 In this episode of the BFR Better for Results podcast, we sit down and talk with exercise physiologist Evan Pykon, who is the co-founder of the NOx device, the first device to be able to reliably and accurately measure nitric oxide release within the muscle. We have an in-depth chat about the importance of measuring nitric oxide, as well as its implementation in an exercise program. We also get pretty nerdy about discussing the mechanistic reasons behind this and how we can leverage this technology to provide better results for our clients and patients. I hope you enjoy the episode. What's up, what's up, what's up, what's up, what's up, everyone? How's it going? Welcome back to another edition of the BFR Better for Results podcast with me, the Human Performance Mechanic, and today I am having a treat getting to talk to Evan Pykon of the NOx and the NOx is something that I'm interested in, because in my research, I'm looking to understand what's happening in the peripheral system regarding oxygenation and nitric oxide and things like that so it can help correlate some of the fatiguing effects of BFR. So I'm very interested for this conversation. We did talk offline briefly, but now I really want to get into it in today's episode to see if this technology might be something that could help you or your athletes, if you're a coach, to optimize programming and performance and everything in between. So first and foremost, welcome to the podcast, Evan. You want to just give like one or two minutes background of who you are, why you're interested or have gotten interested in the NOx, and anything else you find relevant, and then we'll just dig right into your work in the NOx. Absolutely. So first, thank you for having me on. Like I said, my name is Evan Pykon. I spent about seven years working with professional athletes, sports teams, and military. I was previously with training think tank where I was a strength and conditioning coach. I did a lot of their onsite physiologic testing. And then about two years ago, I transitioned out of coaching, consulting full-time, and now I'm a co-founder at a startup company called NOx. So what we do at NOx is we've developed the first and only device that could noninvasively measure nitric oxide levels in your muscles in real time. And we also measure muscle oxygenation. So the reason we got interested in this is, you know, in school, we learned about the respiratory cycle. You breathe in oxygen, you breathe out carbon dioxide. But what most people don't appreciate is that there's actually a third gas in that respiratory cycle, which is nitric oxide. And that's what actually controls the delivery of oxygen to tissues. Now, before we developed this technology, you could measure oxygenation levels in large blood vessels with pulse oximetry, the type of technology that you would have in an apple watch or a loop. You could also measure oxygen levels deep in working muscles with other nearest technologies. You can even measure carbon dioxide if you wanted to. But there was never a way to measure nitric oxide noninvasively and in real time. So what we wanted to do is close that gap and enable people to do that by creating the first device that can measure all of the relevant gases in that human respiratory cycle. So why hasn't there been a noninvasive way to measure nitric oxide before your device, you know, got manufactured? Yes, so the short answer is people were trying to develop this for a really long time. And us being able to do that was really a handful of different factors coming together. One, the technology that goes into different hardware advances very quickly. So it's more than likely that 10 years ago, even if the same team that I was working with tried to build this device, just wouldn't have been possible. So there's just right place at the right time. And it was also having the right people involved with this project. So my team was lucky enough to work with Dr. Jonathan Stammer out of the Harrington Discovery Institute at Case Western, who is a world leading expert on nitric oxide and specifically the form of nitric oxide that we measure. We've also had really amazing experts in bio-optics that were willing to work with our team early on. So it was really getting all these different key players from different fields that were willing to collaborate, be open-minded and explore this new opportunity that allowed us to make this possible. So tell us then about, you mentioned nitric oxide being exhaled as that third gas. Why, what is the function of nitric oxide from a macro perspective and a micro perspective? And you mentioned that you have a specific version of the nitric oxide that you're tracking. Why are you tracking that versus other, versions of nitric oxide? That's a great question. So yeah, like you had said, you can measure nitric oxide through exhaled gases. That's actually not the form that we measure. So up until this point, people hear you can measure nitric oxide through breath, you could put little sticks under your tongue, which between you and me don't actually measure nitric oxide. But nitric oxide is kind of a technically confusing term because when we say nitric oxide, there's really many different forms of nitric oxide in the body. So my team specifically measures the form that rides on red blood cells. The technical name for this molecule is S nitrosohemoglobin or snow hemoglobin. You can imagine why we just use the term nitric oxide. You're not gonna get a lot of SEO on hemoglobin. So really the way that the system works, most people are familiar with nitric oxide released from endothelial cells. And this is really working at the macrobascular level, so in large arteries. So if you were to squeeze your form and start to restrict your blood flow and then release, blood is gonna rush back into that limb and it's gonna press against the walls of large blood vessels and that's going to stimulate the endothelial cells to release nitric oxide. Now that form of nitric oxide is more responsible for controlling bulk blood flow through those large vessels and then doing things like lowering blood pressure. Great for health. The problem is, is that that form of nitric oxide is very short lasting in blood. So if there's a red blood cell passing by that nitric oxide, that red blood cell is gonna scavenge it up. And when that red blood cell travels back to the lungs through the pulmonary capillaries and it releases its CO2, which you breathe out and it picks up oxygen, that nitric oxide is gonna move to a different site on the hemoglobin and it's gonna transform into this active form of nitric oxide, snow hemoglobin. This is the form that, again, knocks measures. Now when that red blood cell goes and travels throughout your body and eventually it's in a small blood vessel, the red blood cells get a sense how much oxygen is present. The oxygen levels in your tissues are high. You know, nothing too interesting happens. Oxygen levels in your tissue are low though. That nitric oxide molecules get a release, which is going to dilate the small blood vessel, get you more blood flow and oxygen delivery. So what we're doing is we're measuring that process of nitric oxide being released in small blood vessels, which is what controls blood flow and oxygen delivery to your muscles tissue. So that's what makes this type of technology so interesting. It's allowing us to peek into your muscle and see a process that no one has ever been able to observe before. So with that, what do you expect to see in a normal like training cycle? So our training sessions. So we start out, we're fresh, we now are doing, let's just say, let's standardize it according to like a max effort, a max effort aerobic type sprint. What patterns would you see in the nitric oxide as time goes on? And from a training perspective, say we now took that test and then we did eight weeks of training. Well, number one, how could you use that information from the max test to then help with programming to optimize the results there? But then two, what would you see or what would you expect to see in a nitric oxide plot post-training? Yeah, so importantly, we're measuring time series data. So throughout a training session, you could observe your measurements in real time. So let's say on that first day, you're doing your performance assessment. The second you start exerting yourself, you're gonna see oxygen levels in your muscle declining. Now, deoxygenation in the muscle is