The Peter Attia Drive - #179 - Jeremy Loenneke, Ph.D.: The science of blood flow restriction—benefits, uses, and what it teaches us about the relationship between muscle size and strength

Episode Date: October 11, 2021

Jeremy Loenneke has a Ph.D. in exercise physiology, a Master’s in nutrition and exercise, and is currently the director of the Kevser Ermin Applied Physiology Laboratory at the University of Mississippi, where he focuses his research on skeletal muscle adaptations to exercise in combination with blood flow restriction (BFR). In this episode, Jeremy explains the science of BFR and the mechanisms by which BFR training can produce hypertrophy using low loads. Here, he reviews anatomy and terminology of muscle structure and discusses the evidence that increasing muscular strength may not be dependent on increasing muscle size. Additionally, Jeremy goes into depth on how one might take advantage of BFR training, including practical applications for athletes and average people, as well as the situations for which BFR training would be most advantageous. We discuss: Jeremy’s interest in exercise and weightlifting and his scientific training [3:30]; The microstructure and physiology of muscle [8:00]; Definitions of fast-twitch and slow-twitch muscle fibers [12:45]; Comparison of strength vs. hypertrophy [21:30]; Blood flow restriction training and the origins of the Kaatsu system [28:30]; The details and metrics related to exercise under blood flow restriction [44:45]; Considerations when training with blood flow restriction: loading, pace, rest, and risks [53:00]; Blood flow restriction studies and the relationship between muscle size and muscle strength [1:04:15]; Evidence that increasing muscular strength is not dependent on increasing the size of the muscle [1:16:30]; Practical applications of blood flow restriction training for athletes and average people [1:27:30]; Situations in which blood flow restriction training is most advantageous [1:35:30]; The mechanisms by which blood flow restriction training can produce so much hypertrophy at such low loads [1:39:45]; Applications of “passive” blood flow restriction training [1:47:15]; What experiments would Jeremy do if he had unlimited resources? [1:51:45]; More. Learn more: https://peterattiamd.com/ Show notes page for this episode: https://peterattiamd.com/JeremyLoenneke  Subscribe to receive exclusive subscriber-only content: https://peterattiamd.com/subscribe/ Sign up to receive Peter's email newsletter: https://peterattiamd.com/newsletter/ Connect with Peter on Facebook | Twitter | Instagram.  

Hey everyone, welcome to the drive podcast. I'm your host, Peter Attia. This podcast, my website, and my weekly newsletter all focus on the goal of translating the science of longevity into something accessible for everyone. Our goal is to provide the best content in health and wellness, full stop. And we've assembled a great team of analysts to make this happen. If you enjoy this podcast, we've created a membership program that brings you far more in-depth content if you want to take your knowledge of this space to the next level. At the end of this episode, I'll explain what those benefits are, or if you want to learn more now, head over to peteratiamd.com forward slash subscribe.

Now, without further delay, here's today's episode. My guest this week is Professor Jeremy Lonecke. Jeremy is an Associate Professor of Exercise Science at the University of Mississippi, better known as Ole Miss. He has a PhD in Exercise Physiology from the University of Oklahoma and a master's in nutrition and exercise from Southeast Missouri State University. He's also a fellow of the American College of Sports Medicine and a member of the American Physiological Society. He's the director of an applied physiology laboratory, and his research focuses on skeletal

muscle adaptations to exercise in combination with blood flow restriction. Now, some of you may have seen me recently posting things on Instagram about blood flow restriction. I've been experimenting with it for some time recently. And in this podcast, I even explained the first time I was exposed to it, which was a little over 10 years ago, it was actually in a swimming pool. Blood flow restriction is a general term that applies to occluding some portion of the arterial inflow to a muscle. We get into the very nitty gritty of this during the podcast. And under these conditions, it becomes harder for the muscle to contract. And what it allows an individual to do is exercise with a lower weight than they would normally do

unoccluded. Now, as we cover in this episode, there are lots of benefits associated with that. There's also other terms that you may have heard associated with that. The most common term associated with this from a brand perspective is Katsu, K-A-A-T-S-U, which is Japanese for basically training with restriction. Anyway, we get into all of that stuff in this episode and more, but perhaps one of the most interesting things that comes out of this discussion, well, at least from an egghead perspective like me, is that blood flow restriction offers a very cool way to study the relationship between muscle size and muscle strength. And that's a topic we explore very deeply in this episode. We also start this episode off assuming that you know very little about muscles. So we explain the physiology of the sarcomere,

the micro anatomy of muscle fibers, the difference between type two and type one fibers. So even if you come into this and you don't know what an actin filament is and a myosin filament is, don't worry about it. We're going to spend quite a bit of time getting you up to speed on that. And of course, if you already have a PhD in exercise physiology and know everything about that stuff and just want to get to the BFR, no problem, get to that too. So anyway, without further delay, please enjoy my conversation with Jeremy. Hey, Jeremy, thanks so much for making time. I've been looking forward to this one for quite a while, both personally and professionally. This is a topic I've wanted to learn a lot more about, something I've been playing with a lot myself, including this morning, particularly painful session this morning of blood flow

