeah. So you're basically measuring the standard deviation or the variability between each R wave. Makes sense. This gives you the heart rate variability. And you might think, why the hell would we want to measure this? So going back to what you said about sympathetic versus parasympathetic at rest,

versus during exercise, which we broadly call the autonomic nervous system control. At rest, your heart rate variability should be variable. It should have wide variation. What that means is there's a good balance at rest between the sympathetic and parasympathetic. Sometimes you might get a little sympathetic tweak every now and then, but mostly it's a parasympathetic. Effectively, the wide variation tells you that

The heart can adapt and change to, you know, what needs to be done at rest. Okay. That's good. Then when you perform exercise, like you said, you tweak, you're turning up the sympathetic volume knob. And turn off the parasympathetic. And turning off the parasympathetic. And as we know, the sympathetic, like we said, tells the sino-atrial node, fire, fire, fire, fire. So it's more rhythmic, but the...

it's a low variation. So the R waves are tighter, but more consistent in their variability because- It's a lower variability. That's right. And that's telling you there's more of a sympathetic drive. Now, the reason why we measure HRV is because-

You can measure somebody's HRV, again, at rest and during exercise. And we've done this before, right? We did this with Chris Hemsworth when we did the first Limitless TV series, right? Because we put him through stressful situations. So what the HRV can tell you is,

If you've got a low HRV at rest, it's telling you, hey, you've probably got more of a sympathetic drive than you should. Yeah, you're in fight and flight whilst you're at rest. That's a bit abnormal. Yes. And it might be reflecting something like, okay, you're not recovering well after exercise or maybe you're in a state of stress or fight or flight. Like emotional stress. Yeah, exactly. So it's

But the thing is clinically as an exercise physiologist, it can reflect or even predict. It has some predictive power for health outcomes. So if somebody has consistently low HRV –

It can be a predictor in some regard for poor health outcomes. Yeah. Does that make sense? Because it would be a surrogate for your system is stressed chronically. Yeah. And that's not a good thing. Well, especially when if you're under sympathetic drive a lot of the time. That's what I mean, yeah. It increases your blood pressure. Yeah. And if your blood pressure is too high for too long, it damages the vessels. Yeah.

And as we know, hypertension, which is chronically elevated blood pressure, is probably the biggest killer on the planet because it leads to... A lot of things. Metabolic disease, cardiovascular disease, a whole range of things, right? I listened to a podcast recently. Oh, was it ours? No, it wasn't ours. Then don't talk about it. So it was Eric Topol. Oh, yeah. Can you explain...

who that is quickly. Oh, okay. So you just, you bring up someone that you listen to. I followed him a lot during COVID because I felt he was fairly balanced. He just reported on studies. He didn't really get involved in the controversy. He just said, he isn't like next study. This is what it is. This is the outcome, blah, blah, blah.

So he's a fairly well-regarded medical professional in America. Yeah, he's a cardiologist by training. He is an active researcher as well within cardiology. So not only does he see patients, but he's a researcher. He understands literature very well, but he also has a particular focus on longevity, but not longevity as people think, like the...

Just ageing well, ageing well. Yeah, it's not about hacking the body. No. It's just about how can I live a long, healthy life? And that might be to 90 years of age with few comorbidities. Yes, that's right. So anyway... So this podcast was... He's apparently got a new book out and it's, you know, around health and ageing, but also...

with bits of AI in it and the focus that I wanted to put here, this is why I brought it up, was the use of AI interpreting both ECG and heart rate variability. Oh yeah. And

It has the potential because AI, these big open source AI models have the potential. In a way, they're just pattern recognizing software, right? So are we. Yes, that's right. But it's starting to do it better than we are. That's true. Now, so in this case, and he's speaking as a cardiologist, is like we can throw an ECG through, which he would have considered to be normal.

through AI and it can look at the pattern of it, which would be seen to be in a sinus rhythm, normal sinus rhythm. However, it's picking up subtle changes that the human eye wouldn't have found that is then finding you may be preclinical cancer.

to go into atrial fibrillation. Right. So you might be a couple of years away, but you may develop AF. Judging on these changes in your rhythm that are still normal, but they're just dynamically different. Which a cardiologist or a cardiac technician couldn't pick up. Right. Right.

