VESPA as an Ergogenic Aid with Peter Defty | Koopcast Episode 127

Trail and ultra runners, what is going on? What's happening? Welcome to another episode of the KoopCast. As always, I am your humble host, Coach Jason Koop. And on this episode of the podcast, it is a little bit of a collision course on the podcast today. I have none other than Peter Defty of OFM, Optimized Fat Metabolism fame and Vespa fame. And you longtime listeners of the podcast and people who follow me on social media will immediately recognize that the folks over at Vespa, I have given no quarter to in some of their commentary and positions around high carbohydrate diets and high carbohydrate interventions. And it might come as a shock that I'm actually inviting Peter on the podcast today. But although I do stand by those criticisms, I'm still not a hater. And I will admit wholeheartedly that I don't know a whole lot about Vespa's products specifically. And that's because there's not a lot of information out there.

And so I wanted to bring Peter on the podcast today to not only explain to me what this product is all about and how it could potentially work, but also to the listeners about what the product is all about. And in addition to that, discuss some of their recent pilot data that they have captured with some of Peter's athletes out in Arizona. So with that as a little bit of a backdrop, I'm getting right out of the way. Here is my conversation with Peter Defty all about Vespa and how it could potentially work for athletes. So we'll, we'll get it rolling then. Um, uh, I think as we're, as I was just alluding to like off air, I think I need to start out by saying that obviously I've leveled, you know, a lot of criticism, not a lot, but a little bit of criticism. It's all good. It's all good, man.

But in it's in, I want, I want you to personally know, and I want to kind of say this on air as well. And I also want the listeners to know something, a few things about that before we really get into anything. Cause let's face it, if we didn't like kind of address it right off the get go, it'd be weird. Right. Cause that's what everybody would be, would be expecting. And I don't want weirdness. I actually want to learn. We have to like rip the awkward bandaid off first, and then we'll get into everything. So we'll do it. So the first thing that I want you to know, but this is really more important for the listeners is some of the criticisms that I leveled. I still stand by that. And, and I know that's a little bit of a super harsh way to start, but give me, give me a little bit of a second with it. Go ahead. Yeah, that that's fine. I mean, a lot of that is just cause you don't know what, what, what's, what's happening or not. I think this will clear it up, clear it up. Okay. Um, but there are going to be a lot of people out there who they're wondering exactly why I'm having you on this podcast when I've leveled some of that criticism. And I don't want people to come away thinking that, that I've changed my perception of that because I feel that that criticism is valid. It's rooted in our current scientific understanding of the physiology and, and it's just common sense. But that being said, I've had, and you, you're aware of this I've had, and I'll continue to have people on my podcast that I have disagreements with it. That's why I don't take on any sponsors. That's part of why I started this podcast in the first place. And you and a lot of other people are examples of people who I want to bring on the

podcast and just, and discuss something, despite me making some criticism about some methodology or intervention or anything like that. Yeah, yeah, yeah. No, it's all good. And you'll find out. Let's just, let's just rip the bandaid off and you'll see about, because one of the things like with you, I haven't taken any external money or anything because, you know, I, I, if I, if I didn't believe in what we're doing with the product and the program wouldn't be, I would have quit, I would have quit doing it a long time ago because there's been a money loser. It's been literally the bleeding edge. Well, I, I appreciate that little bit of it. Yeah. So we got some common ground there is we're not, we're not going to sell out to people just to sell out. And I appreciate that about you professionally. Yeah. So the second thing that everybody needs to understand, but also I want to make mention of this to you specifically on air is it's nothing personal. It's never personal. It's just professional. And I know that when we talk about people's specific interventions, whether that be a nutritional intervention or a supplement, it does, people take it personally and it's nothing of the sort. It's not personal and you need to know. And I, and I just want to make that. I'm good with that. Yeah. And I just want to make it abundantly clear that I don't wish you any ill will or harm. As I mentioned off air, I hope something does come to light from all of this, but it's just a criticism of statements kind of, kind of plain and,

and, and simple. And the third thing that I think I need to mention, and this is more of just a today's culture than anything else is that I'm in no way, shape or form picking on the low carb group or the OFM group. You can pick on the low carb people, the key. I call them, I don't call them key targets for a reason. Yeah. Well, we'll have some common ground there for sure. Yeah. But, but I think that in like the whole diet wars wars culture that we have today, all too often, like I said, it does become personal and does seem that people take it as, as we're picking on one group or another. And really, to be honest with you, I'm kind of indifferent. I mean, the longtime listeners of this podcast will know that I just call it as I see it. And yeah, yeah. You're agnostic. You're trying to be agnostic. Yeah, exactly. And that's, and you're calling it as you see it based on the information you have. Sure. Sure. And, and that's, and if you kind of go through the record, that agnostic, that agnostic viewpoint of that agnostic kind of strategy really prevails where, you know, I've criticized the Western States 100 for their anti-doping policy and spring energy and SF fuels for the exact same, you know, marketing stuff that, that I've, that I've criticized you for. I've criticized the vegans going back to my very first podcast with my late great friend, David Clark. And I even dedicated my book to him, even though he and I vehemently would like go at each other on, you know, in various formats.

Yeah, no, no. I think this will be, I think this will be illuminating for both of us. Cause I think that, um, like, like spring energy and SF fuels, I actually, I actually know there's some problems with them. Well, sure. And so anyway, I wanted to get like all that out of the way, right out of the get go, because I do want to talk about Vespa. And one of the reasons I want to talk about it, and I think you, you realize this as much as I do. So nobody should really take offense to it is I can't, it's hard for me to find information about it. Well, we're going to go into that right now. Let's do it then. Let's get right into it. What is it? What is it fundamentally? You're going to be underwhelmed. Trust me. Let's go. All right, let's do it, Peter. I'm going to turn the floor over to you.

What is it? You can respond to any of that. We're already, we're live now. We're going. Oh, a hundred percent. Yeah. Okay, cool. I'm good. Yeah. All right. Start, start me off. So first off, tell me what Vespa is. Okay. Vespa is a, it's actually classed by the FDA as a dietary food. It just, it's, it's classified as a food. It's not classified as a supplement. So that's really important to know because it's composed of water, honey, bee propolis, royal jelly, and then the, the, the very exotic wasp extract, which is really a bioactive oligo peptide that we literally have a proprietary way of, of extracting from the giant wasp or the murder hornets.

It's a technical name is Vespa mandarinia. And it also has citric or ascorbic acid or orange juice used as a pH buffer because when you're doing food products, you got to keep the pH low to prevent organisms from growing. And so what is the difference between your product and the only other similar thing that I can find in the research, which is Vespa amino acid mixture, which will be abbreviated VAM commonly. Cause this is a source of confusion that I can't, I can't like reconcile. I'm glad you're bringing that up. There's two products out there, VAM, and there used to be a product called Hornet juice was it, which was essentially a knockoff of VAM. And what happened was when Takahashi Abe, the entomologist discovered started, he started tracking the, the, um, giant wasp to, to, to figure out what, what it's about. They were, this is one of these accidental discoveries of nature. Um, what happened was he found these things, wrote some papers, and he was immediately caught contracted by Meiji dairies, which is a big Japanese conglomerate to, and what's the essentially did was hydrolyzed this peptide and then extract out the amino acid compositional profile. And so what they did was they made a synthetic blend of synthesized amino acids that matched that compositional profile. So while VAM has efficacy, um, even in the studies, if you look

hard enough and show that, that they, they admit that the actual natural, um, peptide had greater efficacy. So, so the VAM is a different product. It has, it's, it's, they showed in their research, and we'll get into that, um, that it did have efficacy and I'm not saying it does, but they get less of an effect and they have to use a much higher dose. Okay. I do want to get into dosing a little bit, but let's kind of pivot back to like your product. So do you know what the composition of like those core ingredients are like you list the ingredients on the ingredient deck, but you know what the amino acid composition is or anything? Yeah, I can share, I can share those, uh, papers out of Japan that, but see, see the problem is all those papers reason we haven't put them up.

Uh, and you'll understand this because you're really good at finding those things is, is because they major dairy was paying Abe a lot of money to do this. That's, that's what, why it's all slanted. The papers are all slanted about bam and only scant, um, information, but I can, I can put that all up. It's probably, I can pull it up. Yeah. Yeah. Yeah. Cause what I'm trying to get at is do you, does your product have a similar or the exact same amino acid profile as VAM? And we can, and if so, we can use that as an amino acid analog, right. During, during the discussion. And if not, I kind of want to know like why, because that's really not that hard of a chemical process to do. I mean, you can use chromatography to, to, to distill down what amino acids are in a substance. Yeah. Absolutely. And I had, um, I had these, uh, a series of conversations, my good friend and ultra running legend, Bruce LaBelle about, um, this because Bruce, Bruce happens to be a PhD in organic chemistry and he's the head of the California department of toxic substance labs.

