Welcome to the Empirical Cycling Podcast. I'm your host, Coley Moore, joined as always by my co-host, Kyle Helson. Thanks, everybody, for listening as always and, of course, asking you to subscribe to the podcast and, of course, share it if you are liking what you're hearing here and it's helping you with your training and understanding of, well, everything, really. So five-star iTunes ratings. Thank you so much for all of those or wherever you listen to podcasts. And, of course, we're ad-free, so if you want to donate and support the show, you can do so at empiricalcycling.com. We have some show notes up in the website. We'll have some diagrams and stuff. I highly recommend following along. And of course, if you are in the car or on the bike while you are listening to this, you should probably check that out when you get back. If you have any coaching or consultation inquiries, that is another way to support the podcast because this is, of course, we are a coaching company. And so if you want to get in on that action, you can email me at empiricalcycling at gmail.com. And of course, we are always taking on athletes. And of course, we are always looking to do interesting consultations. So if you want to check me out on Instagram also, up in the stories on the weekends, we have weekend AMAs. So follow me along at Empirical Cycling and you can participate in that. And so, of course, we also have our water bottle collab, which is, of course, just a 10% discount on your entire order. Code ITDEPENDS. So that's W-A-T-R-B-O-D-L. And, of course, we're not making money on that. Just supporting a good organization with really cool stuff. I want one of their pasta shirts now. And of course, we've got some merch up at empiricalcyclingpodcast.threadless.com. So today, let's get to our, well, if you kind of know a little bit about the energy systems, today's podcast title might be a little clickbaity. I don't know. What do you think, Kyle? Phosphocreatine being a critical aerobic energy system? I think it's a little clickbaity, yeah. I don't know if it's really as bad or as good as any other. Kind of clickbait title, though. Well, what if we back it up? What if it's not actually clickbait? Because it actually is. Because we've gone pretty in-depth with anaerobic glycolysis and aerobic metabolism, fuel selection, that kind of stuff. But this is the other anaerobic system of creatine phosphate. And of course, pretty much anything not directly involving oxygen is anaerobic. So the breakdown of fats, that was our clickbait title, is that's anaerobic because there's no oxygen involvement process. And that's where we learned that, of course, reducing equivalence and all of that kind of stuff in the electron transport chain. And so we get this little disconnect between those things. But here, we're actually going to be talking about creatine phosphate and ATP directly. These two things are much more linked directly than a lot of the other kind of stuff. And of course, in this episode, we're also going to be... A lot of this has been briefly covered in the Training Too Hard for Criteriums article and podcast, and that'll be also linked in the show notes. But, you know, the premise of that was that, of course, the replenishment of creatine phosphate, as used for repeated sprintability, is, of course, aerobic. And so what is the highest level of aerobic metabolism we can achieve? Well, sustainably, really, is pretty much FTP. the underappreciated duty of creatine, which is actually as a messenger of sorts. So Kyle, what do we know about creatine and creatine phosphate? And what do you think people who are tuning into the podcast would probably generally have an idea about already? I think for a lot of people who have done any sort of weight training or been exposed to gym bro stuff, have heard of creatine as a supplement or creatine monohydrate and probably therefore mostly associated with either lifting weights or maybe with sprint athletes. Like if you're a track and field runner or something like that, and probably also associated with it being like a gateway supplement, for lack of a better term, where people recommend it. just a lot as something that oh yeah you should you know if you're serious about going to the gym you should you should take creatine and stuff like that and so i think with those associations the idea that it is very important for aerobic work or aerobic systems might seem kind of foreign and i think maybe people also realize that creatine is uh pretty well researched. Like you can search lots of papers about its effects and its safety and all these things. So if nothing else, it's maybe a household name for those reasons. And then maybe if you've had a kidney panel or something in the past for blood work, you've heard of that because So that's one of the things that they'll measure for, like blood levels of that are one of the things they measure for when you get blood work done for kidney function. Oh, interesting. I actually did not know that. Okay. So, yeah. So like, let's see, what is creatine? So creatine is made by combining two amino acids into a special compound. or donate a phosphate group, the P, that's in ATP. And that's pretty much what makes it special. So creatine and ATP and creatine and ADP, they have a kind of relationship in the main cell compartment, which is that creatine phosphate plus ADP makes ATP. And this happens with an enzyme called creatine kinase. And kinase is just something that adds a phosphate group to something. And so we get ATP plus creatine, but without the phosphate. So that's a pretty simple equation, right? And so the reason that this happens, and this is going to sound a lot like some of the metabolic pathways that we've discussed previously, which is that... Creatine phosphate has a higher potential energy than ATP, and it's actually one of the very few things in the cell that does. Offhand, I can actually only think of three things that are capable of directly donating a phosphate to ADP to make ATP. And so the energy rolling downhill, quote unquote, here is easy and rapid because there's just a good high potential energy for creatine phosphate to donate. phosphate to ADP, and now we have our ATP back. And this is kind of supplementary in a lot of ways to all the other pathways that we talked about, like aerobic metabolism, aerobic breakdown of carbs and fats, and anaerobic glycolysis. So are we making sense so far? Yes, I think so. I mean, I think that's an important takeaway you've already hit a couple times is yes, that creatines... primary role is to just donate that phosphorus back to regenerate ATP. Yeah. Phosphate, not phosphorus. Phosphate. Yeah. Pretty close. Yeah. And so one of the hallmarks also here in this particular metabolic