the trigger for nitric oxide release. So when you start exerting yourself, you're utilizing oxygen in the muscle, you're immediately gonna see your NO levels increase in. And one of the really interesting things that we see is let's say someone is doing a 10 minute assault bike or an echo bike for maxcals, they're pushing themselves, the oxygen levels and their muscle are lowering, the nitric oxide levels are increasing. Now, at some point, if they keep pushing themselves, those nitric oxide levels will likely flatten out. They're not gonna be able to just increase the blood flow and oxygen supply to their muscles indefinitely. When that happens is when things start to get pretty intense. So that's one of the things I'm looking at. How long could you keep increasing your NO levels for? How high could you get those levels? And how long before, you know, you reach volitional failure, do those plateau? What we see is the best athletes could effectively keep increasing their NO level until the point of volitional failure during a workout. What that's telling us is there's some kind of limitation that is not related to their ability to get oxygenated blood to the working muscle. Now, there are other athletes where those NO levels will flatten out earlier. That could be a cardiovascular limitation or even in kind of untrained athletes, you often see they just can't really even utilize oxygen in their muscles that well. As a result, you're not gonna see very large increases in oxygen. So one of the things that you could do on that first day is try to identify someone's physiological limitation. So if we're thinking about something like a VO2 max, it's the maximal integrated capacity of the pulmonary system to uptake oxygen, the cardiovascular system to transport it to your muscles and your muscular system to utilize it. We could say which one of those three systems is rate limiting for you? If your cardiovascular system is your limiting factor and you spent eight weeks training to improve your muscular system's ability to utilize oxygen, you're probably not gonna improve your performance. So that's kind of the first component of how do we use that to guide training? Well, we identify your limiter. Now we know what we should be targeting in your training. And then in the subsequent weeks, we could use this data to guide your training in real time. We might say, Hey Nick, I want you to do a maximal steady state session on the Echo Bike today. Well, you're like, how do I do a maximal steady state session? Well, we have you hop on an Echo Bike, increase your speed. You know, your oxygen level might stay flat initially. When you start increasing your speed and you're outstripping your body's own oxygen supplies, you're not at a steady state anymore. So we just find the fastest pace you could hold without your oxygen level changing. Then week to week, we could do things like see how your body's responding to exercise. If you do like four minute assault bike intervals today at 400 Watts, and then you do that same session next week, keep the wattages the same, the rest periods, everything. And we see you're not utilizing as much oxygen on that second week. You've improved your fitness or efficiency. Great. Now we know you have more runway for progressions. There's a lot of ways that we could use this in a very dynamic training program to guide your progressions, guide specific sessions. You name it. That's super exciting because I think a lot of us working in fitness or even rehab get trapped in looking at these macro perspectives, these like not super specific ways to assess some sort of functional outcome. For what I'm hearing, this is almost like, this is the future because you basically have just said that your assessment or your ability to evaluate an athlete, you can look at what are their limiters. And instead of like the default would be, oh, you just need a little bit more cardio or more steady state or whatever that is. You build up more volume, add a little, mix it up, have a little intensity here, a little more steady state here. The assessment process, and I guess that is probably gonna be the most interesting thing in general is how are you differentiating the different limiters because I, and does the NOx help you identify each of those particular limiters because I think that, again, if we can become more specific in our evaluation processes using technologies like the NOx, then that can help elevate the entirety of performance athletics. Yeah, yeah, definitely. So yeah, to answer your question, you can use the technology to identify those limiters and a lot of this is just making the training process simpler. So when we're talking about this, some people might be thinking like, wow, this sounds really complex. My opinion. Oh, I know that. I know that people are doing that because that would be my reaction is like, oh my gosh, like we have guidelines. The big thing just to get slightly, you know, off topic is people want protocols. They want, a lot of people are very challenged in principle based application. Meaning like if you understand this adaptation and you understand this stimulus can promote that adaptation, you can then happen to this stimulus more to produce this adaptation. People just wanna say, oh, well just tell me exactly how many sets and how many reps I need to do. So adding some sort of technology. I mean, even in this, in my own practice as a physical therapist, recently integrating force plates, right? Like that to me, I'm still wrapping my head around a lot of the implications of that. So I can only imagine now with the likely disconnect between some of the cardiovascular stressors, like and the response to those stressors with nitric oxide release, that could be considered pretty complicated and being like, oh, wow, I have this data. What can I do with it now? Yeah. Yeah, I think initially it can make things a little bit more complicated. But I think once you get past that initial hump, it makes things so much simpler. Because for example, like anyone that's been involved in training for a long time, particularly, you know, when you first get into training you're looking at protocols online and there's a lot of paralysis by analysis. And I think everyone has the experience where their friends like, hey, I did this program. I had phenomenal results and then you go do the exact program to a T and you're like, man, that was shit. I did not get any improvements in, you know, the reason that you didn't get improvement is your physiologic system is different. No two people's bodies are the same and no two protocols are gonna impact people the same. So when we have these ideas that this is a protocol for muscle hypertrophy, this is a protocol for you name it. I'm not gonna say it's untrue, but it lacks a lot of context. So what we're doing here is taking a lot of the guess work out. If you want to improve any variable strength, hypertrophy, endurance, there's thousands of potential protocols that you could do. So what this allows us to do is just say, just pick one, take an educated guess. It really doesn't even matter what you pick initially as long as it's not absurd. Just pick one, do it, see how your body responds, and then tweak the protocol based on the response. So if I'm thinking, hey, this is a protocol that's gonna be great for muscle hypertrophy for me. And I put the device on and I go to lift away and I'm like, oh, I actually didn't deoxygenate that much. It's probably not gonna be great for hypertrophy. So for some people, you might see that effectively whatever they do is gonna be great. They go really high reps, really low reps, different exercises and they completely deoxygenate the working muscles on all of those. You're like, that's the person who kind of gets jacked no matter what they do. But for people who are hard gainers, you might see that, wow, they go over 15 reps, 20 reps, they just lose tension and they just can't deoxygenate their muscles. They might respond better to something in the sub 10 rep range with heavier weights and longer rest periods. So you could get as granular as you want, but you could also make these things relatively simple when you're starting out too. Yeah, I mean, I think for me in general, just given the, you know, and it's nice that you talked about hypertrophy because that was kind of the area where I was like, basically for me, for the most part, as long as you exert yourself significantly, you're gonna