Welcome to the Empirical Cycling Podcast. I'm your host, Kolie Moore, joined by Kyle Helson. And as always, I want to thank everyone for listening. Thank you all for the donations. We've got a page up on the website. If you guys would be so kind enough as to give us a good iTunes rating and review, that would be really fantastic. And so for all coaching inquiries or consultations, please email empiricalcycling at gmail.com. And for the show notes, just head over to empiricalcycling.com. and we've got the podcast episodes up there. So today, what we're going to do is we're going to talk about the history of lactate and we're going to kind of correct the historical record because a lot of misconceptions and myths are still very present today. So Kyle, why don't you tell us about your experience with lactate and the popular press and whatnot? Yeah, I think probably Everyone is familiar with the, or they've been told the myth that lactic acid or lactate is what causes your muscles to burn when you're doing intense exercise or that, you know, not warming down after hard efforts or hard workouts and clearing out lactate or lactic acid is what causes muscle soreness the next day and all this stuff. And it turns out that's Probably all wrong. None of that's true. Everything that even a lot of these popular science fitness articles or whatever say about lactate or lactic acid, it's probably all bunk. The other thing is I think people have gotten really into using some sort of massage or compression things, which also... They think might be clearing lactate out of their muscles faster or whatever, and that's also not true. Yeah, and some of the other myths that I see on the coaching side of things, like lactate, it comes from hypoxia or a lack of oxygen in the environment, or that lactate... is a dead-end waste product. And those are just false on their faces. So we're going to go through a lot of the history of the discovery of lactate. And we're going to kind of debunk these as we go. Like we're going to see where these myths came from. And then we're going to talk about the modern science that we have now that really gives us a whole picture that they didn't have up until as late as even the 1990s. So lactate was originally discovered in the late 1700s from spoiled sour milk. So we get the name lactate, you know, the prefix lac, L-A-C, that means milk, and it's the same root as lactose. Lactose is a sugar for milk, lactate is... You know, just a molecule for milk. But they're actually, despite having the same names, they're actually not that similar. Lactate is a three-carbon molecule. And yeah, so lactose is a disaccharide, which means it has 12 carbons. So the first chemist to isolate lactate is a German chemist named Schiele in the late 1700s or early 1800s. And he discovered this with milk fermentation. is a process that we're all familiar with now in terms of brewing beer and whatnot. But fermentation actually has a very specific biochemical definition, which is that it just means happening without oxygen. So in this hypoxic environment, lacking oxygen environment. And so that's where we get fermentation. So lactate was originally thought to form by only fermentation. Fermented. Yeah, so if, you know, like you said, people have been familiar with fermentation for like, you know, probably thousands of years at that point. You know, you hear of ancient monks or whatever brewing beer or wine and things like that. And lots of cultures have fermented foods, sauerkraut, kimchi, things like that. The difference is here, of course, that there are these bacteria that you're taking advantage of that back even in the 18, early 1900s. We didn't really understand what bacteria were. So we didn't really understand how the fermentation was happening. We just knew that, oh, if you mixed yeast and with stuff, you got beer, you got wine, you know, to assume that the same sort of biochemical processes are going on in the yeast as are going on, or the bacteria as are going on in your muscles is sort of, they didn't have the tools to actually figure out and say, oh, is this process going on inside your body different from what's going on inside of bacteria? what's going on in bacteria in East cultures. Yeah, I think that's a good way to put it because in terms of the biochemical pathway, which we'll get to in a minute, it actually is the same biochemical pathway. They just have different fates, but we don't have to get into bacteria biochemistry right now. Just know that for alcohol, bacteria actually have a separate enzyme that if we had it, we would be permanently drunk. That can be fun. Yeah, unfortunately we don't, so we just have to get the yeast to do it for us. Okay, so the first time lactate was found in muscle was in 1807 when it was isolated from the meat in hunted stags. So, you know, you'd chase a stag in a hunt, it would get tired, and, you know, shoot the stag, get the meat, and then, you know, instead of just eating it, now people had all these cool chemistry tools, they were like, let's check out what's in the meat, and they found elevated levels of lactate. and lactate was also found in dead animals and bacteria so like environments that have no oxygen like Louis Pasteur found this as well and what he found was that in environments with no oxygen like you know you cover a bacteria tray with a lighted candle like with a little cup or something then the candle burns out all the oxygen and then the bacteria doesn't grow as fast or as