A

This week on the Training Science podcast, we go deep on the molecule that everyone spent a century trying to get rid. Lactate. For 100 years, we treated it as the enemy. The burn in your legs, the thing to flush out, the reason that you blew up. Then George Brooks flipped the whole picture on us. Lactate isn't the waste, it's the fuel. And now people aren't just clearing it, they're drinking it. My guest this week is ITOR Virabe Morales. And we get into the future of exogenous lactate. That is, imagine drinking it. We cover its signaling properties, the parallels with ketones, and what it all means for training, performance and health. Just another incredible conversation with a pioneer in our field. So without further ado, I now bring you ITOR Virabe Morales. I'm here with Ito Vierbe. Itor, welcome to the podcast.

B

Thank you very much, Paul. Nice to be here.

A

Great, great. Awesome. I'm really looking forward to the conversation. Maybe, you know, we are the Training Science podcast and I know you do my research on it. Sounds like you're into training yourself. You certainly look like you're, you're a fit, fit fella. What's your own personal background and interest in sport? Where did that all sort of start for you? Itor?

B

I'm coming from being a bike rider. Cyclist. I used to compete on sort of high, high level, almost professional even. I had a half a year, almost, almost there. Then I retired. I had this bononucleosis disease, so I had to, you know, stop and, and, but yeah, I've been always moving, you know, around in the mountains, running, biking, you know, bike has been my element. But yeah, more transitioning into running as well. I can say I'm pretty, pretty active.

A

Yeah. That's awesome. Very cool. A classic semi pro, as Martin and I like to like to call it. It's, you know, when you, when you run out of, you know, places to go in the, in the sport world, where do you go? Sport science. Right. So, yeah, we switched the science, exactly.

B

I have to say I started first studying engineering, civil engineering. You know, I used to build bridges and roads and things like that. I used to study engineering while I was competing as a bike rider. And then I changed paths when, when I retired from cycling, I said, you know what I'm saying? I think I like physiology. So I'm going to start with this.

A

That's so cool because so many, I see so many scientists that are innovative. They almost come from that engineering background where they have that first principles philosophy,

B

first and foremost, and I think that's partly something that has defined the way I understand the body and the science as well. I think I've got a lot of kind of mechanisms or way of thinking that are coming from engineering. I don't think you can avoid that. A mine is a mine and sometimes you just think as an engineering problem. And yeah, I see a lot of impact on everything that I do right now on those studies and my mindset.

A

Yeah. Okay, so you went from engineering into physiology and then somewhere along the way, is that right?

B

Yeah, that's right. But I have to say in Spain you don't, you cannot study physiology as a, as a degree. So I went first into, into nutrition, so human nutrition. That's the degree that I, that I studied. And then, yeah, I specialized myself into physiology. I ended up doing my PhD on sports science and physiology and exercise metabolism. That's where I am right now.

A

Very, very cool. So you've got, yeah, I love, I mean I love the background.

B

Right.

A

We got engineering, we got nutrition, we got physiology. We have own personal experience in the, you know, in the, in the high level in the cycling world. And now somehow we're going to get to the, the central concept of lactate. So where did, where did your interest in lactate then begin through all of this?

B

Yeah, well, that's probably, I don't know, I think we all have something that we get somehow obsessed with and I think I can say lactate was one of those concepts for me. I, I started very soon researching on carbohydrates and when you, when you deep, when you study deep or in detail the carbohydrate metabolism, you, you end up studying lactate. So I get, you know, I, I got fascinated by all those studies from groups, you know, Robinovich Gladden, like I've been always a big, big fan of, of them, especially Brooks. I think he's, you know, all, you know, all my kind of honor to him because, you know, he has defined the way we understand lactate right now. Then, you know, I eventually ended up being pretty close to Inigos and beyond learning from, from him a little bit and getting inspired by, by him as well. And you know, I've been always a little bit obsessed with lactate. I remember when I was bike rider myself, I was measuring on myself. He's trying to. And back in the days, I remember I had to go to France to buy. So from the bus country we had to travel to France is to buy a lactate monitor. That wasn't very common. You know, almost 12 years ago. So yeah, I got slightly obsessed with, with lactate and I have to say probably since we started with these studies on the, on the carbohydrate field, I, you know, I had on mind like we need to try to kind of bring lactate to the body. And so that was seven, six, seven years ago I studied with that idea. And the last three, three years we, we founded a lab here in, in, in the Basque country. And we, well, it seems like we arrived to some kind of solutions finally. But it has been a hell of a process on researching and, and developing truly, you know what I'm talking about. But yeah, one of those kind of entrepreneur. Not entrepreneur, because I'm definitely not entrepreneur, but one of those journeys that you start, you know, with an idea that you start developing things and then you find different people thinking different, differently to you and you end up with a potential solution. And that has been the journey.

A

Yeah, I want, that's so cool. I love that. I love the innovation. I've got my friend from the Basque country as well, Inigo, Mexico. And he's been on the podcast and yeah, good friend and it's wonderful to see another passionate individual in this area. That's, that's coming through itor.