create an anabolic stimulus. But there are those people where it's very difficult for them to gain. And whether that's their internal leverages, whether that's their nutrition as well, because that's important. But it's interesting that you said, like with hypertrophy, so you're, when you would put something on for an evaluation, because again, the existing body of literature is basically relatively conclusive that it doesn't matter what weight you use in free flow. BFR is a separate story or blood flow restriction separate story. But generally speaking, 30 to 40% of the one rep max all the way to 80 to 85%, as long as you exert yourself on a set-by-set basis, you'll get equivocal hypertrophy. Strength, obviously different. More specificity, XYZ. So with your hypertrophy and a stimulus there, when you say like certain people, like just don't deoxygenate past a certain level and they're considered quote unquote hard gainers, like what does that actually, does that just mean that they're probably very type one dominance? So they're able to shift really the relative workload to the type ones versus the type twos that really are the ones that are gonna grow? Yes, so this is where getting mechanistic we're a little bit in the realm of speculation, but this is where even starting with that idea of like the 40 to 85% rep range being effective for hypertrophy, that's a statistical average. So for any individual, a range might be 20 to 70% is ideal or 60 to 90%. I mean, that's relatively intuitive that it can move back and forth. One of the things that we've seen, and again, this is anecdotal, but this was a lot of the work that we were doing at Training Think Tank back in the day is we found people that have those cardiovascular limitations tend to be able to respond pretty well to hypertrophy training effectively in any rep range. We tended to ear on the lower side, maybe like a 30 to 80%. I'll get into that in a second. So we for the fact that for these individuals doing a lot of heavier volume would just get them injured, but people who tend to be higher tension, their cardiovascular system is rate limiting for them, they will generally occlude at lower percentages of their one rep max. So whereas for someone whose cardiovascular system is very well-developed, they have less sympathetic nervous system tone, they might not actually occlude blood vessels till 50, 60% of a one rep max. So anything under them that they're just not going to be able to deoxygenate to the degree required to increase peripheral fatigue, increase motor unit recruitment and ultimately get mechanical tension. Or someone who's occluding blood vessels at 30% of a one rep max is going to be able to deoxygenate. Ultimately what we're trying to do with hypertrophy training is get mechanical tension. Well, to get mechanical tension, you need peripheral fatigue. To get peripheral fatigue, you need deoxygenation. It's the oxygen conforming response. So as a rough guideline, what we're looking at is is the person deoxygenating maximally? If not, it's probably not gonna be an effective stimulus. So for most people, we're earing somewhere in the middle of those bell curve percentages. The intensity tends to be relatively intuitive. I think where most of the individualization will come from is the volume. So what you'll see is a lot of people, there's that research factor range of six to 12 sets per muscle group per session is optimal for hypertrophy. You're like, that is a giant range. If you're using a three time per week frequency, that's a difference between 18 and 36 sets for a muscle. Those are not even remotely comparable. So what we tend to see is for those people who are not hard gainers, they'll deoxygenate the muscle first set, second set, third set, maybe towards that fourth set. They're no longer deoxygenating the muscle to the same degree. Now this could be peripheral fatigue impairing deoxygenation. And where is that deoxygenation getting impaired? Do you mean like muscle? Yeah, like so you're saying like they deoxygenate, they deoxygenate, they deoxygenate and then they can't really deoxygenate anymore. Where is that limitation happening? Yeah, so if it is small muscle mass exercise, we could effectively eliminate the possibility that's anything like a cardiovascular limitation. So some of the possibilities are peripheral fatigue. So they're actually not getting as much motor unit recruitment. So they're not recruiting the muscles, not deoxygenating. That's one possibility. Another is that they're accruing muscle damage very quickly and that's going to impair oxidative capacity in muscles. So those are probably two of the most likely causes. Yeah, let's just before you go on, let's talk about the difference. Cause you mentioned, so people think of like you're speaking my language, I understand it. And I know that my audience is on the more educated side and nerdy side, but I still think we should differentiate between something like a central fatigue. Cause if you said peripheral fatigue, then there has to be some, some centrally mediated fatigue. Kind of just briefly talk about the differences between the different types of fatigue and why peripheral fatigue might be something that we're looking to induce in a resistance training program. For me, more importantly at light loads, but why would we look to induce peripheral fatigue and look at that as a marker versus something like central fatigue? Yeah, so very quickly, a lot of times in the strength training world are uncrossed at people. So like I pulled a really heavy deadlift, my CNS is fried, is there rough heuristic any time you hear someone say they have CNS fatigue without talking about his peripheral muscular fatigue. So that would be the easiest way to think of it. Like you just pull the five or at max deadlift, you feel exhausted, you have peripheral fatigue, not central fatigue. Really unless you're working with like ultra marathon runners or populations doing extremely high volume, you probably never have to worry about central nervous system fatigue to any real degree, particularly when we're dealing with strength training, it tends to be pretty hard to centrally fatigue yourself. And that tends to recover relatively quick. Peripheral fatigue would be that the actual fatigue limitation is in the tissue. So you have deoxygenated the tissue to such a degree that you cannot continue working, you cannot get blood to that muscle anymore, you're getting impaired motor unit recruitment, those are the types of things that we're talking about here. Yeah, I mean, I think for me the central nervous system fatigue for the most part is something that happens with prolonged duration of exercise. And the reason why I have kind of gotten into the fatigue literature and understanding fatigue is with light loads, contrary to what your example was, right? Where it's a fibric max of deadlift. You're actually not inducing central fatigue in that regard, because the duration is pretty low. But if we continue on with that and we start to, there's thoughts that the longer duration exercise increases inflammatory myokines that get released that impede motor unit recruitment. Then we also have with the lower loads with the BFR in particular, we have this unpleasant sensations that then ultimately circle back into the brain and the brain then has to overcome those perceptions of discomfort. And the exertion required to maintain motor unit recruitment. So then that kind of comes down. So that the thing with the hypertrophy is you want to induce peripheral fatigue to an extent that's going to give you the stimulus. But then you ultimately don't want to do too much because then you're going to impair the processes and potentially distal muscle groups. Because if it's all centrally mediated, then you might have an impact on other muscle groups. I just wanted to clarify that for the audience because yeah, I mean, this all stuff is super cool with the monitoring. So let's then, let's talk, unless you have anything else to say regarding the limiters, prescriptions or whatever, I do want to get into your abstract that you talked about and what with that we talked about prior, which is in medicine and science and sports and exercise. I think this was the, what the ACSM, the ACSM like a conference poster. But I definitely do want to talk about this because it kind of gets into, you mentioned it before about small muscle mass versus large muscle mass and what that does to