equation of creatine phosphate and ADP and creatine and ATP is that So they're held in equilibrium or kind of a certain equilibrium in that they need to be a certain amount away from equilibrium, right? So one of the reasons, of course, that, for instance, ATP becomes ADP is because... the ATP versus ADP is actually held out of equilibrium. I actually, well, one of the first 10 minute tips actually was basically on this. So listen to the ATP and disequilibrium 10 minute tips. That was a very short one, but it was right to the point. And so basically that's kind of what's happening. And creatine phosphate can rapidly donate its phosphate to ATP, but this is actually the very very simplest thing because of course it takes a minute to get anaerobic glycolysis fired up well not really a minute but creatine phosphates faster than anaerobic glycolysis and it's much much faster than aerobic atp production and so this is why everybody thinks it's well it is a critical piece of the sprinting energy system right just uh so Now we've covered the basics, and we could probably end the podcast here if we really wanted to, right? And scene. All right. See you later, everyone. Now we've got to take a step back. So where is the site of aerobic energy production, right? It's the inner mitochondrial membrane in the electron transport chain. And so remember, complexes one through four take electrons, and they move them down the chain, and they pump protons into the mitochondrial crusti. pump through complex five and spin complex five to make ATP. And it spins really fast. It's like seven or 8,000 RPM, like Ferrari engine, right? And so it's turning out ATP. And so the question is, doesn't the ATP just diffuse directly out into the cell or doesn't it have some kind of transport mechanism, right? And so let's set up the whole picture here because ATP has a long way to diffuse, like longer than most of us might expect. And I didn't even expect this until I really started looking into this. And so deep in the mitochondria, the mitochondria may be set up like right next to places of high demand, like in the sub-circle animal membrane, in the muscle cells, right? So like right next to where all the calcium gets handled. And of course, next to the sarcomeres where, of course, the contracting myosin units will need a lot of ATP to make a lot of contractions happen. And so we have not only that space to diffuse through, we also have the mitochondrial space to diffuse through. Because as you go deeper and deeper into the mitochondria, like into, you know, because they kind of look like worms, right? Most people think about them like beans, but they're longer than that most of the time. And so as you go into the folds, the deep folds, like the things that look like room dividers inside the mitochondria, those are called cristi. And the cristi, where the electron transport chain happens, are far from the surface area, right? And that's why mitochondria aren't like globes, right? Because if they were globes, the center of that stuff would have even further to diffuse. So that's why they're kind of long tubes. But, you know, that's kind of a packaging thing. Regardless, the ATP does have a little ways to diffuse through. And this is actually a current area of research is like ATP diffusion, right? I know, this is riveting stuff, right? So ATP has three problems here. So problem one is that concentrations of ATP in the cell are actually pretty low. like 5 millimolar. It's not a lot. We can look at concentrations of other stuff that's much higher in the cell. Problem two is that ADP concentrations are really low by orders of magnitude. We're talking like 1,000 to 1 ATP to ADP in the cytoplasm because that's how ATP has its potential energy. It's kept away from equilibrium with ADP. And of course, in the mitochondrial matrix, it's actually a little bit better because, you know, deep in the mitochondria, we have, you know, we have to have a lot of ADP. So that way it can become ATP in complex five of the transport chain, right? And so we've got 10 to one in the mitochondrial matrix. And so it's actually something like five micromolar. So now we've got very... Yeah, we've got five micromolar in like the cytoplasm. So we've got very, very small quantities of ADP. And we've got smallish quantities of ATP, right? And so in tissues like skeletal muscle, heart, brain, eyes, rates of demand for energy can get very high. So local levels of ATP can deplete rapidly. And now if we couple this with ATP having a difficult time diffusing... Now we have a real problem, like how do we get the ATP out rapidly enough? So here's where creatine phosphate comes to the rescue. Creatine phosphate concentrations are around 20 millimolar, right? So we've got like four times as much than ATP. And so, of course, the... equilibrium of the reaction of creatine phosphate plus ADP yielding ATP. It's like 180 in favor of the products. So the flow of phosphate from creatine phosphate to ADP to ATP is really, really rapid. And that's part of the reason for it. The other part of the reason is that the diffusability of... creatine and creatine phosphate is actually higher than that of ATP and ADP. And so when we look at how far can it diffuse under normal physiologic conditions, it's actually of something like about 25 to 30% higher. So if we want to measure it in terms of time. creatine phosphate will diffuse approximately 25% further in the same amount of time. Or if we want to look at distance, it'll get there about 25% faster or thereabouts. I've seen a couple different numbers and this is part of what's being looked into with this specific aspect of creatine phosphate. However, one of the other really cool things about this is because of the compartmentalization of the cell, of where creatine stores are high and low and where ATP stores are high and low. Like, for instance, in the mitochondrial matrix, that's the innermost compartment of mitochondria, the ATP to ADP ratio is actually quite low as opposed to out in the cell because ATP doesn't need to do any work inside the mitochondrial matrix. Like, if it's held too far away from equilibrium, it becomes more difficult to make ATP, to regenerate it. And so the compartmentalization and having creatine phosphate as a separate way to transport energy is actually super advantageous in terms of maintaining all the chemical equilibria where they need to be so that way the cell can function optimally. And this is one of the things that is so cool about evolution and how all these systems have developed over time. It's because, you know, if we think about this, like... We don't need ATP to do work inside the mitochondrial matrix. So we can actually have a pretty low delta G. We can actually have a pretty low