Welcome to the Empirical Cycling Podcast. I'm your host, Kolie Moore, joined as always by my co-host, Kyle Helson. Thank you, everybody, for listening as always. And of course, if you like what you're hearing, please subscribe to the podcast. And if you've already done that, a nice rating and five stars on iTunes, wherever you listen to podcasts, goes a long way. Thank you for all of those. And of course, sharing the podcast is really the biggest thing you can do to support the show. We're also ad-free, so if you'd like to donate to the show, you can do so at empiricalcycling.com slash donate. And our listeners have given us a raise recently. Really, really appreciate that. Thank you so much, everybody, for donating. Keeps the lights on here. But of course, if you really want to keep the lights on, we are a coaching company, of course. So reach out to empiricalcyclingatgmail.com. If you have any coaching inquiries, if you are looking for a coach, we're always taking on clients. And if you'd like to hire us for a consult and make sure your season is ready to go, or you just want to ask questions about whatever, our time is your time. So just, again, empiricalcyclingatgmail.com. So reach out for that. and of course if you have any questions or comments comment on my Instagram or reach out to me via email and Instagram is of course Empirical Cycling and that's where we ask for listener questions for the show and so what is going to happen today is we're going to do a 10 minute tips episode right after this episode and we're going to release it a week after this one so keep your eyes out for that but basically what's going to happen is we're going to talk Talk about over-unders, and then we're going to talk about kind of the practical uses I find for over-unders, how I'd like to structure them, and of course alternatives based on what we're talking about here in this Wattstock. So yeah, if you want to ask a question, we will get to the questions in the 10-minute tips episode for next week. But for now, Kyle, why don't we talk about over-unders in general? What are they? What are they supposed to do? What's it got to do with lactate? Why are they popular? When's the first time you heard of over-unders anyway? Honestly, I was trying to think about this and I can't remember exactly the first time I heard about over-unders. I don't think they're mentioned in Friel's book, but I don't remember for sure. They are. Crisscross Threshold. Okay. Yeah, I remember that one exactly. Crisscross Threshold, it's like you start under and then for two or three minutes you work to... going over, and then for two or three minutes you go back down. So it's like a nice even sinusoidal or something like that. Yeah. So maybe that's the first time. I feel like, though, there are enough of a thing in the zeitgeist indoor training, whatever. It's the wintertime. You're going to be stuck on the trainer. If you're bored of sweet spot or doing FTP efforts, like, oh, you should try over-unders because maybe they're more race-like because you do go a little bit harder. They more simulate trying to follow an acceleration, let's say, in the pack. Or people will say, well, because you're going to work over your FTP for a little bit, it's going to get you better at processing lactate or working at that higher intensity level. And then, just like in a race, you don't get to recover at zone one or something in between. You have to go back down to riding a hard but sustainable effort, like a sweet spot or effort. But then I feel like it's weird because I see people prescribe them at wildly different sort of intensity levels for the over. Like sometimes they're like, oh, go like 5% over your FTP or whatever. And you're like, okay, is that going to be that noticeable, like 5%? And then sometimes they're like, oh, you're going to like just... fucking crush it for like a minute and then go back and you're like, oh, that sounds terrible actually. Or they say, oh, it's like VO2 max interval range, so you know, like greater than 120% of FTP or 125 or whatever it is. And so it's kind of all over the map, but it seems like generally it's, you know, it's a sweet spot workout where for a certain period of time you're doing greater than FTP by some margin. And it's not, usually it's those over. periods are shorter, so it might be, I've seen them as low as like, oh, you're just doing like one minute over and then you go back to like, you know, four or five minutes under and then just one minute over or all the way up to something kind of bonkers like, you know, one to two minutes over, one to two minutes under, one to two minutes over, you're just going back and forth and back and forth and back and forth. Yeah, and I think actually the where's the under is actually a very valid question too because one of the things that I noticed here is that There's not a specific study that I found at all looking at over-unders the way that most people do them these days. I've seen a couple that are similar. I've seen a couple studies that can kind of clue us in, but maybe this, and we just talked about this before we hit record too, is like maybe this is a stupid podcast to do for this reason. this there's not like a study a well-done study to pick apart that I've been able to find it's like it's like this is almost like shadowboxing where like we've got the like this thing to talk about that's like theoretical and we're going to spar with this with this type of workout that has theoretical implications on this is why this should work and we're going to talk about the merits of whether or not it actually does work because A lot of the times, like when I've been doing consultations lately, I see a lot of stock workouts where people explain. This is what this workout's purpose is physiologically. And especially with over-unders, I see things like your muscles will be clearing lactate more with this workout, and therefore they'll get better at clearing lactate. So we'll look at that one. Since FTP is the point at which we cannot clear lactate anymore, getting used to clearing lactate means FTP will go up. We'll also talk about that one. I also see things like, you know, we'll get used to dealing with the papillates produced over threshold in association with lactate. And so that's all the kind of stuff that I've seen with these. And in popular media too, like there's a lot of discussion of this and how it should work and like NCT, which are monocoboxylate transporters. And we'll talk about all of this. So I think maybe one of the things that we should think about first too is, you know, the idea that over-unders seem to be endowed with special properties because they create and sustain high levels of lactate and then oxidize it. Miracle intervals. God. So there's a couple things to think about. Like a lot of the mechanisms of adaptation seem to hinge on two things. The first one is bathing a cell in lactate, which I don't know why, that sounds really gross. See, I actually, I have some nostalgia for that idea because back in the day when I was a swimmer, we both in high school and in college and even in club and at a bunch of levels, we would have days that were, they were effectively, you know, anaerobic capacity days, but they were, they were, uh, race pace efforts on like six, seven, eight, 10 minutes. And so you'd be doing fifties or hundreds. So they're very anaerobic. And then the idea was that you'd, yeah, by doing these, you would build your lactate tolerance, which is not. Yeah. Which we now know is bupkis, but you know, it's. But, you know, when, well, that's why there's, I think, in modern theory, there's a couple things that are going on here. Because, you know, if we're gonna look at, you know, the classic view of lactate, which is technically incorrect, because especially in popular media that I've seen in books and whatever, I see two pairs of things. The first pair, yeah, we're either going to Train to reduce lactate production, and then we can do training to increase lactate oxidation, and that's a more modern take. But the old school way to think about it for over-unders, we can increase lactate tolerance and also increase lactate clearance. So there's some overlap in these ideas, obviously, right? Because we've got two things about lactate clearance, and one is tolerance and one is less production. So those are the... two things that I usually see in articles and, you know, in workouts where it's like over-unders are supposed to do one of these two things or both or whatever. So does that kind of make sense about where we're coming from with this? Yeah, I think so. I think that definitely, you know, kind of you're, the idea of you're going from this older perspective of lactate and tolerating lactate and treating it like entirely as a waste product and then That would be theoretically over-unders would be teaching your body to get used to this metabolite waste product, whatever, what have you, or the new school idea where we accept that this is a fuel that your body can use, but your body has to, you know, develop the transporters and all these other things to effectively, rapidly metabolize it for exercise. So again, you could say, oh, well, we're just going to produce more so that our body gets used to using it. Yeah, sure, great. Yeah, so let's start by setting up this whole thing about like the old school way of thinking about lactate, which is actually, you know, has a lot of historical inertia behind it. Even though I think it's technically incorrect, for our purposes today, it really does not matter that much. So the classic view of lactate is that there is a threshold and during steady sit exercise at and under this threshold where blood lactate is steady, so let's say like endurance riding, tempo, sweet spot, FTP, We're producing some lactate glycolysis that is somewhat in proportional to the intensity, but we're also oxidizing the lactate that we make. And once we get over this threshold, we make more lactate than we can oxidize. This is the technically backwards part, but it doesn't matter really. But either way, over the threshold, lactate in the blood always begins to rise disproportionately in relation to intensity. And so, while lactate is building up, We fatigue more rapidly, right? And so that's where our old school thinking comes from is the lactate cause fatigue. We know