restriction, which I might be doing wrong. So I'm looking forward to maybe the end of our discussion when we can get into the practical aspects of it. But I want to take a kind of a step back and get a sense about how you became interested in exercise in general. Obviously, you've devoted your career to it. So when did that become a passion great enough that you decided it was worth all of your study? Yeah. Thanks for having me on Peter. I wrestled early on in my life. So I wrestled from probably the age of five through high school, but I, I wasn't really into training that much. I was in the wrestling, but not really lifting weights or

any of the conditioning. And my coaches would always tell me that you need to try to get in the gym and you just stay in the gym and get stronger, get stronger, get stronger. And I didn't really listen up until towards the end of high school. And then I started, one of my friends was really into bodybuilding, powerlifting. So I started training with him. I do feel like it probably helped me a little bit in wrestling. And then I kind of got interested in just trying to see how to make a muscle get as big as possible. I started reading, you know, muscle magazines, which is kind of the common story, training a little bit. Then I focused on exercise science early on in my undergrad. I was just trying to learn how to make a muscle bigger, how to make a muscle stronger. That's all I was trying to get out of every lecture. Towards the middle of, I guess, my undergrad, you have to make a decision

about, you know, obviously, what do you want to try and do with your career? And I was dead set on working with athletes. But then I did that and quickly realized that's not what I wanted to do. So they suggested that I instead, maybe you're really interested in research. Why don't you try and do an internship related to that? So I landed at the University of Illinois and that's where I met Lane and a couple of other people. And that's where I really came across blood flow restriction. And that's where I started to really read a lot about it and then came back and started to really focus all of my time. So that was around 2007, 2008.

So just about, you know, reading blood flow restriction and how I might be able to do that. So I started off with wrestling and then kind of got interested in bodybuilding, powerlifting, and then came across blood flow restriction when I was up in Illinois. You mentioned briefly that you did a little bit of work with athletes, which was obviously kind of a logical, at least place to look, but it sounds like you didn't find that to be what you wanted. Why is that? I'm a pretty mediocre athlete, but I always trained extremely hard. And I think I had this mindset that everybody was going to train what I thought training was and how everybody was going to train as hard as I thought they should train. And when I was doing a little practicum work with some of these athletes, I mean, they weren't world-class elite athletes,

but they were fairly good collegiate athletes. I didn't get the same vibe that everybody was into training like I was in the training at the time. It doesn't mean they weren't great athletes. They obviously were. It doesn't mean they didn't train hard, but my perception of how they should have been training was not what I thought it was going to be. So I knew I wanted to be in the exercise world, but I quickly learned that I want to do research, but definitely not with animals. So I came back and that's when I got into human research. So where did you do your PhD? University of Oklahoma. And what was the focus of your dissertation?

Looking at different methods of applying blood flow restriction. So looking at, you know, different exercise loads of 20%, 30%, different pressures. In other words, we were trying to get at this idea of, do you actually need higher pressures? So in my dissertation, we were doing a lot of acute work, which has obviously a lot of limitations with applying it to adaptation. But we were trying to really see kind of a short-term characteristic of what that response would give. Acutely, what does this response give? What does this response give? And then try and kind of pick out two of the more promising ones and then study them head to head a little bit later on, which is kind of what we did once I took a job at Ole Miss. I can't wait to talk

more about that. And there's no shortage of questions I have for you. But I was thinking about this last night, that before we jump into a lot of the questions I have, I think it will be important for people to really understand the ins and outs of muscle. What's the structure of a muscle? Not the gross anatomy of a muscle, but obviously the microstructure, the physiology of a muscle. So without worrying about going too deep, I think it's okay to do that. Let's talk about a muscle because I don't think we can get into what we're about to talk about if people don't know what a sarcomere is and what actin and myosin are and what the different types of fibers are. So if I were to sort of take a knife and cut down on my bicep and yank it off the tendon and throw it out there as a muscle,

how would you explain to somebody what's actually going on inside that thing? Yeah, that's a good question. When we talk about a muscle, so like just the whole thing, so it's like a box within a box within a box. The smallest unit of that is, as you said, a sarcomere, which is actin and myosin. And that's the kind of the proteins that we're ultimately synthesizing when we exercise. So we're making more of those. And if you make more of those than you break down, then obviously the muscle will get bigger. So when we actually exercise those actin and myosin interact and that's how we make a muscle contract and that's important because when actin and myosin interact and you have muscle contraction that's where you get a lot of this signaling for ultimate muscle adaptation so the characteristics of muscle we have kind of two broad types is how we typically teach it

we have type one which is more endurance based type two which is more force based but in reality those are probably on a continuum so when we exercise we can shift them we can shift the continuum one way or another, depending upon the type of exercise that you're doing. But in general, when we become more physically active, the overall fiber types shift slower. So they become more oxidative, they become more efficient. That's the general response. So those are the different types of fibers, the actin and myosin, that's the functional unit. They interact to make the muscle contract. Let's explain to people how that works, Jeremy. So you pull out this sort of sarcomere and inside you have these fibers and you've got