deoxygenation. So please just tell the viewers and the listeners about what your conference poster presentation was. Yeah, absolutely. So where this all started is going way back to the beginning of this. So one of the other authors on this paper was Brett Kirby from Nike Sport Research Lab. So originally I saw Brett present maybe six years ago, seven years ago at this point on using muscle oxygenation measurements to predict time to exhaustion in real time. And at the time they were using that for part of Nike's sub two hour marathon project where they were trying to get L. U. Kipchogi to run the sub two hour marathon. Now I started using some of those same methods at training think tank a few years ago in at some point we got to the point where we could predict time to exhaustion real time on cyclic exercise pretty accurately. So that is to say if I had enough data on you I could put a Moxie monitor at the time in your quadricep have you row and I could say in real time you have four and a half minutes until you're going to reach failure. You have seven minutes if you slow down now you sped up you have three minutes. But one of the things that I started to notice in the athletes that I was working with is depending on which leg we put the device on those models may or may not be accurate. So if you were perfectly symmetrical same injury history on both legs our predictive ability great either way but let's say you had an ACL surgery on your right knee five years ago and we have a device on your right leg in your left leg only one of those legs is accurately gonna predict your time to exhaustion. Well that's obviously a problem when you're working with the lead endurance athletes. So I reached out to Brett from Nike with the idea that hey what if we had a way of screening someone at rest to figure out which of their legs is going to be predictive of work capacity or if both legs are the same which in that case things are really easy. So we came up with this idea that well what if we do an occlusion assessment with BFR cuffs? So you pump up the BFR cuff until you get an arterial occlusive pressure and you have a nears device on a working muscle downstream of the cuff and we see okay in a five minute period where you have this BFR cuff cutting off your arterial blood flow how much could you deoxygenate that limb and then when you pull that cuff off how quickly do you reoxygenate that limb? And could we predict work capacity from that? And imagine if you do that on both legs simultaneously and you get the same result on both legs it tells us well if you use either of these legs for these performance predictions you're all good. You have a lot of asymmetry between legs that's where things get kind of funky. So that's where we started out. Turns out you could predict performance really well with just cutting off someone's blood flow and seeing how quickly they reoxygenate. So what we wanted to do is say well how does this apply on small muscle mass exercise versus regional exercise versus whole body exercise? So the way that this experiment works I think the sample size was 10 or 12 people mixed sex performance abilities in this study. So first what we did is we had everyone just in live supine. We put a nears device on their form and we put a BFR. It's a knee edge, I need to cut you off. So the one thing that you said that I wanna just briefly talk about before you continue to go through is you're mentioning nears, you're mentioning moxie like and then nox, right? So talk about the differences between them, the similarities so we can then give more context to the equipment that you're using. Yeah, that's a great idea. So moxie was one of the earlier generations of what's called a nears device and near infrared spectroscopy device to measure oxygen levels deep in muscles. So at the time when I was working at Training Think Tank this goes all the way back to almost six years ago, seven years ago, when we first wanted to start measuring oxygen levels and tissues we were using a moxie monitor. That was kind of the state of the art at the time. The difficulty with that type of instrument is you could only stream data to a laptop. So there's old Training Think Tank videos you could see me like walking around the gym with a laptop with all these squiggly lines streaming on the screen while we're testing athletes. It was also a little bit difficult to analyze that data. You need to export CSV files and actually had to learn how to code just so I could analyze data that I was collecting. Nox is a startup company that I founded now about two and a half years ago. So Nox is what we call like a second generation nears device. It also measures muscle oxygenation like a moxie in addition to other measurements. So the Nox wearable measures nitric oxide levels in tissues. It has accelerometers in it so we could measure movement. It could measure skin temperature, all different factors. And importantly, we really streamline the data collection analysis. So as you're recording data, it's streaming to your mobile phone in real time. As soon as you finish a workout, all of that data automatically goes into a platform online where you could easily analyze it. So this specific study that I'm talking about now, this was done with a moxie. Even though the paper was published in the recent months, we actually did this project about two years ago. If we were to redo it today, I would do things a little bit differently. I would also want to measure. As every good scientist would agree, you go back, you look at what worked, what didn't work, and then the questions that you've gotten from that, which is again, why we're collaborating with this project that I'm going is because I'm looking at like, okay, we need that secondary data to be able to say how is the fatigue process changing? And for background for everybody, we're going to be looking at different BFR cuffs and how they fatigue out and looking to see can we quantify potentially blood flow, but certainly muscle deoxygenation and other things that Evan has kind of been talking about the entire podcast. So that's what excites me about this whole process is just learning about the capabilities and what we can do. So sorry, continue on now with your project now that we have some contacts. Yeah, definitely. So yeah, with this first part of the study, what we did is we had, again, I think it was N equals 10, so 10 different people, we had them lay supine, we put a BFR cuff on their upper arm and we pumped that BFR cuff up to an arterial occlusive pressure. So everyone was wearing pulse oximeters. We confirmed that it zeroed out the reading when you cut off your arterial blood flow. You don't have pulse anymore. So pulse oximeter is going to say nothing whatsoever. Nothing, yeah. So pumped up to occlusive pressure and at this time we were using Moxie monitors. They were on the form on kind of like the flexor digitorum profundus, a kind of inner portion of form. And we just had them sit there for five minutes with their blood flow restricted. Now during that time, we were measuring the oxygen levels in their muscles. So most people, they're starting around 65, 70%. We're seeing how low does that go. Some people get all the way down to 10%, some people 20 or 30, after that five minute period. Oh, from five minutes, yeah, okay. After five minutes, we released that cuff pressure and then we just keep monitoring for another two and a half minutes. And then afterwards, we would process that data and we would say, okay, during that two and a half minute period, after we removed the cuff, what was the rate that you could reoxygenate your muscle? And that's a percent per minute measurements. So what we did is we got each person's reoxygenation rate. Then on a separate day, we had these people perform like a work capacity test with a hand gripping device. It was kind of like a modified grip guillotine type movements and we would get performance data on that. It was kind of like a critical torque measurements that we collected. And what we found is we had in this study, we had like 110 pound females all the way up to 230 pound male power lifters, really wide array. When we controlled for muscle mass, that rate of reoxygenation was almost perfectly predictive of work capacity on that gripping task. That is to say, whoever could reoxygenate the muscle quickest had the best work capacity gripping. I think the correlation was like a 0.95 even. It was something, wow. So