it's not actually true. It's now it's just guilty, like by association. It's like an innocent bystander, like, oops, sorry, sorry, you're there. And so that was part of the lactate buffering or tolerance thing from the old school. And, you know, approaching this whole thing, I think that it's that historical inertia alone. that has made over-unders. And actually, a lot of training methodologies kind of popularized the way they have been. And a lot of them do work. Some of them don't work the way that they're supposed to. But remember, our rubber meets the road thing here is that we are always going to think about, does this improve performance? And when we get into our 10-minute tips episode in a little bit, we're going to talk about... Kind of how I like to program over-unders and how I feel like it improves performance and, you know, how I categorize them also. But for now, we're just going to go with kind of the theoretical underpinnings here. So, let's see. We need to answer a couple questions in this episode. So, can over-unders train any of the things that we listed previously? Which is lactate clearance, which is the same as lactate oxidation, reducing lactate production, or improving lactate tolerance, quote unquote. So for lactate production, I typically wouldn't think about over-unders as reducing lactate production, so we're actually not going to touch on this, but also Wattstock number 40 covers a lot of what matters here anyway. So for more importantly in this podcast, can over-unders train the body to clear more lactate? And then can we train the body to tolerate lactate or more accurately, its associated byproducts? Sorry, lactate, you have been cleared of guilt, so to speak, by a jury of your peers, which are us. I too am a metabolite of the body. All right. Okay, so let's talk about lactate clearance. So here's our section one. And this is probably going to be a somewhat long one. So I apologize to people, but we'll tell you when we're changing sections if you want to hit pause and come back later. So yeah. So what is lactate clearance? Lactate clearance is just removal of lactate from the bloodstream during exercise. What we're going to consider in this podcast is specifically this happening in muscles for the purpose of oxidation. Because lactate can also get used up by the liver and the heart, etc. for energy or other purposes like gluconeogenesis, stuff like that. So there's a lot of different fates of lactate in the blood that are very useful for the entire body. But we really just want to concern ourselves with muscles today. Lactate in the muscle. is not obligately oxidized. It can equilibrate with pyruvate, because remember, lactate dehydrogenase, that's an equilibrium enzyme. And as far as anybody knows, there's no regulatory mechanisms on it. It's 10 to 1 in favor of lactate at rest, 10 to 1 lactate to pyruvate at rest, and 100 to 1 during exercise. And so that means if we import lactate into a muscle that is at rest, The lactatives, of course, like if you have now have 20 to 1 and you're at rest, like a bunch of those are going to become pyruvate just because that's the way that the equilibrium works. It could also become alanine or it could go a bunch of other directions. So there's a lot of different potential fates, but we're focused on oxidation today. And the studies that we're going to look at are concerned with the same thing. And there's at least one really well-known study on lactate clearance and oxidation that we're not going to look at because I don't feel like its methodology actually controlled for this 100%. So a lot of people might be thinking right now, are we talking about lactate shuttling? Lactate shuttle apparently has been getting popular these days. So we're going to look at a study and we're going to talk about lactate shuttling. So the study is called, and there's no dramatic tension with these study titles. I'm so sorry, everybody. It's called Blood Lactate Clearance During Active Recovery After an Intense Running Bout Depends on the Intensity of Active Recovery. So, you know, there we go. The whole thing's in the title. That makes sense. It feels like it is a not a duh but like if you imagine sprinting and then only backing off like 1% it's gonna be worse than if you Get to sit down in between. Anyway, sorry. Yeah, well, here's the thing is even if you think that the premise of this episode is bullshit, and that's fine if you do, honestly, do what works for you. I've always been an advocate of that. This study is actually what's going to tell you where should you do your under and why. So if you are concerned about, not about whatever, if we talk about everything today and you're like, eh, forget that, whatever, I still subscribe to the quote-unquote old school or the traditional way of thinking about over-unders, this is the study that you're going to appreciate because we're going to see where and why we're going to oxidize a large amount of lactate. So if that's something you care about, this is your guy here. This is your study. I like a couple things about the study. That's one of them, is that even if you disagree with me, you can still listen to this and go, okay, I appreciate that. Yeah, that's good. So a lot of the previous ones before the study, looking at lactate oxidation and rates relative to, rates were relative to percentage of VO2 max. And of course, as we know, Lactate Threshold or MLSS or FTP or whatever you want to call it varies relative to VO2 max. And of course, lactate dynamics above and below this threshold vary like we talked about. So I like this one, even though their lactate threshold measurement wasn't my preferred one. It's at least going to underestimate FTP for people or it's going to get it pretty close. So I don't think in this protocol here, nobody's actually in danger of doing lactate threshold quote unquote recovery. Over Threshold, which would really change our reading of this paper. So for the- That would be terrible. I know, right? It's like, all right. If you messed up that bad. Yeah, do this over threshold effort and then recover over threshold. It's like, what do you mean recover? You're going to do VO2 max over unders with anaerobic, with like all out 30 second sprints every few minutes for eight minutes or something, right? Yeah, call them over more overs. Okay. It's called a max heart rate test, right? Oh, God. So what they had people do is they had people do a five-minute effort at 90% of their measured VO2 max. So that just about guarantees everybody's going to be working over threshold. And they had people recover at 0% of their threshold, LT, which basically passive rest, like you do your effort and then you sit on the side of the track. Then you... do it at 40, 60, 80, and 100% of lactate threshold. As a bonus, I like this one, they let people recover at self-regulated pace also, which varied from 50 to 100% of their measured lactate threshold. Average was 80 or like 78, something like that. And so we've got a good over at 90% VO2 max and a good under. which, but they don't repeat it again. So it's not an iterative bout where you go over, under, over, under. It's like over, recovery, that's the end of the protocol. So it's not perfectly illustrative for our purposes, but it's still good because after they sat down or were doing their active recovery, they measured blood lactate every four minutes. out to 32 minutes until the lactate basically returned to baseline values. And they also measured the first derivative of the lactate clearance curves. And they found the peak rate of lactate clearance at each recovery intensity. So Kyle, can we get a quick explainer on what a first derivative is for the people without calc backgrounds or folks who have forgotten what calc was? Yeah, no problem. The first derivative is the change in the... The, you know, basically the difference, it's rise over run. So it's the change from one point to another divided by like the spacing between those two points. So you imagine the derivative is really big if a line is really steep. So lactate is falling faster. Right. Yeah. Like, so you have a big change in lactate for a very short period of time. That's a very steep derivative. That is a very large derivative. you know big number whereas a very shallow derivative would be you have a very very long period of time where the lactate only changes very very slightly where that line is almost might almost be horizontal or looks very very close to horizontal a horizontal line would have no derivative in that it there's no change this is assuming the time is on the horizontal axis here there's can be big changes in time with no change in height whereas a infinitely vertical, a vertical line has an infinitely steep, you know, infinite derivative where no change in time yields an infinite increase in the next points. I have yet to see a perfectly vertical line on lactate clearance, but we have some very steep ones. So the peak lactate percentage removal for the peak first derivative happened at 80% LT. Okay. and also the self-selected one was about the same because it was of course 78% on average. So we're looking at averages here but we got basically a 10 to 12% clearance rate at 80% LT. The second fastest clearance rate was actually at 100% LT. Interesting. Yeah. But we get our fastest one at 80%. So if you want to do over-unders and you are concerned about how fast you are clearing lactate, this is the intensity you want to look at. It's like maybe 80% to 90% of FTP, something like that. Which jives with it being like a sweet spot-ish for the unders. Yeah, yeah. And also, I think when people actually do these workouts, it's around that intensity that they feel like they can actually recover a little bit, depending on how long that step is. And that's something we'll talk about in the 10-minute tips episode. So our third fastest clearance rate was, of course, 60% of LT, which was around 7% clearance rate, and then 40%, and then 0% was the slowest. What we're seeing here is, of course, if you are active, you require fuel and lactate to fuel, so you're going to use the fuel. Okay, pretty obvious. They also fitted an exponential decay curve for each exercise intensity based on the percentage of lactate removed from the peak to 32 minutes. So Kyle, I actually put this graphic up in our show notes and I put it up in