Exercise Physiology | Fuel Sources (Part 3)
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Welcome everybody to another episode of Dr. Matt and Dr. Mike's Medical Podcast. I'm your host, Dr. Mike Todorovic, and today I'm joined by my co-host. Oh my God, it is Winston Churchill. What a dude, got his big cigar. You know the cigar that Churchill was named after him, just so you know, named after him because he smoked cigars that size. My question is, what was it called before then? I am your host, Dr. Mike Todorovic.

And this is Matt, Dr. Matthew Barton. Just if you're listening to us and you don't know who we are, I just told you. That's the introduction. That's the introduction. I'm Associate Professor, Medicine, Bond University. Matt is Senior Lecturer within Health Sciences at Griffith University. We teach students and we've taught students for well over a decade now about how the human body works.

We talk about anatomy, physiology, pathophysiology and pharmacology. And we are in our series at the moment, a special series, Matt, where we're talking about exercise physiology. We're taking physiology and applying it within the context of exercise. So mostly focusing on the muscle tissue itself. So usually when we're talking about all these things, think about the muscle tissue unless we say otherwise.

And today's topic is exercise metabolism. So we're going to have a look at the metabolic responses to exercise. How does the body respond to varying intensities of exercise? And what fuel sources does the body use during these types of exercise? It's going to be a lot of fun until Matt speaks.

And where should we begin, Matt? Should we define the different types of intensities of exercise? We can do. Just generally speaking. So I think it's important to talk about exercise intensity because the physiological reaction to exercise is a function of the intensity of that exercise, meaning whether you're training –

really hard or sort of just meandering around the backyard like you do depends on what your body does. So what fuel sources it utilizes, but also what physiological outcomes occur, you know, breathing, heart rate, things like that. So,

Can you define, so we've categorized them, not we being you and I, but the literature, the scientific organization that is exercise physiology have defined four major categories of exercise intensity. What are they? All right. So these can be termed moderate, right? So moderate exercise. Then we have heavy, very heavy and severe exercise.

It starts pretty high. It starts at moderate. I mean, if these were coffee sizes, this is like Starbucks. It starts with a tall and then ends with a venti. With a severe, which is like a...

What are those big gulps? That's right. Well, now you're talking about 7-Elevens, but yes. They combine the two. Yeah. But I think- You walk out with two liters of coffee. That is severe exercise, I think, walking away with two liters of coffee. Now, you might be thinking going, well, what does moderate mean? What does heavy and very heavy and severe mean? And it's a great question. And there's a couple of different ways that you can categorize it.

So you can have a look at basically the perceived effort of the individual. So what might be perceived as moderate intensity exercise for one may not be for another, but there's more objective ways that we can classify it. And so we tend to look at them according to things like the VO2 max. What is that? Oh, you want me to define it now?

Sure. Yes, please. Okay. So effectively, when we look at the VO2 max, what we're effectively looking at is the maximal capacity to transport and utilize oxygen during exercise. So it's your body's physiological ceiling to consuming oxygen during heavy exercise. Right. So it's to get oxygen in through the lungs, into the blood, and then transported around the body to the muscles, but not only...

To the muscles, into the muscles, to then ultimately... And not only into the muscles, Matt, but to the mitochondria. To the mitochondria's muscles and then to make... The mitochondria's muscles? What are they? The electron transport chain. Are they the biceps of the... Exactly right. And then to produce ATP. Yes, that's right. So all those things have to happen, which is part of the VO2 chain.

And then to max it is the maximum you can reach, right? Yeah. And so, you know, factors that influence. That's the ceiling. That's the ceiling. Exactly. So the factors that can influence VO2 max is your ability, you know, the ability of the cardiovascular and respiratory systems. So that would be, there'll be genetics there. So some people are more efficient than others, I guess. Yeah. We've spoken about your heart. Fair, fair. I was hoping you'd never bring that up again, but thank you.

So genetics is one part, but the other part can be trained for, right? Absolutely. So individuals who are more cardiorespiratorily fit. Yeah, you could say that. Would have a better or higher VO2 max. Yeah. But it's not just the cardiovascular and respiratory systems. It's also the muscles or the muscular system's ability to take up energy.

the O2 as well. So these, you know, these are some variables that influence VO2, but it's a really good measure. The VO2 max, it's a really good measure. Sounds like a radio station. Welcome to Wiener and the schnitzel VO2 max. So I can't remember. Oh yeah. It's a really good measure for both health and fitness. Yep. You know, it's a good indicator of mortality. Aerobic.

ATP. Well, aerobic fitness. Yes, that's right. Yeah, definitely. Because you are utilizing oxygen to produce ATP, which last week we did say that there's two broad systems metabolically. There's an anaerobic systems, which is the phosphocreatine and the glycolysis.

And then there's the aerobic, which is Krebs onwards, right? Yes. So VO2 max is kind of talking about the efficiency, the fitness of your aerobic system. Yeah. And so one way that you can classify whether an exercise intensity is moderate, heavy, very heavy or severe is by taking a look at the VO2 max. So generally speaking, you could say under 60% VO2 max is moderate, severe,

60% to 75% is heavy, 76% to 100% is very heavy, and 100%- And above. And above, which is difficult to do. How do you go above? Yeah, great question. I think it's if you can't. I mean, effectively, you can't go above, but I think it's going above a previously recorded-

VO2 max. That's recognized as severe, going 100. All out, essentially. Going all out. But you know, it's really interesting and I don't want to do an aside too much here because that's just one way that we can classify the intensities. But the VO2 max can be trained in people. So the

It's not like you're born with a particular VO2 max and you're destined for that VO2 max. So while you said, yes, genetics plays a role, you can train your VO2 max. All right. So you can also have a look. Another objective measure of the intensity of the exercise is lactate.

specifically the lactate threshold, and we can define that in a second. And if you have not hit your lactate threshold, generally you'd call that moderate intensity exercise. But if you've hit it,

Well, that could be heavy, very heavy or severe. So all three of those intensities hit the lactate threshold. Okay. And we're going to explain what that means shortly. Yeah. And the reason why is because it's probably going to encompass a big chunk of today's podcast is lactate. So I know that we discussed VO2 max, but we're going to discuss lactate threshold and lactate itself in a sec. What about, sometimes you hear about this for...

of maximum heart rate. Yeah, so you can have a look at percentage of maximum heart rate as well. So for modern... Because that would be easier to do than for most of us at home. Yeah. Exercising and being able to do VO2 max, which would need some elaborate equipment.