And so we were discussing exactly this thing and yeah, you can break down, you can hydrolyze the peptide, get the amino acid compositional profile, but it's not going to have the same efficacy and, um, pathways of action because of the structure. And a lot of that I think has to do with, you know, tight junction signaling, uh, in the stomach and gut lining and things like that, that allow the peptide to pass in if intact. Uh, I, you know, I don't have enough, this is beyond my pay grade, but there's this stuff I've read about and, and, and looked into. So, you know, if you've got the stuff on VAM, that's, that's pretty much what the amino acids are. Okay. Okay. So that's the, so, I mean, it's fair to use that as an amino acid analog, although the structure might be different. This is my chemistry background, like coming through here, by the way. Okay. Okay. Yeah, exactly. Exactly. Yeah. In terms of the ingredients. Yeah. But you know, the special sauce is in that natural structural stuff.

Okay. So you gave, gave a great lead into this. What makes the special sauce so special in terms of the mechanism of action? Well, you're, you're, you're, again, I, I just, for me, it just works. And that's, you know, when I started using it work for me, it's worked for others, but in terms of, um, what I have understood it, because of the, the proline, I think it's the alanine and the glycine, it accelerates, uh, input into the TCA cycle. And especially with, uh, a non-esterified fatty, fatty acids, um, using glycine. Okay. But here's where, so this story has been told a little bit, right? We've tried to use different amino acids as ergogenic aids for five decades now. And they, they, they won't really pan out that well. And here, and here's why is because they have a hard time actually affecting either beta fatty acid oxidation or the Krebs cycle or glycolysis. Now that I'm thinking about it at their rate limiting steps. Right. And this is well-known chemistry, right? I mean, you should know. And I haven't, you've just kind of illuminated some stuff for me because I've always kind of been a little, yeah, the whole branch chain amino acid thing is, is a little overblown. Um, so I,

I agree with you. I just, and that's why I say, I think the structure of that, um, particular peptide. And I think the honey also has an effect in terms of helping to start, you know, how fat burns in the flame of carbohydrate. Uh, every, every freshman level exercise physiology student has just now had that re-conjure up in their head. Right. Right. Right. And, and so exactly. And, and, and, and so, but it's really central, centralized around that particular peptide, um, is efficacy and peptides are a big, big deal right now. Uh, right now in sports, um, supplements and stuff. Yeah. But I understand that. So I'm still trying to like, I'm still, and this was my original question for you that I sent over in the outline, right?

What is the potential mechanism for action that the, where this is going to actually affect anywhere along performance? Yeah. So I, my, my understanding, uh, and observation has been that the biggest effect that this has is it goes right to the liver. And so it's triggering the liver to, um, release free fatty acids and also it, um, depending on the metabolic needed also take, take, um, fat and then, and, you know, with glucagon and it'll, it'll produce, uh, glucose. Right. But, okay. So let's just say that's true. Right. And this is going to get into a little bit of a chemistry lesson. I got to promise myself, I wasn't going to go through Krebs cycle on a podcast, but, but, but stay with me here. Right. Yeah. So I could buy that, right. I could buy that. You can, you can ingest a substance, whether it's an amino acid or a peptide, and somehow it begins the initial catalyst of free of beta fatty acid oxidation. However, the rate limiting step is not the initial step. And everybody should know this. I mean, freshman, once again, freshman level exercise physiology, students will know this, the rate limiting step is getting that acetyl CoA into the mitochondria itself. So it's not the initial step. And this is where very commonly, a lot of these

amino acid supplements have, have failed as they do have a potential mechanism of action, but that mechanism of action doesn't actually affect what matters the most, which are these rate limiting steps within these specific metabolic processes. So that's where I'm failing to understand like where this process is actually going to have an effect. Yeah. You want me, let me pull something up and let's look at that. And, um, yeah, so this, this was the proposed mechanism from Abe initially. Uh, let me pull this up and that this might help because this is, like I said, this stuff's your way ahead of me on the chemistry, Jason. I just, like I said, I make it work in the real world. So let's go.

So for the, for the listeners, while you're doing that, you have to enable me here. You have to enable. Yeah. So, so tee that up a little bit and I'll entertain, I'll entertain the listeners for a second. So the research that you're referring to is the original, uh, as the original research that this is based on that was done in the mid eighties. If I'm correct, if I'm correct, uh, later mid eighties, let me see here. And a lot of it was done, um, on mice and swimming mice as well. And, um, it was kind of done in the same way you do any other mouse study, right? You feed them and you try to, and you try to determine biochemically what's going on. So you, you've pulled it up. What's the proposed mechanism of action from those, from those original studies in the late eighties. Okay. Yeah, here we go. Most disabled participant screen sharing.

Uh, let's see. I might have to, I didn't expect to, do you actually share your screen? So let me enable it on my side. Um, um, uh, I don't have anything to hide here. Normally nobody takes that step. Okay. So all participants can share. So you're good now. All right. Those of you, you can switch over to the YouTube version. You're going to see a, here we go. We're sharing your screen right now. There we go. We're going to see the, Oh, see, look at that. You get to fulfill my fantasy of talking about the Krebs cycle on my podcast. Yeah, no, all roads. No, I I'm totally with you. All roads lead to acetyl CoA and you have to get there before you're going to feed it. So what we're seeing, what we're seeing right now is a graphical representation of the Krebs cycle and how the various biochemical processes actually feed into the Krebs cycles. Let me tee this up, Peter, and you can kind of organize your thoughts a little bit. So for the, for the, for the, for the uninitiated, because we have a lot of lay audience. So let's kind of set the groundwork, right?

So the, the Krebs cycle is the main biochemical process that, um, that describes how we convert energy in the human body and biochemists have spent an inordinate amount of time trying to figure out exactly where these chemical compounds come from, what catalyze the reactions, what the rate limiting steps are. But fundamentally what you're doing is you're taking molecules with big, long chains of carbon and you're breaking those big, long chains of carbon into smaller chains of carbon. And during that process, you convert energy. Peter's got this pulled up. And whenever we do, uh, particularly like nutrition interventions, or sometimes this actually comes out in training interventions. Sometimes we can trace it back to a particular part of the Krebs cycle or any of its biochemical cousins, I'll put it that way, uh, as to how that intervention is actually affecting human metabolism.

So I'll, I'll, with that as a backdrop, Peter, I'll kind of turn, turn it back, like back over to you for what is the purported mechanism of action originally when this research came out? Well, this, this was, this is the purported mechanism and how proline and alanine sort of get things started by going that these amino acids help to drive the demand, um, for acetyl CoA through interventions. I think if you go, if we go up here, uh, this is the part I can send you this paper, Jason. Yeah. I'll link it in the show notes as well. I, I, I pulled it up before the, before the podcast.

So, you know, it has to do with these, these particular amino acids driving it. And I don't, you know, I'll be the first one to tell you, I don't really know all the mechanisms on this. So, but this is the proposal that the proline and the alanine go here, the glycine. Right. They're either Krebs cycle intermediates or Krebs cycle precursors that you're adding to the, the mix of everything. And they are catalyzing these reactions of taking molecules with a lot of carbon and breaking them down to molecules with fewer carbons on them. And then at the same time, harvesting or convert, converting energy. I mean, that's the, and to, yeah. And to a point, I think what you were saying about the rate limiting steps in terms of this particular cocktail that they say, you know, I think the, the actual peptide has shown to do better in, in observational experiences, but it's, it's actually feeding those helps to feed those rate limiting steps from, from this diagram. Well, no, no, because once again, the rate limiting step and beta fatty acid oxidation is getting that acetyl CoA into the mitochondria. And that is catalyzed by a protein called CPT1 and CPT2 that sit on either side of, of the membrane. So if you're

telling me that something is catalyzing the, the proline cycle, right, which happens before acetyl CoA actually gets formed. So once again, we've got big carbons going into smaller carbons. Acetyl CoA is one of the smaller carbons. Proline cycle feed into that. It kind of doesn't, and this is what I've always had. This is my issue that I've always had with nutrition companies. And I'm not, I'm going to actually pick on the ones that use sodium citrate as opposed to sodium chloride. There's a number of drink manufacturers out there that will use sodium citrate as opposed to sodium chloride. And their rationale for that is that it's a Krebs cycle intermediate, right? Citrate is a Krebs cycle, which is true. It's a, that's absolutely true, but it's immaterial in the whole process because there's so much citrate available adding to it is not going to, it's not going to markedly or at all affect the entire process. So when I read, when I read Abe's initial, initial research, and then some of the data that you sent me in advance of this as well, that there might be an area where it affects the proline cycle specifically, or even the alanine cycle, that same, that same mechanism where the choke point is down, is further downstream than that is still, is still apparent.