And the same goes with heart rate variability, which is now speaking to some of these devices that we can buy, which are like the watches and the rings. Yeah, the whoops and the aura rings. That may start to find...

periods in your day that you may be more stressed than you should be, which is inappropriate to what you're currently doing. Again, if you have low heart rate variability, but you're exercising, that's normal. Yeah. But if you're sitting at your desk or relaxing and you having that, that could tell you something that is going on. Yes, exactly right. Um,

So where should we move? We probably should. Okay. So just to close the, the, the chapter on cardiac output in, um, making sure we get enough oxygen to the, uh, to meet the demands of the muscle. We do this by tweaking our heart rate through the autonomic nervous system, but also through affecting our stroke volume, which we said are a multitude of factors. We talked about how, um, uh,

athletes through exercise can remodel the heart and how that can affect stroke volume but also tweak the autonomic nervous system as well. Now, cardiac output is only one aspect of being able to get that. So that's the heart's ability to get that blood out. But we also know that

We're ejecting five liters of blood into the vessels every minute, but that blood needs to go to all the tissues of the body. So now we need to talk about, well, how can we best redistribute this five liters? Well, let's say now during exercise, it might be going up to 25 liters per minute cardiac output, right? Because heart rate and stroke volume has gone up. How do we best redirect it to get to the place it needs to be, i.e. the muscles? So

I want to talk a little bit about if it's okay, if you think it's the best place to say it, that if we were to look at of the five liters per minute that gets ejected, so cardiac output every minute, it goes to the tissues of the body. What percentage goes where? Can we do that? Okay. Yeah. So,

Okay, your heart's pumping out five litres every minute. 20% of that five litres is going to your gastrointestinal tract, right? Because I am in a rest and digest state if I'm at rest. Good point. About 4% to 5% is going to the heart to feed it. About 20% is going to the kidneys for filtration but also feeding the kidneys. And 15% is going to the brain.

And about 15 to 20% is going to the muscle. And this is all at rest. So let's just have a think about this for a sec. So the brain is getting 15% of five liters, right? It's 15 to 20%. So this is 750 mils to a liter of blood. Every minute is going to the brain at rest. Yep. And that's pretty much the same as the muscles. That's getting the same amount as the brain at rest. 750 mils to a liter. Yeah.

But the brain is only a kilo and a half. That's true. Whereas muscle would be 20 kilos. Well, it depends if it's you, a kilo and a half. But for me, 90% of my body weight. So now I tell you to exercise. Now because of what we said before, all those various factors, your cardiac output goes to let's say 25 litres per minute is now getting ejected from your heart.

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Right. Now, the...

Distribution changes. So while your gut got 20% at rest, it's now getting 3% to 5%. It's saying digestion isn't an issue. We're not dealing with that right now. So it's shunting that blood elsewhere. The heart, which originally got 4% to 5% at rest, still gets 4% to 5%. Even though it's working hard. Even though it's working hard, but it's 4% to 5% of a greater volume. So it's getting a lot more blood to meet its demands.

The kidneys go from 20% to 2% to 4%, which effectively is making it stay around about the same-ish to what it was originally getting, maybe a bit less. But here's the interesting with the brain and the muscle. So the brain was getting 15% of cardiac output at rest, which is about 750 mils. It then, during exercise, drops from 15% to 3%. But 3% of 25 litres is still 750 mils. Oh, sorry. Same amount of volume...