And often you get that. And like take threshold, but you'd have to be taking blood samples. Yes, exactly. And so what you'd probably find is when you get, you know, like online training programs and they're asking you to perform things at particular intensities, they have their own ways of defining that. So if it's weight training, they might say a percentage of your one RM.

for a certain amount of reps sort of thing. But yes, you could do a percentage of the max heart rate. So moderate could be classified as 50% to 75% of the max heart rate. And what is max heart rate? So 220 minus age? Yeah, you could do it that way. That's for your age. That's relative to your age. But you could...

measure your own max heart rate, right? And then do it off that. Heavy would be 76 to 85% max. Very heavy is 86 to 100%. And then severe is your 100% of your max heart rate. So effectively severe training, severe intensity training is you're topping out on all your physiological measures, right? Because exercise is a stressor and severe means you're stressing your body as much as you possibly can through this exercise. And like we mentioned earlier,

a couple of episodes ago, the steady state. You're not going to hold steady state at a severe exercise intensity level very long. Not possible. Not possible to do. So that's the different exercise intensities. But I think what we need to talk about is...

And what a lot of people don't talk about is going from rest to exercise and then going from exercise to rest. And then we can talk about what's happening during exercise. Okay. Because some of the important things physiologically is going from rest to exercise and then going from exercise to rest. Don't you think? Yeah. Yeah. So, um, going from rest to exercise, I'm going to ask you, let me ask, I'm going to give you a scenario and ask you a question. Okay. So,

Firstly, so I've set up a treadmill in our studio. So unfortunately, the listener can't see it. That's what it was there for. Yeah, so if you hear that whirring sound, there's a treadmill next to Matt that's going 200 meters a minute, right? So how fast would that be per hour, do you reckon? 12Ks. 12Ks an hour? Yeah. Do you reckon you could run 12Ks an hour? I do that on my treadmill. Okay, yeah.

All right. That was great. That was better than the joke at the beginning of the episode. So we've got this treadmill next to Matt going 200 meters a minute. But Matt's sitting next to it. Now, not exercising. So, Matt, you would say that you right now, your body is in... Rest and stay. Yep. But also...

Oh, homeostasis. Yeah, it's in homeostasis. Okay, so the ATP that's in your body right now and available to you, do you think that you have, is the ATP that's being made, is it being made in preparation for exercise or is it being made right now to meet your current energy demands? The latter, yeah. Yeah, that's right. So you're only producing the ATP needed for right now. But then the question is- Do you reckon you could be making an increased amount of ATP through the thought of what you're about to do?

Oh, that's a great question. I'm sure there's a bit of... I would never say never. Yeah. I mean, yeah, I don't see why not. I mean, you through thought can... Oh, but that's also sort of solidifying neuronal pathways. When you're thinking about doing or performing a movement prior to doing it, you tend to do that task a little bit better. Great question. But it would be like if you could...

perceive it well enough that you would have a change in stress hormones, then that would increase ATP beyond the requirements at that time. But it's probably not doing it in preparation. It's probably doing it because your heart rate's gone up and to meet the demands of your heart increasing its workload. But as we will speak to shortly, if you were just to put noradrenaline into your blood, your metabolic pathways would start to be more efficient. Yeah.

produce an ATP. Yeah. And when Matt says put neuroadrenaline into your blood, he means that your adrenal gland is releasing it endogenously, not you're injecting it into yourself, making you more efficient. Okay. So don't do that at home. Now you're standing next to that treadmill, right? You're only making enough energy to meet your current energy demands. But if I said, Matt quickly jump on that treadmill right now, you go from rest to exercise and not just rest exercise. You're going from rest to running 200 meters per minute.

which means that you immediately require performing an increased workload and require more ATP immediately, which means your body must immediately

produce enough ATP in that moment to hit the new energy demands. So it's spontaneous, right? Because if you didn't, you'd fall off the back of the treadmill because your muscles aren't going to be contracting properly. So then the question is, how do we, in such a short period of time, produce enough ATP to meet those immediate energy demands? And we alluded to it last episode, right? Which is what? Phosphorocreatine and then glycolysis. Those two systems are

Yeah. So they technically don't need oxygen, so they are fast recruiters of producing ATP. Yeah, it's amazing. If you have a look at an ATP consumption graph, you'll see that

Matt's ATP consumption will be low at rest. And as soon as he hops on that treadmill, it matches. It is basically in sync with him and his movements going 200 meters a minute. Right? So there's no delay. There's no lag period there. And that tells us that we have immediate systems that can provide that ATP. Like you said, the phosphocreatine system will be the predominant one within the first 15 seconds.

Now, that doesn't say that glycolysis isn't happening in the first 15 seconds. Effectively, you could make an argument that glycolysis is in some degree always happening. So it's just as a percentage of what's providing the ATP, it's mostly the phosphocreatine system. Yeah, so...

Just to reiterate, any activity less than 20 seconds would be a combination of both the phosphocreatine and the glycolysis, but you would assume that in that first...

burst would be more phosphocreatine. Yeah, exactly right. Now, so we've gone from nothing to something, but let's just say you stay on that treadmill for a little bit, right? So you start going, okay, first 15 odd seconds, phosphocreatine predominant pathway. Then you start to utilize glycolysis. You're getting ATP from glucose turning into pyruvate, making ATP. Not a lot, but you're making enough to maintain for another couple of minutes. And

And then after, let's just say five, six, seven, eight minutes, we start to measure your oxygen consumption.