big as the bacteria with the oxygen supply. And in the early 1900s, a lot of scientists actually did experiments that showed that lactate occurs in muscles without oxygen and then disappears again in the reappearance of oxygen. So we have a really interesting data point here. And this is actually the beginning of the theory that Lactate occurs in these oxygen-less environments. And also, in 1907, it was found that exercise made muscles acidic, so it lowers the pH. And this also happened at the same time lactate formation increased. So this is our first really big myth to bust. because this is the origin of the phrase lactic acidosis because the lactate happened at the same time that the pH was decreasing so people figured it went hand in hand and you know you really can't blame them they had very crude tools and at the same time there was little knowledge about acid-based chemistry and acid-based chemistry is just like where the protons are so like an acid is something with a proton on it and then when it dissociates it sends that Proton Out, now that thing acts as base, and that proton is going to go, you know, be caustic to something. So that's how an acid works, and that's one of the first things that you learn in Chem 101, and, you know, I took it for granted for sure until I started, you know, learning about the origins of lactate a couple years ago, and I was going, oh my god, these guys didn't know acid-based chemistry, like, you know, I really feel like I... No wonder it was so hard. Yeah, exactly, like, you know, we take it for granted. So right now, but at the time, you know, that was like cutting-edge science. And in one of the papers that I've got up on the website in the show notes called The Biochemistry of Exercise-Induced Metabolic Acidosis, it's kind of an easy read if you've had some chemistry. If you have not, it might be a little rough. They go through All of the origins of every proton that occurs during exercise. They go through all of the steps of metabolism and they show how lactate is formed and how it doesn't actually form as an acid. So lactate is not an acid. So acids have hydrogen ions on them, they have hydrogens attached, and lactate is made without this hydrogen on it. And so this just really means it's not an acid. If it was an acid, it would be made with that proton attached. And then the proton would dissociate and go elsewhere and be caustic. So I actually did a really basic chem calculation with this. I used the Henderson-Hasselbalch equation. So the equivalence point of lactate as an acid, meaning An equal number of them have the proton on them as have the proton dissociated is 3.8, and that's the pH. So at that pH, you've got one lactate to each lactic acid. In normal conditions, it's actually pretty different from this, but just by this equation, in quote-unquote normal conditions, you've got... 25 in the non-acid form to every one in the acid form. And under the very worst possible conditions I could conjure for a cell, you had one acid to the 10 not-acid form. And that's very, very brief, those states. And like I said, it's actually more complicated than that, so the ratios are actually much wider. So you actually have very, very few in the acid form. So actually, lactate is therefore a base. Yeah, it is formed, and the way it is formed, it actually can absorb a little bit of protons, which means it's going to act as a base and buffer some of that acid, you know, the same way that baking soda buffers acid. And so the other myth that we mentioned here already... is that we've seen the experiments that show that lactate forms in low oxygen environments. So what happened was scientists assumed that the opposite was true. And, you know, Kyle, what's that old saying about correlation and causation? Correlation does not equal causation. It's the classic. So this paradigm here that we have with lactate and low oxygen... The phrase is low O2 evokes high lactate. So low oxygen environments means lactate is going to form. The idea that low O2 evokes high lactate is extrapolating the phenomenon seen with lactobacteria fermenting milk in the absence of air to the functioning of human muscles. So yes, while it's true that human muscles can Ferment Sugars to Survive for Short Periods of Time. That's nowhere near our preferred method of burning sugars, and it's not enough for us to actually subsist on for long periods of time. And it turns out that actually fermentation is a pretty inefficient way to generate energy, which is why all of the bacteria and yeast that actually only use fermentation to survive are all... single-celled organisms. And all the big organisms you can think of don't survive just on fermentations. All the multicellular organisms are using aerobic respiration or photosynthesis or something like that. And so they actually conjured up some interesting mechanisms for how this happens in a human muscle. So they figured that... There was, you know, maybe like muscle swelling happens, muscle damage, muscle occlusion, and occlusion is just a fancy way of saying no blood's getting to it because like, you know, you've got a pump on or something that's so awesome that you can't get blood to your muscle, which makes like no sense. But so they had these interesting theories about how this happened, about how, you know, during intense exercise, you could exercise so hard that no oxygen is getting to your muscle. And so it's this that's actually the origin of what we know as anaerobic