the... in the show notes up on the website at empiricalcycling.com under the podcast episode notes. So here, basically, a lower number is better because we're looking at the time constant of DRDT, the percentage of recovery per minute. So lower is better. And of course, at 80% LT, we have the lowest number. And our second lowest is at 100%. And then third is 60 and then 40 and then zero. But the little, it is interesting because the little error bar that sticks up above 80%, or not error bar, it's probably the one standard deviation range, basically almost equals the number for the self-regulated. So they're like, they are different, but they're very close. Yeah, and I think the significantly different yada yada, like that's in the... So I encourage people to go read this paper. It's actually open text. So yeah, it's, you know, read the caption on what they have as significantly different. But we're just looking at basic rates here. And we're not too concerned about what's significantly different from whatever. We're just looking at, okay, you're clearing the most lactate here on average for all the people. And actually, the error bars aren't that big. It's not like everything kind of overlaps. It's like the self-regulated 100% LT and 80% might as well. Of course, as usual, a small test group here. But once we get to 60, 40, and zero, it's like, wow, those bars are much bigger in terms of being slower clearance rates. Yeah, yeah, yeah. They would be like several standard deviations away. So those are definitely. So I think a lot of people would think about this as being lactate shuttling. So what is lactate shuttling really? It means that we make lactate in one tissue bed, it goes into the bloodstream, and then it gets used elsewhere. And that's fine. My question is, is this special in terms of adaptation? Of course, everybody saw the title, so I don't think it is. So in popular lore, it seems to be. Because seemingly, the act of oxidizing lactate itself... Endows us with the ability to get better at oxidizing lactate, right? And one of the adaptations we're supposed to get here is the greater expression of MCTs, monocarboxylate transporters. And so now we are going to look at answering the question, does oxidizing lactate make us better at oxidizing lactate? And if this sounds familiar to you, does this sound a lot like burning fat makes us better at burning fat? Doing something makes you better at doing that thing. Is that true? I think that's true for like tennis. Yeah. Skills. Skills and like... Yeah. Deliberate practice is very useful for skills, memorizing things. When it comes to burning lactate, like that was kind of the premise of Wattstock 40 and a lot of the stuff before that, like looking at like the keto episode. And we did one way back in the day. I think it was Wattstock like... 8 or something like that. Like does a low fat or sorry, does a like a high fat diet encourage glycogen sparing? And, you know, basically we saw it doesn't improve performance really. It actually just like decreases it. And so this is the same question here. And if you know my thoughts on fat burning, you can guess what I think. But if you don't, well, keep listening because We should probably talk about the properties of monoproxelite transporters first and lactate shuttling because this is supposed to be the big adaptation with over-unders that I see most commonly. It's like, we're going to increase MCT expression. Okay, so we're going to look at whether it does and if this is special or not. So maybe in a twist of irony, I spent like three months just reading up on MCTs. You know, just lactate transport in general. And so compared to the amount of time I invested, this section is going to be painfully short. But I think that's probably for the benefit of the listeners. So I feel like that's how research always goes. You spend like a sentence in the paper on the thing that took you like the most frustrating time for one various reason or another. You're like, cool. I know, but it's I think it's I mean, this is. Everybody knows I studied biochem. I have a biology degree. And so I'm a dyed-in-the-wool trained scientist. And so if I'm going to make a statement, I want to make sure that I qualify it as best I possibly can to the best of my knowledge. And if I'm wrong, I'll straight up say I'm wrong. We've been wrong on the podcast before, several times. Several, some people are like, many. Yeah, okay, fair. So with MCTs, let's get back to business. One of the big issues that I found with this section of the scientific literature is that training status has an outsized influence on expression of lactate transporters, monocarboxylate transporters. And fundamentally, let's talk about a couple of the properties of these things first. They're often specific to lactate, and so for biochem folks, they have a low KM value. It basically says at a lower concentration, we're going to have higher specificity for this thing rather than something else. And so these transporters can also transport pyruvate, ketone bodies, and chemically similar things. But usually a lot of the time, they're somewhat very specific to lactate. And if we look at just lactate and pyruvate, all the ones that I looked at very specifically in terms of their activity levels are at least... at least 50% more specific to lactate if not like a full order of magnitude. So MCT4 and MCT1 are usually the big ones that are talked about. There's a large family of these, by the way. The number I always saw in the literature was 14. And as far as I know, I've only seen MCT1, 4, and 2 in the scientific literature. And actually, When it comes to the expression of these in mitochondria, it's very interesting, but a little wonky for us today, although hopefully we'll get to it at another point because I think it's really, really cool research. So MCT4, you will usually see it as having a higher capacity for lactate flux. Which means the VMAX is higher, so it can actually flow a larger amount of lactate per second or minute, but it has a lower absolute specificity, so its KM value is 25 millimoles or thereabouts. MCT1 has a lower capacity for lactate flux, but higher specificity, so it's not going to move as much per unit time, but the KM value is around 5 millimolar, so it's much more specific. generate higher levels of activity here. And now here comes the problem is that there are conflicting descriptions of these transporters in the literature in terms of what's expressed, where, why, how, and also in the change of expression relative to exercise interventions. And what I can say for sure based on all the biochemistry stuff that I read is that they're both bi-directional. based on the concentration gradient. It's not like one only imports lactate and one only exports lactate. It has to be based on what's the difference between the two sides of the transporter we're looking at. So if it's on the sarcolemma, the muscle cell membrane, we're going to be looking at is the concentration gradient between the bloodstream and the cell larger, same as like O2 from the VO2max series. And so it's going to flow in. If it's smaller, if it's greater in the cell, it's going to flow out. And the same thing goes with mitochondria. But presumably, with mitochondria, inside the mitochondria, it's always going to be oxidizing the lactate. And this means that probably the flow into the mitochondria is always going to be high instead of going the other way. And if it goes the other way, I would presume the cell is about to die. Just presumably, I have not seen anything confirming or denying that. So looking at the runner's study, right? Right at about their LT, we see less oxidation of blood lactate than at 80%. So why is this? Because the concentration gradient. Because at 80%, knowing that the monocarboxylate transporters are bidirectional and gradient-based, We've got a larger gradient between the blood and the cell than we do at 100% LT. Even though at 100% LT, we have a higher workload. So the work rate at 80% is high enough that we can get a better clearance rate out of the blood. But if we go down to 60%, the gradient delta is bigger, but our workload is smaller. And so the oxidation rate lowers. Does that all make sense so far about why we saw that result? Yeah, and I think, you know, not, this is like a tangent, but it, that kind of makes me think, oh, you know, this is probably why, this may be why people were like, oh, you know, back in the day, oh, you know, always warm down after really hard efforts, like you'll, you know, get rid of lactate or whatever. And you're like, well. I see that to this day. Yeah. To this day. You have to, you have to have passive recovery because you need to combust the lactate. It's exactly what I hear. Lactate doesn't, it doesn't. So what? So what? You're burning lactate, you're not burning lactate. Like, one of the experiments we're going to look at is they put a lactate clamp on people. Like, here, we're going to keep this, the concentration of lactate at a certain, like, concentration, regardless of what you're doing. So, anyway, sorry. Anyway, yeah, no, it's, no, no, it's okay. So, I think, Thinking about why we have MCTs in our muscles anyway should be discussed as well. Because the prevailing theory is in the literature, which I have no reason to disagree with this. The two main transporters on muscle, out of the 14 known, the MCT1 and 4, they are for encompassing the physiologic range of lactate concentrations that we're going to find. So for MCT1s, this is going to be for lower concentrations where rates of oxidation are going to be presumably lower, and MCT4 for higher concentrations when the rates of lactate flux need to be higher. So if you read the literature at first and if you spend like 10 minutes of Googling, it seems like slow-twitch fibers have a lot of MCT1, fast-twitch fibers have a lot of MCT4 because This is what we'll usually see, is MCT1 imports lactate into the slow-twitch fibers for oxidation, and MCT4 exports it from glycolytic fast-twitch fibers. So I think that's something that people have heard a lot. Kyle, you barely pay attention to the popular stuff like I do, but I'm sure you even heard of this, right? Yeah, definitely. It seems like a... It's in the... I don't know. It's in the air. Yeah, and it kind of makes sense, right? If you just say that to