potential energy of ATP. And so if we have creatine phosphate being made there or being regenerated somewhere between there and the cell surface... then once we send creatine phosphate out into the cell, now it can actually fairly rapidly diffuse and fairly rapidly rephosphorylate ATP, whereas we're going to see in a couple experiments in a little bit that without this system specifically, it becomes very, very difficult for an organism to have a normal and healthy life. And so thinking about... the very small quantity of ATP in the cell, this is why it's so crucial to have all these metabolic pathways so we can have different ways to supply ATP so that way we don't actually kill the cell because otherwise we will, right? Yeah, right. The ATP is needed for more than just pedaling your bike. Yes. It is needed for all things requiring energy. Even like building. And repairing and the immune system. Take your pick. Metabolic processes in the liver. The body has passive systems everywhere that it possibly can in terms of diffusion and filtration. The kidneys, like you brought up before. Kidneys. You want to talk about an efficient system, you look at kidney filtration. That is one of my favorite things in all of biology. Nerd. I know, right? Excuse me. So ATP really wants to become ADP so badly that keeping it out of equilibrium is like holding back water in a dam. And so we've got like 60 kilojoule per mole of potential energy in ATP if that remains high. But if ATP levels drop like two orders of magnitude, for instance, like to 0.05 millimolar in the cell, we lose more than 10% of the potential energy ATP has. And also the ATP and ADP ratios change. And the same ATP that we had like just a couple seconds ago is now like 45 kilojoules per mole instead of like 60, right? So we've got an energetic value that's dropping faster than cryptocurrency values. Oh no, my Dogecoin. Yeah, my... I don't even know what... Just pick a random word and put coin after it, and I bet there is one. Okay, so now... Now we have... We actually have... We've never imagined this before, but this is probably as good a time as any to bring this up, but we have an additional system that actually keeps ATP and ADP levels far away from each other as possible. So ADP, those are the last levels in the cell to rise, actually. AMP levels rise first. Why do you think that is, Kyle? Probably to help maintain that, what do you call it, disequilibrium, because it's not equilibrium. Exactly, yeah. So we actually have an additional enzyme that's called adenylate kinase. And adenylate kinase... takes two ADP and it makes an ATP and an AMP. So we have an additional system here that is trying to keep that equilibrium separate. Like it's removing ADP from the cell as rapidly as possible. So that way we can keep that potential energy in ATP. So like, how cool is all this stuff? Yeah. I mean, I think that's, it's also interesting to think, right, that the, for the theory of the origin of mitochondria is that they were separate. single-celled organisms that your body was just like, well, we're going to absorb this and turn this into something useful. And now all this stuff goes on. That is actually what happens. And the same with chloroplasts. Lynn Margulis. I believe she won a Nobel for that. I'm not entirely sure. But I believe she has passed on now. But if you see one of those Darwin fish with another thing in it that says Margulis, that's what it's referring to. All right, so now we've kind of set the stakes. So we've got a problem with ATP diffusing out of the mitochondria. And we also have potential energy systems that are set up to make sure that ATP levels stay high. So we have the aerobic replenishment of creatine phosphate. We have creatine phosphate in the cell. We have adenylate kinase in the cell. But now we have a transport problem. This is logistics. This is cellular logistics. It's like supplying an army. How do you do this? Okay, here's the thing. How rapidly does this stuff deplete actually? So it might help to really put some numbers to this. So in a three to five second sprint, we're probably going to see more than 50% of our energy supplied by creatine phosphate. We're going to see like 30% from anaerobic glycolysis. Maybe probably a little more and a smattering from aerobic ATP production. And of course, like resting ATP levels. So, you know, some places might say you get 10% of your energy from stored ATP, et cetera, et cetera. So there's a little bit of a little bit of fuzzy math that goes on with this kind of stuff. But let's say after a 30 second sprint, Kyle, you and me, we're both familiar with 30 second sprints, probably all too well. In a 30-second sprint after one that's full gas, an average person will probably see cellular creatine phosphate stores depleted by 60% to 80%. That's how crucial their job is. Keeping ATP levels high, right? And so textbooks and papers will call this temporal energy buffering. So it means it's, you know, covering, quote unquote, for anaerobic glycolysis and oxidative phosphorylation until they really get going. But it's a temporal buffer. It buffers in time. So when we start doing activity and we don't have any of our other systems quite fired up yet, creatine phosphate, it covers the over. It's an incredibly useful system. And when we start pedaling from a warm-up or we're not warmed up or whatever it is, even if we are warmed up, we start pedaling, creatine phosphate gets used. And if we really want to get nitty-gritty about it, and why not, every contraction probably starts with the use of creatine phosphate. Every single contraction. Because it's not like you're contracting one muscle continuously for an hour as you ride, right? So it's on and off. Yeah. This is also why for people who have seen anything about creatine with strength training or something, a lot of the studies show that taking creatine or supplementing creatine doesn't mean that you can, it won't make your one rep max better, but it might make you more able to turn that set of 10 into like a set of 11 or something like that. Yeah. Where it's not helping you. Yeah, with higher force production, it's helping you with not blowing up and dying quite as early. Yeah, right, exactly, because force production comes from how much muscle do you have, to some degree, like what is the fiber type composition, how much neural drive do you have, all that kind of stuff. But yeah, creatine phosphate, as we see, is not going to add additional contractile force. You're not going to add sarcomeres like this. But yeah, like in my experience with taking creatine for strength training and sprinting, yeah, it doesn't help your one rep max. It really does not, but it'll probably badly affect your watts per kilo, but also it's going