threshold. So we hear the words anaerobic threshold thrown around for the point at which you start burning carbohydrates, or it's the point at which lactate accumulates in the blood exponentially. But it's really neither of these things because they thought that if you exercise hard enough, at a certain point, your muscles were just going to start using energy anaerobically as opposed to aerobically like it was like a switch or something like a binary state and if we know for a fact now that it's not but you know for a long time they assumed that that's what happened and so some of the experiments that they did was they would like you know make a muscle exercise hard or they would constrict the blood supply of it and then lactate would form. And then they would allow oxygen back via blood supply or however they were doing it with their experimental model, lactate would go away. They thought that oxygen was actually necessary for the combustion of lactate. You know, that's untrue also. Potentially the other assumption here that people are making is that, oh, maybe if you exercise hard enough, you're exercising at a point where like you're, Heart and Lungs, your cardiovascular system couldn't keep up with the energy demands and so then your body was like, oh, somehow it was monitoring this fact or something and then switching over to this anaerobic burn. You're actually more on the money than you might think. But we're actually going to get into that at some point in another episode when we look at the physiology and biochemistry of FTP. So for now, one of the significant findings on anaerobic threshold was in a 1964 paper called Detecting the Threshold of Anaerobic Metabolism in Cardiac Patients During Exercise. And then, you know, from this paper to like 10 years on, this scientist named Wasserman, he defined, quote unquote, anaerobic threshold as the, quote, level of work or O2 consumption just below that at which metabolic acidosis and the associated changes in gas exchange occur. This, to me, sounds like FTP, because FTP is where, you know, lactate starts accumulating, and, you know, to him, quote-unquote metabolic acidosis. So, okay, so to quote one of the papers that we've got up on the show notes, Quote, Wasserman's anaerobic threshold hypothesis implies that the accumulation of lactate during muscular exercise is due to, quote unquote, dysoxia. Dysoxia, as defined by Conant et al., is a sufficiently low level of O2 such that cytochrome turnover is limited and therefore there is O2 limited oxidative phosphorylation. So what they're saying is, like, at this point, your aerobic... Your true aerobic metabolism, the electron transport chain, is tapped out. It's pinned at the top of the meter. There's no more that they could possibly work. Actually, we know now that that is very untrue because now we know that the appearance of lactate, the exponential accumulation in the blood, happens much sooner than you actually hit your VO2 max. and we can actually measure power output at these levels and FTP can happen anywhere from like 60, 70 to like 90% of VO2 max. 90% would be in the super elite athletes but the point is essentially the same. So Wasserman's hypothesis, and again, you can't blame them. They didn't know how it worked but it's calmed down in the exercise and coaching communities and the medical communities too as canon, like as if this is how it really works. Like as soon as you hit the onset of lactate, you are aerobically tapped out. You can't deliver any more oxygen or your machinery can't work even if you can. And we just know that that's not true. I think it's worth noting too, like you said, if the rise in lactate is appearing, is correlated with the onset of FTP, You can work very aerobically above your FTP for relatively long periods of time, you know, 3, 4, 5, 6, 10 minutes, 20 minutes, something like that. And you're very much still working aerobically. You're not, you're anaerobic for 15 minute pills or something, you know. Yeah. Yeah. And so like, so actually some, there's been some really good experimental data on what is a truly anaerobic effort, meaning anaerobic meaning happening without oxygen. So even in. Like a one-minute all-out effort. You know, depending on the athlete, you can still get like 20 or 30 up to like 50, 60% contribution of oxygen and oxygen-derived ATP into that effort. You know, like the low end is probably a track sprinter. The high end is like a track enduro if you want to go for like the very fastest kilo times. in the world, like about a minute, minute one, 59 seconds, something like that. So even in a minute, there is a good deal of oxygen being used, even though a lot of people think it's like the true anaerobic effort, but it's really not. And we're going to get into that also in another episode, because there's just so much to get into. So the reality is that hypoxia, like the lack of oxygen, inducing an increase in lactate is a real thing. What they got wrong is that it's not a prerequisite for the lactate appearance. So in about 1927, separately, the two Corys and another scientist named Warburg looked at animal models with glucose-consuming tumors and they had high lactate despite normal oxygen conditions. So everybody kind of figured like this is just like a weird thing that happens in tumors and it doesn't happen in, you know, normal tissue. But, you know, like in 1966 or so, about the same time that Wasserman published his paper on dysoxia, there was an experiment showing