B

So if I'm not wrong, we are, we are both from the, from the same city.

A

Oh, you're kidding. Which, which city is that?

B

Yeah, no, I'm not kidding. Victoria. Victoria.

A

Yes, yes. And yeah, I feel, I feel the passion whenever I speak to him about it. So I'm sure you share that.

B

Yeah, yeah, definitely.

A

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B

Yes, I'm probably not the best person to, you know, I'm 32 years old so I, I didn't, I wasn't alive when that those initial kind of research or studies or results were obtained even by Brooks. But yeah, I've read quite a lot and I think we can say, you know, from when lactic was kind of not well discovered, we can say like the lactic acid was introduced as a term and mostly coming from food and compounds that were kind of. Because before physiology, the human physiology that was identified on foods we can even now find in every, any yogurt or milk. Actually you know, part of that field of or food categories, you know the name is coming from lactic acid. Well that are all, you know, evolved and I think one of the first definition of lactic acid is related to the fatigue of anaerobic muscles. So when they identified that lactic acid was present in some, let's say, cells that were under anaerobic conditions, something that probably right now we could change the interpretation or the definition of that term that has been hopefully evolved as well, and that has massively kind of traveled to the scientific literature into. I think a milestone is definitely those studies run by Brooks and the definition of the lactate subtle theory, which has allowed us to understand that lactate is far from being the devil, is really an instrumental molecule on the human metabolism.

A

And I'll stop you right there, Itar, I want you to. Let's bring everyone onto the same page. I think we've understood what you're saying at first, but break down the lactate shuttle for us. What is the whole thing about the lactate shuttle? What does the listener have to understand?

B

Well, it is probably hard to explain that very, very fondly, But I could say just to summarize and make it super practical, I think Brooks discovered that lactate can travel through the body, that can be produced in certain cells and can be consumed or oxidized on some others. And that opened a new research field to understand how lactate essentially travels preferentially through the body, as we could say, like with the VIP kind of tech. So I can come in and out depending on what I want to do. And I think that's what essentially defines, you know, lactate can travel from the production sites to the oxidation sites or clearance sites that are essentially fibers or tissues, organs. And that way it define or help understanding why lactate could travel. You know, that we ended up with these three important concepts around lactate, which is not only a source of energy. I think lactate subtlety theory is very important to understand that lactate is a source of energy. So it is produced and is converted into energy somewhere else that is a major gluconeogenic precursor. So that lactate can also be converted into more glucose. Okay. So that the whole purpose behind that travel that the lactic does, for example, between cell of the. Of the triceps muscle, that I'm. That I'm making a contraction, and it goes all the way down to the liver, and it creates more glucose there. That's the gluconeogenic process. And then something more important, and I think it will open a massive. It's already opening a massive research of a field of research, which is the signaling properties of lactate. So the fact that lactate is traveling doesn't mean only that it is Going to be used to create more glucose or to be used as a source of energy. But also on that trouble is going to make some impact on the environment. It is going to say, I'm here, so I'm going to make that effect. And that's very evident, for example, on them, on the consuming cells. When lactate is present there, it sends a message to the whole cell. It says, I'm here. So maybe glycolysis, maybe think twice, you can stop a little bit down or mitochondria, you know, think twice, you can use me. And that means more conversion into ATP or even genetically, we know that it can trigger some epigenetic and some transcriptional processes.

A

Amazing.

B

So that's the third leg of, or the third role, the third cup of lactate. That is, I find it extremely fascinating.

A

Yeah, well, we often talk about signals like that happen in the muscle cell that make training adaptations. We talk about the calcium calmodulin and the AMPK 2 PGC 1 Alpha to make more mitochondria. So you're saying basically that lactate can do a similar function all around the body. And I think you mentioned, you mentioned them briefly, but I missed them. What were the main things? So if lactate's passing through the various cells and touching them and signaling them, what is it causing later on? What is it signaling them to do later on?

B

Well, many things that depends on the cells. I think lactate is, you know, I learned from Inigo and Brooks that lactate is, it plays a big role on the big physiological processes of the body. So you can find different roles on a cancer cell or on an immune system T cell, for example, or on the muscle cell that we use to contract and then make some power into the pedals on the bike or on our shoes on the run. So there are different mechanisms which by lactate can trigger certain kind of potential adaptations when it comes to, for example, exercise. One of them that I find extremely interesting is that it can modulate the substrate utilization in the muscle cell, for example. Okay, so when exogenous lactate is introduced into that cell, it can say, okay, I'm here. The fact that I'm here says something. And that means you have been using carbohydrates or glycolysis at this rate. You have been converting, transforming energy through fatty acids this way. But I'm here now and that is going to change. Okay, so when we say that lactate is preferential source of energy is because it contains that VIP pass and it says and preferential. So I'm going to go first and that is going to make an impact on how you glucose or fatty acids, you go after me. Okay, so for example, something that we, we have even, we have already seen on some of our pilot studies with sodium lactate is that when you ingest that. And we, there are some other studies in animals and humans as well. When you, for example, inject lactate into a cell, let's say the glycolysis is inhibited. So it says stop. Why? Because I'm already here as the main source of carbons, which is essentially glucose. So you don't need to push more. I mean, glycolysis, you can stop. I'm here, I'm going to do that job. By doing that, lactate can potentially promote fat oxidation or it can open kind of the door of oxphos utilization, like stimulating the Oxford system. And I find that extremely interesting because that role of being the organizer internally in the cell of the substrate partitioning, it is something that I think we haven't explored yet when it comes to major physiological potential adaptations.