to positively affect how many reps you can do. Like I usually find it, I get a good like one or two reps in sets of like 10 to 15, something like that. That's completely anecdotal by the way. So do not quote me. All right, so that's why I think it's pretty common for creatine phosphate to be seen as used for high-intensity sprints. And so we've kind of set this up twice now, right? And now it's a temporal energy buffer. But the reason I brought up the problem with ATP diffusion is that creatine phosphate is also a spatial energy buffer. And so it's actually... kind of a messenger molecule. It's like money almost. It's like, we've got ATP here in the mitochondria. All right, we're going to exchange this for creatine phosphate and then we're going to exchange it back from ATP out in the cell. Like that's kind of how it works, right? So that's our blueprint here. So again, cells being highly organized, we can look at under a microscope, we've got myofibrils like sarcomere chains that have mitochondria packed tightly around it, but we need that. diffusion to happen from the deep recesses of the mitochondria. And it has to get not only to the surface and out of the surface, but it also has to get, if we're like looking at myofibrils, it has to get deep into the fibrils. It has to get in there, like to where the myosin units are contracting. So let's see. Yeah. So there's actually a really cool what I think of as the creatine conveyor belt paper. It's linked in the show notes, and there are actually a couple papers that have a very similar diagram, but this is the one that I think does the best background info, and then the rest of the article is not really pertinent to us at the moment, if at all. But I will link in the show notes, but the actually first reference I can find for this is 1984. And I'll have a link to that up in the show notes as well because I think that's probably a cool paper because that's how long we've known about this. It's nearly 40 years now. Which makes it actually probably one of the older things that we would still say is valid and relevant today. Like lots of things from, I don't know, 60 years ago, you're like, ah, lactic acid, ha, ha, ha. Okay, so anyway, so one of the things that I think is cool about the experimentation that's been done on this and these poor mice, we'll talk about these poor mice in detail in a little bit, but creatine kinase mice, so creatine kinase being the enzyme that transfers, does the proper transferring of the phosphate from creatine phosphate to ATP and deep in the mitochondria the other way around. from ATP to creatine phosphate, when we have to regenerate creatine phosphate, they live short and very languid lives. Oh, no. You could just ask the paper, impaired voluntary running capacity of creatine kinase deficient mice. Ugh, sounds hard. I know. Okay, so, all right, why don't we just get into this? Here's some background info. So there are different versions of creatine kinase in mammals. They're made out of different rehashings, as it were, of particular subunits. So a gene will encode a certain protein, and you can put these proteins back together in a couple different ways to make the same enzyme that actually operates just a little bit differently, and that'll be used in different tissues or different compartments of different tissues. Well, the genetics being such as they are, the experiment in this paper, they either knocked out the kind of creatine kinase that's expressed in just the cytoplasm, or they knocked out the ones that are expressed in both the cytoplasm and the mitochondria, because there are two slightly different versions, and we can knock out either one or both. And they probably could have knocked out the mitochondria one, but they didn't. And so... Kyle, can you give me a prediction on how losing your regular muscle creatine, the one in the regular cytosol, how would this affect voluntary running exercise in mice? Or how about losing both? How would it affect you, do you think? Oh, I mean, you would be able to sprint. for your, I don't know, three to five seconds, and then you start to get really tired. It would be really hard. What about aerobic exercise, though? If you're going to go for an hour easy spin, how do you think that would affect you? Oh, I mean, well, getting started, you would get started and you'd feel fine at a relatively low intensity, but then you wouldn't have this creatine to cover until your aerobic system. you know, got warmed up, so to speak. And so it would either be really hard and you'd be really tired or you just, you just like would stop just because you wouldn't, you'd feel so fatigued because you didn't actually have enough time to get your aerobic system up and running. Well, thing is like, well, you're, you're really close cause you can get your aerobic system up and running. Um, but the double knockout mice in this study, Voluntarily, you know, because mice don't like, they don't really, they can kind of sprint, but they'll just run for a while. And they only run, the double knockout mice would only run 10% as far as wild type mice and expend 10% as much energy. And the single knockout was in the middle. Yeah, so like they're just... Extreme lethargy all the time. Pretty much, yeah. Like they don't want to do anything and they really can't when they decide to get up and do something. So the other thing is that the double knockout mice showed decreased muscle and heart mass and the inability to grow mass in either in response to a given workload, which of course shows again, as always, that muscle mass and things like that always responds to a stimulus. You never actually... get muscle mass for free, like within a certain genetic limitation. Like if we look at gorillas or something like that, okay, sure. They have tons of muscle mass, but we are not gorillas and neither are mice. So what they did find was that there was some compensation from the gastrocnemius, that's the mice calf muscle, where citrate synthase increased threefold. This is a mitochondrial mass marker. And of course, cytochrome oxidase, that's the electron transport chain complex four, increased tenfold. So we actually saw a direct physical compensation by the muscle for a double creatine kinase knockout. And it sounds impressive, right? But it still didn't help. It's just a compensatory mechanism. Yeah. So even without that, I guess, and maybe that's why the single knockout. mice were able to run farther than only 10%, but not 100. Yeah, because if you think about what's really going on, is that if you're missing the creatine kinase deep in the folds of the mitochondria, the ATP has a hard time diffusing out, but also that is exactly how crucial the ATP is, or the creatine kinase is, for regular function. 