an animal model flexing constantly for periods of time up to like 60 minutes or so. And what they found was an increase in lactate that was transient. Like it went up for a couple minutes and then it went down. And so this, like we talked about in the 2x20 FTP episode, is just what we were talking about with the first couple of minutes not quote unquote counting towards your time at FTP aerobically because when your muscles start working they cover that anaerobically like any immediate onset of exercise of work output is covered anaerobically by your muscles until it can get this slower moving aerobic stuff Like going up to speed, which is in a way, you know, it actually makes our aerobic systems kind of lazy, like you got to like roust it out of bed, like for your FTP efforts. And so that's what they saw with this, is that transient increase in lactate at first, and then they saw it decline. It went down to like near zero, or the muscle that was working that they had contracting constantly. would actually become a net lactate consumer. It would start to take in lactate with these continued contractions at an unchanged metabolic rate and unchanged oxygen delivery. It goes completely against everything else that was thought at the time. But they didn't have enough to really get a theory for what was going on, right? Yeah, they just knew that like that in these muscles if they just kept them going long enough you know submaximally they would just start taking in lactate at some point and they're like they're scratching their heads like why does this happen like is this just like a passive diffusion thing because there's like at some point there's less lactate in the cells and it's just accumulated in the blood or like like who knows well we do now the joys of being 50 years ahead of them in Biochemical Understanding. Okay, and so going forward, we actually have to gloss over the next set of experiments because unfortunately there's so much biochemistry now because the tools start getting better that it's not worth the time or the energy to really explain without like a whiteboard or something like that. However, if anyone is interested in that kind of thing, I am more than happy. to do a consultation or to start a Patreon or something like that where I actually go through all of these pathways and show people how we can use this knowledge to become better cyclists. So if you're interested in that, give me an email, give me a shout and let me know. And if there's demand out there, I will be absolutely happy to do it. So going on from there though, We can't get into the mechanisms of some of these experiments, but with fatigue and lactate, the thought that lactate causes fatigue because when you exercise maximally, you get tired very quick, and this happens at the same time as lactate accumulation. But some really good experiments showed that it's... probably other conditions with like, you know, the lowering pH, high levels of phosphate, high levels of calcium, you know, neurotransmitter reuptake that's, you know, not fast enough, stuff like that, depending on the exercise intensity, but not lactate. But, you know, even with these things, fatigue has a lot of different factors and it's debatable like what actually causes fatigue and to what degree because Also, some of these chemicals can act as regulators of the pathway glycolysis that creates lactate at some point. And so these things might actually be more of like a feedback mechanism. And if you've ever studied any sort of pathways, signal pathways or metabolic pathways, you know that regulation is a super important part. of energy expenditure and control of energy expenditure. So just that it's lactate is, you know, once you see kind of how the body works, it's too simple of an explanation. Like all the very, very simplest things about our bodies were discovered like by the Greeks, pretty much. And after that, it gets much more complicated very quickly. There are some experiments. on rat muscle contractions that show that lactic acid, now the actual acid version, and propanoic acid also actually restores force production of fatiguing muscles. So you can think about this as like a sprint. And so these rat muscles, they've got isolated and they're basically sprinting for all they're worth because you can electrically stimulate a muscle to contract on its own. And that's exactly the same as a nerve, like a brain, sending the signal to it. they're making these right muscles contract and when they pour this acid on the muscle like the contractions get stronger again because as it fatigues the contractions get weaker they produce less force put this acid on and they get stronger again so yeah this is one of those weird things that like maybe like the actual acid version isn't so bad yeah But, I mean, it's very complicated. So we cannot say that, you know, pouring acid on your muscles is going to be great for sprinting. Like, it's not that simple. Don't go around, like, adding lactic acid to your, like, water bottles, like, mid-race. No, no. Aside from making your drinks taste horribly. Yeah, definitely. There's another really interesting experiment with lactate and fatigue. And this is actually, I read this in a paper. that was meant to present this experiment like they've done it and it's a very easy one to do and it is very illustrative of how lactate doesn't cause fatigue when it's elevated in the blood. So what they did was they had groups of students do eight 30-meter sprints