someone out loud, you're like, yeah, okay, I can see why that could make sense. There's no glaring inconsistency on the face of it. And so here's the other thing is that you usually read, is that MCT4, our quote-unquote fast twitch transporter, is less sensitive to training, and MCT1 is more sensitive to training. but this is one of the things is that I started seeing some things that didn't quite make this line up because and I've got a couple links to some of these references in the show notes so this is probably going to be our most reference heavy episode yet but apologies for that so one of the things that I found is that from an untrained state both transporters are actually highly sensitive to training and especially from an untrained state pretty much anything is going to increase expression of both MCT1 and 4, both. And then, after we're somewhat trained, MCT1 expression, our high specificity, low rate thing, correlates really well to mitochondrial content. Really well. Like, R squared is like, I think it's like 0.8. Oh, wow. And if, Kyle, scroll down in our show notes quite a while. I think it's on page like 14 or something like that. 15. Yeah. Page 15. So that's the graphic. And this is going to be up in the show notes, by the way. It's trained versus untrained people looking at MCT1 relative to Synthase activity, which is a... Decent but not perfect marker for mitochondrial mass, and then MCT4. So Kyle, describe what you are seeing with these. So for the citrate synthase activity, it's almost a tongue twister, it is a pretty good correlation between more MCT1 in your favorite arbitrary units show a higher degree of Citrate Synthase, Activity, and you can, like, if there wasn't a line there, if you saw it, you'd be like, oh, there's a clear correlation. Like, it's not drawing constellations in the sky where you're like, that doesn't look like a dog to me at all. That's like four lines. This is a clear line. And it is interesting, though, because the intercept, the Y-intercept is negative. Yeah. on the lines. So you would have negative, at some level of positive MCT1, but albeit very low, you would have negative citrate synthase activity, which is kind of weird. Yeah. I think it shows that it's either the sample group, because it actually encompassed a bunch of studies to come up with that graphic. But it also, I think, says that it's not exactly proportional. Sure. Where like if you've got some level of citrate synthesis activity, some level of mitochondrial density, you're going to have some sort of outsized proportion of MCT-1s because I think MCT-1 is not only found in mitochondria, in the mitochondrial lactate oxidation complex, but it's also found in the muscle cell circle lemma. And I don't think that they controlled for that in that graphic. I see. And there's also a clear distinction between the trained and untrained groups. Like the trained groups have, all of them have higher MCT1 and also then higher citrate synthase activity. And so there's a very clear line too where that sort of 10 in arbitrary MCT1 units to the left, so lower than 10 is all of the untrained and then to the right or higher than 10 are all of the trained. And you're like, okay. That makes sense. Yeah. In a, you know. Yeah. So, that plot, and then the second plot, which is the same axes, so, but MCT4 across the X or the bottom, and then Citrate Synthase Activity on the Y-axis, there's no, like, there's maybe a very, very weak correlation where you could draw a line that's not just like, a horizontal line, but it doesn't, there, I would be hard-pressed to say that you could fit a line to that data, and like, I think fitting a line to that data would be academically disingenuous at best. Yeah, R squared is going to be like 0.15 or something like that. Yeah, and also there is, previously where I said there was this distinction between the trained and untrained having a very, there's a line, a vertical line between all of the Untrained always had lower MCT1 and the trained always had higher. Here that distinction is gone and the trained always have or tend to have more citrate synthase activity but it doesn't correlate with where their MCT4 is at all. So it's not clear that there is a correlation here aside from the fact that, yeah, generally speaking, trained people have more citrate synthase activity and untrained do not. That was true in the previous graph as well. Yeah, and so one of the things that we usually see when we look at, this is part of what has conflicting results, is like people, because most of the studies I saw with an exercise intervention started with basically untrained people, or they had people take like four weeks off or something like that, then they trained them. There's not a lot on like well-trained people and doing more stuff. And so this is an unfortunate. Point where we have to use our knowledge and like make an extrapolation where we say, okay, if having more mitochondria means having more monocarboxylate transporters, perhaps that their regulation is linked in some way. Because, right, if we're going to make mitochondria, you might as well make some lactate transporters, right? Because what You know, if we just think about the host of adaptations that we get, like if we're going to get aerobically better, we need to import fuel. So I bet we could find a similar thing with like, you know, fat importers and all sorts of stuff. Like if we pyruvate dehydrogenase complex, like I bet we could find a similar correlation, meaning that if we're going to increase expression of mitochondria, we need stuff. It's like there's going to be a correlation between houses and beds. Right? Exactly, yeah. It would be silly to build all these mitochondria and then starve them. Like, you know, like, okay. Please, sir, can I have some lactate? Yeah. Okay, so here's the thing about the fast twitch, slow twitch fiber thing. Because as we saw in Wattstock number 37, which was talking about how... How much synthase activity and how much even fat oxidation capacity we can have in fast twitch fibers, which are, you know, they were not histochemically stained. These were myosin heavy chain typed. So fast twitch fibers can have a very, very large aerobic capacity and aerobic potential. And so I think that this kind of spoils the nice and easy picture of slow twitch fibers have MC. MCT1, and fast-switch fibers have MCT4, and that, you know, fast-switch fibers are only going to produce lactate, and slow-switch fibers are only going to oxidize lactate. I think that picture is too neat for the data that we have these days. It's definitely true, though, in, like, untrained rats, which I saw a lot of studies on, and it was like, okay, yeah, I see why they get this correlation. What does all this mean for lactate shuttling? Because it means that lactate is oxidized by the trained and active fibers, whatever type they are. At least that's my interpretation of all this data. So let's say if you're at sweet spot, and I typically just call this like straight up 90% of FTP. And depending on a host of other factors, you're probably recruiting a good deal of fast twitch fibers like type IIa fibers, which are also oxidizing lactate. Because if this were not the case, What would we see as we increase our active recovery rate for our runners? Like at 60%, we might expect to see, okay, if this is going to recruit all the slow-twitch fibers and start getting into our fast-twitch fibers at that point, we would expect to see if only slow-twitch fibers oxidize the lactate, we would see a plateau in lactate oxidation at that point. Instead, we see lactate oxidation rise because even though we can never say for sure what kind of muscle fibers we're using at whatever power output we have, it's likely that a lot of those people are getting into their Type IIa fibers, which are oxidizing lactate. Yeah. Yeah, and also remember, it's not like a... It's not like a sharp cliff for the type of fibers you use. It's not like all of a sudden you tick one watt over and then you use all of your type II ones or whatever. There's this continuum as you start to work harder and harder and have to generate more force, more power. You're going to start recruiting larger and larger motor units more and more. Yeah, I know. And actually the question of how many hybrid fiber types there are based on Myosin Heavy Chain, there is no good data on that right now. There are a lot of conflicting studies. about people saying like, okay, all the, you know, there are very few intermediate fibers like that express both type one and type two Myosin Heavy Chains or, you know, vice versa. So it's, it's a very active area of research and I haven't looked at any papers on that in like probably a year, but I cannot imagine that there's been any huge advancements, although I hope there have. And if somebody knows about them, please let me know. I'd love to read that. So do we have any more thoughts on all of this so far before we get into like the big factors that actually have to do with lactate clearance. I don't think so. Okay, cool. Just curious if I missed something so far. All right, so we're on the same page. Hopefully our listeners are on the same page at this point too. So thank you all for bearing with us. This would be a good point to pause the podcast, by the way, if you need to do so. So now let's talk about lactate clearance. What factors matter? And is it in fact having more MCTs, more monocarboxylate transporters? So thankfully, this is where a lot of the popular media seems to agree more with modern data and science and whatnot. We mentioned in a lot of previous episodes, particularly Wattstock 40, that the best thing for lactate clearance, along with fat oxidation, is increasing mitochondrial mass. Because more surface area means more oxidative potential. And as we kind of saw before, if we get more surface area, we're going to increase MCT expression as well. It correlates pretty well with citrate synthase activity. And so, how do we increase mitochondrial mass? Exercise more. Right. Thank you. Spoiler alert. Another scientist right here. So one of the things that I went and looked at was there's a great study by Granada and a bunch of folks on Training Induced Changes in Mitochondrial Content and Respiratory Function in Human Skeletal Muscle. We're going to get deeper into this paper in another