So anyway, the paper does conclude... Oh, by the way, they referenced another study that showed double knockout mice also had only 50% of the ATP production ability as wild-type mice. So it all really... The creatine conveyor belt, as it's called, is super, super crucial. And this is just a regular experiment that shows that the... problems that cells have when they are lacking creatine kinase system is very high, and the cell does attempt to compensate for it because we would expect certain stressors in the cell to increase mitochondrial mass and all that kind of stuff, but it's sort of like changing your technique for trying to pick up a rock that you can't lift. It's like, you might get a little better leverage on it, but it's really not going to lift the thing up. Yeah. So the paper, anyway, concludes that it states the creatine kinase system is not redundant, which... Seems obvious to us now, but actually may not have been previously. Because if we think about what happens if we remove the creatine kinase system, it's sort of like your initial hypothesis on getting going. It's like you can't really get going, but then once you kind of get up there, it might be like okay-ish. That's really not the case. So it's not redundant. It's not like... You get a little impaired as you sprint or as you start exercise, but then once your aerobic system starts moving, everything's fine. It's not fine, right? Yeah, yeah, yeah. You just don't have that potential, that energy gradient anymore, and so everything is harder regardless whether it's a sprint or aerobic or in between. Yeah, that spatial energy buffer is, yeah, super, super critical. So how does this information help us out? Okay. If we want to rehash the last podcast and article on this, the period too hard for criteriums, oxidative capacity limits how much ATP and of course creatine phosphate that can be generated aerobically, right? So what's our sustainable limit again? It's FTP. And so should we expect that recovery? Between intermittent efforts over FTP should be improved with better aerobic training. Of course. Yes, definitely. Yeah. And this training is not just about having a higher FTP. And we're going to talk about more in depth on that in probably the next Wattstock, I think. We're going to probably just do a wrap-up episode and answer some questions. So again, having a massive sprint is fine, but Kyle, what's the rest of this thought? If you can't make it to the end of a crit or the end of a race, or if your aerobic capacity is not high enough such that when you sprint out of every corner in a crit, you don't actually recover, you're just going to keep losing sprint watts as the race goes on, and then you're not going to... Have a good time. Precisely. Yeah. Um, and that's why you could, sorry, go ahead. You could run this experiment by like taking some, you know, like crack sprinter and just having them. Yeah. Yeah. All right. Have fun. Like the first, you know, 20, 30, you know, corners or whatever. Fine. But like, if you got to do a hundred of them, it's going to get bleak real fast. Yeah. Um, that's. You know, that's exactly where I was going with that, too, is I was thinking, you know, everybody's first thought, oh, my God, Chris Hoy can do 2,500 watts. What? And then it's like, why doesn't he just go to the tour and just win all the sprints? It's like, he's never going to make it. He doesn't have any aerobic training. All right. So now because I think we want to top the last time we did this, which I think was Wattstock number two. We're going to look at a study that really supports this point in particular. The title is Relationship Between Different Measures of Aerobic Fitness and Repeated Sprintability in Elite Soccer Players. Again, link up in the show notes at empiricalcycling.com. The intro to this paper is a good read, I think, since they look at other similar papers conflicting results because we've got a lot of variables when we look at repeated sprint efforts. Sprint protocol is not the same. you know, looking for correlations with things like VO2 max and stuff and, you know, rest intervals. And there's a thousand things that we can do. Like, just look at all the books that have been written on like high intensity training and intermittent kind of effort kind of things. So this paper notes in particular, and I quote, this may not be the most appropriate index, talking about VO2 max, because VO2max is believed to be determined mainly by central factors, whereas RSA, repeated sprintability, has been more strongly associated with peripheral factors. So muscular metabolism, FTP. So consequently, it may be hypothesized that an index of aerobic capacity more strongly associated with peripheral factors, yada yada, is a better metric for repeated sprintability. or a better correlation, right? And so they want to look at how well-repeated sprintability correlates to OBLA, our old friend, onset of blood lactate accumulation. I know. Okay. It's... It's an easy thing to measure. Yes. So why not measure it? Yeah. Well, I thought that they were going to measure four millimole. They actually went for three and a half millimole for some reason. I don't know why. But I think we mentioned this before a couple times. If you use it as a population average marker, you're probably going to do fine. As soon as you start trying to treat individuals with this, you're probably not going to do so fine. So this paper, while it has this particular flaw, I don't think it really disqualifies it entirely. So let's kind of look through our protocol and our results and see what happens. What did they do? Well, who were they? They had 29 well-trained Brazilian soccer players from two national level teams. So Brazilian soccer, national level teams. These guys are really good. These guys are good. So what they did was seven by 34.2 meter. I don't know why it was that exactly, but 34.2 meter maximal sprint efforts with 25 second recoveries. So the efforts were actually about six ish seconds long. And so they also did a ramp test with running, and they determined OBLA velocity, and they also determined VO2 max, and they used three-minute stages. So from the sprints, from the seven sprints they did, they looked at fastest time, mean time, and sprint decrement percentage. So like what percentage did the sprints fall off with? So it's a simple and a good study, not perfect. Obviously, it's not as long as the criterium. If it were a criteria, I think we would see an even higher correlation here, right? So if you are looking at the paper yourself, you would want to look at tables two, three, and four. And so across the board, low correlation is between the fastest time and anything else. And of course, mean time and sprint time decrement. percentages should be our biggest things right so kyle um i put up in our show notes table two for your viewing pleasure and i could probably toss this up into this to the show notes on the website too so um we have fastest time and vo2 max velocity of vo2 max and velocity of onset of blood lactate accumulation so we have our correlations for fastest time it's like our highest one is like 0.2 so not great not great yeah and Likewise, you wouldn't expect, even if with no prompting, you were like, how correlated do you think a fast sprint time would be with VO2 max? You're like, not so correlated. Yes. Running, you're like, okay, if I gave you a bunch of milers, how well do you think their mile