we're like, okay, it's very clear on small muscle mass exercise that your ability to reoxygenate the muscle is a very strong predictor of performance. That makes sense. It kind of recapitulates, you know, 30 years of cardiovascular physiology. So next, we essentially did that same experiment, but this time we did a single leg measurement. So we included the upper thigh, same data collection process, and then we did a single leg knee extension. Now, what we found is when controlling for muscle mass, that rate of reoxygenation, I think it brought the correlation down from like a 0.95 to like a 0.85-ish. So still strong of a performance, but it's getting lesser as you add muscle mass. Then we did a third protocol where now we occluded both legs controlled for muscle mass and got the reoxygenation rate on both legs. And then we correlated that to work capacity on like a cycling test, so more full body exercise. It was actually like a modified echo bike where we removed the handlebars from the echo bike and rigged up this weird contraption so you could kind of hold yourself stable brought the correlation down even more. So essentially what we found is as you add more and more muscle mass, your reoxygenation rate is less predictive of work capacity. And part of the reason why is that when you're exercising is you add more and more muscle mass, the sympathetic nervous system is gonna become more and more active. Your sympathetic nervous system wants to restrain your blood flow. I'll actually get back to a funny Kyle Ruth related story with this in a second. So the reason for that is if you were to vasodilate all of your skeletal muscle during exercise, yep, arterial blood pressure will get so low that you won't be, or you'll vasodilate so much that you don't have enough blood in your body to maintain your blood pressure. You'll go unconscious very quickly. So the sympathetic nervous system protects that from occurring. So basically that's what we found. The important part of this is that in years is actually a tool that allows you to assess these things. So this was all part of like a bigger study touching on a Kyle Ruth related story real quick. Brenda both of ours from Training Think Tank. So this was years ago, Kyle and I, he was getting really into BFR training and we decided to do like a lower body BFR session. So double cuff on both, a cup on both eyes. We did like a bunch of trap bar deadlifts or something. All good. So Kyle's like, okay, now let's do a upper body BFR session right after that. I'm like, okay, he's like, I do this all the time. So we start doing it. I have the cuffs on my upper arm. And after a few minutes, I'm like, I can't swallow right now. He was like, what are you talking about? And I'm like, I can't like physically swallow. And then all of a sudden I'm like, I'm in trouble talking. It's like, what the hell is going on right now? And took the cuffs off and I essentially lost the ability to swallow or talk for about a five minute period. I later on realized that I had induced so much vasodilation that my blood pressure was dropping so low and I was essentially progressively blacking out. Wow. This is why you do not do a. Yeah. I mean, I think that's really, really, really important from a side note that since you're, we're talking about BFR, that there is this reactive hyperemic response that occurs particularly more with greater muscle mass involvement than the upper body. But we get like a lot of times, people disregard the potential for post acute hypotensive response following a BFR episode or BFR training episode. So anybody listening that does BFR that knows me or has taken any of the courses is as I always recommend being in a stable environment, whether that's sitting, whether that's leaning against the wall, whether that's anything lying down before you deflate the cups because I'll tell you a funny story now. So I was at CSM, which is combined sections meeting the largest physical therapy meeting. This is like five or six years ago. And one of my ex partners of the BFR pros was doing an LOP assessment. So simply it's just basically a blood pressure cuff is applied to the arm. They find out what your systolic blood pressure is based on whatever cuff it is, and then it deflates. This poor PT student was getting her blood, like getting her LOP assessed, and then you just see her lights out. And luckily it was, we were there to support her and she was fine, but just simply getting a limb occlusion pressure or atrial occlusion pressure assessment, you have to protect against the acute post-hypotensive response from the reactive hyperemia that you get from oxygen-starved muscles, even if you're not doing anything. So that just is a good segue to just remind and nothing about that with Kyle Ruth surprises me. Nothing because he is one of those people like me that will try everything because number one, you wanna understand what your athletes are doing and you wanna be the first person to be able to say, hey, this works, I'm confident in X, Y, Z and understanding how you're feeling. And number two is just why not? Like why not just go through and try this? There's a couple of things like talking with Kyle where I'm just like, wow, okay. All right, well, he was talking about, he was talking about on one of the podcasts that he was doing some BFR combined with sauna. And I'm just like, come on. Like just again, Kyle in a nutshell. So Kyle, eventually I know you're gonna listen to this or watch this, we love you, we're just poking fun. So yeah, so I guess for us then with this, the practical conclusions in terms of what you can draw from your study and where are you going next with this data? Yes, so the practical conclusions that you could draw, this was really more of like, I'd say, I don't know the proper term for this, but it's like a tool study. So it's essentially figuring out ways that we could use this new tool. So what we're specifically looking at is, a lot of different sports, you do performance assessments. And the problem with doing like preseason performance assessments is you could train for the assessments and then the assessments not doing what you were doing with the assessment. So we're trying to get a very objective insight as to could we just cough someone up, look at their reoxygenation rate and predict performance with that. It's not something you could game. And then that way we could both say, okay, we could do a quick screen on people, rank them relatively speaking, but secondary to that, could we use this as a performance assessment post-injury? So if you have someone they tear their ACL, they're in a rehab period and you want to know, are they regrung blood vessels? Are they getting all the adaptations that you want them to get, but you don't want them to go on an assault bike and do a 10 minute maxcals or something that could hurt them? Could we do something like this reactive hybremia assessment every other week, track changes in their reoxygenation rate and use that to assess if they're actually improving their, let's say fitness or performance during that return to play period. That's kind of where we were going with this study. I think there's a lot of other potential things that we could do there though. Could you, do you think based on your experience that you could, and I don't honestly think that this has ever been done, but could you do repeated reactive hyperemic testing and expect that there may be some adaptations that occur simply from the repeated exposure to the reactive hyperemic response? So what I'm getting at is, could that be a practical application potentially in and of itself, and what would the limitations of that approach be? Obviously beyond just, yeah, you're not exercising. You're not doing anything with that. Yes, sir. Are we saying like repeated is in like occlude, release, occlude, release? Yeah, so basically you take that same protocol. So in the BFR world, IPC, I'm sure you're familiar with, ischemic preconditioning is very high pressure. So 100 plus percent of the limb occlusion pressure. And for five minutes on, three to five minutes off repeat three to four times. And that has been, and again, I'd be interested to actually hear your thoughts here too, that they've looked at an application of IPC and have shown, hey, like we actually can reduce the muscle damage that happens following a strenuous bout of eccentric bicep curls, for example, exercise. Or we see that there may be variably, and