And what we end up seeing is that unlike the ATP going straight up, reflective of phosphocreatine and glycolysis, there's a lag period for the oxygen to hit a steady state, right? Meaning that if I measured your oxygen at the rest, you'd have a certain oxygen consumption. And then I'd chuck you on the treadmill and measure your oxygen consumption. So your VO2, not VO2 max, but your VO2.

Which is the litres per minute. Yep. What we'll find is that it gradually increases. It's fast, but it's not immediate. So it's not spontaneous. So there's a lag period, which we call the oxygen deficit. Right. In which not the debt, we'll talk about that in a sec, but the oxygen deficit. And this is important because it's telling us that in the first few minutes...

aerobic metabolism... Takes a while to kick in. Yeah, isn't the predominant fuel source. And we know that. We alluded to that last episode. So then...

My question to you is, why is there a lag period? So why doesn't the oxygen consumption immediately? So are we not breathing in fast enough at the beginning? Are we not, is our cardiorespiratory system not efficient enough? Are our muscles not good enough at taking it in? Like, do we know why there is a lag period at all?

Well, there would be means to get more efficient. So I'm sure if you're a trained athlete, that debt would shorten. Not debt, deficit. Deficit, should I say? Yeah. That would narrow. Yeah, that's true. So you could train. Yeah. Which tells us that it is something at least partially physiological that we could tweak. Yeah. All right.

But you can't get rid of the deficit. So it's always going to be a lag phase, right? So do we know? Well, my assumption, working back from first principles, is you've just gone from nothing, which you're at homeostasis for, in your whole body, not just your muscles, but your cardiorespiratory system is also homeostatically in place. Yep. You jumped on the treadmill and running at 12 k's an hour. Yeah. You've...

broken off those phosphate molecules to be producing ATP in the sarcoplasm through the phosphocreatine. That's enough for the immediate. That starts to deplete and glycolysis takes over, which is still enough to do what you need to do in the moment, right? So it's not like you are running out of, or you're encountering problems here. You're still doing what your muscles need to do. Still performing work, yeah. Yeah.

But as all these metabolic pathways are becoming more active and there's byproducts being produced like ADP, then that's going to be a stimulator for the further down pathways, the aerobic pathways to go, oh, something's happening higher up. We better start to kick into gear. And so that then necessitates them to say, well, if we want to kick in, we need oxygen to be part of our system.

Electron donor. So we will need to start to utilize oxygen. So that will then require certain requirements for oxygen. And I guess there probably would be enough oxygen in the muscle at that given time to start the aerobic system off. But then the stimulus comes about that maybe we're becoming a little bit hypoxic.

or hypercapnic and then the cardiorespiratory system has to kick in to kind of counter that. So that takes a lag period. Yeah, yeah, exactly right. It's all those things. It's a multitude of things. Theories have been thrown around saying it's an –

and an adequate supply of oxygen to the contracting muscle at the onset of exercise. So we might have enough oxygen bound to their red blood cells because, you know, you and I both know it was saturated. Yeah, that's right. Right? So our red blood cells are saturated just from normal breathing. So it's not like our lungs aren't getting enough oxygen in, right?

So why isn't it that from the very onset of exercise, we don't have enough oxygen and we don't have a deficit and just kick in to aerobic metabolism straight away. But yeah, like you said, it's...

The muscles take up the oxygen. There's a little bit of a delay there. The electron transport chain, oxidative phosphorylation might take a little bit to kick in. The triggers, the stimuli for it aren't there. Often the stimuli, like you said, is ADP accumulating in the body, but we've got phosphocreatine and glycolysis that is not

that is making up for the ADP, right? So you've got enough ATP. So we don't exactly know what the answer is, but like you said, it's a multitude of things. But you could go the opposite way and say, well, if you're talking about that there's a lag period to start it off, there's going to be a lag period afterwards.

After the exercise. So then if you were to jump off the treadmill and then stay stationary, it's not like that VO2 goes back to the level of standing still immediately. So that's a great segue. It will taper off. So we spoke about going from rest exercise and now...

You've brought us to going from exercise to rest. So just describe that again. So you've been on the treadmill for a couple of minutes now, right? So let's say I've been running the treadmill for up to six minutes. Okay. Now let's just say during that time, we noticed that

you continued to maintain your pace, which means your body was supplying enough ATP for itself. We know within the first 15 odd seconds, phosphocreatine pathway was providing that ATP and glycolysis. So probably for the first few minutes, it was predominantly those two sources. We saw that your oxygen levels increased.

So your VO2, it took a while to go up. So you had that oxygen deficit, a bit of a lag period until your oxygen, your VO2, not VO2 max again, but your VO2 hit a steady state. And like we said, the VO2 is a really good indicator of aerobic metabolism. And then we saw when your VO2 hit the steady state, okay, Matt's utilizing aerobic metabolism now. And so for the rest of that time, you were probably more predominantly in aerobic metabolism. Would you say that this is the...

You know how they talk about the second, not the second wind, but you know how like when you initially start exercising, you feel a bit out of breath, but then if you keep going, you kind of feel like I'm in the rhythm now. Yeah. I don't think that would happen so soon. Okay. If you're getting a second breath at six minutes. No, no. I just mean like in the first couple of minutes of performing an exercise, sometimes you feel, Oh, today I feel a bit out of shape. Yeah. I don't know what that is. It could be like a big hormonal dump. Uh, it could be, uh, uh,

I don't know what the second window. I think there's some evidence out there that it indicates a couple of things, but I'm not privy. I'm not read up on that. All right. So you've been running for six minutes, right? Yep. Are you impressed, by the way? I'm extremely impressed. I'm falling off the back of the treadmill. No, not yet. Now, after this, so you've hit your steady state oxygen consumption. So you've undergone all those ATP producing pathways. So I've gone from...

Under half a litre a minute of oxygen to up to two and a half litres a minute. Of oxygen consumption? Okay. Is that it? Yep. For me, I'm pretty efficient. Yeah, okay, okay. So now you jump off the treadmill.