time is correlated with their 100-meter time? You're like, well, it's not going to be completely random, but it's not going to be like. Yeah, it's not tight. Yeah, every fast miler is also a fast 100-meter dash or something like that. Yeah. All right, so we have mean time. Mean time correlates as 0.08 to VO2 max. So, again, not so great. Sprint decrement, 0.39. Not bad. Not bad, yeah. I mean, now you're getting into the situation where... If you think about it a little bit, it does make some sense that if you have a high VO2 max, you likely have a higher level of aerobic conditioning for these soccer players. And so the decrement in time should be, or I guess like slowing down as the sprints go on should go, should be less bad for the people who are more aerobically fit. because that greater aerobic fitness will help them recover faster in between efforts. Right. And so, well, we've got kind of an interesting one with velocity at VO2max here, because we have actually a pretty good correlation in our velocities at VO2max, but we're going to tackle that in just a second, because that does need a little bit of explaining. But for velocity at OBLA, fastest time again, as predicted, 0.2 correlation. Our mean time is 0.49 and our sprint decrement percentage is 0.54. Yeah. So now you're getting into much more well core. And keep in mind, this is not a number between zero and 100. This would be a number between zero and one. Yes. Yeah. One is our 100 in this case. Yeah. One would be that definitely, you know, the fastest time correlates with the fastest. V-O-B-L-A or vice versa. Yeah. And so we actually have a decent correlation with velocity at V2 max. In here, we have our sprint decrement percentage as a 0.49 and our meantime as a 0.38. So okay-ish. But I think this is explained because when you have a higher O-B-L-A velocity, so a higher... quote-unquote threshold velocity, you're not using your anaerobic stores earlier. And so that way you actually get to, and I think this was our very first VO2max podcast on, you know, there's basically no such thing as VO2max power, really. And so that's kind of how that gets explained. It's like you hit your threshold a little later in the test, you're going to have a higher velocity at VO2max. That's why I think that has that correlation. But the most telling table, I think, in all of this paper is table four. So we have a multiple regression with repeated sprintability. So our fastest time R squared with repeated sprintability is 0.78. But our fastest time plus velocity of OBLA is 0.89. Yeah. And so keep in mind, R squared is also... Not a number between zero and 100. Zero and one. It's a number between zero and one. Yeah. Yeah. So we have a really tight correlation here between, you know, we have basically two variables that put together do a lot of explaining about somebody's repeated sprint ability. And so we have 89% of the variance. explained by these two variables. So this points to things that we know about fast criterion racers. They have a high sprint and they have a high threshold, right? It's pretty simple. Yes, exactly. And you can imagine if you just think about fast sprints, well, okay, you're going to have generally more spread in your... your sprint times, right? Because if you have a super fast time and not enough, not enough threshold, then you're, you're going to lose speed as these go on. Right. Chris. Yeah. Your favorite track sprinter. Yeah. Yeah. Yeah. And so you're just not going to have as tight a correlation because the times will be, we'll have a larger spread, even just with one athlete, let alone a bunch of athletes. Yeah. All right. So, um, All right. So do we have any other learnings from this paper here? Because I think that's a pretty good conclusion. But I think also the VO2max context here is pretty interesting to note because it's a central limiter of oxygen supply. But muscularly, aerobic training is about utilization of oxygen. And in our case, to replenish ATP and creatine phosphate. So when you have better aerobic conditioning, better aerobic training, You can do this better and faster. Yeah, I guess maybe the VO2 max would be interesting if you had to recover above threshold. If they made you sprint and then recover above threshold, but below VO2 max so that the higher your VO2 max was, the more ceiling you would have or something. I don't know. Now I'm changing the study. Yeah. Well, we can look at heart rate and something like that to kind of give us a good idea about that kind of thing sometimes. It's not obviously a great correlation, but when somebody's heart rate is super, super high for a long time, that usually says that you're supplying oxygen for recovery from efforts. And that's why you can go to a cyclocross race and... slam it for 40 to 60 minutes, and you're going to see a higher heart rate than you can do on any single one-hour effort that's not in the Sahara Desert. Oh, God. That would be awful, yeah. I also think about that, too. I'll do a 30-second effort, and you're not breathing that hard at the end of 30 seconds, but... 10 seconds after you're done with a 30 second all effort, you're at like ventilatory threshold. You're just like, oh God. At least I am because I'm not aerobically well conditioned. Yeah. All right. So this is a really, really short one. So we're going to look at one more paper here. This is actually about the muscular kinetics of what's happening. So again, link up in the show notes. This is called the recovery of repeated sprint exercise is associated with PCR resynthesis while muscle pH and EMG amplitude remain depressed. So this was actually a fairly elaborate paper and they look at a lot more stuff than we're going to be concerned with here. And it's a cool paper if you're interested in this kind of stuff. If the title sounds interesting, they look at exactly that. pH and EMG amplitude remain depressed, et cetera, et cetera. But they had people do six. Sorry, 10 by six second all out sprints with 30 second recoveries and then six minute rest. Then they did six by five second sprints again. And they got biopsies taken at rest before the efforts, after the first set of sprints, and then after the six minutes of recovery before their next set of sprints. So we have 10 by six seconds, six minutes recovery, six by five seconds. Something like that. What I said before. I think I got that one wrong. So what they look at in their biopsies is they're looking at creatine phosphate levels, ATP, and total work done in the sprints in kilojoules. And they compare various measures from sets one and two. But for our purposes in this paper, you want to look at figure five. They look at phosphocreatine recovery during the first period between the first 10 sprints. and the work done for Sprint 11, so the first one of the second set. And the PCR recovery correlation with the work done during Sprint 11 is 0.79. Quite high. Yeah, and the correlation for the average for Sprints 11 to 15, so the second set, is 0.67. Also quite high. Yeah. So the authors put a nice bow on it. They quote, Thus, we conclude that much of the inability to produce power output during repeated sprints is mediated by intramuscular fatigue factors probably related with the control of high-energy phosphate metabolism, as in ATP and phosphocreatine. So basically how fast you can... How fast you can recover is how much power output you can put out when you get back to putting out power again. 