And once again, this happens all the time in biochemistry and the way the listeners can, can think about this is if you have a garden hose and that garden hose is producing energy and you have two valves on that garden hose, one valve will let the water out at three gallons per minute. And the other, and the other will let the, will, uh, let water through at five gallons per minute. If you open up the five gallon per minute valve to 10 or 20 or 30 gallons, it doesn't matter because it still has to go through that three gallon per minute choke point. That analogy is what we're talking about with these rate limiting steps in biochemistry, where we, we have tried to push and pull on them for, for, for years with interventions and supplements. And just as it turns out, unless you're directly affecting that rate limiting step, it's just not that you can't do it because there are other synergistic effects. I'm not trying to like isolate biochemistry into the only thing that matters here, but it just becomes really, really, really hard to do. And I agree with you. I mean, um, I'll stop the share. So let's, let's, let's kind of like back up a little bit. So you've said in your, in your observation, right. And, and I'm not going to discount that, you know, I give athletes interventions all the time that I can't track back to one exact scientific paper or methodology or whatever. We try to base it. We try to base things in science, but, but ultimately what we're doing at

the end of the day as coaches and in, in your coach as well, is we have to create reasonable, reasonable extensions of the research, right? We have to look at what science is telling us and make a reasonable extension of that to try, to try to apply an intervention or a supplement or a regimen or kind of whatever. So we'll go back to your like observation of how the supplement actually, actually affects athletes. Why don't you start to describe that? And if you need to kind of go through a little bit of an origin story of how these different products have kind of emerged in sports science over the years, like going back to the eighties, you can, you can go ahead and describe that as well. Um, well, I think the first appearance of Vespa came in the late nineties, early two thousands in Japan. And so, uh, you know, a number of marathoners used it in the early two thousands successfully. Um, and, uh, then for me, I, uh, you know, everything here is sort of accidental with me. So, um, I, uh, did my first marathon in 2000 and I did the whole carb loading thing. And, and that just turned into a big bonk, had a sub three hour marathon going and I still finished and got a BQ, but, but it was ugly the last six miles. And I thought, well, this didn't work and it didn't appear in training because I wasn't carb loading. And that set me off on this whole journey of, of fat metabolism. Um, so I was open to that idea. And in 2006, I got in,

I got into the 2006 Western States and I was training for it. And my friend, Paul charter is at the Western States Memorial day training camp. Um, uh, threw me a couple of pouches of Vespa and said, Hey, my friend Mojo swears by this stuff. And it, it, you know, I'd read the label on the back and talked about fat oxidation. And so since I was open to the idea and I was basically, my experience was that consuming a lot of carbs is chronically wasn't working that, um, I was open to using the Vespa and I used it, um, for two in the 2006 Western States, it was my first hundred. Uh, that was the year, the hottest year in the history of the race. I ran without a shirt from the very start to the very finish. And it got up, you know, I think Miller's defeat, they said it got up to 115 or 118 that year. Um, anyway, I had no, I had no issues and it, it, everything worked fine. And, um, that's, that was my first empirical thing. And then I made it my day job in 2008 formally.

Um, did the product change when you took it over, like in terms of where you're getting it sourced from or no, no, no, no. It's a single source proprietary thing. I work very closely with my manufacturing partner in Japan. Um, and it's, you know, we're, and, and it's, it's, it's, it's a food facility. It's not a supplement manufacturer. Um, and so the, the, once again, I need to be mindful that some of the listeners aren't going to know what it is. It comes in a pouch. Yeah. Forgive me for the, forgive me for the analogy, but it looks like a gel pouch, but it's bigger. Yep. And so what's the size? There's a, there's a 2.7 ounce, 80 milliliter, uh, pouches, the junior and the CV 25. And then we have a little one called the ultra concentrate.

Um, but it's a little tiny carry pouch that, but you don't take it like a gel. That's one of the biggest mistakes people make. Cause it's, it's, it's, it's actually got enough. It's got a 175 milligrams of wasp extract. And so that's as much as a CV 25 or a junior together. So if people just take it like a gel, they might get a little stomach, uh, issues. Whereas if they dilute it, like you're supposed to, it works just fine. So along both of those delivery mechanisms, how did you determine that that's the right amount to be delivered? I didn't, I didn't, that was just how it was presented to me. And it, it worked for me and I'll be, I'll be frank and honest about it, but it's just the way it came. And so you were like, we're just going to use this dosing. We're going to run with it literally. Yeah. Cause, cause once again, so I'll tell you like my experience as a coach, right? I have an athlete that comes to me and says, Hey, I want to take this supplement. It doesn't matter kind of what it is.

I kind of go through a few things right out of the gate for first, first off what's in it, right? I need to go and figure out like chemically, like what's in it. And you know, the supplement, I hate to use the supplement analogy because I know your product is not a supplement. Yeah. But, but as you know, the supplement industry is just rife with bullshit, right? I mean, there's so many products that don't contain what they're supposed to contain on the label. Listen, when I, when I did my due diligence to become a partner, equity partner in the company and take over the distribution in the U S and Europe and all, I almost didn't do it because when I did look at the supplement industry, it's like, it's fucked. I mean, it's like, it's yeah. And the profits, it's like, we don't have a profit margin, like other supplements, because the cost of ingredients for what we're doing is just, you know, exponentially like, you know, 10 X 20 X higher than.

I get it. No, I get it. I mean, CTS was involved in, uh, in the supplement industry in the early two thousands. And so I got to see the very backside of that. And trust me, I don't want any piece of it either. But my point with that is, is my run of show as a coach and athletes approach me with this all the time, whether I work with them or whether I just kind of interact with them, I always want to know what's in it. And sometimes it's easy to figure out and other times it's difficult. And then the second thing I want to know is what is the correct dosing based on what the literature says and what's in it? Because we know that everything in, you know, chemistry and in particularly with, with supplements is all about, is all about correct dosing. And, you know, you just mentioned the supplement industry earlier. This is one of like the dirty little secrets is everybody hides behind proprietary blends. And the reason that they hide behind proprietary blends is they're trying to, they're trying to use as little of the really expensive ingredients as possible, yet still make all of their claims. And that's a total aside that we don't really talk about.

No, and I get you because what they'll do is they'll cite papers on that specific ingredient. A hundred percent. A hundred percent. And, but it's not directly tied to the efficacy of the product. A hundred percent. A hundred percent. Yeah, yeah, no, we're on board with that. And so I carry that forward. And once again, I hate to use a supplement analogy with vestibule. Yeah, no, we're good. I know it's, I know it's a food product, but I still, I still have a hard time, A, determining what's in it, like we talked about earlier, but B, you've got this dosing that's just based off of history, you know, more than anything else. Somebody at some point in time came up with a correct. There was no formal, yeah, there's no formal stuff. And really what, what's kind of interesting about this, Jason is the fact of the matter is for you and your listeners, it's kind of exciting for me because at the time I took over, it was mainly being distributed to hockey and figure skating, which was really a dead end, even though, even because the guys were Canadian, they wanted out, they just gotten tired of it. They were totally new what the potential for the product was, but they only knew how to market it to hockey players. And it had a pretty, pretty interesting underground following in hockey. But what's happened here, the point I want to make is the exciting thing is we're doing that empirical science right here in ultra running. I mean, it's, you know, ultra running's kind of on that for what we're doing, we're, we're literally on that edge of the human performance envelope to see what happens. And that's, that's where the empirical

science is. And, and, you know, the reason we got this conversation is because I'm, I've finally gotten to the point where I can start to put some money into, to, to developing data. And, you know, this is going to lead to a study. We can talk about that in a, in a bit, but I mean, I have a researcher who actually wants, who's really keen on doing a, a, a, a, a research project. And so that's, that's where we are, but, but it's really, you know, it's fellow ultra runners, not just myself, but fellow ultra runners over the last 12 years, who 12, 14 years, who've, who have kind of brought it to this because, uh, you know, the first time I did a online interview, it was with Scott, Scott Dunlap. Yeah. And we got, he and I, and he uses the product, he swears by it. And he was using, he was one of the early adopters and he says, yeah, it works. This works great. Had me on. And we got, we got absolutely skewered in the comments. And so, and, and it's okay. I get it. I get it because all the science is, is, is based on carbohydrate physiology. And, and so, um, this is not, you have to be fair. There's no science on this. And I say that the point I'm making is we're, we're doing the empirical science because science starts with observation. And now, you know, at this point, we're getting enough data points and we're developing data to, to get it to that science.

So I want to give you the opportunity to, to go over some of that observation, because once again, I observe things as a coach and sometimes that's all I have to go by. I always try to trace it back to something logical or research that I've reviewed or something like fundamental about physiology, but sometimes all you have to go off of is observation. I'm kind of completely with you on there. So I do want to give you the opportunity to kind of go through that observation so that the listeners can kind of understand this is what you are seeing in the field with athletes who have tried this, this food product. So you want to go ahead and, and, and describe that in any way that you want to, whether it's an early adopter or some of the current athletes that are using it.