Just less percentage. Exactly. But the muscle goes from 15%, 750 mils, to 80%, 85%, which is about 20 litres of that 25 litres is going to the muscles. Huge. So we need to talk about – thank you, I've been working out. So we need to talk about what happens in the vasculature, the vascular bed, to say, nope, don't go there, yes, go there, to the muscles. Yeah. How would you – would you say that it's both –

Local changes and systemic changes? I would say so, yes. So let's start systemically. So just generally how we dictate blood flow through the body and we'll just focus here on the systemic loop. So this is basically going from the left ventricle back to the right atrium. You happy with that? Left ventricle out by the aorta, then all the branches, feeds the tissues and then jumps back to the right atrium via the venous system. Okay. Okay.

Now, the way that it flows in that one directional path is it needs to have a pressure difference between the start and the end. You alluded to that earlier. Yes, yes, yes. So the pressure, and now let's change blood pressure because we know blood pressure is systole and diastole. So there's a high and low. Yeah, we don't want to keep saying 120 over 80. Yeah, let's do a mean value, meaning an average, not...

You know, unfair. Be cruel. The YMTA. Yes. So this is termed MAP, M-A-P, mean arterial pressure. Yeah. Now the way we work this out is we take the diastole value. Yes. And then we, do we plus it or time it? We plus it. Plus it to a third. Yeah.

Of pulse pressure. Okay. And the pulse pressure is the difference between systole and diastole. So you deduct your diastolic value from your systolic value. Yeah, which is ballpark 40 millimeters of mercury. So 120 minus 80, 40 millimeters of mercury, and then you multiply that by a third. So why a third? Why are we multiplying it by 0.33? This is the fraction of time that...

Systole... Is in. ...is in during the cardiac cycle. Because we said earlier, at rest, 33% of that, what, 0.8 of a second was systole. Yeah. Right? So now... But what this also means, just very quickly, is that the mean arterial pressure, if we were to calculate it at rest, that's fine. Diastolic plus one-third of the pulse pressure. But because we said that during exercise, the fraction of systole changes...

we can't use the exact same equation to calculate the mean arterial pressure during exercise. Yeah. That's just an important point. It's different. That's right. But generally speaking, so we do that, that's going to give us a mean arterial blood pressure of 90-ish, between 90 and 100 at the A audit, let's say. Which, just so everyone knows, because we just said this complex, confusing equation without justifying why. The reason why we're talking about mean arterial pressure now is it effectively gives us

the pressure value that's required to feed the tissues, right? Yeah. So it's basically saying, look, this is the mean pressure that is required to deliver oxygen and nutrients to the tissues of the body. We don't really want it to go too high. We don't really want it to go too low under resting conditions. Yeah. Are you cool with that? That's fine. All right. So 90 in the A order. That's right. All right.

Now, if you go right to the end of the circuit at the right atrium. So would this be like inferior superior vena cava, bringing the blood back to the right atrium? It would be zero. Zero millimeters of mercury. Almost zero. Right. One or two. So that's a big pressure difference. So that then means because of that pressure difference, you'll have a flow in that direction only. Now, just to see how it breaks down as we move through, we leave the left ventricle and we go into the big ventricle.

resistant vessels. So they are vessels... Well, not even resistant vessels yet. So in the aorta? Yeah, let's say the aorta. Okay. What would you call those vessels? What are they termed? I call them elastic vessels. Elastic? Yeah. Okay. And then we go into the larger... So they're the larger arteries and we go into, I guess, the arterioles. Yes. Now these are... The resistant vessels. Smaller diameter and they start to put resistance against the blood flow. So just quickly, so...

While the arterioles are smaller, they're more numerous than the arteries. So effectively, Matt decides to cough and then coughed in the microphone as opposed to away. The arterioles, they're more numerous, but they're smaller. But like you said, they're surrounded by smooth muscle. So they're the ones that can change the diameter. And that's really relevant here, right? Yeah, that's right. So once we get into these arterioles,

the MAP or the MAP or the blood pressure drops, can drop by 60%. So it's diminishing the pressure quite significantly as we get into the arterioles. And then we get into the pre-capillary vessels. So these are just the vessels before we get into a capillary bed.