A

Yeah.

B

Wow.

A

Where do we go with this? There's so many different angles. So you mentioned some big words there that we should clarify. You mentioned exogenous and of course there's the word endogenous. So let's just define those two key points for the user.

B

I think that's a very important point because to be fair, all the knowledge or the majority of the knowledge we've got on the lactate is it relies on the endogenous lactate. So we know that lactate is produced in a cell. For example, when you are contracting a fiber two type cell, you are, you know, your glycolysis is producing lactate and that lactate is going to exit that cell and it's going to go into somewhere else where it can oxidize normally, some other sites that oxidative capacity is higher. Okay. So because at the end of the day, lactate has to be oxidized into mitochondria mitochondrial complex. Well, that said, we have studied that. So we know that endogenous lactate, we know the behavior of that endogenous lactate and we know that to produce lactate you have to pay a cost, which is activating D glycolysis. Okay. So when you activate that glycolysis or you break down the glucose, then you create lactate. However, over the history, I think that the knowledge around the exogenous lactate is very limited because we, let's say we have been limited on the capacity to ingest or put through the body that exogenous lactate. So basically, nowadays we've got a lot of knowledge on endogenous lactate. We've got a very limited knowledge on exogenous lactate. The difference between both of them is exactly what I said. You have to pay the cost of producing it, which is activating your glycolysis, for example, on the environment of an exercise, you have to go into zone 3 or zone 4, zone 2, high zone 2 intensity, just to produce lactate and extra lactate or exogenous lactate. It comes for free. Somehow. You know, it's just like something that you are putting into the body, whether that's, you know, injection or medical studies, for example, or orally. And that comes from for free. So we still don't know very well that behavior. We understand very well what happens with lactate when you produce it internally, because that's the natural way of doing that. But we still don't know how that behavior is going to be with exogenous lactate. And I think you can use different analogies. The ketones is a good one. We understand very well how we produce ketones. When you reduce your carbohydrate availability and you go into a certain physiological state, you produce ketone bodies internally. But then we also have exogenous ketone supplementation, which are ketones that we commonly use for. I know that kind of bottle that I'm sure you have seen somewhere. The knowledge is very different. We know a lot about how you can create endogenous ketosis and the effect of that. We know a little bit more than lactic, but still limited information around how exogenous ketones can work. So it's exactly the same analogy.

A

Yeah. We've had Shilpafi on the podcast for the exogenous ketones. He's a real leader in that. That area. But it's fascinating the more. The more they go. Those rabbit holes and the studies that they're doing. There's just one I saw came out the other the other day. We're gonna have chill back on. But. But you know, it was signaling for angiogenesis, I believe was the. The latest one. There's. And then of course there's the EPO findings as well. So there's more of these. And again, back to where you led off with the signaling. Right. Itor, like the. The signaling is. Is likely causing these. And we're probably, like you said, just at the very beginning of figuring out the potential signaling benefits of exogenous out from outside in terms of the lactate. Maybe just to begin, I always think when I look to the ketone, the exogenous ketones, supplementations, I always think it's a really great opportunity to think about, oh man, imagine if I'm doing something like that endogenously for myself. Let's just think of the potential, the potentials of fasting or fasted training that might induce a bunch of ketones, right? In, in terms of just naturally as, you know, sometimes difficult as that can be. But you know, you know, in the cycling, in the cycling world of coaches, they've prescribed fasted rides for, you know, decades and decades and decades, right? Like they, they've, they sort of found something there. Now, um, it's kind of, to me, I'm, I'm thinking the same sort of way now with, with lactate and you know, with my, with my hit science hat on. And almost like the benefit of, the potential benefit of properly calibrated high intensity interval training in order to induce natural endogenous high lactates from time to time, that again has to be a positive signaling environment. Of course, now we're also now potentially able to manipulate this exogenously. So I think there's benefits in improving our understanding on all these different areas of how to live and perform. So it's cool.