So that's pretty much what we got for the big science stuff. So let's, we could do actually a lot more studies. Like you said, it's been very well studied, but we're going to spare everybody. But let's get into a little bit of kind of questions and conclusions we can think about just from this kind of stuff. So why isn't VO2 max going to be the best way to improve a phosphocreatine resynthesis? 

Well, it's not – VO2 max, like you're not – like I said, kind of said before, it's not like you're restricted to only operating at maximal oxygen uptake to restore these systems, especially with a situation like we just described where you get 30-second recoveries and then a longer period, like six minutes rest, where you can just sit and you don't have to exert yourself at all. you're you're gonna race toad or intelli or something where you got a bunch of crits it's not like you have eight crits in a day you have a long period of time to recover those those stores when you're at aerobic relatively low aerobic work rates right like even off days or something like that yeah the rest of the day after your race for example it's not like your body has stopped recovering or something because you're not at the race anymore your body's like oh we're just going for a walk like no you're gonna recover all of that, the glycogen and the ATP all the time, not just when you're wearing kit. Well, like Andy Coggin has said, for VO2max, it is necessary but not sufficient for high levels of performance. And so when we think about VO2max versus something like peripheral aerobic conditioning, having high VO2max is great if you're going to do a pursuit. You're going to do like a short running race, like five to eight minute kind of range, 12 minute, whatever. But as soon as we get to something longer like a criterium, yeah, you need that aerobic ability to sustainably regenerate ATP and phosphocreatine. And we can actually think about... work rates at like FTP and like TTE, like how long can you sustain that sustainable work rate? We don't have to think about it in terms of power output also. We can think about it as an indicator of recovery ability. Like we don't have to turn that ATP directly into work on the pedals again. That ATP and phosphocreatine that we regenerate can just be recovery from our efforts. how fast and how quickly and how easily can we do it? And FTP and TTE and general fatigue resistance, so your aerobic ability, your endurance, these are things that are great indicators of repeatability. Yeah. One way to think about it, too, is if you have a very high FTP and you're cruising around at a lower fraction, you know, at some relatively low fraction of FTP, you have a lot of headroom to do the recovering in addition to the sitting in. Whereas if you have a relatively low FTP and you're working at a much higher percentage, you don't have a lot of headroom above the effort it's taking just to sit in. Yeah. Well, actually, that's something that I've been asked quite commonly is like, hey, can we improve my ability to ride over FTP? And, you know, if you're doing like... In a 40-minute crit, let's say you're doing 25 minutes over FTP, maybe even 30 minutes, there's not much more ability we can do. And if you could do more, that would be your FTP probably because you would be riding sustainably at that level. At 40 minutes. Yeah, 40 minutes. You're like, is that your FTP? Okay, so I think another good question that probably will come up from listening to this episode is can we just do endurance training? and have good repeated sprintability? Maybe? I would say probably not, because obviously there are a lot of other things that we need to work on, right? Because we need to be able to generate high power outputs, of course. We need to have buffering capacity in our muscles. We have to have... The short answer is really fatigue is complicated. And so that especially goes for over FTP, but also around FTP as well. And with repeated efforts, it gets even more complicated. And so I think it might be interesting, this little factoid that was in the research I was reading. So the half-life of phosphocreatine resynthesis is 21 to 57 seconds. What's a factor of two between friends? It's a little bit of a range. And so, yeah, so like we, you know, people like you and me, like when we do like a 30, 40, 50 second effort, we're going to lie on the ground for quite some time. And somebody who's really well aerobically trained is going to be walking around instead. Like you look at, like if you look at what was the last, the old Omnium style format on the track at the Olympics, like. When people did the kilo, you can do a 101 kilo and you're walking around afterwards. A pure sprinter who does a 101 kilo is going to be gasping for air for at least 10 minutes, if not 20, and barely able to walk. They're like, maybe not going to make it to the podium to stand there. They're like, no, no, no. Just leave me here. I'll send someone in my steed. It's fine. Get me a wheelchair. Yeah. Roll me up. As an aside, there is some interesting research that shows that active recovery might actually impede phosphocreatine resynthesis and decrease the time to exhaustion that you can do repeated sprint efforts. Interesting. So you're saying that track sprinters who just sit after every effort have it right? I think so. So after every corner in a criterium, you need to sit down. Great. Get your lawn chair out. But that's just one of the thoughts here, because if you are creating muscular work, you are using ATP, and that will put strain on your phosphocreatine. So it's a pretty simple thing. You do work, ATP levels fall, other things have to fill in, and so now you've got to do double time of aerobic resynthesis to have the same power output again. So it kind of makes sense. So the other thing here... High raw power, of course, can still be quite necessary because the soccer paper has correlation between highest sprint velocity and repeated sprint velocity, but granted it was a short set. So I think it just points to the fact that you need balance between the sprint watts and the aerobic stuff, right? Yes. I think the other thing is that is... What was summed up when Andy Coggin retweeted your article. Oh, yeah. Where he said, it's still an aerobic sport, damn it. That was a big day for me, by the way. Wake up and see Andy Coggin tweeting out my Training Peaks article on you're training too hard for criteriums. And I tweeted, like, wow, it's a big day for me. And thanks for sharing or something. And he was like, yeah, it deserves to be shared. I was like, oh, my God. It was actually extremely validating for me because I wrote that article. I didn't run that across anybody. I just wrote it myself based on the research I had done. And I was like, this makes sense to me. Publish. Yeah, that was a scary moment. But it turns out I was right. So that's nice. Well, according to Annie Coggin, I was right anyway. All right. So last thing. Do you need to supplement creatine? 