episode because it's well worth considering. There's a lot of really interesting takeaways from it that kind of match with our experience. And I only ran into this paper to really read it deeply a couple months ago because I read it basically when it came out and I was like, oh, okay, well, I didn't really get it. And I think I get it. a lot better now. So it's going to be worth digging into. But yeah, anyway, so it matches really well with our experience. So the graphic I included in our show notes, Kyle, and I'm going to put this up in the podcast notes too for everybody. What we're basically seeing is training volume in arbitrary units, not astronomical units, Kyle, versus citrate synthase activity. and what we're seeing is not a perfect response but it's basically about as linear as you're probably ever going to see. So they took a bunch of studies on mixed intensity, sprint intensity, HIIT and moderate intensity. So basically endurance riding studies and they put them all together in a pile. and on the left we have it with the sprint interval training and on the right we have it sans sprint interval training studies without it. So Kyle, why don't you describe what we're looking at in these graphs? Okay, so they're a little busy certainly because of the different points. So what they've tried to do is they've tried to Group, like make little different icons for the different studies for the different points that are with the, you know, medium intensity, high intensity, you know, mixed, whatever, and so try to segregate them out that way. But generally speaking, more training volume is more and shows a higher degree of activity, although it is not perfect. Like if you... The training volume in arbitrary units goes from sort of zero all the way up to 250,000 somethings. And so the 250,000 somethings, like there are a few data points up there near the very top, but they are not, it's not all one type of training or another, like you, especially down toward the lower. half where more of the training volume is. So that's sort of 50 to 100,000. There's a ton of data points. But the different types of training are kind of smeared out over everywhere. So it's not like one type of training is definitely better than the other. There's not a clear trend, at least. And also, some studies show more response than others for a very similar amount of training volume, which is sort of interesting. Yeah. Which maybe is like a, you know, includes genetic outliers and things like that. Yeah, and I like to think about the ranges that we see too, because at the very, very low training volume, what's on the Y-axis is the full change from pre-exercise citrate synthase activities. So we go from 1.0, meaning no change whatsoever, they're the same, up to 1.8. Basically what we're looking at is down near the zero for basically very little training, we can get anywhere from like a 1.005, you know, mixed intensity there, but all the way up at the top, like, you know, or for the zero, we've got as much as like 1.45, 1.48 fold change, but that's a big range and the range gets smaller as we go up. So at the 100,000 arbitrary units, Our range is more like 1.2-fold change up to 1.6-fold change. And if we go all the way up to our 225,000, which is basically the top of our arbitrary unit scale, we've got a 1.5 up to a 1.75-fold change. So it basically says more is more. And the R for the everything included is 0.59. But if we take out the sprint interval training, The ranges actually get smaller and our R gets to 0.71. So it basically says more is more, just like you said. So while more training volume doesn't necessarily guarantee anything, it is very highly correlated with more mitochondrial mass. It doesn't guarantee anything about like VO2 max or anything like that. But you know, of course, rubber meets the road. This kind of training supports VO2 max adaptations really well. So if we wanted to dig deeper here, we would get into a big volume versus intensity thing. And that was probably going to be the, you know, when we really deconstruct this paper, that's probably going to be our focus. But anyway, training a lot is what's going to increase lactate clearance rates by having more mitochondria. That's it. That's, it's that simple. This is one of the reasons I don't think over-unders, this is part of the reason I don't think over-unders are that special. Because while we can look at a study and say, okay, from an untrained state, doing over-unders is going to improve, blah, blah, blah, like, okay, sure. Even though we don't have a proper study that I'm aware of that actually shows that. But, you know, for its mythical properties, well, not even mythical, for the properties that it's supposed to have, you know, it is definitely effective training in a lot of ways. You know, there's nothing so far that is special about over-unders. Because if we want to clear lactate, do we do over-unders or do we just ride easy more? I know what I would pick. Wimp. Wimp. So that brings us to our next question is, if over-unders, increase MCT expression. And an increased MCT expression alone, is that going to increase lactate oxidation? Right? And then we'll consider this and we'll consider it also with them being coupled to more mitochondria. But that one's pretty obvious. We've already said yes. But this brings us to another study. We've only got two studies left to deconstruct. That's why we're going short on the study deconstruction here. This is one that shows, yes, indeed, general aerobic training increases lactate oxidation rates. So you don't just have to take it from me. This is actually very common in the literature. If you're expecting the 1983 study from Brooks, I am not going to include that paper. I actually find problems with how they did the tracer calculations in the blood. So I found a better study. This one is called Direct and Indirect Lactate Oxidation in Trained and Untrained Men. So they use the same kind of type of isotope labeled lactate measurements, but they looked at the CO2 evolution from breath. So that's like an actual efflux of CO2. And that doesn't mean that they got all of it out because, you know, the CO2, blah, blah, blah in the blood. But anyway, it's a... Good correlation. It's not perfect by any means, but it's better than the Burke study by a long shot to me, at least. So, I'm not going to go too far into the details of the procedures. It's open text, so I recommend people read it. But they basically had 12 cyclists who were either, six were untrained and recreationally active with a VO2 peak of under 50, and the other six were trained members of the Berkeley cycling team during race season. All with a VO2 peak over 55. So, yeah, good stuff. I think the coolest part of the whole procedure was when they infused the participants with labeled lactate. This is the lactate clamp. And they had them ride at 10% below threshold with the lactate infusion clamp, but they raised their blood lactate levels to the same ones at LT, at their lactate threshold. So you're riding easier, but now you've got extra lactate. and it's not from riding harder. They are just giving it to you. You don't have to work for this lactate. It's just there. So you don't have to ride at 90% VO2 max. It's just here, have some in your antecubital vein. That must be kind of weird riding, but you're sitting on a trainer or whatever stationary bike and they're injecting you with lactate. I know. Actually, in the study, they mentioned that like one of their participants didn't. finished the study because during one of the procedures like there was excessive bleeding from something during this so another reason to not you know to be careful with these kind of studies but most of them I've never heard of usually never heard of bad stuff happening anyway so one of the things that I think is illustrative about this study is it's somewhat equivalent to having consistently elevated lactate levels from doing an over and then going under threshold. So now you're under threshold, but you've got elevated lactate. And one of the things that this shows is, of course, being well-trained without whatever training they were doing increased lactate oxidation rates. And the highest lactate oxidation rate they had was at 10% below lactate threshold. So what we would call a sweet spot. 

So we've got another one here. So if this is what you're concerned about for over-unders, there you go, 80% to 90% of FTP, that's where you oxidize the most lactate. And of course, they went into a bunch of other stuff that we're not going to get too far into, or not really at all. But basically, everybody trained for very general aerobic training, cycling training, oxidized more lactate than the untrained or recreationally active people. So it shouldn't be so surprising. Yeah, not really, but it definitely shows kind of what we're talking about is just general aerobic training will increase lactate oxidation. And so I think it's time to consider, here's another good spot to pause, by the way, for folks. Let's consider the adaptations that improve lactate transport and oxidation and compare them to our other stuff. So this is our, like, let's compare general stuff to the apparent adaptations of over-unders. And what should they do versus what do they do? Is there anything that seems unique about over-unders to increase MCT expression and lactate oxidation at this point? The thing that stands out right that makes them different than Sweet Spot is that little bit of extra intensity. So if there was clear evidence that like more intensity meant more MCT expression, then maybe. So then you're sprinkling in a little bit of extra intensity, but then the argument becomes, well, if it's extra intensity, then just do more intensity. Well, one of the things that we saw in the, that we didn't look at in that paper before with the training volume is that intensity is not a big factor. It's really, really, really not a big factor. The correlation line is pretty much flat. So if you want to look at that study, listeners, please go ahead. You can get ahead of the podcast on that one because it might be a little bit before we get into that. It might not. Who knows? But Kyle, you're actually getting a little bit ahead of us because I have that as a... Later point. But okay, so let's build our way into it. This won't take long. So, so far, I