with either 20-second rests or 120-second rests. And what was interesting about this is that blood lactate increased By similar amounts from the start to the end of the test in both groups. But the difference is the 20-second rest group, their speeds tanked. And the group doing 120-second rests showed actually no fatigue between each of the sprints. Like their sprint times even got a little bit faster. And so with the same amount of lactate in their blood, you might expect that the 120-second rest group would have fatigued and they didn't. Also in this paper they go over, you know, what are the other possible mechanisms that would cause this fatigue? And so one of the cool things that they were talking about is the recovery of phosphocreatine. So it's not lactate, but the inability to reproduce phosphocreatine between these sprints that caused their times to decrease. So also there have been other experiments that show that muscle occlusion, you know, just putting a band around your muscle, like just stopping the oxygen blood supply, muscles under these conditions cannot recover phosphocreatine. So the next good question is, how does lactate accumulate and why does it accumulate? So during exercise, glucose, a sugar, gets broken down into pyruvate. So glucose gets split in two at some point. and makes one glucose makes two molecules of pyruvate. So this is always happening at a certain level at every exercise intensity, even at rest. So at the zero watts exercise intensity of just existing, you are making a little bit of lactate. Now, pyruvate has two choices. It could go into the mitochondria and to the Krebs cycle, and this is the quote unquote aerobic cycle, or it could get turned into lactate. And a note on the Krebs cycle being aerobic, technically, The entire Krebs cycle happens without oxygen. So very pedantically in biochemical terms, we could actually consider it fermentation, even though it happens in the mitochondria and in just general biochemistry parlance, just talking to each other, we just say the Krebs cycle is aerobic. It's good enough. So the enzyme that makes pyruvate Turn into lactate is called lactate dehydrogenase. And it's always active. You can't really turn it off. So that's why you're always producing a little bit of lactate. The balance of pyruvate and lactate are actually a little in favor of lactate. So if we let this reaction, just if we stop everything below pyruvate and we just let this reaction run out, we actually end up with a little bit more lactate than pyruvate. Not a significant amount though. So during periods of intense exercise when pyruvate's backing up and getting turned into lactate, why don't we send pyruvate into the bloodstream? And this is a very good question because there are transporters on cells in every tissue or almost every tissue that send out and take in three carbon molecules. with a carboxyl group on them called a monocarboxylate transporter. And MCT1 and MCT4 are the very most common ones. And I believe it's with training, MCT4 actually becomes much more prevalent on your muscle cells. And this is both to send out lactate and bring in lactate. And we'll get to that in a little bit. But why does the pyruvate get turned into lactate? It's a very good question. Because, you know, we could just... Leave it at pyruvate, couldn't we? But we don't. So what's the deal? So there's another molecule that's very, very important in metabolism. It's called NAD+, or nicotinamide adenine dinucleotide. And there's also a second one called FADH and FADH2, but they're not involved in this specific reaction. But know that they're important because they are what supplies The Electron Transport Chain, the actual thing that ends with oxygen and water. When there's a backup in the mitochondria, you can't get enough pyruvate in, and you still have to push hard, you still have to exercise hard, and you're burning a lot of glucose, NAD is actually very necessary for this process. So in the breakdown of glucose to pyruvate, we use a lot of NAD, and it gets turned into NADH. and in order for this process to happen because we're pushing really hard over threshold we need to have a lot of NAD and as it gets turned into NADH through this process we would actually run out if we didn't turn it back and the process of breaking down sugar would slow down very significantly which means we wouldn't be able to exercise that hard over what we could do aerobically okay so evolution's solution because evolution is if nothing else very very clever It takes pyruvate and it takes NADH and it takes another proton from the cell. So this is actually reducing acidity at the same time it's freeing up an NAD to go help break down more sugar. And then these two protons get put onto pyruvate and that gets turned into lactate. So lactate is used to free up more NAD for more breakdown of sugar. And it's used as a slight buffer by absorbing a little bit of protons that cause acidity. So even more proof that lactate is indeed not an acid and it's not actually what's causing your muscles to burn there. No, not a bit. And also, it's not a waste product. This on its face seems like it's a waste product because it gets turned into lactate and it gets sent out into the bloodstream. As we mentioned before, other cells take up lactate. And the reason they do is because lactate dehydrogenase is always active. And if you have a lot more lactate than you have pyruvate, you're actually going to make pyruvate. And now you can send