Um, well, I think what, what let's just talk about in general principles, like what's consistent, what we're seeing consistent with, with all these athletes. And the listeners should know that I've worked with people from, you know, elite people all the way to back of the Packers. You know, we have people in their seventies and eighties or just back of the Packers and they're finding they can have it. But, um, what they noted, what we've noticed with the Vespa is one of the reasons why it's easier to develop some form of empirical data in ultra running, not, not the testing we've done. We'll get into that, but is the fact that you can put a metric on it. You know, a hockey player can say, yeah, I played my third period a lot better. Uh, but that's not gonna, I get it. That's not science, but with ultra running, you know, we can see people running a hundred miles on less than a thousand calories of intake. Um, that's a pretty, pretty hard metric. Uh, and, and that just, you know, it precludes the risk of, of GI distress. Um, people, people observe that they're much steadier in terms of the ups and downs and energy, um, mental focus, but that's not really, that's, you know, that's more of a perceived thing. And then the other thing is the recovery is markedly, uh, better. And I, I, I want to reframe this. The reason people actually recover better is because they haven't done the damage in the first place from the oxidative stress and lactate

load. Okay. Um, that's reasonable. Um, I, I want to get into some of the pilot data that you have recently released and a previous guest on this podcast, uh, Jeff Browning, who introduced me to who was responsible for my introduction to ultra running. Let's put it that way. Oh, uh, participate in this. And like I said, I've had them on the podcast earlier. Why don't you take the listeners through like the kind of the origin story behind collecting this pilot data and then what the design was. I'm going to call it data collection. It's not, but it's not science. I want people to know it's not formal science. Um, we do have a, we'll have a pilot data sheet. I think I sent that to you from, yep. From St. Mary's on cyclists, but, um, over the, so I'll back up. Yeah. I hope you don't like detours down different rabbit holes. You get you, it's your rabbit hole, man. Go ahead.

Okay. Well, you know, I finally got, um, okay. The rabbit hole started in 2010 when somebody said to me, Hey, you ought to go talk to this guy. He's kind of on board with what you're doing. And it was an article in the SACB about Steve Finney and, um, about fat, fat burning and all. So I had lunch with him and that started a series of conversations. He, he found out, he goes, you, you're doing empirically what, what the science shows. And, and Steve is a big, he's like totally into the ketogenic diet. Um, and you know, he had his, his cycling study out and he's just, um, was big on it. So what he'd found with me was, and I, so I've found a researcher who actually knew what I was doing actually worked. Cause I, you know, being in Davis at the time, you know, Liz Applegate, all that, it was total dismissal. Um, so I started, we started getting together because Steve's secret passion was athletes and that led to the 2012 Western state study. Um, and so that study was done on a cohort of high carb conventional athletes and, and athletes I was working with who were, uh, fat adapted and using Vespa and that data never got published, but what they, what happened out of that data. And it, you know, it was, it was ultra running that was doing it. This was science.

So they were taking cheek cells, blood samples post or pre pre-race and then post-race and then post-race out a few days. And then they were taking, uh, cheek cell swabs, uh, to look at oxidative fatty acid, fatty acid compositional profile changes and oxidation, uh, at the start, uh, at, at Forest Hill post-race. And then they did it for, I think three days after, and then they sent a kit to everybody has sent two weeks after. So what they saw in that study, they, they didn't, they didn't want to publish it in a low tier journal because it was Steve and Jeff, Jeff Bollock and Steve Finney. So they didn't want to publish it in a low tier journal. So they didn't publish it. So, and I think you can confirm with the readers that there's, there's a whole tiering of, of in academia of ranking system of publications. And, you know, people can get stuff like you alluded to with the supplement industry. You can get put stuff published in a crap journal and people won't know the difference. Yes. I agree with that.

Yeah. So anyway, that data was pretty stark in that on the recovery side, what was statistically significant and I can share, send you that data was the people in the OFM VESPA cohort recovered really fast, really fast based on what markers, uh, recovering fatty acid compositional profile. So were they looking at like creatine kinase levels or interleukin six or no, they were looking at fatty acids, the fatty acids and the oxidative stress. Okay. Going back to the old King Cooper days. I grew up right next to King Cooper's, uh, the Cooper clinic in Dallas, Texas, where I grew up.

I did an internship there a long time ago. Anyway. Okay. So the, that research never got published. So they keep going down the rabbit hole. So, but that, that so impressed them that that led to the faster stuff. Okay. So origin story, the faster origin story for VESPA is an origin story for the faster study. Well, it's not, yeah, it's, uh, yeah, we're good. We're getting there. Okay. We're talking about the research. Okay. So let's lay the groundwork for the faster study, because once again, I'm familiar with it. You're obviously familiar with it. Let's, let's give the listeners just the nickel version of its significance. Why don't you give your nickel version and then I'll add context. Oh, sweet. So the faster study took, took a, took, took a cohort of athletes, well-designed study in terms of they had them, uh, in a nutritional ward for your, your testing, my memory on the week, six weeks. Is that right? No, no, no, they were, no, they weren't even an award. They were just tracking their data and they were, they were only there for, I think two or three days for the actual testing, but they were keeping them on a pretty tight record in terms of their, their diet. You know, it was, it was pretty, they didn't have any nutritional awards.

Okay. So the, the fundamental part of the study is, is they, they had them exercise at 60%. You're going to have to correct me on the percentages here. 60% of their VO2 max for three hours. 60 or 65. Yeah. For three hours before a low carbohydrate intervention, would you call it low carbohydrate or optimized fat? Actually, actually it was a, it was no, they, this is where we need to talk. This is where we get the, the meter. Okay. So what it was, it's obviously been a while since I've reviewed the study. So go ahead. No, it's all good. Since I was part of the design and, um, recruiting, I've got a little bit more, and I don't probably look as near as many papers as you do. So they had two cohorts. They were comparing two cohorts. They had a, we recruited a bunch of people who were your normal, normal diet, normal fueling ultra runners, people like Mike Wardian.

Sure. Um, and they recruited a bunch of people, uh, who were essentially on my program or doing carbohydrate restriction. Um, and they matched them very carefully in terms of age ranking their, you know, their profile in terms of how well they did in races. And then they, they tested them on a three hour treadmill. They did a VO two max test in a three hour treadmill test. Um, and then they, they did a bunch of, you know, blood draws biomarkers, including a muscle biopsy. And, um, the, the, the take home was the, the, the take home data is it shifted the science because previous to faster, uh, the, the, the science up to that date basically suggested that, that humans can burn up to one gram a minute, um, in peak fatty, peak fat oxidation. And the crossover was right in line with George Brooks crossover concept of 65, a well-conditioned athlete, 65% of their VO two max cell crossover from fat to carbohydrate faster changed all that with an average of 1.54, um, grams per minute. And, um, the crossover shifting to 75 to 80%. Now, and this is leading up to what, what, why, why, why are we doing research? I told you. Okay. So it, it led up to this. Um,

so it changed the science in terms of what human potential is. Um, but to control variables and I get, I get it. I, the control variables, they kept it at a ketogenic diet, the, the low carb cohort. Yeah. But here's, okay. So you're saying that, that, that, that study shifted the science from what we previously thought was the highest rate of fat oxidation to a new rate of fat oxidation intensity, intensity, intensity, intensity level of crossover. Totally get that. But if you're looking at it, this is a, the sky is blue type of result. If you put people on a low fat or a ketogenic diet, you I'm totally with you, Jason. Yeah. So totally this, this was, this was the problem with faster is they were matching them up based on performance, but that performance, you know, I, I knew I actually coached, I think all but one or two, maybe, I don't know. I don't know a couple of the guys in there, but all the other people, I actually either coached them and got them started on their fat adapted journey. And in their races, they were OFM and Vespa, which means when they're OFM, once you get them fat adapted, you got to bring the carbs back in. And there's no, you'll have no argument with me. And that was the, so this is where we're getting to the point of the, your question is the problem with faster

was the inference was you can perform as well on keto as you can on fat. And, and, and it really has set the, to me, it's, it's really set us back in terms of everybody trying to move things forward in terms of both performance and health, because you, you're right. You're absolutely right. You cannot perform on a straight keto diet because it's a conservation physiology and it's, it's, it's, it's basically turning the governor down. But, but in addition to that, I can test this whole notion that regular mixed macronutrient athletes can achieve carbohydrate or fat oxidation rates of above 1.5, because I have that data and I just reanalyzed it. Sorry, this is, I'm kind of like springing this on. But I have a good cohort of, of very, very similar to the faster study.