B

Yeah, no, absolutely. I think, I mean, not only the, it's not the only pathway, but one of those pathways that we used to adapt from training definitely is the signaling properties of lactate. We produce lactate and that makes us bigger, let's say, or better, you know, lactate is part of the, you know, some of the major or the biggest physiological adaptational processes in the body. You know, hypertrophy, for example, likely plays a big role in that, potentially angiogenesis as well, mitochondrial biogenesis. So we, we push the body to the zone, 3, 4, 5, whatever zone it is, like at the high intensity, of course, to create a lot of messages to the body that might be interlocking stress, different other kind of stimulus for the body, but lattice is one of them. So lattice drives a certain kind of group of adaptations that comes from training. So the same as fasting that you can get some potential adaptations from fasting and that's through sometimes through ketone bodies. Lactate is one of the drivers of adaptations and that's one of the reasons why we exercise at high intensity. The only problem that is the one million dollar question is how much high intensity volume we can do. I mean, if we could just imagine this ideal world where we could do 20 hours of zone four, that might be incredible stimulus for the body. Incredible. And we could grow on rates that we cannot even imagine right now. But the reality is that that is not possible. It's not suitable for the body. So it's not something that you can sustain. You cannot train 20 hours at zone four. You basically, you're going to destroy yourself. But I suspect, and this is just a potential hypothesis that exogenous lactate can potentially help on the kind of, on maybe mimicking those efforts of the exercise. Like how we can at the end of the day make the body count more hours of high intensity without doing them. So essentially creating a metabolic state that is associated to zone three, but without paying the price of, or the cost of the mechanical load, for example, in running. So that's a potential hypothesis that I suspect there might be something.

A

Yeah, I love it. And I'm thinking, or I'm thinking about our other colleague Martin and I, as a PhD student formerly when he did his PhD with Dan Plews with the rowing team at New Zealand, and one of the observations we made, he was totally looking at heart rate variability across that. He found the general gist that came out of that data with the Olympic program was that low intensity exercise, zone 2 training and below was exceptional at raising HRV and ultimately probably facilitating an adaptive state. And then when the key sessions, the high intensity, likely lactate producing sessions were performed, well, that flattened the HRV line, you know, thinking that there, there's some association between these high lactate levels and a larger parasympathetic withdrawal or sympathetic, you know, appearance. And, but correlation does not prove causation. And certainly I'm imagining that someone's going to have exogenous lactate at high levels. Well, that's not necessarily unlikely. If there's no stress that's induced, that's probably not going to be inducing anything in hrv. So it's a nice one to just sort of be aware of there. Just a random thought.

B

No, no, but that's a very interesting standpoint, I think. You know, of course that correlation I would say has nothing to do with lactate, but with the cost of producing that lactate. You know, HIV is, let's say, signal of the nervous system. And of course, if you have to activate a cell, the cost of the nervous system is very high. So you have to. And that's the reason why it's so expensive to spend a lot of time zone 3, 1, 4. That's a very, you know, cognitive, not only cognitive cognitive, but also nervous system Cost is very high. So I think it's mostly related to that. But that's a little bit, I don't know, this is all questions, I'm not saying anything here. But just imagine creating that metabolic state that can induce adaptations without making any impact on your nervous system, for example, estimating that that's those kind of things, you know, make me dream somehow. Yeah. Which by the way, I have no evidences and I have no clue how that could be. But you know, potentially there are mechanisms, they are, you know, there's some logic there. And, and that's also. Maybe we can keep researching around. I can say, by the way, on this, Paul, you know, we have been well for, for more than year, two years right now, trialing exogenous, likely with different athletes. This new solution that we came up with, it seems like a common response to that exogenous lactase implementation that is certain positive impact on the hrv, for example. And that's interesting and I don't know why, but I don't know how, but I suspect nervous system loves lactate. And again, there are some elegant studies on the brain that the preferential source of energy and the brain, when lactate is available, is for lactate. So you spur glucose on your astrocytes, on those kind of helpers cells for the neurons. And there is a very nice study that was published I think a couple of years ago. So they induced hyperlactotemia in two different ways. One through exercise. So basically doing a high intensity mode of exercise and another one passive infusion. Okay, so they match the same concentration on the blood. And what they saw is that when the brain is exposed to 4 millimoles of lactate concentration in the blood, it quickly shifts metabolism. And out of 10% of the, let's say ATP demands, 25 is taken by lactate. But when you produce that hyper lactidemia, up to eight minimals, I think that can, that goes up to 60 or 70%. So that shows that when LAPT is available in the brain, in the nervous system, which is the biggest organ of the nervous system is the brain? Of course, not the only one. A lactid is a preferential source of energy. So the brain is going to decide, I've got lactate here, I'm going to use lactate and I'm going to save some glucose here. So I suspect the nervous system gets very happy when lactate is produced. And actually there are some elegant studies why high intensity produces that dopamine release. And that, you know, happiness is certainly related to the Lactate release into the brain. So it makes me, I don't know, dream a little bit about that as well.