that into the mitochondria for the Krebs cycle. It's very, very efficient. And this is the reason that we don't pee out a ton of lactate after intense exercise because the body's like, no, there's still energy in that. It's like not wasting your food. This is like your mother telling you to finish your dinner and if you don't, you're going to have it for breakfast. Right. Yeah, I think the other way you can think about it is if you look at what a lactate or a pyruvate molecule looks like, it's got many carbon bonds. a lot of them are bonded to hydrogen but it's a much more complex molecule than what the normal true waste products from aerobic respiration are which are carbon dioxide and water so if it's a more complex molecule that means more energy can be derived from the breakdown of the molecule and your body's not just going to let you let that go to waste exactly like you said especially you can think humans back in the day were kind of apex predators which means we definitely need to Conserve energy, you know, trying to track or hunt or even farm food is very labor intensive and requires a lot of work. And so if it requires a lot of work to get food, you're going to want to be really skimpy on wasting energy, even at the cellular level. Yeah, exactly. Okay. And so now that we know that lactate gets used as a fuel also, So like, really, where does it go? You know, to what degree does it get taken up by working muscles and other tissues? So it was actually thought to be a dead-end waste product up until about the 70s. As a side note, it was also wrongly assumed to be the cause of the slow component of oxygen uptake, but we're going to do another episode on that later. We're going to give the slow component its own special look. Okay, so now that we know... that lactate is not a dead-end waste product and it's not an acid and it doesn't cause fatigue. So why do we have workouts like quote-unquote lactate tolerance workouts? Yes, I think these are actually pretty common amongst many forms of aerobic or even aerobic slash anaerobic exercise and sports ranging from running, swimming, cycling. Everything. I even remember back to my, even all the way through my collegiate swimming days, we would have quote-unquote lactate tolerance workouts where there would be hard race pace efforts, one to two minutes long, so typically 100 to 200 yards, where you'd get almost full rest, so like three, four, five, six, seven minutes in between to recover, the idea being that these really hard efforts would generate a lot of lactate. Yeah, yeah. Yeah, and so actually Joe Friel has a lactate tolerance workout in the cyclist training bible. So what was the protocol on that? So I actually have that book open right here. I have the third edition. So for people playing along at home, it's the third edition, page 259, which is an appendix C. A5, lactate tolerance reps. This is to be done on a flat or slightly uphill course into the wind. After a long warm-up and several jumps, do four to eight repetitions of 90 seconds to two minutes each. Intensity zone is 5C, which I think is pretty close to all out. Yeah, that's max. Cadence is high. The total of all work intervals must not exceed 12 minutes. Recovery intervals are two and a half times as long as the preceding work, so that means if you did... a two-minute interval, you'd have five minutes to recover, which actually pretty well jives that I was saying that I did when I was swimming. And then he talks about how, you know, you'd build, you wouldn't do this more than twice a week, and you'd first start off with, you know, only a few reps, then you'd kind of add them as the... Training Cycle Goes On, and he real recommends doing these in the build and the peak phases, and curiously enough, he recommends to not do these if you're in the first two years of training for cycling, which I think is a little weird, but you know. We're not really developing the ability to tolerate lactate because there's nothing to tolerate. Right, it's actually something useful that your body is like, oh, yeah, we can do something with this, hey. Yeah, so your heart... takes up a lot of lactate because the heart is a very predictable machine because it's just beating all the time. So it's very, very slow twitch. It's got a ton of mitochondria. That's why like if you've ever eaten heart, it's like the very, very, very darkest meat you've ever eaten. So lactate is... is a great thing because it's full of mitochondria and so it can just like turn lactate into pyruvate and like, voila, you have more food for the Krebs cycle and the brain likes lactate and you know, muscles that are working sub-maximally like lactate too, like they'll take it up too. One of my pet peeves about the misconceptions in lactate, like the Michael Phelps thing, Kyle, like what's the Michael Phelps thing that's happening recently compared to? Oh, the Michael Phelps thing is like, oh, he was tested to have like, twice or either it was either twice the lactate clearance rate or produce half as much lactate or something as the average person and so that must be why he was able to win like 97 gold medals or something like that yeah and you know who else has uh you know has like twice the lactate clearance rate of the average person is any trained cyclist right yeah the other thing is like even like Even if you think that about, like, if you think about the events that he was swimming, it's not even like he was doing, he was rarely doing those short, you