In terms of, you know, how good they are, if you want to think about it like that. And when I analyze the top 10, eight, eight out of the top 10 are above 1.5. And what I'll also say is we use a different protocol, shorter protocol, which is, is you're very well aware of is going to blunt that the absolute number that you get from, or the highest number that you'll get from a fat, uh, from a fat oxidation study. And the second thing is we use a 20 second rolling average versus a two second or a three second rolling average, which is always going to bring the maxes down. So when I look at that, I'm like, well, wait a minute, hold on. You're not rewriting textbooks, which is something that I hear out of that study, right? You're not rewriting textbooks. Like we've got this data that already exists. Yeah. It might not be as well known, but let's like, you know, temper the jets a little bit on the significance of all this. So let's, let's get, let's get back to the observational piece, right? You gone, you went down the rabbit hole.

Now we have the fastest, faster study. How does that lead into Vespa in terms of people's use research? Okay. So here's the thing because faster inferred, you know, and I got dropped. I mean, I, unfortunately, Steve and Jeff, they got what they needed and, and, and cause they thought it was really all about the diet and Vespa really doesn't have it because you know, you're, he, they were asking the same questions you are. Vespa doesn't have any science behind it. So they thought all this performance gains were, I think that they're, they're thinking was all the performance gains had to do with the ketogenic diet. And I would say, I would offer that, you know, carb restriction at certain times is important, but using carbs is that, is that so post faster, I'm like, where are we going to go with this? So I knew that the performance that these athletes were seeing, you know, the people like, let's just talk elite level, they're winning races, setting records, um, that, um, you know, it had to do it. So that's where I started, started my journey to try and get, um, some data developed.

And, you know, it was, it's just, it's just hard. And I didn't have like tons of money to throw at this. Um, so that's, so it's led to, so from 2015, 16, when faster was published, I started looking around and then, oh, 2017 or 18, we started to try to develop some of that data. And then we, I finally met Dr. Marks and then Jeff had his, his, some testing done on him, which you've seen and you brought that up. And then we tested Jeff a couple of years ago at Utah state university. And I I'm getting, I'm going to get that data processed and up to, so that's, and then, so Dr. Marks started, uh, a study in the late 2019 and 2020, uh, using cyclists. And that, that of course got nixed. Uh, so with the whole COVID thing. So, so here's, so here's my thing though, even with that, you've got a product that's been on the marketplace for 20 years and there's, there's not one single solitary modern day research intervention, research intervention study that has analyzed it. Like the time, like you've got to understand that I'm, I'm not only representing like my opinion of this, but there's a lot of people that have like told me this as well. They're like, why has this been on the shelves for so long?

And the claims are, you know, so incredible yet there's not one scant piece of research to actually show for it. Because to be frank with you, I mean, until 2015, when I started looking for it, I personally didn't, I'm like, it's work. It works for these people. They're winning races. Observational evidence is the start of science. And I think people forget that Jason. Uh, and I'm not, I don't want to get a back and forth on that, but I had to, I had to get reality. Yeah. We need to develop some science around this. Okay. But the other thing is, because this has been, this is so, um, you know, uh, disruptive, the product is so disruptive in its approach and it's, it's manufacturer. Um, it's, it's tough because we don't, like I said, we don't have the margins to throw a lot of money at research to show that it works. Okay. All right. Well, I get the real time limitations in the, in the financial limitations of small business. Trust me, I've been in small business my whole life going back to my grandfather's shoe store and the, you know, the sixties and seventies. So I get it. I mean, I, and I'm not, I'm not going to knock you for not, you know, throwing around capital to get research done, but you have to understand that that's a reasonable criticism. The gap is absolutely reasonable. And this is exactly why I spent the money this February

to start developing some real data. And we're actually going to continue that because the data is really interesting now that I'm, I'm kind of nutting into it. And I actually have you to thank for that because you hadn't got this interview going, wouldn't gotten me off my butt to really start new nutting into it. Well, I had to, I had to hack together the raw data to make sense of it. I couldn't just rely on it already being done. So, all right. I could be like, no, no. And I've got some, I've got some graphs. I found a package of, uh, uh, there's a company that was just acquired by Canva that, that does, that has a program. So I just really crudely, uh, took the raw data and we can show some screen shares of what, what that data is seeing. So, I mean, I would offer to you that this is like a big opportunity for you to participate as, as part of the research team, because you're the guy that's going to say, Oh, look at this. This isn't it. You got to have bidding and I'm not, I'm not scared to have somebody who has a different voice. I actually want that because if you don't know to, if everybody's saying, Oh yes, that looks wonderful.

You don't know to dot your eyes and cross your T's. Well, here. Okay. So here's what I'll offer up, right? You want to send me a placebo and actual Vespa that I can't tell the difference. I'll go down to my metabolic cart that I've got three blocks from now and I'll do whatever test design you want on it. And I'll do it within three days. I was going to offer you that and say, if you want to come do testing and do that, um, uh, you're welcome. I do that all the time. That's not a big deal. Um, okay. Let's so we, we've beaten around the bush with this pilot data a little bit, and I I'm glad, I'm glad that you're taking the right tone with this, that it's just very simplistic pilot data that you're gathering. In fact, you probably have a hard time even just saying data, right? Cause it's just numbers at this point, but I do take a little bit of time to explain to the listeners why you're being so cautious around it first off. And then also let's kind of go into the mechanics of how you're gathering that data. And then what initially you were, what initially you're drawing from it? Because once again, this is, it's not the first time because you've got to, you know, the graduate, uh, uh, work from St. Mary's, um, that, that exists, but it is of the limited information that exists around this product. It's at least something to grab onto. And I think we've got to, you got to start somewhere. We got to start somewhere. And, and there's, we'll, we'll, we'll nut into the data here in a second, but, but the reason I'm being cautious with it is frankly, I've got my BS in biology from UC Davis. I don't have a biochemical

degree or anything like that. And I struggled just to get out of UC Davis. I got hammered the first two years by the pre-med. You and I are the same way, man. I was solid C student on my best day. So yeah, I know that the first two years I had to take all the general coursework with the pre-med, pre-med students at Davis. And it was like getting slaughtered. So, um, and some of the people I run with like Bruce LaBelle, uh, he was like one of the top finishers in Western States in the early eighties. Anyway, he's, you know, he's a, he's a PhD biochemist. And then another gal I ran with Wing Roo, uh, she's a PhD, uh, in animal behavior. And then my former wife is a, is a basic researcher and gets her in her field. She, um, and it's plant pathology, soil science. She gets all her stuff published in top tier journals. And I've also worked with Steve Finney and Jeff Follick. So, um, I know what good science is and I'm not the one to do it, you know, in terms of experimental design, controlling the variables, all those things. It's like, that's why when you said pilot, pilot study, it's like, no, it's not a pilot study. It's just pilot data.

I had to cross that out like five times on my outline, pilot data, pilot data, because that's, you know, cause you know, enough to know how studies can be designed a certain way. And the stats, you know, the old saying about statistics, there's lies, there's damn lies and there's statistics. Um, so I know enough to know how, why I have to be very careful with this because it is what it is. And, and really most of what this is doing is going to, it's, it's providing a lot of insights for the athletes who've got tested and it's going to provide, uh, insights to athletes who want to look at it and it'll all be on the Vespa site next week. Um, next week. So we're, sorry, I didn't know I cut you off. I, uh, I'm always reminded of this cause there's a delay between recording that push out. So we're recording this April 28th. So it'll be out first week in May.

Yeah. Probably, probably before, or just as this podcast is actually coming up. Right, right, right. So, and that was my goal all along is to make, make all this stuff transparent, but just it's data. But, but as we go along, I want to do it. And when we talk about this data, I'll show, you know, we'll talk about some stuff and this is why we're going to be doing some testing. And, and in terms of scientific method, it's, it's, yeah, it's a little bit kind of sort of, and if we wanted to, you know, if I had a PhD and looked like a guy, I could probably fool a lot of people. Right. And thinking it's science, but it's, it's not, you know, there's, there's, I'm sitting there and looking at, well, what about this? What about this? Because you, you know, it's hard to control, control the variables. And that's, that's a big part of doing well done. Hey, listen, I get all that. Like, trust me, I've been in those situations a lot where we have companies come and approach us and want to use our lab to gather this type of stuff. And sometimes you do what the client says. And then sometimes you're like, no, this is kind of dumb. This is the way you need to do it and offer, you know, kind of counsel that way. And I get it. I guess what I'm trying to say is I get it. Cause I've been in that consulting role, not in a role where I own the product, but I've been in that consulting role a number of times where you got to get something on the board. And a lot of times you have to make kind of compromises or sacrifices for what would be viewed as a proper scientific method, scientifically controlled studies. So, so I get it.