mean, there's no evidence that they do any better than other types of aerobic training, but we also don't have any evidence that they don't. So we can really only conclude this by the inference that burning lactate or having high lactate concentrations makes you better at burning lactate or quote-unquote dealing with it. That's the theory behind over-unders in the first place, right? The baked-in assumption that burning a fuel makes you better at oxidizing that fuel even further, and that increasing lactate transporters could help. So what does all the scientific literature so far, in my reading of it anyway, and all my hands-on coaching experience actually tell us? Well, to me, it says there's no unique adaptation to over-unders about clearing lactate. Especially when we consider compared to all other types of aerobic training. So here's the kicker. This is what I was talking about with the, you know, if you're going to build houses, there are going to be beds in those houses. If we look at the actual switches that seem to control the expression of MCT1 and MCT4, they're the same molecular pathways responsible for a large host of other aerobic. Adaptations. PGC1-alpha, hypoxia-inducible factor, et cetera, et cetera. So there's so far no evidence that MCT expression is a singular or unique adaptation to a cell, especially if we think that lactate itself is a trigger for the expression of just MCTs. I see. Okay. Yeah. Seems to have mythical properties, even though we know now, all modern people, it's just a fuel. And while it certainly does provide a link between glycolysis and aerobic metabolism, and it is important for that and many other reasons, of course, it's not, as far as I can tell, it's not special in the way that the mythology builds it up to be. Which means flooding your cells with lactate, Oxidizing Lactate. These are not the triggers for vermic adaptation of MCT1 and MCT4. And I need to, at this point, also mention that in my reading of all this stuff, I looked at a bunch of papers on cancer cells and what happens when we give cancer cells more lactate. Like, for instance, You take some sort of like HeLa cells or whatever and then you bathe them in 0, 5, 15, 30 millimolars lactate. And you look at, oh, there's this gene that I want to see if it's expressed more. And it turns out, yes, if you give cancer cells more food, they're going to express more genes in proportion. Does this sound silly to do with cancer cells, Kyle? Because I think one of the other things that bugs me about a lot of these studies that I saw is that they didn't actually control for energy availability. They didn't control for like, they didn't look at lactate versus ketones or like palmitate or fructose or glucose or anything like that. They just looked at lactate. So the controls for this to me aren't really that good for being able to interpret lactate causes differential gene expression. That makes sense. I mean, I think I always think back to lactate is from like earpricks, fingerpricks, whatever, blood in real time, relatively easy to measure. So it was a convenient proxy for something. And it's figuring out whether that it actually means what you think it, whether measuring lactate or the presence of lactate means what you think it means or what you hope it means. It's not that there's something, it's not like they discovered lactate. and discovered it because there was something magical, right? Like it exists in the popular lore because it's a relatively easy test and it became this reliable marker for something. And not saying this is exactly how it happens, but a lot of times when you've got a reliable marker for something like that, because it's easy to measure, you start looking for things that you can correlate with it because it is easy to measure, right? Why go searching for something that's hard to measure when you've got this something easy to measure? You know, this easy thing right in your lap. Yeah, because before measuring lactate, there was measuring oxygen consumption. Because, you know, before the, I think there was a mid or late 50s or early 60s or something like that. Before that, measuring oxygen was easier than measuring lactate. So after that, we saw the thing switch. We no longer had people breathing into giant Douglas bags. We just had a little finger prick. So yeah, I think also branching from this discussion, like what happens if indeed we do, like let's say we can increase MCT expression just by exposing something to lactate. Let's say we can. The question is, does this actually oxidize more lactate and does this matter? What's it going to physiologically change? What's the performance implication if this adaptation actually proves to be true? because like I said, we don't have any evidence for it, but the evidence against it is not insubstantial. It's not a slam dunk, but it's certainly there because I don't think it is going to improve anything, right? So if we have the same VO2 max, if we have the same mitochondrial density, if we just have more MCTs, both in the cell membranes and on lactate, okay, we've got a higher rate of flux of the fuel. The thing that's limiting our threshold is not our ability to burn lactate. It's not like a fuel availability problem. Right. And I feel like we kind of talked about this in the talking about like VO2 max, right? It's not that your body doesn't have enough. Sugar to support that VO2 Max, right? Like we did the, you know, we look at the pedaling with one leg versus two, right? Like one leg is like, you know, ready and able to use almost all of the oxygen that you're, you know, that two legs will because you've got all this, you know, available. Yeah, the one leg like VO2 Max or VO2 Peak rather was like three liters a minute. But if we go up to... Four, sorry, if we could use two legs, we had like, it was like four liters a minute, like as our VO2 max, with a plateau and not just like a peak. And so yeah, that showed that when, you know, there's, you know, of course, if we're going to use one leg cycling, like there's, you know, like there, I'm sure there's a bunch of para-athletes who are interested in this right now, because I know we've got a bunch to listen to the podcast. You know, if you're riding with one leg, you've probably got a different You know, strategy for training than you've got as somebody with more muscle mass and two legs. So like central factors like heart stroke volume actually have an outsized influence on VO2 max and FTP, you know, assuming we're riding with both legs. And so chewing through lactate is not going to raise the oxygen limitation. We have to improve the O2 supply aspect. And especially in well-trained people, you can do FTP intervals until the cows come home. And a lot of people do. If you don't improve the O2 supply, like if you don't increase your VO2 max, you're not going to increase that threshold. So... Dang. I know. Because I had one of my pro clients had her doing a bunch of VO2 max efforts. And she was like, why am I doing this? Aren't I supposed to be like... I thought I was supposed to be increasing my threshold at this point in the season. I'm like, we are. She was like, what? I'm doing like three minute efforts. I'm like, yeah, I know. Just wait. Yeah. And just wait, she did. And suddenly she's got 20 more watts of threshold. Big surprise. Oh, 20 watts. That's pretty great. I know. I think average threshold increase for my pro clients this year was about 15, 20 watts. The biggest was like 30. I know. Anyway, so. Again, substrate supply is not the limiting factor. And so being able to transport more lactate into the same amount of mitochondria and the same amount of oxygen supply, it's not going to make a big difference. It really goes back to we have to do the basics. We have to focus on the basics. And if you do the basics, like all this other little stuff. is going to take care of itself, which does not mean that we shouldn't do over-unders, of course. That's what the next episode, the 10-minute tips, is going to be exactly about, about how I think about over-unders and how I program them. So also, if we increase MCT1, for instance, with mitochondrial mass, is this going to alone improve threshold? The answer is it's probably not. Because again, We're increasing our clearance rate, but it's not the oxidative supply rate because for this we still need oxygen, as always. It'd be cool if it did. I know, right? Because I think the thing to really understand here about why over-unders themselves do not, and oxidizing more lactate... So if we get more MCT expression, even if we get it with mitochondrial mass, it's not going to necessarily increase threshold because threshold is not a function of we need to transport more lactate. Because that was our thing right at the beginning was defining the threshold is like, oh, we're creating more lactate, we just can't oxidize it. So if we do more over-unders, we will oxidize it more and therefore get better at oxidizing it. But that's not threshold. Threshold is maximal aerobic ATP production. The substrate is secondary to this. Which is why, of course, we see people on keto diets at 50% fat oxidation at threshold. It's not like, oh, they're making too much lactate. It's like, it doesn't matter what they're burning. The threshold is threshold. All right, do we have any more thoughts on this before we get to our last section? This is a good spot to pause for folks. No, I think it's, fortunately or unfortunately, I feel like several of these episodes talking about some of these trendy, popular things have boiled down to like, it's not that it's bad, it's just not that it's magical or special. Over-Unders are a perfectly fine workout, and if it works for you, that's great, but the belief that they are substantially different than FTP or sweet spot work is just not there. It seems semi-analogous, but not exactly the same, to doing a tempo or Endurance Ride that's kind of a fart-like one where you go above tempo or endurance pace for a little bit and then come back down, but it's still all in all generally at the end of the day like a tempo or an endurance ride, right? Like it's not like, oh, because you sprinkled in a handful of minutes here and there above that it like drastically changes the impact of this workout, right? Yeah. It's similarly for over-unders. Right. And so you didn't see these