know, approximately one minute long efforts. Most of his races were actually longer than that, and so quite aerobic. Yeah, yeah. You race a 200 or a 400 like he was doing, like the majority of his races were in, you were not. They were not terribly anaerobic in lactate. And you're not, yeah, you're not critically anaerobic for those races. Yeah. The test I actually did, I found out, was they tested his blood lactate after a 100-meter fly, and anybody who's done blood lactate testing will tell you that that doesn't really reflect anything about the person's physiologic state, but not only that, it doesn't matter, because it's not a harmful thing. And yeah, so that's like, that's one of the pet peeves I've had lately, it's just in the popular press, is that. Okay, and so what is... What does the training do? How does this work? So trained cyclists have a high rate of flux of lactate, which means trained cyclists make more lactate, but also use more lactate. So this is a very, very important distinction because it's not that you make less when you get stronger. You make more, but you use more. I mean, this is a critical distinction. So lactate clearance from the blood varies by intensity and training status. So this is from a paper called Lactate Kinetics at the Lactate Threshold in Trained and Untrained Men. So at FTP, or their approximation of FTP, trained subjects had 34% higher clearance rate than the untrained subjects. At 10% below FTP, trained subjects had a 64% 97% higher clearance rate than at FTP and 97% greater clearance than in the untrained subjects at the same intensity. So the reason that the clearance rate is increasing is because the intensity is decreasing. So you're not making quite as much lactate. So your cells take in more to use it aerobically. I think this also kind of makes sense if you consider that The more you're trained, the more your body and all of your cells are going to be exposed to lactate. So your body is going to respond in a way that allows it to handle those lactate molecules better and more efficiently and higher flux rates than if you're just sitting on a couch all the time. Yeah, exactly. And they tested the muscles of the trained cyclists and they had a greater percentage of MCT4. Big, the big transporter in and out of lactate. And so, you know... And so it's not just to like get rid of lactate, just stick it in the bloodstream so you can pee it out. It's very much the opposite. It's like depending on the intensity, your working muscles are going to be the biggest consumer of lactate. So when you test somebody for, you know, lactate tolerance, quote unquote, and you do like a ramp test or you do a whatever test and you look at, you know, lower, like an FTP. A trained cyclist has a lower level of lactate than an untrained cyclist. Or like a more aerobic cyclist has a lower level of blood lactate at FTP than like a really good sprinter has. And so it doesn't necessarily mean that one is, well, it does a little bit mean one is making more lactate than the other, but like the level that's in the blood... has two components to it that are very important that we measure separately. So I think you're basically saying that when you measure blood lactate, that is a number that is affected by both your utilization rate of lactate and the transport rate of lactate in and out of the cells. Yeah. And so also, let's also consider... Let's say we have a hypothetical cyclist who does a 30-second or one-minute all-out hill rep, and we look at his or her blood lactate from before and after and during a couple minutes after the hill rep. Because lactate is just a fuel, and the appearance and clearance rates are different for different cyclists depending on training state, it doesn't actually provide us with that much actionable information. We have so much more data Just from power alone, that can give us actionable data about a cyclist, way more than blood lactate. And just personally, I think this is one of the ways in which lactate is completely overblown. Or to put it another way, as Dean Golich once told me, everything you want to know is in the power data. Every physiological parameter that you... Can train or that you want to see improving or changing as an athlete trains? It's all in there. You just have to know what to look for in the patterns emerging from the training data and the racing data. Granted, it does take a long time to get used to seeing these patterns and knowing what you're looking for and why they happen and how they affect the power data, but I personally think that this is a point that every coach out there should be trying to achieve. So how do you feel that understanding the process of discovery of lactate and metabolism has kind of affected the way that we view exercise and training now? Okay, so I think like a lot of things in science, having a even Shallow understanding of the historical context in which these scientific measurements were made or discoveries were made gives you a much deeper understanding for why things are the way they are or maybe why misconceptions are the way they are. So, you know, being a physicist, one of the famous things is, of course, that when you study electrical current, the first thing they tell you is that conventional current is the direction positive charges flow even though you know now it's like electrons that move and those are negative anyway you can also see why these things sort of permeate into the popular culture like it's much easier