Yeah. So let's kind of run through like just what you were doing with the athletes, a group of athletes that you kind of picked out that, that, that, you know, that you work with, what did they do? Well, this, you know, in my, in my hunting around for how we can get some testing done. One of the guys I work with a cycle coach named John Benson up in Flagstaff said, Hey, I was asking about getting testing done because as you know, I've got a pocket of athletes in the Phoenix Flagstaff area in, you know, Nick Curry, Jeff Browning, Peter Mortimer, and then Anthony Kunkel spends a fair amount of time in the Phoenix area. So I had these, you know, athletes who'd been on the program a long time. So, um, we organized in February to do it. And we had, we had actually up to nine or 10 people. Uh, but you know, like Michael McKnight, uh, he, he, he, he got COVID, right. He was coming down. So Jeff said, don't come down. And then the buddy he was going to drive down with from Utah, you know, of course, wasn't going to come down there. Right. Right. Ben light, Ben light didn't have COVID, but he wasn't going to ride in a car with Mike. Right.

So, um, this is what happens when you, this is what happens when, by the way, for all the listeners out there, this is a realistic story of when you're gathering initial information about a product or intervention, you get volunteers to do it just based off of goodwill. You're usually not paying them. You're running something in a very simplistic format with not a lot of money and it's easy for people to bail. I'd still trust me, man. I like that part of it. Is cat herding on a, on a high level, right? You're very, you're correct with that. Okay. So you're getting these, you're getting these athletes down there. So, so we, you know, we had like over, I think we had over 10 and it got pared down to six. So it was Peter, Jeff, uh, Anthony, uh, Nick and Lauren Curry, Nick's wife. And then, uh, we got Jesse to come out, Jesse Haynes from, uh, Southern California. Right. So we got, we got the athletes lined up. Um, and based on testing that Jeff had done previously, the couple of tests we'd done before and, and just knowing, thinking about what works and what didn't we, we designed a protocol like this, um, you know, like 20, 30 minutes before the warmup they did, they took a vest ball to concentrate.

Um, and then they did a half hour outdoor warmup at the facility. So just, just easy jog warmup. Uh, cause the data, the data I see, and once again, this is empirical data. I've kind of, I kind of look for at least a half hour warmup, uh, for, for workouts and everything else. Cause what we see in the data is what I call the switch where you were, you're really uprate, regulating your fat oxidation occurs around 32 to 33 minutes. So we do a half hour and that, and that's been corroborated by these athletes. They, they just feel this switch when you get this really sharp up regulation of fat oxidation. Um, so we did a 30 minute warmup and then got on the treadmill, uh, a couple minutes to, you know, calibrate, right. To make sure the machine's working.

And then, um, the, the, the treadmill was set at 2% grade, which simulated, I guess, flat surface. That's what the, we'd worked, worked out for wind resistance, but that's right. Exactly. So, um, 2% grade and six miles and six miles an hour, uh, speed. Okay. So your starting point is easy. The success starting point is easy. And it was four minutes. And then, uh, what was the data? Was it half, half a month, half a, so four minute, four minute stages. And you, I think that's immaterial. You increase the intensity. No, we increase the speed, right? So, right. So increase the speed up to nine miles an hour. And the problem we had was this particular treadmill would shut off at 10 miles an hour. Anything over 10 miles an hour would shut off. It would just, did you get a lemon or something? Come on. I don't know. I mean, this was what's available and they, you know, the, the facility was this really fancy facility in Scottsdale, but yeah, they had this janky and I'll tell you that it gets better actually, but it gets better, but it's, you know, you, you, you take lemons and make lemonade. I'll tell you that story later. But, um, so we have a great, you have a graded exercise test every four minutes. The speed is increasing miles an hour. And then after that we raised it 1% every four minutes till they tapped out. Okay. And you're taking, so, so that's an important part.

So it's volitional exhaustion, right? They have to jump off, jump off the treadmill, straddle treadmill, right? Right. It's not shutting down. I think that's, I'm going to bring that up in a second. You're taking gas exchange, right? Gas exchange. Yep. Anything else? Uh, we didn't take blood, no blood samples, no blood samples, no lactate. So no lactate, nothing like that at this point. And it was also my understanding. You can correct me if I'm wrong. You had the participants come into the tests fasted like from an, from an overnight fast. So they slept, this test was mid morning, I'm assuming. Yeah. Okay. What was that? Just because we wanted to control variables. Yeah. But you could just tell them to eat the same thing they always eat. Most of these guys do fasted. Remember we're in my world, Jason. All right. That's good. All right.

I'll take that. I'll take that. Most of these guys are, their normal training is fasted. They, they pop a Vespa and hit the, hit the trail or they have a coffee. So you're doing the same thing. Do what you normally do. Yeah. Yeah. Yeah. They might have a coffee. Like Jeff might have a coffee or something. Now, the other thing that's important to know is I, I purposely, because of the timeframe, we had to do this testing, I purposely scheduled things to rig it against Vespa because we did one test and then approximately 24 hours later, the second test occurred and you've done plenty of these tests. I've done a test or two of these. Everybody knows when you do a VO2 max test, you burn some matches. It, you know, it's, it's, it's not like, it's not the same as going out on it for a three or four hour trail run, but okay, hold on. Let's pause there. Cause I do want to bring this up. So you designed the intervention such that the control. So the non Vespa condition was the first test. And then 24 hours later was the Vespa condition, not placebo controlled, right? So they know they're getting, there's no placebo control. Yeah. Okay. At this point. Yeah.

So which is fine. I mean, you could probably get a placebo controlled it, but that's neither here nor there, but this contention that you're stacking the deck against Vespa, it's actually the opposite. So first off, how out of the athletes besides Jeff have done exercise testing before? Um, well, Anthony Kunkel was in the faster study. Oh, okay. So you got two of them that were in the study. Okay. Yeah. I think Nick, Nick's probably, Nick's probably done it, but I, Nick's probably done a VO2 max test. I don't know that for sure, but Jesse hasn't Peter hasn't. Okay. So I get, I understand the conventional wisdom that if you do two back-to-back VO2 max tests, can the conventional wisdom would say, yeah, of course you're worse on the second one, because the first one is hard and you're telling people to go as hard as they can. And then you're telling them to come back at the second day and go as hard as they can. Yeah. Naturally you would say in your words, they've burned a few matches, but the data is actually the opposite, particularly if all you're concerned about is, is, is VO2 max. And you can understand that particularly in nutrition intervention studies where they don't want a training effect to occur between test one and test two, they have to get the right amount of time between those two tests to not have a training or detraining effect so that the tests are fair across each other. And so, and so my point with that is, is research is kind of,

research is kind of like looked at this ad nauseum. Do we need to wait one day? Do we need to wait three days? Do we need to wait four days? And kind of the common one is you want to wait three or four days. Yeah. Yeah. And that would be up with that. Yeah. And that, and that once again, that's common, but if you really look into the data, you can see up to four tests in a day, in a single day with no deterioration in VO2 max, the staging might be different, but the VO2 max numbers will not be, but, but in addition to that, in addition to, hold on, hold on, I'm not done. In addition to that, particularly with athletes where the testing is novel, there is either a learning effect from one test to the next, because you know what you're in for. And you can imagine everybody out there can, you know, put their imagination hats on and think about this. You're going as hard as you can on a treadmill with all this gear hooked up to you that you've never experienced before. And you're asked to voluntarily jump off the treadmill when you think you're done. Anybody who's ever done that one time, once they get off the first time, they're like, shit, I could have gone 30 more seconds. And you've been around enough testing that, you know, that that's a common, that's a common piece of feedback. And we actually see the data actually play that out as well, where if you have somebody do consecutive tests, even in a day, they will either perform the same on the second test or even better. So I would, once again, you haven't published this, so now you can like take that information with what, what you will.

But this notion that the, that the way that you ordered the test was stacked against Vespa, I would, I would completely contest that notion, but you could have just switched it. Like you could have just said, you're going first and you're going, like you could have controlled that. So it's just like that whole piece of the, of the data collection. That's fair enough. And I think in terms of VO2 max, I'm not sure that there's a big change. I just think that, um, But even in the staging, because the athletes know what they're aiming at, right? So for the athletes who have never been through it, they, they kind of don't know. But then once they go through the test, they're like, Oh, I got to stage 10 or six miles or 10 miles an hour or what, like whatever it is, they have something to aim at, you know, competitive athletes, they want to always, especially now that they have, you know, the metrics to shoot for, they have some metrics to shoot for, but now they have an intervention, right? That's like, Oh, this is supposed to make me better anyway. So it's, so anyway, I mean, I would, once again, I would definitely.

And that's fair enough. And that's why, you know, that's why we have to do placebo controlled, double blind, you know, sampling so that people don't know whether they're using the Vespa or not and space out the, I think that spacing it out three or four days, um, is, that's a better product. But any, but anyway, I, I use that because I heard a couple of athletes bring that up, that the testing stacked against Vespa to which I was like, I've been around testing enough. That's not the case at all. In fact, usually it's the opposite. Whenever you bring in somebody for two consecutive tests, usually they're trying to beat their previous time, irrespective of an intervention or not. And sometimes you just do the test just to get the first one out of the way. Like that's just part of it. Right. So anyway, so let's get back to the fundamental piece. So graded exercise test first time around, there was no intervention. Second time around they had, they took a Vespa 30 minutes before.