Then we move into a capillary bed. And once we're at the capillary bed, which is where all the exchange happens, and in today's case, this is in the muscle now. So now the mean arterial pressure is only around 25 millimeters of mercury. That's enough to get plasma out of the blood, deliver the oxygen, and pull the carbon dioxide back. Then when we get to the venous end of the capillary, now we're below 20.

Then we go into the large veins and by the time we get back to the right atrium, we're really looking at almost zero. Right. So this is a pressure difference. So that allows blood flow to go in that one direction. But the thing that also determines how well the blood flows, and this is a bigger determinant, is the resistance. Mm-hmm.

So how much resistance are the vessels placing on the blood flow? Yes. And so if you think about a hose attached to a, a garden hose attached to a tap, but that hose, let's say was the end of that hose was connected to, let's say 50 smaller hoses, right? So you turn the tap on and you've got water squirting at the end of 50 little hoses, right?

You would say that, okay, they're all at the same diameter, same amount of water is exiting each of those hoses. But let's just say you had the ability to narrow or...

increase the diameter of each of those hoses. What that effectively does is not only limit or increase the amount of water leaving a hose, it redirects, if you're limiting it, it redirects water to other hoses, increasing the pressure in the other hoses as well. So because if you're closing one hose off, the water backs up and the pressure goes up.

Right? And then it can push it out another hose at a higher pressure. Yeah. And so the arterioles are no different, right? So not only do they redirect like you said, but by narrowing them, you can increase the blood pressure as well. And the big things that add the resistance, because the resistance is more of a profound effect on blood flow than the pressure is. Yep. The big things that, well, the determinants of resistance will be the length of the hose. Yes. This...

Generally it's considered static, but you would say that individuals that put on weight, most notably adipose tissue, that you will increase the length of blood vessels. And in doing so... Why? Explain. Well, if you've got more tissue, more adipose tissue, you need to bring more blood to it. Therefore, you need to make more blood vessels. Therefore, more blood vessels add length, more length adds resistance, more resistance...

changes flow, therefore probably needs more blood pressure. So if I use my hose analogy, if I've got a five meter hose attached to the tap and turn the hose on, let's say 50%, the water will come out the end of the hose at a particular pressure. If I then make that hose, not five meters, but 500 meters and turn the hose on 50%, the water will probably dribble out the other end. So in order to get the water to the other end of that hose, you've got to put a lot of pressure in because as the water moves through, it's excretionally

experiencing resistance from the wall of the hose. Blood's no different. That's right. Now, another factor that can add to resistance, if you change water into custard, viscosity. The Jesus Christ of biology. So if you were to change...

the liquid component and make it thicker, that would also add resistance. So increase the viscosity. So by doing that, decreasing the water volume or increasing the solute. So decrease the solvent water or increase the solute, which is whatever's dissolved in the blood. So it could be more red blood cells. Yeah, so the hematocrit, if you had a high hematocrit, that would make it a bit thicker or

Solutes would be in – I wouldn't think solutes would make a big change. But saying that if you're dehydrated, you'd have thicker blood. Yes. And then lastly, and this is the most profound one. Pretty much the only really significant one in this context. Is the radius of the blood vessel. Yeah. So by changing the radius, you profoundly change the resistance. Yeah.

narrow it, increase resistance, relax it, decrease the resistance. All right, so let's talk about how we are redirecting all this blood, right? So we said that at rest that the blood is, you know, 15% going to the muscles, but now during exercise 80% to 85% is going to the muscles. So we can assume that the blood vessels have dilated actively

At the muscle. That's right. Right? But we've got things like the GIT, which have gone from 20% to 3%. So you'd say that they've constricted. That's right. So there'll be receptors located in those regions that would have, an example would be alpha-1 receptors that respond to noradrenaline. And when they respond to it, they constrict the smooth muscle. And that means the radius decreases, resistance increases, therefore blood flow decreases.