this kind of gets into your area where you've kind of commented on this, where now, this is where kind of my head is going, is like, all right, well, we see that there's a variable response to ischemic preconditioning following, preceding a performance test. We generally see that there is some sort of improvement, but it's completely variable. So where my head's going after our conversation is saying, okay, well, it might not necessarily be that the IPC is the issue, but the IPC might be targeting a limitation in some athletes versus other athletes where they're actually not having a limitation in their peripheral oxygenation or deoxygenation to reoxygenation response. And thus, this is just a stimulus that's not gonna have an adaptation. Yeah, yeah, totally. So first, let's talk about who's gonna benefit from IPC most and then ways that we could individualize the IPC stimulus. So yeah, first, let's start with the, in some way, simple activity like sport climbing. Sport climbing, one of the best predictors of performance is surprisingly, no shit, finger strength, but a lot of that is how much could you deoxygenate the finger flexors and form flexors? Now, IPC is really commonly used in sport climbing among high level climbers because you cut off blood flow, you get all of this release of nitric oxide, you essentially get like a rebound effect where now you have more blood flow and oxygen delivery to them. And to increase your capacity. Exactly, but if you have a beginner climber, remember they don't have very good deoxygenation capacity in those muscles. If they do IPC, it's really not gonna improve their performance to any meaningful degree because guess what? You just improved the blood flow and oxygen delivery to muscles that are incapable of utilizing oxygen at a fast rate, no performance improvement, very high level sport climber, they will completely deoxygenate their finger and form flexors. So using IPC is gonna be an advantage to them. So now that we know a population that it's gonna work for specifically people that have some kind of oxygen supply limitation, generally intermediate to advanced athletes, we wanna know about how do we individualize this stimulus? So two things that I've seen, I use IPC quite a bit, that was actually introduced to me from none other than Kyle Ruth years back. So one thing that I found in myself and a handful of other people, it's not for everyone, is that in order to get the same level of deoxygenation with each application of the cuff, I need to use increasing pressures. So the process of deoxygenation. Now why? Now, we haven't obviously talked about any of this before this, but I had an idea that you were gonna say that, why? Yeah, so that first time you do IPC and you deoxygenate your limb and then you release, you have all these vasodilating factors flooding the muscle and that's going to expand your blood vessels and improve blood flow. Well, now you have so much more blood flowing through that muscle that you're gonna need even more pressure to restrict blood flow. And then if you do that again, you're gonna need even more pressure to restrict blood flow. So one thing that I've used is this like staggering approach where you have first set, I'll use a little bit over 100% of limb occlusive pressure. Next set, I might have to increase that by another five to 10% and so on. So that's one way to individualize it. The second is how many occlusions you do. So this is at least for myself, I've seen this being variable on different days. Some days I do the first occlusion. Where are you occluding? So I'll generally do this for sport climbing. So I'm gonna occlude upper arm, so brachial artery and I'll be measuring on my form. You could do the same thing for lower body. If you were occluding the upper thigh, obviously it would have to make sense for the activity that you're doing. So something with lower body work capacity. But what we'll see is during that occlusive period, we could see what are your peak nitric oxide levels. You do the second occlusion, generally they're a little bit higher and then you do that third occlusion, they're higher again. That would be the response that you would want to see. For some people what you'll see is their NO levels will actually go down occlusion to occlusion or they'll go up from one to two, but then from two to three they'll go down. If that's something that you regularly see on someone that after the second occlusion, they actually have lower NO levels on the third, that means that you probably don't wanna go for three with that person. What's happening is if you have enough hypoxia in this nitric oxide release, you could actually deplete your NO levels and that's something that we can look into. So for a given person is to the ideal stimulus to get a lot of azodilation without depleting NO. For other people, three might be fine. So that's also something that can be looked into. So I know that there are gonna be researchers that are gonna be listening or watching this and my passion is getting good evidence-based blood flow restriction in particular research done. So what you're saying is a couple of things. Number one, we have this overcoming of the cardiovascular system to a repeated ischemic conditioning stimulus due to the fact that we have this vasodilation and we have all of this blood flow that's now gonna need to be constricted relative to a proceeding bout of high pressure. So at one end, we need to increase the pressure. We probably need to increase the pressure over time. And I actually don't think that to my knowledge that that's ever even been looked at. Typically they prescribe a 220 millimeter of mercury prescription with an arbitrary cough or they do 100% LOP. Number one, I think that's a takeaway is that we actually should look at the using something like the NOx where we can look at the deoxygenation, the nitric oxide levels to individualize an IPC stimulus and see now my head's going wild. Cause I'm like, all right, well, what if we only need one bout for this person but we need two bouts for somebody else and how does that then impact performance? And then the second bit is the personalizing of the, whatever your IPC stimulus is, but I'm interested in hearing your thoughts if you have any regarding some of the work that's been done that's been shown two things. Number one, reduce muscle damage. How could that, how could the IPC stimulus reduce the occurrence of muscle damage? And number two, how could the IPC application enhance performance in those particular individuals that it's beneficial? Yes, so the reduced muscle damage could largely be attributed to less time spent in a deeply deoxygenated state. So when you do IPC, you're again, flooding the tissue with vasodilating factors and that's allowing for more blood flow and oxygen delivery to tissues. So on the subsequent work bout, you're going to deoxygenate the tissue less and that's going to result in less muscle damage. It's almost like a protective effect. That's also the same mechanism that is going to give you that performance benefit as well. It's going to be the fact that you have increased blood flow and oxygen supply. So as long as you are not limited by your ability to utilize oxygen in the muscle, you're essentially providing the muscle with more of the substrate that it needs to do muscle work. That's also where with IPC, it becomes interesting is the greater the total muscle mass used in an activity, the smaller the performance benefit will be for these reasons related to cardiovascular control mechanisms. So if you're climbing, doing a grip, fatiguing workout, IPC is going to be phenomenal. A lot of CrossFit athletes will use it for this. If they know there's going to be like an open workout that has power snatches, toes to bar rowing, something that's very grip intensive, it's a great workout to use IPC for. But if you're about to do a workout that let's say it's thrusters, bar-facing burpees, and let's think of another- Yeah, I mean, honestly, so this is an important conversation to have. Because a lot of people are like, oh, I'm going to do IPC for CrossFit athletes because IPC can help with maintaining oxygenation in the muscle. But I want you to comment on the cardiovascular control mechanisms that separate a multi-mass, or a multi-joint, multi-muscle mass movement from a single joint movement and why performance is going to differ potentially between a large muscle mass exercise and a small muscle