What, what, what does, what the, what does the metabolic heart tell you? Let's see. Let's have a look. Do you want to have a look? Yeah, go ahead and put it up on the screen. This might be the first time I've seen it. I've just seen the raw data. So. You've seen the raw data. So let's, um, let me go ahead and hold on. Let me pull this up. Let's start with Jeff Browning. So Jeff Browning, he just did that grand Canyon crossing, cut the weather, right? Uh, this is okay. This is his first one fasted and he came into this pretty well conditioned and staying pretty low carb into the thing. Let me see. Can I pull this up? Yeah. So while you're resizing that for those of you on the YouTube version. So what you're looking at is a graph where the X axis is time and the Y axis is the metabolic data. It looks like you've got it kind of, I can't see it anymore. It just looks like it was the carb fat or the macrodutrient split, right? Yeah, there we go.

Right. There's your carb. He actually didn't cross over on the fasted test and his data is showing him burning. This is 1100, uh, K cows. I can't get the sizing to work for me. Okay. So this is 1100 kilo. Here's 1100 kilocalories right here. That's two grams a minute. Which is consistent with this previous test, right? Came on my podcast earlier. Right. Well, he wasn't, he didn't pull it that long for that long, but yeah, that's consistent with what, but this is faster. This isn't even faster with Vespa. Um, and he pushed it pretty hard, but Jeff and I were talking about this and he, he feels that because he uses Vespa all the time in training. It also helps him in terms of his level of fat absent adaptation now.

So hold on, hold on. What's remarkable about that? Um, well, well, I think these data points showing that he's pushing above two grams a minute for a pretty substantial portion of that test is remarkable. Once again, I'll give you a little bit of that, but what you have to understand, you have an athlete who's going into this fasted. And I think this is a point that I'll make it now because I'll make it across the board. Sure. Whenever you're doing exercise testing on athletes that are in a fasted state versus a non-fasted state, they're always going to burn more fat in a fasted state because they don't have carbohydrate on board.

I mean, that's been universally shown for, uh, for years. And as I indicated to, to just in the data that I have, I'm S when I see this, you know, quote unquote, remarkable two grams per minute, I don't look at it as that anomalous within an ultra marathon cohort, because there are a lot of ultra marathon athletes that go into these types of tests. And actually, now that I'm thinking about, I had Chris Roche, who you should be familiar with, uh, on my podcast a few weeks ago that has ultra endurance and ultra marathon data. That's, that's not quite a two, but, but, but indicates that people can get up that high in a non-fasted, non quote unquote, fat, fat adapted. Sure. I mean, I w I won't disagree with you because a well conditioned, well, aerobically conditioned ultra endurance athlete, they're going to burn fat by, because deep by default, because glyc glucose isn't going to, isn't going to do it, you know, entirely that there's no, there's no, there's no debate there. Okay. So this is, is just his baseline.

We'll call it that right. Baseline, baseline, you know, but he's burning, like, even when you go up here to the 1200, which that's around two and a half grams, that's pretty remarkable. And that's a, and it's not like he's, he's dipping down or it's just a peak fat oxidation. This is pretty steady. It's pretty, pretty steady amount of time. We're talking, we're about 22 minutes all the way up to when he taps out at, at, at 33, 36 minutes. Okay. So, so let me kind of rephrase the remarkable part of this because freshman exercise physiology students will recognize this as well. When you do a maximal fat, uh, oxidation test on a person, not that it's not going to be this intervention. It's going to be, it's going to look slightly different in terms of the intensities that they're going at. You see different curves, uh, emerge based on the subject that you are testing.

So most of those curves look like an inverted N no look like an N and inverted U. Sorry. I'm having hard time with the alphabet this morning, right? Where there is a P and this is what you're, this is what you're referring to, uh, Peter. There's a peak amount of fat oxidation at a particular point. And then once you continue to increase intensity, that fat oxidation starts to tail off and carbohydrate oxidation, uh, uh, subsequently increases, which you're saying to paraphrase it, that's remarkable is that you don't see that in that inverted U shape with Jeff. It just keeps going up and up and up and up. Is that a fair chemical reconciliation of that description? Yeah. And he holds it. And that's consistent with some of the other data we got, which we'll, we'll go through. But then we, we, if we go to data, uh, here with the fasted with Vespa, what's remarkable here is, you know, he does cross over because like I said, his, I don't think his VO two changed much, but his, his substrate utilization did. And part of that's from not being recovered from the first day is what I, what I surmise, but you'll disagree with me.

It's okay. We can, we can have different positions, but he also went, uh, a couple of minutes, two minutes, about two minutes fat longer to exhaustion, which, um, but once again, in terms of his output, it's, it's still, you know, very, you know, very high output. Is this, so let me ask you this, cause we're going to, since, since they're, since most of the people are going to be listening to the podcast version of this versus looking at the YouTube is this result similar across this group of a group of athletes, where when you compare the baseline condition, the baseline fasted condition to the Vespa condition, you see higher rates of carbohydrate oxidation and the crossover point start to emerge a little bit earlier, or is it inconsistent across this cohort where that's happening? There's, um, let's look at Anthony's cause he was probably the best, um, best, uh, condition. Cause he had just come off the, um, the Phoenix marathon a week earlier.

So that's his fasted. Uh, it's not up on the screen. I've got the data. Sure. Sorry. Sorry. It's all good. There we go. All right. There's his fasted. Um, then let's go ahead. So similar. I mean, I'm just eyeballing it, but yeah, very similar. Yeah. Yeah. But the crossovers also, you know, at a, at a, they're all crossing over like 85 to 90, low 90% of their O2 max. Here's the deal. Here's the deal. You're testing the Vespa condition, right? I mean, that's the thing that you're changing from athlete to athlete. So what I'm trying to, what I'm trying to pinpoint is, is not, not where the crossover point or how much, uh, of a particular substrate is being oxidized at any one particular point, but how it changes from the control to the intervention.

Yeah. And that's interesting because here's one of the things where this comes back to the whole lame, um, lame treadmill test. So, uh, I'll show you Peter's stuff here. This is Peter's, um, you changed more than on your, uh, on the, on the, I'll share it right now. Sorry. Sorry. Oh, all right. There's Peter Mortimer's fasted, um, treadmill test. Now what happened was, uh, okay. So what happened with him was when he went to do a second test, the next day he got to the nine mile an hour mark. And it's the, the moment they raised the gradient, the machine shut down. So we had to reschedule. So this I've had that happen before, by the way.

Oh, actually I'll tell you a better story. Uh, we were filming it one day and one of the cameramen kicked the plug out like right, probably one or two stages after threshold. So the athlete was actually going really hard and the machine all of a sudden came to an abrupt start and I had to catch him. And he was a regular size human being, like not a little wispy 130 pound person. Like I had to like come in and make sure he didn't slam against the, and luckily I was paying attention, right? But he was going to like literally take a step and slam himself and like face point against a wall, right? He would have hit the control board before we would hit the wall. But, uh, it was really bad. The camera guy felt awful and got an earful. So anyway, I feel your pain there. Yeah. Yeah. Yeah. So, so we had to reschedule. So this was taken the end of March, the 25th of March. So, and this was after he said his week, he'd done a big volume, big volume trail running training week. Um, so we got that training effect. Okay. So he wasn't doing anything high intensity to burn mitochondrial matches or anything like that. But when you look at this, this, so, and then the day before he took seven vials of blood, they took seven vials of blood.