A

That's so cool. We've had this exact conversation. So we see the wind trainer bike here beside me and we do this session on Velocity, which is like an online platform where everyone kind of gets to train together and we all do our athletica session there. And we were having this exact same conversation as we were doing our 30, 30 sets of 30, 30 ultimately. And we was basically encouraging everyone. And then you do kind of, you've got, you know, shortly after where whatever you're in some sort of an endorphin, dopamine, maybe lactate high. And it's like, and it's like you can be quite creative and you feel quite good and tired, but good. And I think everyone listening is probably experiencing that and it would be, it's probably impossible to know, but you know, it's interesting to hypothesize how much lactate is contributing to that state, that nice flow state that we often feel. I had one other thought and again, this is the training science podcast. We recently had the great Marius back in on the podcast, recently published the Norwegian Method. And you know, this, this is, you know, it was, it was fascinating to listen to his 30 year history on just being obsessed with lactate and kind of like yourself itar and you know, really just doing his best to understanding where his own sort of sweet spot was lying for, for him. And then we talked about the muscle state as well. But why is it that people like Marius and yourself itor are, are finding and the thousands of coaches out there that use lactate as a tool. So what, what, why is this a beneficial, I would call it an internal load response. And why is it still valid to, to, to do that? Art and science.

B

Well, let me make a note or a point here first because you know, my, I mean I'm pretty young, my contributions to science is very humble compared to these guys that you're talking about and of course Brooks and you know, these, these big names. You know, if you, if you search my name on Ahmed, you're only gonna see some, some studies. But my contribution and my scientific kind of career is very humble. So I, I don't think I need to kind of speak on, on, on their level, but I think I can, I can reply to that question by a very simple kind of question. Sorry, answer. It's just like, you know, lactate is part of the, is a molecule that talks about the cell stress. So if everything that we do in our daily life, not only in training, but also when we are sick or when we're just overthinking or when we are stressed, we are constraining our capacity to transform energy. Lactate is going to be involved in that process. There are few molecules that are part of that process. There is an emerging protein that is called GDP. GDF15. That's. Sorry, I lost the name in English. Anyway, GDF15, which is an internal biomarker that talks basically about how the energy goes to the mitochondria, how the mitochondria is reacting to that flow of electrons. Lactate is one of them. So basically measuring and tracking that molecule, lactate, it gives you a sense of what is happening on that cell. So when lactate, we know this very well, it's not oxidized. So let's say when mitochondria cannot meet the, let's say the demands of, of the ATP and it cannot transform more energy, lactate is gonna, is gonna get accumulated. And that's something that we know very well. We see that race in the blood concentration. So tracking lactate is just a way to track the stress, the metabolic stress of a cell. And it basically, you know, it's just like, it's the sign of what is happening on that cell. So of course it makes sense. And that's the reason, I think, why all the practitioners and coaches with long careers, like people from 50 years ago, they have been already kind of thinking about lactate. And on top of that is something that we, well, technology has allowed to measure lactate, which other components are not possible to measure in such a kind of quick and available way. So that makes the perfect molecule to track, let's say, fitness or training adaptations. And also the internal load.

A

Yeah, no, I think it's really well, really well said. Makes me reflect on some of my, my time with the late and great Laurent Vidal. I was a, a French triathlete. He placed fifth at the London Olympics. He was then became a coach. He was training his, his wife, Andrea Hewitt from New Zealand. And I was there visiting them in Fontremo at altitude, in a training camp. And he just told me just that. He goes, paul, it's really all about managing stress at the end of the day, is what I've discovered. And to your point, Idar, the lactate is one marker that coaches can use to determine where that level of stress is lying. And that is what Marius, Dr. Bakken discovered and others. So very, very cool. I think this is a perfect point now with all that Being said, is to transfer now to your pioneering, innovative world of exogenous lactate. Now we've established that it's not a waste product, it's a signal and a stress indicator. And now how do we potentially also leverage this for either a training or an acute performance effect from the exogenous drinking standpoint, where we might envision that in the very near future, you know, drinks with lactate, exogenous lactate in them are coming into the body and facilitating this in either training or acute performance.

B

Well, let me explain first that lactate, exogenous lactate is not anything new. I mean, definitely I haven't invented that. Not at all. Please, no. You know, the knowledge and the rationale behind that has been there for at least 25 or 30 years. And actually George Brooks, he holds a couple of patents on lactate delivering. The problem has been always that the technical barrier to deliver the lactate safely in a palatable way and insignificant amounts to the body. Okay. And that's kind of the refinement of that solution. What we have achieved, let's say, well,

A

we can say itar that it's not mainstream commercial, right? Like I can't walk up at the 711 and buy, and buy a.