And for our North American audience, noradrenaline is norepinephrine. And so the way I think about it is that if we just focus on the vasculature at the muscle, at rest, we have our sympathetic nervous system innervating the blood vessels of the muscle. They have those alpha-1 receptors in those blood vessels. The noradrenaline is released from the sympathetic neuron, binding to alpha-1, and it's

tells the blood vessel to constrict. So you have at rest what we call a sympathetic tone of the blood vessel, which keeps it narrowed-ish, right? So alpha-1 stimulation narrows the blood vessel.

At the same time, the capillary beds at the muscle, they're only partly open, right? It's basically saying you're on the highway going through the tolls. And when it's busier, back in the day when we had toll bridges, right? Toll booths. Toll booths. Thank you. We've still got toll bridges, but toll booths.

Remember when it was super busy peak hour, they would open all the toll booths up so that more can get through and then when it wasn't busy, it would have three toll booths open. So it's sort of the same when at rest you've only got – what percentage of capillaries are open at rest-ish? 50%, 60%. Yeah. Now when we start talking about exercise –

a couple of things happen. One, when the muscle contracts and relaxes, it produces metabolic byproducts. And these can include things like nitric oxide and prostaglandins and ATP and adenosine. And these are all vasodilatory chemicals. So they're more paracrinal.

Meaning? They're working in their local environment. Perfect. So they're released by the local tissue affecting the local tissue. And it tells those blood vessels, hey, you know what? I know you've got this default relaxation thing going on, but just dilate so we can let more blood in. And I think some of these chemicals also have a sympathetic lytic. Yeah, sympatholytic. So they kind of block blood.

The alpha one bit as well. Exactly. But here's the... So again, talking like you said earlier, incremental exercise. So we've just started some exercise and we're releasing these chemicals. Then we're going, all right, I'm doing a full-blown hardcore training, heavy training right now. This is a stress that the body senses. So it stimulates a fight or flight response from the hypothalamus. And so what we end up getting is...

activation of the sympathetic nervous system. Now you might think, because I just said, well, you just said the sympathetic nervous system innervates the blood vessels of the muscles through the alpha-1 receptors to constrict. True. But when you get a full-blown stress response, the sympathetic nervous system innervates the adrenal gland, right? The medulla and says, time to release adrenaline or epinephrine. And so you get...

adrenaline, aka epinephrine, just being dumped into the bloodstream. And adrenaline is slightly different to noradrenaline. So noradrenaline, you could broadly say, is the neurotransmitter. And adrenaline is the hormone from the adrenal gland. And so it will bind...

to different sympathetic or adrenergic receptors. Just different effects on the receptors, yeah. So it binds to beta-2 receptors on the blood vessels of the skeletal muscle and tells them to relax. And so not only do you get those beautiful, like you said, sympatholytic receptors,

that are also vasodilatory, nitric oxide, ATP, prostaglandins, adenosine, you also get adrenaline telling the beta-2 to tell the muscle vessels to relax as well. Yeah, and I'd imagine at this state when you're pumping out the adrenaline is only sustainable for a short period of time in exercise. Absolutely. And that's probably speaking more to a very profound fight and flight response as well. So when you've got a lot of adrenaline in the system...

opposed to just noradrenaline from a sympathetic response to exercise, you're going to even clamp down even more on those blood vessels that you don't want blood to go to. Yes. Hence kidney, skin. GRT. GRT. And this is why you see...

to individuals that kind of have shock because they're not taking blood to the kidneys or the gut in those, not exercise I'm talking, I'm just actually talking about a different situation, but it's still adrenaline based and therefore you can get kind of damage to those organs if you're

continuing that real profound fight and flight situation. Because you kind of think if you were having something like, say, anaphylactic shock where you have vasodilation everywhere and everything's leaky, we know that a treatment to that is epinephrine. Yeah. Right? Adrenaline. And you give it as a bolus. And that would constrict all blood vessels because you're trying to get central blood pressure up. Okay? But that would be a very acute condition.