So what we see is that, like you said before, there was a lag to begin with, but now you've also got a lag to end with. And that lag's referring to the VO2. Yeah, so let's think about this because I think we take this for granted, right? If we have stopped exercising, we no longer require ATP for the contracting muscles. And if most of the ATP is coming from aerobic metabolism now,

Why don't we just immediately stop huffing and puffing the way that we do? You know that when you finish exercise, we huff and puff for many minutes. You, I've seen days later, you're holding, you're bent over. I've still got a stit. Yeah, that's right. But, you know, for many minutes after the exercise, you're still breathing heavily. Yeah. And so then the question is, why is that the case?

This is where the term oxygen, not deficit, but oxygen debt. Now that's an older term I think coined in like the 60s or maybe even earlier, but that's changed now because we use the term EPOC, which is excess post-exercise oxygen consumption. So effectively what they thought was, you know... You just need to replenish the oxygen in the muscle or something. Well, paying back the oxygen deficit that incurred at the onset of the exercise, right? Yeah.

We don't necessarily think that that's the case now, right? So what we think with the EPOC, excess post-exercise oxygen consumption, is that if you have a look at a graph of the oxygen consumption, you might have stopped exercise, but you've got this, again, lag period on the back end where it sort of peters off, right? It drops down the tail of the curve. You've got the rapid phase immediately after. And so this is two to three minutes after exercise.

And what this is, so the oxygen that we're consuming here, we generally think it's mostly there to resynthesize our stored ATP and phosphocreatine, but it's also there to replace the oxygen, the tissue oxygen that's been lost during exercise. Okay. So that's probably the sort of rapid- I think rapid R as replacement. Rapid for replacement. Oh, yeah, that's a good idea. Right? And that's everything in the muscle. So almost resetting the muscle back-

For the next bout of exercise. Yeah, that's a good way of thinking about it. Imagine a world without borders, where money moves between countries fast and securely, all without having to build or manage a complex infrastructure. Introducing Visa Direct. With Visa Direct, you can move money securely to and from 195 countries in 160 currencies.

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relatively heavy but not as heavy and so this is called the slow phase. How about this one? Slow S for systemic. Oh, that's good. Okay, so explain that. So why, what is this oxygen consumption for then? You said systemic. Like whole body stuff. So your heart's still contracting so it still needs more oxygen than normal. You know, other body systems are still requiring more things because it's been part of this energy bout and so it needs to also reset plus

You're probably hotter than you were when you started your exercise. So that is also doing systemic changes and altering certain metabolic capacities as well as hormonal changes during the exercise. Adrenaline's been dumped into the body through the adrenal gland.

That's important because it vasodilates, it helps mobilize energy stores, things like that, but also increases the metabolic demand on tissues. So yeah, I like that. And maybe also probably depending on... I'm sure it's gone up a little bit. Like considering that you have exercised or I exercised aerobically, most people would think I haven't really used much lactate in that process, but it would have still gone up like...

A little bit. Yeah, and we'll talk about that. So that lactate that has been produced has to be re-synthesized into other things. So that also will... Converted. So that would also require oxygen to be there through that conversion. Yeah, so 20% of EPOC...

towards converting lactate to glucose. Okay. So that would typically be called the Cori cycle, would you say? Yeah, which is part of gluconeogenesis. But that gives us a nice segue into lactate because I think now is a good time, don't you think, to talk about lactate? Okay, so...

We'll talk about what lactate is and then we'll talk about lactate. Let's talk about lactate threshold first. So we spoke about earlier on that one of the ways that you can define the intensity of the exercise is whether somebody's hit their lactate threshold. The lactate threshold isn't like the VO2 max in which it's the ceiling, right? The lactate threshold isn't the most lactate that you can produce.

The lactate threshold is effectively when your body has an uptick, a rapid uptick in lactate production. So it might have a relatively stable lactate production, but as you increase the exercise, incrementally increase the exercise intensity, your blood lactate will also increase. And then when you get this sudden rise in lactate during this incremental exercise, that's the lactate threshold. And that can keep going up, right? Yeah.

Now it doesn't go up infinitely, but it can keep going up. Now the reason why we produce lactate as we incrementally increase the intensity of the exercise is for a couple of reasons. So the dogma was, as you probably learned at uni. Because it was studies in dogs. Well, you do talk a lot about dogs and experiments in dogs in our podcast. Probably was to be honest. Yeah. And they probably did do it in dogs. Um,

We know that glycolysis takes glucose, a six-carbon molecule. It's C6H12O6, six carbons, 12 hydrogens, six oxygens. Its job effectively is to rearrange that molecule in a multitude of steps called glycolysis to be able to pluck off the hydrogens. We've spoken previously that glycolysis

The hydrogens need to get shuttled to the mitochondria where the proton, which is just the positive part of the hydrogen, and the electron, the negative part of the hydrogen, can be utilized by the electron transport chain to produce ATP through the oxidative phosphorylation pathway or chain, right? The electron transport chain. What do you call that as a shortened term?

ETC. Oh, okay. Or oxfos. Oxfos. Oxfos. Well, oxidative phosphorylation, yeah, you could refer to it as oxfos. So glycolysis ultimately, we're trying to pluck hydrogens off. Now the carriers for that are NAD+, which when it plucks the hydrogens off becomes NADH.

And then FAD, which plucks it off and becomes FADH2. But that's in Krebs cycle though. Well, that happens in glycolysis. Oh, does it? Yeah, definitely. It happens in... So NAD... So...

If you're referring to FAD specifically, that's only Krebs. Yeah, that's what I meant. My apologies, yeah. So NAD is NAD plus will pluck hydrogens, become NADH and carry those hydrogens from the sarcoplasm, so the cytoplasm of the muscle, into the mitochondria and hand those hydrogens off to the- So how does it get in there? There's a shuttle. There's a base NADH shuttle. You say shuttle, you mean like a-

A bus? There's a channel for it. Oh, okay. Yeah. I prefer the bus, but yeah. Sorry. So there's a bus. There's a specific bus for it. All right. So again, we haven't spoken about lactate yet, but the textbook used to say that

When we have enough oxygen, this is exactly what happens. Glucose turns into pyruvate. Through that process, hydrogens have been stolen by NAD+. It forms NADH, gets shuttled into the mitochondria, hands the hydrogens, protons and electrons to the electron transport chain, and with the help of oxygen, produces huge amounts of ATP. That's aerobic respiration.