B

It is not available right now. It's not even in the market. Exactly, it's not even available in the market at all right now on this. That's a category of solutions so palatable, safe and insignificant amounts that it can make some real effects on the physiology of the human body. That said, in the implications of exogenous lactate, there are many difference and there are different angles. You can apply that into recovery, into performance, potentially into health. So at the end of the day, the mechanisms in the body, they are the same. They are the same when you are stressed, they are the same when you are jumping or running, and they are very similar when you are recovering or when you have disease. The body somehow fights in similar ways against what is coming. So because Latif participates on all those kind of physiological mechanisms that are essentially related to converting energy, which is everything that we do, we transform energy and then we live. And the difference between a dead body and a light body is just the energy is not flowing anymore, but the material is still there. So that's the only thing that we do, is transforming energy continuously. So therefore lactate can impact on many different aspects of life if we bring that into performance. There is some data and there are some mechanisms and logic to think that it can impact, for example, on endurance performance, high intensity performance, How? Well, probably by providing energy as simple as that, by creating a higher efficiency environment, for example, or simply by protecting nervous function, nervous system function, or neuromuscular function. Okay. You can extend that as well into recovery because at the end of the day what you want from recovery is to optimize the energy transformation, to allocate energy to those processes of recovery so that it can help there and to recover quickly the nerve, the nervous system function. So those, let's say systems are ready to push again. So the same principles, very similar mechanisms, they can be applied to performance. Let's say a race or a given training session or a recovery phase. It can be three, four hours or even 10 hours after a certain port of exercise. But also you could extend that into health and other areas. Like we know, for example diabetes patients or people with diabetes. They, let's say, let's make it easy. They cannot manage really well the glucose. Well, not really well. They cannot manage it basically, especially the type 1 diabetes. They basically lacto, insulin, lactate can fill a massive gap there. I, I suspect lactate doesn't need insulin at all.

A

It's a bit like ketones, right? It just kind of diffuses through.

B

Yeah, exactly.

A

Yeah.

B

So at least on, on the first phase of how, how, how you put the, the sutra into the body, that can be a good element. Then of course lactate success in the body in depends, it depends on your oxidative capacity. So if you can oxidize it, you can convert it into energy. But there are potential implications. But yeah, just talking about performance, which is probably our field of study and what we do, essentially we advise athletes and we're mostly into this world, we still don't know how and how much, but it is pretty logic to think that lactate could contribute to different performance, endurance or high intensity, for example. And the mechanisms are clear, you know, source of energy, which is already a thing when energy is a problem, for example, endurance, exercise, efficiency. So we can't create high efficiency environment simply because it is, let's say, less expensive to convert energy from lactate than to convert energy from glucose, fructose or even fatty acids and so on for different contexts. And finally the nervous system, which I think is a major target for insulin exogenous lattice supplementation.

A

Yeah, and they're, if you get them in as well, they're the preferential. A bit like ketones, aren't they? Aren't ketones preferential too? Like in terms of a substrate?

B

But I'm gonna say something here. You tell me, allow me to Say yeah, as far as I know, lactate and ketones, they serve the same transporter or some of them to go into the cells. So let's say they open the same door to go into the room. The affinity of that transporter is much higher for lactate than for ketones. So what we call it the km, which is the marker of affinity of a protein towards something else that can be a carbon containing molecule, can be the lactate or the ketones. Those transporters, the mct, the different numbers that we've got, there are different types of MCT transporters. They prefer lactate over ketones always. So they always are going to prioritize lactate over ketones. Why is that? Well, essentially because ketones are a very good and very efficient source of energy when there is a specific context which is, you know, the absence of glucose and fructose, that might be fasting, that might be, you know, a ketogenic diet, et cetera. But when lactate is available biologically, biochemistry shows us that lactate is preferential over ketones. And that's something that we also have to consider. And that's the reason why, for example the brain, which is a very sensible tissue to ketones, for example, when there is a big trauma, let's say a concussion and that brain is damaged, that means that that brain probably creates very rapidly, it creates resistance to insulin so it cannot receive the glucose or, or well, mostly the glucose to meet the demands. And that's why ketones, they are so important under those circumstances because ketones, they don't need the insulin, they can just bypass all that process and they go in. There are so many studies as well on post trauma with lactate and lactate makes exactly the same. So the, the only problem let's say that we've got is a naturally both of them, I'm not going to say they don't, they don't exist because the body is a continuum mix of things. But they're not used to coexist together. And that's something that can inform how we think about, for example, exogenous lactate versus exogenous ketones.

A

Well, that's interesting because you've been talking here and I've been thinking about the Jeff Volek faster study. I'm not sure if you've seen the data from it, but it's fascinating. In the three hour prolonged run in the keto group, call them that. You know, these guys have been low carb for low carb mountain runners for like a year or more and they, the Lactate response in those keto athletes is huge. So it's almost like the, I mean, it's, it's super cool. Right? Like they're, and it must be their liver that is outputting a higher dosage of lactate. Now isn't. Isn't that a fascinating, fascinating finding?