profound response in the adrenaline. But when we exercise in, it's this kind of combination between no adrenaline, adrenaline from neurological as well as hormonal. Yes. Tweaking, tweaking all these different systems. Is there anything else you'd like to speak to?

on this topic. We've gone through the fact that, you know, one of the main reasons why we've got the cardiovascular system for exercise physiology is to ensure that the muscles meet their demand of oxygen. We do this through increasing cardiac output, but also by blood redistribution. I think we've nicely spoken about those two points. But is there anything, any final points that you'd like to add? Well, we spoke about, I think we spoke about the changes in exercise. We've spoke about how that can be impacted effectively

I guess, over time in the exercise. And as we start to, I guess we spoke about incremental increase, right? Where we said as a VO2 of the intensity increases, the cardiac output changes, but that's at least in the untrained, the stroke volume isn't as profound as the heart rate. And that's something that I have to have a consideration on patients or individuals with

cardiovascular disease, but we also have situations where what happens if we draw out the activity, the exercise? So what happens if we make it a longer duration?

Well, what would you expect to see from a cardiac output standpoint if you're making it? Instead of a high-intensity bout of 20 minutes, now you're doing it beyond 90 minutes. Untrained, trained? Yeah, well, let's just say untrained. Okay, untrained individual and you're telling them to, let's just say, jump.

jog 20 kilometres or something. Yeah, yeah, just sustaining activity for 90 minutes to two hours. Well, effectively, if that's the case, then you would hit a particular cardiac output plateau. So your, we know cardiac output is heart rate times stroke volume. So your heart rate would hit a plateau and your stroke volume would hit a plateau because it's just going to the point in which it's meeting the energy demands and

but it doesn't need to go any higher. That's my assumption. Yeah, that's true. But then you start to have... So that would be fine if you wanted to sustain it for 30 minutes. Yeah. But if you want to draw that out for two hours, you're starting to have changes in your homeostatic system as well. Right. Like thermodynamics is...

Thermoregulation, should I say. Right, so you keep producing a lot of heat and also you're reducing the amount of energy from glycogen, for example. So you're also switching energy sources. And so things are now changing as well. Like you've got less blood volume to work with because you're trying to regulate your temperature. Oh, so you're sweating. So you're losing blood volume. That's right. But more volume of blood is staying in the tissue, not in the circulation. Right.

And so your stroke volume is going down. So your heart rate can only continue to go up to a certain point. So basically, you know, the first little bit, you've hit this nice, happy, healthy sort of rhythm where it's all in balance. But then you hit a point where the tipping point effectively, where stroke volume goes down due to those things you just said. And to compensate, because you're still maintaining the work effort, heart rate has to go up. But that can't continue indefinitely. So then what happens? Yeah.

Well, that will then essentially lead you to your... Full fatigue. That's right. And then you'll have to slow down and stop. Slap on the floor. Now, that goes with duration, but then you could also go to situations where you do intermittent exercise. So you kind of go...

do like a CrossFit kind of workout where you do high-intensity rest, high-intensity rest, high-intensity rest. But every time you go to the intensity peak and then go to rest, when you come back to your rest, you might have a one-minute rest. You're not going back to the baseline. You're kind of working on it. Additive. And then that will also lead you quicker to your VO2 as well, VO2 max. So that's another consideration you have to think about with exercise. Yeah.

duration, the intensity incrementally, and then also the type of exercise. So there's a difference in stroke volume between you doing activity like running, cycling,

And maybe something like swimming. Right. Because swimming, you're in a, what, supine, horizontal position? Laid down. So you have a different dynamics in blood return because you're not working against gravity. Wait, so you're saying that if I'm doing exercise standing up...

Because we said that stroke volume, which is very important for cardiac output, in part has to do with the blood returning to the heart. If I'm standing up, it's harder for the blood to return to the heart. Correct. So it's pulling down the bottom. So stroke volume is probably going to be lower standing up. So you're going to have all these other compensatory mechanisms like your heart rate is probably going to have to be higher to begin with. But you're saying that swimming –

Are you saying that... Or something supine. Okay, let's say I'm swimming... Or horizontal. Or horizontal that my stroke volume will probably be as high as it needs to be from the beginning. That's right, yeah. Right? Exactly. Because there's no pooling of the blood. It doesn't have to do any of those compensatory things per se.