So he was coming into this in good shape, but not great shape. And this is, this is the data we got from that. And yeah, but you could throw the comparison out. Come on, man. I'm just being honest. Oh, no, no, no. I'm just saying it's data. Two weeks later, two weeks later, big training camp in between vials of blood, just throw the data out. Like it's not even worth trying to compare. Right. But it's, it's, it's not worth comparison, but it's, it's kind of good to guide like, okay, this is interesting. What can we, what does this show that we can do to, to refine it? And that's, that's kind of where I want to take it. And that's why we're going to retest because, you know, this data, like you say, you got to start somewhere. And this data has given us some, some guidelines in which to do that. And, and it's also going to be shared with Dr. Marks. So we can kind of figure it out because he's got the same conundrum because he's using the Vespa and he's a mountain, he's an avid mountain biker. And he, he, you know, he's like, as a scientist, he's like you, he's like, I don't want to believe this is working, but it's working. And then he's trying to figure out how to do it. Cause he, now he's using it. Um, but his, you know, his science background is like, this isn't supposed to work, but so let me help the listeners kind of understand this is you now have some, some data, and this is probably the most robust data that exists on a Vespa intervention. What does it initially tell you about how the product affects a human's

physiology? Like how, like, cause you can see some of it in the respiratory data, like in your, in your eyes, what can you glean from this? And I mean, you could even turn that into a pitch, like, Hey, listen, we did this with this small group of athletes and this is what we saw. Yeah. So from the pilot data from St. Mary's from this pilot data, um, from the stuff Jeff's done before, you know, we're seeing, you know, increases in VO2 max time to exhaustion, um, real high rates of fatty acid utilization. And, and also like with these tests, except for Jesse Haynes, who had some variables in there that influenced everybody went to a greater time to exhaustion on the, on the treadmill test. And that seems to be, be corroborated by the data that Dr. Marks had, um, when he began the data collection. Yeah. So that, okay. All right. So that fair, I mean, fair, like I said, if you, that's consistent with the, the, you know, the empirical real world, uh, evidence, you know, that, that athletes are seeing and the, and the results in their races are showing, but needless to say a long way to go in terms of the, in terms of the research. Sure. But I mean, you can't argue with the results that some of these athletes are getting.

I mean, you know, especially a guy like Jeff, who's older, um, and Peter, I mean, Peter won hurt this year and he's, he's a big guy and he's 40 years old. So the, the, you know, these aren't the young fast guys. Um, so I think that there's some validity in that. Well, I, and I'm first, first off, I'm all about performance and if athletes are performing, I'm a happy person, right? That's how I make my living is getting athletes, silver buckles at Western States and, you know, get them to qualify for the Boston marathon and win races, kind of whatever is on that, uh, whatever's on that continuum. But there's a lot of different ways that you can justify performance or increases in performance. And sometimes it's good athletes. Sometimes it's good training. Sometimes it's nutrition intervention. Usually it's a little bit of all of the above. And so whenever, whenever, whenever there is a case of an athlete did this and then achieved that, and you are essentially giving credit to whatever the intervention is, I always say, wait, wait, wait, hold up. Performance is always a multifactorial phenomenon and it is, and it is never due to one specific thing. It's due to a lot of specific things adding up, but never one specific thing.

So I agree with you that we can't ignore performance, but I will not take it as far as to say that this is the catalyst or the only catalyst. And I think that you would agree with that as well. There's a lot of training and a lot of talent that goes into it also. Absolutely. But I think Jeff Browning story is a pretty good way to highlight it because when he came to me in late 2014, Zach said, you need to talk to Peter because he was struggling with his GI stuff and race stuff. And, you know, the addition of Vespa and OFM has been, you know, you know, basically resurrected his career and got him. And he's, you know, he's just, he's just consistently performed well. And, and, and Nick Curry's seen the same sort of things by, by adding these interventions and, and to, to your point about, it's not only a thing, one of the first things, you know, if I was just here schlepping Vespa and that was my only goal was to schlepping Vespa, I would have never gone down the rabbit hole of developing programs that took fat adaptation to another level because it's, it's not, you know, Vespa is Vespa a great tool. I, you know, the more I work with it, the more impressed I am with it.

Just from an honest thing, it's just, it's, it's, it's amazing, but it's not the only tool carbohydrate restriction at certain times to get certain adaptations is important. Carbohydrate use is important. You can't, you can't just do one training modality. You know, a lot of people in the gym or the CrossFit thing, you know, they, they, they poo poo aerobic endurance training. It's like, no, you got to do that. But at the same time, you got to do resistance. You got to do intensity interval training and tempo training. You're, you're absolutely right that there's all these things. And, and that's what we try to work with here at Vespa is how do we incorporate that in, in a way to get that, those synergies to not just get performance, but, but long-term health. Cause one of the things that, that, you know, that I saw early on, cause the only people like some of the early adopters were, were pukers. Sure. Um, like John Olson and Jenny Capelle. And, um, you know, that it, it literally turned them around. But when I started looking in the physiology of that, it's just like, you know, I'm not, I'm not against using carbohydrates when you need them, but if you're just using them all the time, it just can turn into a mess. Well, I'll, I'll get, I'll give you the last word, but just to, to kind of wrap it up, here's where I, where I've come to, to things I'm surrounded in anecdote. I have athletes and even myself go and experience things that I can't explain. I trained good on one day and this

happened. I trained bad on another day. And I have that wealth of experience from 20 years of coaching of all of these athletes and all the interventions and all the nutritional trials and things like that, that, that, that I've tried. I could go any direction with any of those anecdotes as, as, as I can. And some of them I try to try in some of them I explore and I, and I incorporate with athletes and then other ones I do not. And the, the key difference between those two, the anecdotes that I think deserve a little bit more fleshing out and trial trial and error with athletes. And the ones that don't is if I can tie it back to a specific mechanism or there is physiology underpinning what that athlete is actually experiencing and best if there's research actually underpinning. And what I'll say with Vespa specifically, and we'll leave OFM for another three hour podcast, but I'll say with Vespa specifically, and I think you admit that, that those three underpinning things that I'm looking for just aren't there.

And they're not there. They're not yet, but yet, but there we go. Right. Right. But, but, but here's the great thing for this, this audience. I mean, this is, this is ground zero. I mean, we're, you know, I think ultra running prides itself on being sort of boundary pushing. Right. And so, but you get the last word. So if that's the last word, it being ground zero, great. I'll take it. And maybe 20 years from now, we'll be at like level one. And the last word is at this point is those underpinnings aren't there, but you know, like I said before, science begins with observation and that observation has taken place right now. We've got that observation to the point where we've got so many real world empirical data points that this begs to be looked at. And, and, and to a point you're, you're, you're saying we got to look at this and we got to start researching it because, you know, it's, it's so different from the normal course action that people have just sort of said, Ooh, what is this stuff? So, I mean, I, I understand the skepticism, but at this point, when you look at how well people are doing, particularly the older athletes, you know, it, it, it should be an, and I hope that we can do that. And, you know, where can I send you some Vespa? I'll, I'll send you my, my physical address later. I'll take you up on it. You want to send me a placebo and Vespa? I'll go with Dr. Marks and see if we can get that mixed up. Yeah. I'm, I'm totally, I'm totally game for it. We can connect with that after the fact.

I appreciate you coming on. You are a good sport about it. You know, like I said, there's a lot of people that I reach out to that I want to have a civil conversation with that just tell me to F off and that's their right to do it. But, um, uh, I, I honestly do wish that something comes out of this one way or the other. Right. I do hope that you explore more of it. And I do hope that we have some more definitive things to talk about. Yeah, no. And I think we're in this because we're passionate about it. We're certainly not in it for the money and the ultra running sport. Right. And so, so, you know, it's an opportunity for you to be part of, part of this change, you know, uh, like I said, you know, I need people to, to show, tell me I got to dot my eyes and cross my T's. And, you know, those eyes and T's are the, those underpinnings you're talking about. And we're trying to work towards that, but you know, my, my bias is towards working with athletes and getting them results and enjoying that. And then just thinking about, uh, what's the underlying physiology, what's going on here, what's going to, what are the implications for long-term health? Um, and, and so that's, that's where I'm coming from with this. And, and so, you know, we'll just kind of try to move it forward with this. Well, I appreciate it, Peter. Like I said, well stated.

And, uh, I look forward to not only seeing these results, which will probably be on your website by the time this podcast comes out, I'll give a link to that. But also if there's any information on any of the studies that are coming up, I'm happy to put those in the show notes as well. So if you kick those, yeah, we'll continue to do this. And I'm sure as we develop this, we'll, we'll, we'll have other conversations. Cool. Thanks again, Peter. Appreciate it. All right. Thank you. All right, folks, there you have it. There you go. Much thanks and a lot of respect to Peter for coming on the podcast today. Um, I always give a lot of credit for people who come on this podcast and know that they're going to face a reasonable amount of pointed criticism that really comes from an area where I'm just trying to understand these things just like anybody else out there. So ton of respect for Peter for agreeing to do this interview. As I mentioned during the podcast, this is an intervention and it's a nutrition product that is extremely difficult for me to recommend as a coach.

Whenever I get these things fly across my desk and I do so numerous times throughout the week, I always take the standard run of show. I want to know what's in the product. I want to know what the effective doses are. I want to know what the mechanism, what the mechanism or potential mechanism of action is. And I want to know what the literature says about applying these interventions to athletes. And this is a case where I don't have any of those. I don't have any, anything across those four steps. So it's very hard for me to wrap my head around it and actually recommend it to athletes in order to potentially improve their performance. But y'all are grown adults out there and you can make your own decisions. You can go to the, you can go to the website, you can go to Vespa's website and look at the information that they have there. You can take the information from this podcast, glean from it, what you may and make your own decisions about it. That is it for today, folks. I appreciate the heck out of each and every one of the listeners. And as always, we will see you out on the trails.