notes before we recorded. So do you think I at least laid this out in a fair manner? And I know people think that you're some sort of like yes man for me, but you're really not. So like you give me a shit appropriately as I need to be given shit. So how did I do? I think so. I think, you know, obviously like you laid it out before the exact, you could not find an exact study that was like, oh, we had people do. 2x20, where every, you know, for three minutes they did sweet spot and 90% FTP or something, and then for three minutes, for the other three minutes, or two minutes, I guess, right, 20 minutes, so for two minutes they did 120% or something like that, nothing perfect, but at least looking at the assumption of, okay, does, is there something special or something really, really interesting to be gained by spending that handful of minutes per block? above threshold. If it is the idea that lactate utilization, lactate clearance, lactate shuttling, whatever the trendy phrase is for that now, hopefully you would see that maybe in the study they looked at different exercise intensities. Oh, the higher intensity really does it. It really helps with this lactate utilization. And it turns out it kind of doesn't. Then there wasn't a ton of clear trends with that sort of meta-analysis, but aside from the trend that more aerobic exercise generally seems better. And then, you know, I think it's unfortunate that no one has done a study exactly on this, but I think you gave it a fair shake in that you're like, okay, so this assumption logically means that X, Y, or Z must be true. Like, if you're going to be lactate shuttling, lactate transporting, whatever you want to call it, better, then you should see more transporters when you do higher intensities above threshold, right? Because, oh, you're working above threshold, you're generating more lactate, so if you're going to transport it, utilize it, whatever, dump it into the bloodstream, let your other cells use it, things like that, like, there are... things that have to be in place in order for your body to be able to do that. And so you go out looking for those things. Yeah. Yeah. Okay, cool. All right. So we have one more section and this is a shorter section. Don't worry, folks. People are looking at, oh God, how much more of this podcast? There used to be an hour or less. I actually thought about breaking this up into like two or three episodes and I was like, you know what? It's just not gonna flow well. Now let's look at lactate tolerance, right? Lactate is not a problem. There's no dealing with it. Yes, yes, we know. So let's talk about anaerobic capacity because that is basically what we're talking about when we're looking at dealing with the bonus metabolites we get over the threshold when we are making a lot of lactate. So we're going to look at maybe a study that is ironically famous for VO2 max training. But it was originally supposed to be looking for anaerobic capacity. And how did they do it? Is they were actually looking at oxygen consumption. And this was a very old method at this point. Like, I think it was developed in like the 20s, 1920s. Oh, interesting. Not 2020s, because this study was from 1996, I think. But it's the Tabata study. It's called Effect on... Moderate Intensity Endurance and High Intensity Intermittent Training on Anaerobic Capacity and VO2 Max. Is it interesting? I always find this one interesting because, yeah, it wasn't, I feel like that was, the original Tabata study was for speed skaters, like Olympic speed skaters, which is kind of cool. You know, it's like, it's different. I feel like a lot of, so many studies are, oh, cycling or running or, you know. because those are easier to control and it makes sense cycling, running treadmills, stationary bikes, much easier to use for studies. But it's like, oh, speed skaters, that's kind of fun. Yeah, yeah. And there's a lot of crossover, especially if you're a Dutch athlete. Yeah. All right. So, well, in this Tabata study, they recruited young male phys ed students, seven for... for the endurance group and seven for the intermittent high intensity group. They did a VO2 max test and they also did anaerobic capacity as measured by accumulated O2 deficit in milliliters per kilogram during a max two to three minute effort. And so the test groups were either one hour at 70% VO2 max, five days a week for six weeks. or 30 minutes at 70% VO2 max and then four sets of the intermittent efforts at 170% of VO2 max power, which is what the speed skaters had done too. Yeah. And I think that's actually one of the places where people call things Tabatas and they're not actually Tabatas because 170% of VO2 max intensity is like... a lot. You know, you know, you're like, oh, if people like misread it or something as like 100%, 170% of like FTP or something like that, you know, that's just not the same workout. Like, you know, 170% of VO2 max is like by the end, like bleeding through your eyes, like pedaling really, really hard. Yeah, and what they did is, I think it was 30 second. They looked at what was the power output for the average of the last 30 seconds at VO2max. So that's how they decided how to do it. Because as we saw like way back in the day, like the Adami study on like, basically you can predict somebody's peak power output during a ramp test based on their W-prime critical power model and how long the test was. Yeah. Go figure. So anyway, besides the fact that there really is no such thing as Vita Max Power, we all know that, but I like the study anyway. I like all the Tabata studies. So they measured anaerobic capacity at weeks two, four, and the end. The intermittent group's anaerobic capacity increased an average of 28%, with a P of less than 0.01. And the aerobic group did not budge. Go figure. Comparing the VO2 max improvements, both groups started at 70, but the aerobic groups went up by 5 milliliters per minute per kilogram, and the HIT group went up by 7. So, the anaerobic capacity group also, their anaerobic capacity, their pre-test 2-3 minute power could be done for 6 afterwards. Um, and as a side note, this is why improvements in efforts over FTP can be both anaerobic and aerobic in nature, which is why every time somebody asks me, how do I train for the individual pursuit? Um, maximize your view to max, maximize your anaerobic capacity. There you go. Yeah, it's a lot, a lot of different types of training to do both of those all at the same time, but, uh, you know, periodize it, blah, blah, blah. My favorite part of Tabatas and all anaerobic capacity type intermittent efforts is that they're like very spicy over unders. Very spicy. Yeah. The downside of this is that if you care about actually physically clearing lactate, you're not moving much in between. Like you're spinning your legs because you got to, you know, the muscle pump helps, you know, bring the oxygen back to your heart and blah, blah, blah. Riding at like 90% for anaerobic capacity intervals. And one of the things that I kind of like about this is that it shows that if you want to increase anaerobic capacity, you should do anaerobic capacity efforts versus doing over-unders. They certainly can help. It's not like they don't, obviously, because you are doing a bunch of riding over threshold. But I find that rubber meets road, and we'll talk more about this in the next episode, it's better to do anaerobic capacity efforts. Yeah, I think that makes sense. If your goal is to increase anaerobic capacity, do anaerobic capacity work. If your goal is to increase threshold power, do threshold work. Saying that you're going to try to... save time and compromise. And I certainly understand people who are time limited and in a position where they don't have a ton of time to do all the different types of training. But picking a workout because you think it's like splitting the difference may actually mean it's... It's doing neither as well as it could. Doing, yeah, exactly. Two dedicated workouts. Yeah, like, what's the saying? Like, you chase two rabbits and both will escape. I did not know that one. You haven't heard that one? Oh, okay. I'm not from Michigan. We don't hunt rabbits in Massachusetts. If you're, if you are really time crunched, right, you almost want to pick very effective, very specific workouts. And yeah, if you're time crunched, you know, it's things you can bang out and, you know, two hours or less type thing. Not, not... Even though it's very attractive to be like, oh, what if I can get both, right? That would be really awesome, but you might not be getting what you actually think you're getting. Yeah. Well, it's because this is another way of looking at, see, this aspect of training is not necessarily only available to over-unders. Yes. Yeah, yeah, for sure. Like, the over-unders seem nice because It at least is a, it's like a, it's a fun twist on a, on a workout that people probably sick of doing, especially if they spend a long time on the trainer in the winter, staring at the wall, like doing sweet spot workouts. Like, I understand it's like a, it's a nice change up for pace from, um, just straight sweet spot. And so that's great. You know, if you, if it helps break the boredom, then have at it, you know? Yeah. Seems fine. But don't do it fooling yourself into thinking like, oh, I'm getting a bunch of anaerobic capacity workout too. Like having done a ton of anaerobic capacity work fairly recently and also having previously done a lot of threshold work, they feel very different. And like, you know immediately from doing one workout versus the other, whether this workout is an anaerobic capacity workout or whether it's like a more steady state like threshold type. Workout. Yeah, and, you know, we'll get more into this in the next 10 minute tips, but, you know, one of the hallmarks of a good anaerobic capacity effort is you can barely pedal at the end. You're fucking dying. Like, that is a good hallmark of, like, this is effective anaerobic capacity work. So if you're doing over-unders to that degree, yeah, sure, you're probably getting a good bit of anaerobic capacity adaptation, but maybe in an ironic twist. Like if we're looking at something like one minute power or something like that, I actually find that as long as people are well rested enough, they can actually do a huge improvement in one minute power just off steady state