B

It is, absolutely. And I honestly think we, you know, whatever we say in Spanish, we fill our mouth with good words, but probably we know very little about that, how that is happening and metabolism, we've got pretty good knowledge, but we don't know why. And you know, how that is happening. You know, we've got very, a lot of limitations. Like sometimes we take conclusions from the, the blue lactate concentration, but that's essentially a volumetric variable, just something that is measuring the concentration. So it can be the same number for different context of, you know, the, the exercise, for example. Yeah, but I, for me, it is fascinating and I have to say I am coming back to some of the, those studies that I read when I was learning and, you know, on my university degree, and I'm definitely, I can interpret now those studies and those results from a different angle. And I, I don't know if I've got more questions or more answers. I don't know, definitely. But I could say it is, you know, it makes it fascinating. Yeah, absolutely.

A

You can think, I mean, logically, in the keto context, athlete, they don't have a lot of glucose going into that brain. And the brain, you know, usually usually needs glucose. So in that context, it's got. The body has to figure out a different pathway to get energy into that. It must. Right. And ketones, of course, is one, but lactate, of course, as you're illustrating, emphasizing on the whole podcast, it has to be another one. And it's, it's almost. And the body has to figure out something. It has to figure out a means because it has to survive. So.

B

Yeah, so. No, no, absolutely. It has to be. It has to be one. Of course, because, you know, we have demonstrated and on, on those studies, we, we know that even if you restrict your carbohydrate intake, you can still activate your 5, your type 2 fibers, of course, I mean, it's not that you cannot make a spring. I mean, you are still running on, on glycolysis, but through different elements as well. Probably on gluconeogenic pathway is extremely activated. So you are obtaining the glucose that you need from different sources of energy. So luckily, it must be there, of course, because, you know, otherwise I think you could stop Running or biking or whatever.

A

Yeah. Another. I just read one of your recent blog posts. Love your, Love your work, Love your work there. What is it called is the glute four. So it's a fantastic need to check that out. Listener. And your latest one, you were really kind of going back into an area that I, I used to be fascinated in as well. And it was really where you were looking at the different limitations to carbohydrate absorption around the different, you know, glucose requires a certain transporter that, that basically caps out at about, you know, 60 grams, 60 grams an hour. And then fructose you get, you can get another 30 in that way. And that's typically where they got to 90 grams an hour. But now you're sort of, you're capping, you're throwing lactate into potentially the mix here too with its own, with its own transporter and potentially, you know, if from, from the model of taking in larger glucose lactate amounts, you're again increasing the delivery. So do you want to talk about that briefly?

B

Yeah, well, that's, I mean we, we know from the last 20 years of research of the carbohydrate, exogenous carbohydrate, let's say, fueling studies that the, the absorption rates of glucose and fructose are limited essentially. Actually the biggest barrier is, is, is the absorption. So the, the customer kind of barrier. And that was limited. We can discuss if that can be challenged if, you know, you can absorb more or less, if you know, those participated in the tour, the France or whatever. Okay, that's a discussion. But definitely there is a limitation. That's the reason why we kind of feel whatever. 400 grams of carbohydrates per hour lactate can, exogenous lactate goes to different routes, so to different pathways. And I find this very interesting because you can support or change or stimulate the body through different pathways on the exogenous, let's say energy availability. And that's something that we probably still needs to be understood properly. But yeah, we know the mechanisms that, you know, the MCT one is probably the, the, the biggest contributor to that lactate transporting through the intestine or. Yeah, the digestive system cells. And that follows a different route. That is not, so far we don't know if that is saturable or not, if that is saturated or not.

A

That's.

B

So that it is, it is something pretty, pretty cool that we need to research and we need to see. There are some studies in animals. There's something very fascinating as well that is that lactate can cross the barrier on the opposite way as well. So it doesn't only go on that way but it can also do the opposite direction. So for example, we know that from the microbiota, you know, lactate is also produced down there in the, in the colon for example, and that goes all the way and travels across the, the different membranes, you know, bidirectionally. So it is, it is something very, very interesting and I think genuinely that can open a new potential window for fueling sports nutrition, fueling in sports. And I'm fascinated about researching that.