So are you saying that the stroke volume of a swimmer compared to the stroke volume of maybe a runner or a cyclist at the beginning of their exercise, that the swimmer, their stroke volume will probably begin higher than the runner? Yes, that's right. Because they've got more central volume to work with preload as opposed to the upright positioning requires better strength

vaso, venoconstriction and muscle pump return to get greater volume back to the preload. And then you can add further variability in are you using more leg or more arm? Because if you're more dominant in arm activity. Yeah, why are you looking at me? The arm activity seems to, apparently, like the sensory going back from moving the muscles...

seem to have a bigger effect on the sympathetic nervous system. So you'll have a greater heart or a higher heart rate from doing arm activities than you would from doing leg activities. So you get a greater sympathetic from that. At least from a heart rate standpoint. Is that just an anatomical proximity thing? I think so, yeah. Right. It's probably a bit like, you know, how visceral, like if you get visceral pain symptoms,

in your chest, it can sometimes go into arm. So referred. In a way. So in a similar way, it probably comes in in a similar. Because obviously sympathetic thoracolumbar nerves. Yeah, that's right. And that's sort of. And arms in that region as well. Yeah. And then you look at blood pressure changes and with leg, because you are using a greater volume of muscle with those localised muscles

paracrine effects, you're getting more vasodilation. So you're actually getting a lower blood pressure by doing

by doing leg dominant exercise than you do with arm because you've got less muscle volume in arm compared to leg. So he's basically saying that if I were to wear, you know, put on some wearable tech that measured heart rate and blood pressure, that I go do arm curls, that I might find that my heart rate's higher because of the stimulation of the sympathetic nervous system. But if I find that I'm just doing leg work, because of the size of the muscle, I get pronounced vasodilation below the heart. I get...

obviously decrease blood pressure. Yeah, less blood pressure. Because of legs. In that dominant type of activity. So you're saying that not all activity is created equally? Not perfectly, no. These are just considerations to be mindful of because these again can be important for if you are an exercise physiologist and you need to provide prescriptive activities for people, then these things can change around these dynamics which can have effect on the

the homeostasis of the system. Absolutely. All right, Matty, you did a great job. I'm proud of you for once. Listener, thank you so much for listening to us. We hope you're enjoying this series. You can send us an email, admin at drmattdrmike.com.au. You can follow us on social media. It's just me at drmikedorovich at D-R-M-I-K-E-T-O-D-O-R-O-V-I-C or you can just type in drmike.com.

Todorovic on all social media platforms. There's another Dr. Mike in America. He's the, well, the smarter, more attractive version of me, I have to admit. And also the version of me that's more famous and probably has far more money. So let's just say he's the successful version of me. But if you don't want to follow him or you also want to follow me. There is a Matt Barton who's a tennis player.

Oh, yeah, there is a Bob Arntesman. Relatively successful in Australia. There's Barton's Car Sales. I don't know if you're related to them. Use car dealership. I think there's also Matt Barton Motorcyclist. Really? That's not you? There was also Dr. Matt Barton who worked in the same hospital as I worked in. What? So I used to get his paychecks. Wow, two paychecks. I didn't get paid, but I just got his flips. Sure, buddy. Yeah. Okay. And also I got, you know when you publish an article and they send you like,

Invitations to review or whatever it might be. Yeah, I get his stuff. Oh, that's funny. Wow. See? Haven't surname like Todorovic and that won't happen. All right. Thank you, everyone. We will see you for our next episode. We have to do a Q&A very soon, but we are still continuing our series on exercise physiology. Again, if you enjoy, let us know. If you don't, just keep quiet. All right. Thanks, everyone. Bye. Bye. Bye. Bye.

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