threshold intervals. So like if you do a threshold block, rest for a week, like really walk it like up until like Friday, do a little opener set and then Saturday, go out and slam a one minute effort. If you're actually well rested, You're going to see a really big number. A lot of people PR this way. They're one minute and can do this like year on year, incredibly somehow. Yeah. And, you know, we're not talking about like, oh, it's the same 20 and once the threshold went up. Like, no, we're talking about 50 or more. And so steady state threshold efforts in this respect seem to have some adaptations that increase anaerobic. Power, Capacity, something like that. And if we're going to make a scale of like endurance riding up to like, you know, Tabata, anaerobic capacity, HIT, intermittent stuff, where that's our 100% and anaerobic, sorry, anaerobic like endurance riding is like 0% effective for increasing anaerobic capacity. I would put threshold stuff at like 40 to 50% effective. As long as, you know, they're done appropriately. It's not like you get one threshold workout and like, oh, wow, I increased anaerobic capacity. No, we're talking about like weeks. Yeah, like a proper block of that. Yeah, and over-under type stuff, even like intermittent type things, and I'm going to qualify that as a type of over-under. Like I would put that at like 50 to 60% effective. So a little more effective than regular. Steady State Threshold Training for Improving Anaerobic Capacity, the way I assign them. Now, if you're doing them like a minute over and a minute under and you can barely get through eight minutes, I might give this like a 70% to 80% as effective as true anaerobic capacity. So it's not like they're not effective, and I'm not saying not to do them, but I'm just saying like if you are looking for a specific adaptation, You do not have to do over-unders. They're not special as the premise here, and I think that's kind of what we're getting at. Yeah. And I think that it's, you know, if people are worried that this was going to turn into just, I don't know, some previous episodes where we've said like, oh, this thing is total crap and doesn't actually do anything, it's not true. And yeah, I think, unfortunately, like a lot of popular Well, it's not fair to call this like a fitness myth, but a lot of popular things that border on bro science do come out a lot, literally false, metaphorically true type things, right? Where you're like, oh, that, you know, like, you know, when we talk about why is 2x20 special or 5x5 special or, you know, people talk about this in like a lot of like Weightlifting and strength training stuff. Like, oh, why does three sets of 8 to 12 seem to do, you know, like, you know, really good for a lot of, like, general strength and also hypertrophy? You're like, oh, well, it turns out that's kind of, like, in the middle of the range, blah, blah, blah. Like, it's not because there's something magical about it, but it's an effective thing for most people, and it's just that it's not magic. It's just to, you know, it happens to be that... whether people realized that this was, you know, through trial and error or whatever, what have you, realized that this, oh, this, like, works, and if their reasoning, like you said, literally false, metaphorically true is bad, but, oh, it seemed to work, well, just keep doing them. Oh, it works, okay, you know? Yeah. You can be a little ignorant on why, and as long as you know that it works and know when to... When to do them and when to not, like, seems fine. Yeah, like that was the recent podcast with Patrick is like, like a lot of it was talking about that feedback loop of you've got to, you've got to do the training and make sure it's, you know, on the other side of it is doing what you think it is. And you've got to have performance markers for that. And if you don't have any performance markers, then like, then really, you're just, you're just, it's, you're just going in a circle. Like, you're just spinning your wheels in the mud, like, and literally not going anywhere. Like, you can change your physiology inside. You can teach the test or whatever. But, you know, at the end of the day, you've got to see that the performance is increasing. And that's really what I care the most about is, you know, because we're not selling anything. You know, you can hire us to coaching. Buy my book. Look at my data. What was that? If you buy my book, you can look at my data. Yeah, I'm not writing a book. I'm not writing a book. I don't have anything to sell. I'm not selling training plans. We coach people. We're here if you want it. We're not if you don't. But this is also, of course, my opinion. I'm presenting data about why this is my opinion. And yeah, I just don't think over-unders are unique or special. They are certainly different. They certainly have a standard place in training. But it's like when I am training people, some people get over-unders as their regular training. And some people have literally never done them, and we're getting the same improvements over time. And the question is, what do people need? That's really what it comes down to. Does somebody need to do more intermittent-type efforts? Does somebody have ADHD and they can't pay attention unless they do over-unders? These are real questions that I ask myself. I love over-unders personally because yeah it's as much as I love steady state threshold intervals I would rather do over-unders and I find them to be rather equivalent even though they're not exactly so I think that's another good point like if you if you have done them and you're like oh I just don't get the hype don't feel pressured to keep doing them if you're like oh but people say they're good eh? Like, if it doesn't work for you or if you don't find it better or whatever, then like, eh, don't do it. Yeah. Yeah. Okay. So let's wrap up some bullet points before we beat this horse to death because we're going to beat it really to death in the next episode. So my bullet points here, the act of oxidizing lactate itself does not have a special property to elicit performance improvements during exercise. Nor does having... a high lactate concentration itself, the bathing a cell in lactate thing. Honestly, though, that would be really cool if you could get training benefit just by having like IV infusions of lactate. Oh my God, right? And like pedaling at like 100 watts. Like I'm going to sit on the trainer, I'm going to pedal at 100 watts and... Yeah, it's like Scrooge McDuck diving into the pool of coins, which I think in reality that would hurt, but like imagine diving into a pool of lactate and just being like, ah, adaptations. So what about things that actually improve lactate oxidation, if we're going to care about that as a performance marker, which personally I don't, I'd rather see performance itself, but if we just care about the lactate oxidation improvements, we need regular old endurance training. Because the same things that improve, you know, generalized aerobic adaptation, PGC-1 alpha, HIF, et cetera, et cetera, they all work just fine. They always worked just fine. And we don't need to reinvent the wheel. Because, you know, even if we think about MCT-1 being proportional to mitochondrial mass, just think about generalized aerobic adaptation. There you go. Like, okay, I'm getting good aerobic adaptation. I will increase my lactate oxidation capacity. Maybe you need to do some specific intervals. Maybe you're bad at accelerating from threshold in a crit. Okay, great. Do over-unders. Highly recommended. We'll talk about that in the next episode. But I don't think people should forget the forest for the trees because caring about specific and niche adaptations is not what evolution has decided to do. because Evolution gave these things the same control mechanisms and adaptive switches as all the other aerobic adaptations that we need. So we don't need to reinvent the wheel. Just do your training. We got to come up with a cool name for them. Like you said, like Crisscross Threshold. I totally have memory hold that. But yeah, cool names sound cool. You get more excited for workouts, right, if they sound cool? Yeah, true. No? and if they're fun and if you just think over-unders are fun, do them. But if you're really training for performance, have that feedback loop. Does this work? Does this improve what I think it's improving? Have markers to show whether or not that's happening. Be able to differentiate aerobic versus anaerobic adaptation, et cetera, et cetera. So we are going to record a 10-minute tips episode soon and what we're going to talk about is how do I structure, me personally, Kolie, how do I structure over-under workouts? What other workouts am I going to give to make people better at clearing lactate? What other workouts would make us better at not producing as much lactate? We'll talk about that too. Why not? Spoiler alert, there's probably going to be a lot of overlap with some of these workouts. And what other workouts make us better at tolerating metabolic byproducts? We'll talk about anaerobic capacity stuff. So we're just going to do just like a straight up. Alternatives to Over Unders type episode. So we're going to get to that and we're going to get to all of our listener questions for that and that's Empirical Cycling. on Instagram for all of our questions, of course. So thank you everybody for listening as always. If you have any coaching or consultation inquiries, shoot me an email, empiricalcycling at gmail.com. Again, like I said, we're here if you want us. We're not if you don't. So hire us for a consult, hire us for coaching. Just give us a shout out if things have been going well. Let me know if things are not going well. Happy to help. DM me on Instagram, email me, et cetera, et cetera. So donations to the show are always appreciated. We are not selling any alternatives to over-unders. There is no stock canned plans or anything like that. I like to work with people one-on-one. So that's what we all do here at Empirical Cycling. So empiricalcycling.com slash donate helps keep the lights on, helps our hosting fees, et cetera, et cetera. Thank you all for that. Of course, we can AMAs up on Instagram, at empiricalcycling, and that's where you ask all of the questions. So we will see you all next week for 10 minutes. Thanks, everyone.