to digest these small little tidbits of like oh lactic acid is is what causes your muscles to burn during exercise and you should warm down after exercise like that's a very concise soundbite that's much easier for you to digest whereas actually going into all this biochemistry and all these physiological measurements took Many, many minutes and obviously that we've been talking about it here and even more time spent in the lab and then digesting all these papers. And so I think fortunately, unfortunately, like a lot of things related to training and physiology, like it's never as simple as you think it is when you first read it. And that's good, I think, because hopefully us trying to break these things down. has provided a good route into some deeper understanding about lactate and the origins of all these myths. I think it also should hopefully give people a good appreciation for how far we've come. People think, oh, it's really cool because, you know, we've got the internet and all these other things. But if you think about how much we've learned even in the last 40, 50, 60 years about the way the human body works compared to, you know, what the peak of medicine looked like in the 18 or even early 1900s, it was bleak. You know, we've come a long way and even just the things, the sort of whirlwind we've done here from early 1800s, oh, sour milk. Lactate, fermentation, all the way up to now being able to say something about how your body is actually utilizing these molecules instead of just guessing. I think my favorite thing that we covered today is actually quote-unquote anaerobic threshold. Because once you go over FTP and your blood lactate starts climbing, does that mean you're breaking down more sugar since glucose is where the lactate comes from originally? And the answer is yes. But does that mean that that it's fully anaerobic, that it's a hypoxic thing. And the answer is that even when you're in zone two, when you're just going for an easy spin and you're like, oh, this is quote unquote aerobic, you're still breaking down glucose and you're still making some lactate. The difference is not like once you go over a certain intensity and you start burning more carbohydrates, that that's anaerobic. The honest answer is that Even at the easiest pace riding that you can be doing, you still have anaerobic processes going on. You're breaking down glucose, you're creating lactate. The Krebs cycle technically is anaerobic. The breakdown of fats, technically anaerobic. The only place where you get oxygen in the entire chain of metabolism is in the electron transport chain, which happens in the mitochondrial inner membrane. So the important thing to know is that the anaerobic threshold, quote unquote, isn't really anaerobic. It's not like you go over this and you're anaerobic. Anaerobic processes are happening all the time at every intensity. So this actually makes a very inconvenient picture for people trying to describe these things in these very simple terms. But now we have a historical context for why that is. And in another episode, as usual, but we will get to it, I promise, we're going to go over, like, what is aerobic? And, you know, we just sort of touched on it here, so, like, let's let that be a little bit of a preview. I think the other thing is that I always interpreted when people would say aerobic or anaerobic threshold that that was also somehow, like, the tipping point, like, oh, once you, way back in the day, once you exceed this level, that means you're, you know, You know, you've shifted to 51% anaerobic contribution and 50% aerobic, you know, 49% aerobic contribution, which also isn't even true. Like, as you said, as we said earlier, that's actually more right around the, like, one minute-ish all-out effort. And so, you're still quite, quite, quite aerobically dominated at this anaerobic threshold, quote-unquote. Yeah, or put another way, like, you know, the old... Coggin Training Zones of, you know, 120% of FTP is your VO2 max and over that is your anaerobic. So if your VO2 max power is 300 watts and you shift to 301 watts, it's not like everything like flips all of a sudden and now you're totally anaerobic. Like it's not at all how it happens. It's very much a sliding scale. And it, you know, it just depends on how fast are the processes happening. I think the other thing is that your body is actually really adaptable. And so I think the cool thing about training is that you're taking advantage of these evolutionarily enabled adaptations to make yourself good at this thing that isn't required for you to live at all. Whereas your body developed all of these things to help you stay alive. And now we're going to take advantage of that to help you pedal bikes faster. Okay, so I want to thank everybody for listening and we've got the show notes up at empiricalcycling.com and we've got the podcast episodes up there. We've also got a donations page so if you like the show you just heard and want to donate to the podcast we are advertising free so if you want to show us some love we would really love you back for that by producing more shows that you're enjoying. So if you have any questions, comments or coaching inquiries please send an email to empiricalcycling at gmail.com and if you'd be so kind also as to give us a good iTunes rating we would really love that and if you want to tell your friends especially alright yeah and so as always everybody thank you all for listening so much bye bye thanks everyone