mass exercise. Yeah, definitely. Let's say you're doing a small muscle mass exercise and again, you're an advanced athlete, so you're going to outstrip the oxygen supply in those muscles. The more you could increase blood flow, the better for the sole reason that you are never going to be able to vasodilate your forms enough to lower your systemic blood pressure that you black out. There's just not that much muscle mass unless you're like pop-ying your forms or the size of your quads. Crop. Okay, you might actually have that problem. I do not have that problem, so let me rephrase. But if you were to do a full-body workout, you're not delivering blood to all of your working muscles already. So once you reach about 40 to 60% of your skeletal muscle mass engaged, this is why you don't see increases in VO2 max above that. It's because your brain is having to sympathetically vasoconstrict some of that working muscle to limit your blood supply. If you were to deliver blood to 70% or 80% of your total muscle mass, your blood pressure would get so low that you would very quickly black out. So for the same reason, if you're doing IPC on a thruster bar-facing barbie workout, it's not going to benefit you because those muscles, if you do it on your legs, being vasodilated, is just going to mean that your brain is gonna have to restrict the blood flow to other muscles even more. Those muscles could be your paraspinal muscles that are allowing you to stabilize yourself with the upper body musculature that's used for pressing. So there's going to be some kind of trade-off. And which you don't, so you don't have that trade-off with small muscle mass. So that is awesome because I think that there is this blanket approach to the research that is like saying, oh, IPC could benefit performance, right? But I think what you're saying is we really need to look at what exactly that performance is. Is it a whole body movement like a thruster where you're looking for increasing thruster rest? Which to be fair, you might get a little bit of an improvement, but is it something that is gonna be dramatic for an elite athlete? Who knows? But when you mention climbers, small muscle mass, that's due to the sympathetic control and not having to divert as much blood flow because you have small muscle mass that's gonna be activated. So maybe a grip endurance test might be a better performance metric for the impact of IPC versus something like an assault bike. But at what point does the, and this is obviously arbitrary in speculation, right? Where you have, obviously there's a dramatic difference in total muscle mass between something like an assault arm bike versus an assault leg workout versus an assault arm bike and leg workout. So what would you anticipate based on your expertise in the area that if we do IPC that we would probably get a greater benefit for muscles like the calves or the dorsiflexors or the wrist extensors or even like a bicep task, right? But we would then get progressively less benefit with a forearm and bicep tasks, right? Or then a forearm and bicep and shoulder or something like a pushup or then you start to get into a whole body exercise based on the cardiovascular responses to controlling because at the end of the day the most important thing is not to black out so our system is gonna be creating that vasoconstriction somewhere to be able to help with maintenance of blood pressure. Yeah, yes, I think if we're going really small muscle form task, really big performance benefit as we get larger even a full single leg task you're likely gonna see some significant performance improvement, full double leg task like legs only cycling, you're probably still good. I think once we get over that 40 to 60% hump is where things get more complex with CrossFit. I don't know how you would quantify how much muscles used in something like a thruster bar facing burpee but it is certainly greater than 60% of skeletal muscles engaged. So that's where those benefits are likely to decrease. It also just adds more complexity because some people may benefit if their legs are the limiting factor for them but another individual with the same amount of muscle mass relatively speaking doing that same workout, it may be of detriment to them if they're vasodilating their legs with IPC but their upper body strength is a limiting factor on a thruster for some reason. Now they're just restricting blood for where they need it most. This is where even doing some of these types of studies could become really challenging because we're mixing populations of people with different physiologies, different limitations the stimuluses are impacting them differently. So I think there's definitely a place for obviously we need these studies to be done but then in a very like applied performance setting looking at that individual specifically in saying I know the research says this but is that true for you? And if it is not, what is true for you? What do we need to modify to get the result that we want? No, I think that's tremendously relevant because if you have studies that you know and I go off on this for the BFR stuff where people are getting into BFR they're doing BFR research but without understanding the differences between cuffs but features can potentially impact the acute responses to BFR exercise and they're designing studies that are just that don't help us understand the nuances with BFR. At the end of the day, BFR is applying a cup to an arm inflating it but there are a number of factors that can impact that stimulus. What's interesting based on this conversation and is something that we have to consider is if we understand that even though somebody could be for example, like a CrossFit athlete for five years, all right, whatever that is. We understand that, yeah, CrossFit has a variety of different exercises, domains that they need to be fluent in but just because if we have an arbitrary cutoff in a study that says, oh, I want people that are at least five years experiencing CrossFit to then do this if we're gonna use IPC as the intervention that we're gonna then test and even if it's an assault bike task, whatever, that they're all not gonna be equal, right? Because CrossFit is a multimodal type exercise regimen they could be very strong but have a moderate cardiovascular system they can have a massive cardiovascular system and be strong or they could be not as strong. So there's other of these domains that I think what you're trying to say and I totally now I'm like, agree but have to figure out how you can even get like to stratify these athletes because then if you wanna say, hey, is IPC effective? Yeah, you can use a blanket approach and we generally see such mixed results from IPC particularly because we don't, we have researchers that are not understanding that there's, hey, like there's nuances associated with these athletes in particular but also in the BFR stimulus but even if they recognize that there are nuances, right? We're now creating a bucket that's very wide and instead if we understand that, hey, these limiters might be present in 25 to 30% of athletes, okay, well, then we take this bucket and now we test them pre and say, hey, how can we identify that the peripheral deoxygenation is the limiter for this athlete and then include those in the IPC studies and then we can really start to laser our research to then the practical application for coaches and clinicians that are reading these, these important bodies of literature. Yeah, I think that's really key because for example, let's say we had a study with 30 people, is IPC effective for improving performance? Some people, yes, some people know, it's a variance. And you see the data, I mean, you definitely looked at the IPC studies, you see that there is this very heterogeneous response to IPC and now it's making me think, well, wait a second, like if everything, we wanna relate back everything to physiology, well, then maybe those people that are having, cause you see those strong responses, like there was a performance study that I was looking at with a cycle and I was like, and they plot all the individual data and you just see like three or four where pre to post massive improvements and then you have these like middle ground where they're kind of improving a little bit but then you have people that actually decrease. Yeah, and that's where we have to ask, well, what is the mechanism by which IPC works? What are those different individual