The textbook used to say, ah, yes, but if your ATP demands exceed the amount of oxygen you have available to create ATP through aerobic respiration, we need an alternate pathway to make energy. And so we produce lactate. It actually used to say we produce lactic acid, which we don't. We produce lactate straight from pyruvate. There's no evidence. There's no strong evidence, I should say, that we produce lactic acid. Just so you know.

So what happens is pyruvate will just turn into lactic acid. And lactic acid, and the reason why it turns into lactic acid is because when... Donates hydrogen? Yeah. So think about it like this, right? There are negative regulators like glycolysis. Glycolysis is a really great pathway. So going from glucose to pyruvate is a really great pathway to produce some energy very quickly without the need for oxygen. Okay.

What it produces is NADH, like we spoke about. Now, everything needs negative and positive regulators. When NADH goes up, that's a negative regulator of glycolysis. It says, hey, stop, I've got enough of the end product, right? But if you're still exercising and you need, so let's say you're exercising and you're exercising intensely, you know, so very heavy or severe, you're in the gym training really, really hard, you need glucose for energy, right?

You don't want to inhibit it. So we need a way to get rid of this NADH. And if that NADH can't shuttle into the mitochondria fast enough, it goes, crap, what am I going to do? I'm going to accidentally inhibit glucose. Pyruvate goes, don't stress, brother. Give me your hydrogen. And so the NADH gives its hydrogen to pyruvate.

replenishing it into NAD+, which can go back to the glycolysis and keep it going, right? But now pyruvate has hydrogen and it's become lactate. So when pyruvate gains hydrogen, it's now lactate. Okay. So it's buffering out hydrogen. But in doing so, that makes ATP as well, right?

Well, no, it doesn't. What it does is it regenerates NAD+, which allows for more ATP to be produced through glycolysis. And then that lactate can do a couple of different things. So...

In the textbooks, it's like, yeah, this is a byproduct, right? We're doing this because we've got nothing else we can do, right? It's just happening because we need it to happen. And it's a waste product. It makes muscles sore. We just don't want it. That's not true, right? So once we make this lactate, it can do a couple of things that are really helpful and really important, right? So you've undergone exercise. You've made all this lactate.

Now, it can happen because there's not enough oxygen, but it also happens when you just accumulate too much NADH, like in this scenario we just said.

Yes, 70% of the lactate that's produced during exercise is oxidized, meaning that it just will ultimately turn back into pyruvate and then pyruvate jumps into, you know, turns into acetyl-CoA, jumps into the Krebs cycle in the mitochondria and produces heaps of ATP. That's 70%. And what does that? An enzyme called lactate dehydrogenase. Okay, but what I mean is what tissue can do that?

Oh, great question. So the muscle tissue itself can do that. We can take the lactate that's accumulated, but the liver can do it as well. So the liver is probably the biggest handler of lactate. Right.

per size of you know the organ obviously we've got a lot of muscle compared to the liver but that lactate the thing about lactate is it can leave the muscle and go into the bloodstream very easily and in the bloodstream the liver can can manage it turn it back to pyruvate and so forth but the muscle can do that as well so 70 is oxidized meaning that's what it does 20 of the lactate undergoes gluconeogenesis so can you just break that word up for the listener

Glucose, neo, new, genesis, production of. Read it backwards. Genesis, production, neo, new, glucose. So the production of new glucose. So what does that mean though? The production isn't all glucose that's produced new glucose. I don't get what that means. Well, a lot of the glucose that's available in our blood have come through eating and

then it also comes about from the liver breaking down glycogen, which is its longer storage method of glucose. But if you are wanting to generate glucose from a different source, say you want to make it from proteins. Tomato sauce.

Or in this case, lactate, that would be neogenesis because you created it from something else. Yeah. So producing glucose from a non-carbohydrate-based source, that's gluconeogenesis. And lactate is a non-carbohydrate-based source. If you look at it, it's more like an amino acid than it is a carbohydrate. So 20% will do this. That happens mostly in the liver. Then the last 10% basically produces amino acids. So what happens is that the lactate...

through its conversion to pyruvate because that's reversible, right? Pyruvate to lactate, lactate to pyruvate. And is that done by the same enzyme? Yep, lactate dehydrogenase is reversible. So during muscle metabolism, you've got amino acids and amino acids are utilized and they're also metabolized and we know amino acids have an amine side chain, which is NH3. Now, NH3 is ammonia.

We don't want, through the metabolism of amino acids, ammonia to accumulate in the muscle, nor do we want it to accumulate in the blood. So we need a way to be able to get rid of the ammonia from the muscle and also have something to carry it in the blood to ultimately pee out. Because that's what we do with most of our ammonia. We pee it out.

So what can happen is in the muscle, the ammonia or amine side chain gets linked to an amino acid, glutamate, and that glutamate hands it off to pyruvate and produces a

alanine, which is another amino acid. And that alanine jumps into the bloodstream. You know, basically it's holding on tightly to the amine. It's not damaging. It's not a problem. Sends it to the liver. The liver plucks that amine off, throws it to the urea cycle. We pee it out and the alanine is converted ultimately back to pyruvate. For glucose.

Or for energy, let's say. Yeah, for energy. So that pyruvate can turn back into glucose or it can undergo Krebs cycle by turning into acetyl-CoA. So 70% is oxidized, meaning turns back to pyruvate. 20% undergoes gluconeogenesis, so lactate turns back into glucose or turns into glucose. And last 10% is amino acids to be able to get rid of the amine. So...

You can't tell me that lactate isn't useful. Yeah, yeah. It's not a byproduct. And so with that said, if you did do a heavy bout of exercise and you had produced a lot of lactate, is there an efficient way of getting rid of it? Or a more efficient way? Like is it just by jumping off the treadmill and sitting down on the couch? All right, well, let's work through this anecdotally. Okay. I'm sure that at some point in your life you've done exercise, right? I mean there's no evidence to suggest but –

I get in trouble so much from the listeners for teasing you. I should stop, but I won't. So let's say, so you've obviously done intense exercise before and I'm sure you've done warm down or cool down periods or, you know, cool down exercises. And I'm sure there's been times where you've just stopped. Yeah, I've never enjoyed them, but yes. Right. As in the cool downs. Yeah. Yeah.