Kyle, would you recommend a Criterium Racer supplement creatine? Not necessarily. Dietary-wise, you get some creatine just by eating meat because that's where it's stored in your body. Analogously, it's stored in muscle tissue of animal proteins. If you're eating meat and you're a crit racer, probably not. If you're like a vegetarian crit racer, then maybe because you're maybe not getting any. Whereas if you eat a diet of meat, like you're actually going to get a fairly reasonable daily intake. Yeah. And this means like, you know, you don't have to even be like a... The carnivore diet guy who only eats raw meat. What's his name? Don't say his name. Let's not give him their time. Okay, yeah. You don't have to be the guy who's only eating raw meat to get a measurable quantity of creatine daily in your diet. Actually, have you ever Googled what kind of meat has the most creatine in it? It's red meat. That makes sense. I would say, is it liver or red meat? Because that made no sense to me a while ago because I didn't... I didn't remember, or I didn't know at the time, whatever the deal was, because I was like, it's slow-twitch stuff. Why would it have creatine? It should be like chicken and fast-twitch muscles, like white meat. That should have the most creatine because it's fast-twitch fibers, right? Creatine is for sprinting, right? No, it's the opposite. This is another thing that shows how crucial it is for aerobic stuff is because in red meat and in red muscle, like heart, There's a lot of creatine because it is this critical spatial energy buffer. That's really cool. Or not cool. Fascinating. Yeah. Fun fact. Yeah. And I would say probably not for most endurance athletes because the associated water weight gain with phosphoric creatine loading is very high. Yes. Yeah, yeah. taking creatine and not for my lifting whenever it's been safe to go to the gym with COVID and not. And for me, I usually put on anywhere between four and six pounds. And some of my athletes who have experimented with creatine loading, mountain bikers, crit racers, who are around 150 pounds or so, they'll also gain about five pounds. Yeah. Yeah. I noticed I'll gain about five pounds. Yeah. I think one thing, though, is if you were considering that, like if you are considering supplementing with creatine and you are concerned about weight gain, one thing you can do is not supplement nearly as much. Like if you're a gym bro, bodybuilder, whatever, sprinter, a lot of times they say like five grams a day, which – That's a lot. Which is a lot. And that's – one of the reasons why they suggest five is because it guarantees you for – Almost everyone, even a very high muscle mass percentage, is that that is enough creatine for you to reach saturation levels within a reasonable amount of time. Whereas if you're a 150-pound crit racer, you may be able to get by on a gram, a gram and a half a day, not five. Yeah, and we're looking at, of course, remember that we're looking at muscle quantities of 20 millimolar. And supplementing creatine, you might go up to like, I didn't look at the numbers, but I'm just guessing it'll be like 22 millimolar. Like maybe as high as 25, but I doubt it. I could be wrong. Like I said, I didn't look at the numbers, but it's just a little bit of extra. And it doesn't make much sense in terms of, to me, it doesn't make much sense in terms of power output gain. Like I think you're not going to gain enough power relative to the water weight that you're going to put on. And if you want more of that power, do some proper anaerobic capacity stuff, and you're going to get it, no doubt. Because sometimes creating the demand on those systems by doing good anaerobic capacity stuff is going to, as long as you've got some creatine in your diet, it's going to increase the resting levels in your muscles. And whatever else is doing that may or may not actually be increasing creatine levels. If you want more power in like the 30, 60 second range, rest, do some good training with good power output. Which is, it's another feather in the cap of like, there is no, well, there's no legal supplement like this that will give you these, you know, factor of two improvements and stuff like training and like basics. It turns out there aren't too many shortcuts. Yeah, there's no shortcuts. Yeah. And so, yeah, again, that's why you might be training too hard for crits because more oxygen supply and more mitochondrial mass and more aerobic enzymes means faster aerobic recovery of both ATP and phosphocreatine, which, of course, now we know are basically indistinguishable for a lot of our intents and purposes. So there you go. Phosphocreatine is not just for sprinting anymore. Happy sprints, everyone. Yeah, happy sprints. All right, everybody, thank you for listening. As always, again, subscribe to the podcast. Check me out on Instagram at Empirical Cycling for the weekend AMAs. Reach out if you are interested in coaching or a consultation. We can answer any questions on training or endurance training philosophy or programming or pretty much whatever you want. We'll be happy to do that for you. So reach out to empiricalcycling at gmail.com. And of course, we've got all our show notes up on empiricalcycling.com. And of course, what else didn't we talk about yet? Oh, yeah. 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