in the studies of physiologic states? And then we could either investigate or make some assumptions or new hypotheses. Why does IPC that works on these mechanisms improve people with these physiologic limitations performance, it becomes much more apparent. Honestly, at training think tank when I was there, a lot of people are like there, we would take these athletes that have been in the game for a long time and suddenly they get much better and people thought we were doing like some super special protocols. I don't think what people realized is we are just matching protocols that people's physiology. It's like the same protocols that people already know exist. Yeah, but you're creating what would be the, so the buzzword in the medical community is precision medicine. You're creating when you were at training think tank, you're creating precision fitness. And I think that's super important to appreciate is that there doesn't need to be these complex protocols. Given you understand the baseline physiology of whatever athlete you're working with, their demands of the sport and where they're developed or underdeveloped and then all you're doing is you're creating based on your assessment, you're then creating an intervention that's gonna specifically target those impairments. I think that that's a massive oversight and not to get into my other passion of mine which is the volume debate with exercise, right? All over social media, it's the same thing. And I think that if we get down to the nitty gritty, we can kind of see based on an individual's portfolio for whatever their cardiovascular and muscular physiology is that we may need more volume in some because again, it's the generic recommendation, right? Like I'm sure you've seen it all over social media. Like we're looking at 10 to 12 sets per week per muscle group to give a generally very good robust response. Some people might need less, some people might need more, some people might need a lot more. And I think that with your approach and using precision fitness, I think that it could really aid in the stratification of individuals in research. I mean, think about the potential implications of looking at implementing something like the NOx and seeing, all right, well, we understand that this happens with hypertrophy and our study, our main outcome is hypertrophy. Okay, well then this person might not be an appropriate person for this study based upon their initial assessment in terms of their deoxygenation rates. This person might be best responsive to more volume and we're trying to do a low volume study and we're trying to match or mismatch, right? There's so many things that can happen. And I think that that's why like when we started to talk that was so exciting to me because it was like, oh my gosh, actually we can create more precision fitness and get potentially better results. Yeah, absolutely. So what the last question that I have before I hand it over to you to plug and play with whatever you want is, of course, I'm a physical therapist. I'm interested in getting people back to the activities that they love as quickly as possible. NOx is clearly one of the technologies that can be able to do that. What would you expect to see? Somebody comes, you mentioned it a couple of times, post-op ACL and what would, you're not a physical therapist but you're an extra physiologist and we can look at the physiologic status of those patients. What would you expect to see in somebody that's post-op or post-injury and how would the NOx come into play in terms of exercise prescription? Yeah, definitely. So this is where I need to stand my lane because again, I am not the PT but I could speak to- You can speculate. I'm giving you permission to speculate given the topic of the NOx. Yeah, so general patterns that I've seen. So after injury and the interesting thing is this could even be like one or two years following injury if someone hasn't rehabbed properly is you're gonna see impaired deoxygenation in those muscles. That could be a whole host of different reasons. It could be shortly after injury the muscle fibers are torn. Of course, they're not going to be recruited and deoxygening optimally. It could be, a lot of times you'll see these hypothermic asymmetries. So if you ever look at like a heat map of a tissue following surgery you see these big blue regions on the tissue, regions of cold. Cold temperatures are going to impair deoxygenation of muscles. It's gonna actually change the history of blood and cause what's called a left shifted oxygen dissociation curve. Essentially means your hemoglobin is gonna be more sticky. It's not gonna release oxygen as readily. So in general, we see impaired deoxygenation. We also tend to see lower nitric oxide levels in those tissues. Again, this could be a whole host of reasons. It could be that left shifted state. The nitric oxide is not going to release from red blood cells as readily. It could be that the blood vessels are torn and damaged. Most people don't think about that. When you tear an ACL or you tear a muscle you're also tearing your blood vessels and those need to be regenerated. So that's another factor. We also typically see that as people recover over time these factors are going to improve. There could be able to deoxygenate the muscle to a greater degree. Their nitric oxide levels will increase. Now, what I don't know is for a given individual how do we make sure that those things happen in the most optimal way? That's where we're gonna need to do some leg work and research over time. Because again, I've only been looking at these things observationally. I haven't been in charge of anyone's rehab programs. We haven't looked at these things in an individualized and controlled setting. It's just general patterns that we could observe. So the question is, if we use this technology could a skilled practitioner figure out the best way to heal that tissue using these metrics over time? That would be the hope. No, I mean, I think it's super exciting definitely because the more we can introduce objective measures to track the rehab or fitness outcomes of interest, the better. I think that the biggest limitation and you kind of mentioned it before with the Moxie where you're in the clinic and you're in the gym and you're like following the athlete with a laptop. And I think that given where technology is going and everything is going to the cloud and everything is going on the phone that being able to have instantaneous data that's easy to analyze. Because I think that that's another barrier when you're trying to look at adoption is do we want to have this data and then export it to a CSV file and then now open it up in Excel and now we have to do an algorithm, whatever and then it's just not going to get adopted. So I think the most important thing as a practitioner speaking is it needs to be accessible it needs to obviously be valid and certainly or needs to be reliable and most certainly valid. So it's actually giving you consistent measures and the measures are doing what it says that's the reliability and then validity specifically. But yeah, no, it's super, super exciting. I'm very, very much looking forward to seeing what we find with the NOx and looking at all these different outcomes and obviously our collaboration is just starting. But I'm excited and I thought that this conversation was really, really informative. I'm sure a lot of people are going to be like, whoa, I need to listen to this again, which is perfectly fine. But yeah, if there's any last things that you want to just comment on for the viewers or the listeners, where they can find you on social, where they can find out more information about the NOx, anything in between, now's your time to speak your piece. Yeah, first off, I appreciate you having me on. That was a lot of fun. If anyone wants to check out NOx, you could find that on NOx's website, it's N-N-O-X-X. That'd be the best place to find what I'm doing as well. I'm not super active on any other social media platforms these days, so that'd be the best place to stay up to date. Okay. All right, well, everyone, that's the episode. Thanks so much. And Evan, I'm sure we're gonna be talking very, very, very soon. Thank you. And that was today's episode of the BFR Better For Results podcast. If you enjoyed the episode, I would love if you subscribed to the podcast on whatever platform you're watching or listening on. I really appreciate the support.