Anecdotally, do you find that the next day or the day after you have – and again, this is working off anecdote. You've got more muscle soreness.

from not cooling down or more muscle soreness? Well, first of all, I think I need to pull you up here and say that there's no real, from my understanding, there's no real evidence of soreness associated with lactate. Yes, and that's true. That's true. I can see what you're doing here. What I'm trying to do is people do link lactate or lactic acid to muscle soreness. You're right. What effectively is predominantly or possibly happening with muscle soreness

It's an accumulation of hydrogen ions that we know is going to be there when we pluck them off.

glucose and other molecules. Also, they're produced by the mitochondria. Muscle damage itself, micro tears that happen in the muscle itself. Inflammatory. So, you know, pH changes, other metabolic byproducts, ATP could be, you know, we know that ATP can stimulate nociceptors. So, you know, it could be muscle soreness is likely a multitude of things. So yeah, you're right. You pulled me up. Okay, fine. Lactate isn't causing muscle soreness.

I'm going to throw the question back at you. What is the best way for that lactate to, you know, of those three things, you know, oxidize, gluconeogenesis, amino acids, you know, we want to turn that lactate back into something else. What's the best, what's the fastest, most efficient way to do it? Is it from just stop exercising or is it doing something else? Well, it goes back to partly your explanation of what happens to lactate whilst we're exercising and what the body does to it.

And you spoke about muscles, both the heart and skeletal muscles, having the capacity to oxidize lactate. And the muscles that do that most efficiently, the slow twitch, which presumably is heart and certain fibers within our skeletal muscle, right? So less fatigable. That's right. Don't mind using lactate. And they can use lactate as that energy source. So if you were to... But you need to be using that muscle. Yes, that's right. So if you were to be doing exercise at higher intensity...

Where you are using the fast twitch fibers, which are using more lactate dehydrogenase, which is producing more lactate. So technically you're making more. But then you stop that intensity or you're still on the treadmill and you dial it right down to 6 k's an hour. You've now switched back to the slow fibers. Predominantly. Predominantly. And they're...

sucking up the lactate to then be used oxidizing into energy. So what you're saying is the best way to reduce the lactate is effectively to exercise. Yeah, a low moderate exercise.

Or moderate, should I say. Yeah, moderate. Moderate intensity exercise and a lot of that has to do with the slow and fast twitch. Yes. Oh, great. Okay, so we've spoken about lactate and we've spoken about lactate threshold. So you can probably see why people want to measure lactate threshold because it gives – when you get that uptick in lactate, it gives you that indication as to –

when things are sort of... That's the intensity. So if you combine the two, so if you're a trainer or you're an athlete and you're trying to figure out where's your happy medium, the VO2 max will give you an idea of endurance, whereas lactate threshold's more about intensity. So you can try to figure out the two together. It'll give you an idea of...

how heavy can you exercise, but kind of like what's your aerobic kind of endurance for the VO2. But just one final thing with VO2 before we move on to maybe the fuels is VO2. If you, even, even if you're at a steady state, so even if you were to be holding it at that 2.5, I think that's what I said, the 2.5, um,

liters per minute of oxygen. Okay. But you kept that going for a period of time. It would be at a degree of a steady state, but it would be slowly drifting up.

Right, okay. Explain that. What do you mean? Well, you're going to be slowly consuming more and more oxygen. But is that as you incrementally increase? No, it can just be at that steady state. And the reason for that is, well, it could be the ambient environment. And so if you are in particularly humidity...

Queensland, Australia. Then your body at the same time is trying to regulate and, you know, your thermoregulation is trying to be going on all the time. So can I just clarify? So you're saying that if I had you on a treadmill in an environment controlled, sorry, a temperature and humidity controlled environment, you know, and we found your body

uh, intensity that, so it's obviously a moderate intensity that allows for you to maintain a steady state VO two again, not VO two max. And then I could change the environment and I cranked up the temperature and cranked up the humidity, even though you're doing the same amount of quote unquote work consuming the same amount of oxygen. Um,

That your VO2 would go up. It starts to uptick. That's right. Now, that makes sense because there's, in a way, effectively a greater demand on your body because now temperature's going up, so your body needs to work more efficiently to remove that temperature. That's one part. So your cardiovascular system is blood vessels are dilating. Heart probably has to pump harder and faster. You're probably breathing a lot more. Yep.

So that's definitely one part. Okay, what else? But there also would be at a higher temperature than physiological temperature, your enzymes are working more efficiently. Mine specifically or the athletes? Your muscle. Everyone. Okay. Your...

In your muscle, your metabolic enzymes are becoming even more active. So metabolism is cranked up a bit. That's right. And so therefore need more oxygen. Right, right, right. Does that make sense? Yeah, yeah, yeah. On top of that, you are also producing more catecholamines and they are also dialing up the pathway. So that's adrenaline. That's right. Yeah.

Right. And so they've done studies here where they've given, so that would also account for that VO2 drift, which is a slight increase. And that's what it's called. Yeah. And they've given people beta blockers and that dampens off a bit of the drifting.

So that tells me that beta blockers stop adrenaline binding to its receptors. So if that stops the drift, then it tells me that the biggest driver of the drift is hormonal. Well, there's a degree. I'm not sure if it's the biggest, but there's an influence there. And this is where training would come in. So athletes, they would have a more blunted hormonal response.

Okay, so they're used to it. So effectively is what you're saying that this can't be maintained? Yeah, yeah, that's right. So this isn't – because it's not a steady state. So you can't maintain this? Effectively not, no. That's right. Okay. But exercise training can – again, typical adaptations, your body just can handle the temperature and humidity better. But if right now you went out in 39 degrees Celsius, a Queensland summer, 99% humidity –

You wouldn't be able to maintain the exact same intensity that you would perform on the treadmill inside the house. That's right. And then, you know, the enzymes go the opposite way where once they get over a certain temperature, they then start to go towards more denaturing. True. And the whole system will start to slow down and fatigue. Should we talk about some of the fuel sources? So how do you want to do this?