A

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B

Paul, I heard that you and actually, well, you told me on a couple of previous messages that you are fascinated about the the impact of exogenous energy supplementation on the neuromuscular function. Yes, I have to say we were back in 2020 we published one of the first papers, I could say very humbly I say that because I know some others that were already researching on that. But one of the first papers that was published exploring the 120 grams of cow har intake on professional or elite trial runners, one of the main results that we obtained it was, we don't know because we didn't run any biopsy analysis and all that, but we measured performance and we measured neuromuscular function. You can go and check the paper. There was a big correlation into the muscle damage, for example. Pretty crazy actually, on the internal load of the athletes, but most importantly on the neuromuscular function. So I have to say I read a lot about what Tim knows. I've been following him for a long time and I know in certain kind of post on on on X he he has been appealing you on your NER nervous system and I've been kind of reading those things. I believe one of the biggest impact that exogenous C supplementation makes in the body has to do with neuromuscular function. And I cannot tell you on on what kind of level compared with muscle kind of environmental conditions, let's say, or metabolic conditions. Sorry, it can be whatever, glycogen or whatever. But definitely there's a big, big thing to study on the impact of exogenous carcinitis and lactate supplementation on neuromuscular function. We have learned that what we call durability. I was fortunate to participate in a paper led by some very smart researchers in, in the Netherlands, where we studied durability in scientists. And I think that was published from 2022 or 2023 if I'm wrong. No, sorry, 2024, I think it was anyway. So I think that contributed to understand that durability, what we call durability, it is not a matter of energy. You know, when you stop running, if we look at your muscle and we make biopsy, there is still plenty of energy that you can still keep running. You're not stopping because you are running out of energy. That's what animals, they do, they keep running and suddenly they plop. They die. We stop because the brain, and that's where Tim knows, has inspired us, the brain decides to stop. And that's because there is probably certain environment for the nervous system that it cannot hold its activation. So we know that durability is probably a neuromuscular function thing. I think exogenous alpha hydrated supplementation plus exogenous lactis supplementation can trigger that. And that's one of the reasons why performance can be improved potentially with exogenous lactitis. So because I know that you're fascinated about that and I read one of your, some of your exchanges with Tim Noakes on Twitter, I just wanted to touch on that point.

A

Well, you've opened, you've opened the can of worms, so why don't I share where I was? So I was. So it came actually after my podcast with Marius Backhan and Marius was really. I read his book and then had him on the podcast and we spoke quite a bit offline as well about just how much performance improvement he would get, he would receive when he monitored his muscle status, that is his muscle tone, elasticity and stiffness through. I think it's called a myoton meter. And that was another part of it. So we often talk about the double thresholds and the lactate stuff. We talk. But it was really muscular status. And Marius, his belief is that, yes, central governor is key, but you also, like, there's a gate. If your muscles are not working, you're. There's a gate on that. So you've gotta, you said you need to have the neuromuscular functioning as, as well. So then I'm, I think I was off for a, for a ride or whatever and I was pondering things and I, and I kind of And I was seeing all of the, you know, the, the, the tweets about the, the performances in marathon performances in London and, and Boston and the high doses in them. And I kind of potentially with Marius in, in mind I put the, the two together and I, I wondered is there, is there something here where the high carbohydrate doses are provide. Providing some sort of a neuromodulatory effect on the, on the neuromuscular system? And then I did I actually read that I just in prep for this podcast either I read your study. I, and I was like, oh, there's more evidence.

B

Thank you.

A

So congrats on that. You've. Yeah, you've known all along that a potential mechanism. And then Tim of course is tweeting, tweeting all about it because I shared with him too and he definitely thinks there's something there as well. So I think we have to collaborate on this on a future high dose study there maybe with lactate as well.

B

I could be, definitely I'm up for it. I could be so excited about this.

A

Yes, fantastic.

B

Definitely.

A

Ido, we're hitting close to ida. Where can people reach out to you follow your work and the exciting things that you're doing and can you hint more about what you and your team are sort of doing as well, maybe even first?

B

Yeah, yeah. Well, we're now mostly focused on this exogenous lactate solution, let's say. And I think it opens a new field of study for everyone, you know, regardless of the potential product or solution in the market. You know, I'm more interested into the scientific progress that it makes. Sodium is likely available for everyone that people, they can start studying and that is going to open a new, a new window. So we're mostly focused on that. But I have to say from the last five years I've been spending a lot of time researching on the, let's say energy allocation into the body. So working on this concept of the energy budget and measuring energy transformation with Adobe Global at water isotopes technique. So I've got, you know, some very good ideas there and they're mostly related to the, you know, my practitioner side of things rather than research because unfortunately I'm very, let's say humble on the way we can research. We don't have good resources here on our place and we are limited on that. But I'm fascinated about developing that line as well. Understanding the body as, you know, as finite resource of energy that you cannot spend continuously energy on things. You have to make decisions, you have to allocate energy on different processes that might be a stress exercise, recovery adaptation. I'm fascinated about understanding the body as an energy kind of budget that is dynamic and flexible. So those are my main, let's say interest, you know, energy budget and of course exogenous lactate supplementation. And I'm not a big name, definitely, but you can find me on Twitter, my profile, I think it is Mvator. You can also find me on Instagram Glue for Science, my website. It was three years ago that I wrote the last article and then I said I have to write down about Lockdit again. So I did it. But I'm mostly active on x Instagram LinkedIn. That's what I could say. But you can find me. Perfect.

A

Well, that was an awesome hour, Idar. I just thoroughly enjoyed it. I've been enlightened. You really got me thinking about different things and I hope the listener feels feels the same. I know they do. And we've got some collaboration to do in the future. So. Yeah. On behalf of my colleague Martin, team at Hitscience and listeners, thank you so much for your incredible contributions at such a young age. I can't believe you're only 32 and you're doing all this stuff. I know Ingo would certainly be proud of a fellow Basque countryman doing that work. So congrats and all the best for the continued work.

B

Thank you for the opportunity, Paul.

A

Cheers.