Um, well, in terms of how we, how we produce in the ATP, like what's the... Well, we've spoken about that more so, um, we know that we ingest... Like the input product. Yeah. We ingest proteins, fats, and carbohydrates, right? To ultimately produce energy.

in the form of ATP. And we know that they are our fuels for energy production. And it's important for athletes to understand or exercise physiologists or physiotherapists or doctors and nurses to understand what those fuel sources are and how they contribute to maintaining, or at least in an attempt to maintain homeostasis during exercise, right? So creating ATP. Straight off the bat, proteins, amino acids.

Do they contribute much to ATP production during exercise? In the early duration, negligible. As it's drawn out, so we're talking hours. So if you were to go from less than an hour of exercise, you would say the amount of energy produced from proteins would be less than 2%. Right. But then if you do exercise for three hours and beyond... Yeah, that's not happening. You're going...

much higher. So up to 10% are coming from proteins. Okay. And that's a process of proteolysis, breaking down proteins into amino acids? Possibly, or there's just amino acid pools that they're drawing from. And amino acids can jump into the Krebs cycle. Yep, that's right. Hence how it can contribute. Okay. So that means for most people, most of the time, it's carbohydrates and fats. Right.

Yes, that's right. As the fuel source. And generally speaking, so if we have a look at the muscle fiber types, you know, slow twitch, fast twitch, there's obviously subcategories of each we're not going to jump into in this episode, but the slow twitch fibers are

They are called slow twitch. They don't have a stronger contractile force. You can't generate as much force through those contractions, power through those contractions. They tend to be less fatigable. They can contract for longer, obviously, because of that.

And it means they need a consistent and constant fuel and energy supply to produce enough ATP over a long period of time. These are usually aerobic, so aerobically driven, so it requires oxygen and tends to most often be predominantly fatty acid driven as a fuel source. So...

Okay, compare that to fast twitch. Fast twitch generate more power, more force. They can't contract for as long, but they can contract hard and they don't usually use oxygen. However, there's a mixed type that can and they're mostly what we call glycolytic. So they use glucose or carbohydrates as an energy source. Our body is a composition of both muscle fiber types and I'm not saying that the quads are type one or slow twitch and this is type...

All muscle groups have a combination of both. A lot of it's genetic and some of it can be trained and changed, right? But not completely, right? But they can be trained and changed. So the point I'm trying to get across is here, if you were to jump on the treadmill and start walking on the treadmill and then I were to incrementally increase your exercise intensity from moderate to heavy to very heavy and severe, right?

In the beginning, you would be firstly recruiting more of the slow twitch fibers. They're less fatigable. They don't generate as much force. Maintaining posture, balance, allowing for you to walk without using a lot of energy. It's going to be aerobic predominantly, right? So you could maintain that for a long period of time. You could walk for a long period of time. So moderate intensity,

for long periods of time, tends to utilize aerobic respiration and the major fuel source of fats, fatty acids. Fatty acids, yeah. Right. Does that make sense? It does. If you were then to go to a high-intensity diet

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So, and I'll say just to add on to that, with the fatty acids at that lower intensity, let's say, let's say 25% of VO2. Yep.

you would say most of it's coming from fatty acids in the blood. Oh, that's a great point. Opposed to fatty acids from the muscle itself. Right. That's a great point. So it's utilizing, you could effectively say that it's using what's provided to it readily. So however, the blood's like your drink bottle, right? It's there. It's readily there. Yeah. However, a caveat to that would be also duration. So it,

If you were to be exercising on the, so you're saying walking on the treadmill at 25% VO2, initially you would probably say it's pretty much similar of plasma fatty acids versus fatty acids in your muscle itself. At what intensity? Moderate for how long?

Just in the immediate, but as it extends. So if you were to run it out to four hours, most of the fatty acids it's still using, but it's coming from the blood. And that would make sense because you're needing to be recruited from fat stores. Yeah, so those fatty acids aren't just – they haven't just been there for the four hours. They've been mobilized from adipose tissue, fat tissue. And this is where you would have heard the term that –

working at a low intensity burns fat. Yes, which is true, but also not. Yeah, there's a caveat to that, which we can come back to in a second. But at this point in time, what you would say is at low intensity exercise, yes, the predominant fuel source for ATP would be fatty acids. Yep.

And then if you were still on that treadmill, I'm like, okay, Matt, you're going to go as hard as you possibly can, right? Or just slightly, let's just say you slowly increase it. Yeah. So as you slowly increase it then, as the demand on the muscle increases and you need to recruit more force and more power, you start to then go, I need to start recruiting more fast-twitch fibers for this. They're more fatigable, but they generate more force. They utilize glucose as their energy source, so carbohydrates. Right.

And that's important because now if we think about what we've spoken about previously, as we incrementally increase the exercise intensity and we're now using glucose, we're also going to be starting to produce more lactate at the same time. So as the intensity goes up, the lactate goes up as well. But also because you're using aerobic respiration to try and maintain your

ATP through aerobic means because it's not like the aerobic respiration switches off. No, no. Your VO2 also goes up as well. But it's about talking about what fuel sources are predominantly used. So all three are going to be used during exercise but there's going to be a predominance of which one. That's right. I think at about 40, VO2 is the crossover between where carbohydrates are starting to become more dominant...

and fat's starting to drop away. Yeah, as you go above 40% VO2 max, yeah. So let's just talk about – so you alluded to before that if you have moderate intensity –

For a longer period of time, people say it burns more fat. And that's true in the sense that the major fuel utilized are fatty acids during this type of exercise. But it doesn't necessarily mean it's always the best way to burn fat. Potentially, if you look at it from a time benefit perspective,

sort of thing. So I'll try and do it as an analogy. Okay. I mean, I'm not sure how well this will work, but so shoot me down. Let's just say you, now, listeners, we live in Queensland and we've just survived a cyclone. Survived, yes. Suppose we did survive it. So we had a cyclone this time last week. Yeah. Anyway, that was an experience, but where I'm getting to in this is we lost power. Yeah. And so...

A lot of people as a backup source, they have a generator. Yep. So let's say, so the generator is running off a fuel to generate electricity. Yep. Right. So this is going to be my analogy. Let's say you have your generator running and you'll run it at a low intensity. So it's running, you know, at its peak,

At its 30% capacity. Okay. At this particular intensity, the fuel source that I'm pouring to the generator is all olive oil. Okay. Does that make sense? Yeah. That's a cool generator. So it's doing what it needs to do at 30% of its max intensity. But all of a sudden, I need to...

increase its output because I want to run a whole lot of things in the house. You want to do the washing machine, the TV. You also want to start playing video games. That's right. So I dial up its intensity to 70%. Okay. Now the source of fuel I've got to put into it is now –

with syrupy glucose with only 30% olive oil. Okay. Okay. So the olive oil isn't enough to maintain the output for that intent, for that, those many device, that many devices. That's right. So you need something that gives you more energy in the shorter period of time. That's right. It may not be, you might utilize heaps of it,

But it's giving you more energy faster. That's right. Okay. So the take-home difference now, what you can see, is when it's working really at a low intensity, it's 100... It's not completely like this, but it's 100% olive oil fat. Whereas when it's working really hard, it needs more sugar with still some olive oil in there to do what it needs to do. Now, most people would say, see, it's burning more fat at a lower intensity. However...

When the generator's working really hard, it's chewing through the fuel. Yeah, you've got to put that mix of glucose and what was it? Vegetable oil in more often than you would when it was running at 30%. So you're actually going through the fuel quicker. Yeah. Okay. So is your take-home point this? So...

The point here is if you actually look at absolute amounts, you're actually burning through more fat at the high intensity just at a lower proportion of it. So at the end of the day, it's about calories in, calories out. So you end up for the time period for the exercise intensity that you're performing, you could do –

...very heavy or severe for a shorter period of time... ...and it burns large amounts of calories including fatty acids... ...those derived from fatty acids... ...compared to doing moderate intensity for longer periods of time... ...yes, while fatty acids are the predominant source there... ...if you looked at how much fat was burnt per minute let's say... ...you're burning more fat per minute with the higher intensity... ...than you are with the lower intensity...

It's just the predominant fuel. Yeah. That's just the caveat. I just wanted to bring into it. That's fair. That's fair. Um,

Look, I think that's pretty much touching upon all the important points. Anything you'd like to add before we... A few other things. I mean, just if you wanted to look at the... And so going back to these fuel sources, they don't only change with intensity that we just spoke about, but they also change in the duration. So as you start to lengthen the time of exercise, they're going to...

start to change their dynamics as well. So yes, if you're exercising for four hours, you would be using a lot of fatty acids, but the glucose that you are also using has shifted from muscle glucose in the shorter term, which is coming from muscle glycogen to now glucose from the blood.

Right. Does that make sense? Is that sort of the opposite for the fats where it starts taking fatty acids from the blood first? Yeah, that's right. So for glucose, it's going to utilize the glucose in the blood but then it utilizes glycogen stored in the muscle and then it goes back and utilizes glycogen that's been mobilized from other tissues like the liver and potentially kidneys that have then been released into the blood. That's right. Okay.

And I guess that makes sense because a lot of the energy stores that we do have that is for long, long term would be our adipose tissue, which has a lot of energy there for long periods of time. And just to plug our upcoming book, there is a chapter in that book where we talk about starvation and the person who fasted the longest, which was over one year,

he started off now, I can't remember the specific weights, but I think he lost around about 80, 90 kilograms of fat tissue. Well, predominantly it would be fat and water and other things, but fatty mass because there's so many calories present within his fat tissue that he was able to utilize that for energy. So he didn't eat, he just had-

Like multivitamins and fluids? Yeah, I had some barley sugars every now and then. Okay. Had tea and coffee and multivitamins, but that was it for a year. Wow. A year. Yeah. Yeah. So there you go. All right, Matty. That is – I think that's part three or four. I can't remember now. Yeah.

of exercise physiology. We're going to be back for more. There's multiple parts to this. I hope everyone's enjoying it. Please leave a comment if you like it. Please give us a five-star rating. Please send us an email at admin at drmattdrmike.com.au. You can visit our website, drmattdrmike.com.au. You can... Website's been upgraded and we're

diverting. So there's a bit of a lag period between our Q&A sessions, but we hope to do one of those shortly. So if you are wondering where your emails are going, we have them on bank and we will cover them in our Q&A sessions, but we've just been a bit behind in that. It is what it is. We will get there. Do we have an, we read your emails. We enjoy them. We thank you for your emails. We just get a lot of them and we don't,

We don't have a lot of time. We don't have a lot of time. So we do apologize. And I know that I tease Matt a lot. And I know that we talk over the top of each other. That's me more than you. We're passionate. Shut up, man. We're passionate. We care. We've got a lot of information to get across. A lot of people also don't like our banter. They don't like the way- A lot of people like our banter. Do they? Yeah. I don't know. I get a lot of emails that say that they love our, you know,

Back and forth. Well, I hope so. The only thing they don't like is our geography. That's for sure. We're bad, especially with the North American geography. But... You know what we should do is just get a globe or a big...

of the world. So it's right in front of us. So we never make these mistakes. That's true. We'll still make them. So anyway, thank you. You know that we do this for free. We know that we do this for fun. We do it just to help people. We've got to make it enjoyable for ourselves as well. And if it was just dry and content-based, I'm sure that you'd be like, yeah, that's cool. That's all I want. I just want the information. It's talking for over an hour is not

necessarily fun when it's just over an hour now so you're now going into more fat stores very good Matt look at that always bringing it back always bringing it back anyway thank you everybody thank you Maddy and we'll see you on the next episode

I don't know.

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