these Z lines. Explain to people how the actin and myosin actually interact with each other relative to the Z line, what the contraction looks like. And frankly, even one of the more interesting things that I think is a bit counterintuitive the first time people learn it is which part of the interaction between actin and myosin requires ATP. It's a bit counterintuitive when you're first presented with it. Right. So when we decide to exercise, we have a signal that goes from the

nerve to the muscle. Basically, we have a release of calcium and that calcium is going to expose the binding site. So basically, we have these filaments, they slide past each other. That's the general dogma, at least with concentric actions. Eccentric is a little bit more complex. I think they're still trying to figure that out with Titan. But just in general, when a muscle contracts, so the myosin is interacting with the actin and it's causing it to pull in. Now, ATP is required to break that bond.

So the ATP comes in, it breaks it off, it gets hydrolyzed, which re- cocks it and allows it to be able to reattach assuming there's more calcium on board. So that's the the general basic physiology of muscle contraction. So as long as calcium is there, or as long as the signals being sent, those sarcomeres, those actinomyosin will keep interacting. So they don't all interact at the same time. Otherwise you couldn't really sustain exercise, but you have them, you know, in a

textbook, we talk about, we have kind of like an image and we have myosin head, but those myosin heads are on all the way around that myosin and they're all interacting at different times. So that's how we're able to actually move through kind of a fluid motion. times. So that's how we're able to actually move through kind of a fluid motion. And what's interesting, as you said, is that the ATP is required to actually release the actin myosin complex, which we learned in medical school explains why a corpse is experiencing rigor mortis, right? When a person is dead and they're no longer able to produce ATP, they don't have the ability to release the actin myosin filaments. That's why a body gets stiff, sort of a morbid thought, but it explains

physiologically what's happening. So let's now talk a little bit about this difference in fibers, because again, I think most people have probably heard of the idea of a type one and a type two fiber. But as you said, it's probably more complex than that. And there's more of a continuum. I think even by the time I was in med school, the teaching was really, it's a type one and then a two A and a two B, and then it became a two A, a two A B, a two B. You could argue it's even more complex now. Let's start with the term fast versus slow twitch. I've read conflicting things, so I'm hoping you can clarify this for me. I've read that there's no difference in the twitch speed. They all twitch at the same speed. It's the force of contraction and the speed to fatigue

that's being referred to. So the faster twitch muscle has a higher contractile force, but it also fatigues quickly, hence fast twitch. Is there actually a difference in the neurologic signal that's happening there or the speed of contraction for that matter? Yeah, that's a good question. This is not work that I actually do. I have a lot of confusion surrounding this myself and a lot of it reading some of the work by Andy Galpin and some others. A lot of it comes from the old methods are still being used. And the limitations of those is that we don't have we can't do hybrids. And some people say we should be using these new methods. And I think it all depends on how you're actually identifying the fibers.

What are you doing to call it a fast or slow? How are you ultimately deciding that with your methodology? So I don't honestly know the ins and outs of all those. The general idea, I think, as you said, the type two fibers. So for example, type two X, those typically are bigger. They're typically stronger, but they fatigue much faster. The type 2a, it's a little bit more oxidative. They're pretty forceful and they can sustain it for quite some time. So in general, when we exercise, it's thought that type 2x usually transitions to type 2a. You don't have a whole lot of type 2x left over.

That's my general understanding. Type 1 fibers, generally a little bit slower, and they're not as forceful, but they don't fatigue. It takes a lot to fatigue those fibers. So I think that's the general characteristics. I think how you go about identifying that, you might get a little bit of different things, but that was the general idea as I understand it, at least. And what accounts for the difference in contractile strength between a type one fiber and say a type two X take two opposite ends of the spectrum. I mean, sometimes using the extremes is helpful, right? So the type one fiber has lots of mitochondria surrounding the fibrils within the sarcomere. As you said, it is readily able to access glucose

and fatty acid oxidatively. Conversely, the type 2X fiber, I don't even think it has mitochondria surrounding it. It's purely a glycolytic tool, meaning it's going to basically have to go glucose to lactate. What accounts mechanically for the difference? That's a good question. I think most people would say that perhaps the overall just size difference, whether or not there are other things, how it may interact and the speed of it, that might be different as well. But the big characteristic difference, at least in young people, is that the size of the fiber is just distinctly different. And I think when you look at fiber mechanics outside of the body and you test a type one or test a type two, they will be different.

How those interact within the body as a whole, I think, is quite a bit different. whole, I think is quite a bit different. And that's always been an interest of mine with respect to dynamic strength, moving the whole person, not necessarily saying, well, their fiber is still nice and strong, but what about when the fiber is in the person? What's going on then? So I think there are, I think both of those are very important. I'm not, I don't want to come across like I'm talking down to that type of work. I think that's very important work, but I think they're just different. How genetically set is this? It seems that there's clearly a difference in individual's capacity for work, meaning aerobic work versus explosive strength anaerobic work.

But do you have a sense of how genetically diverse the fiber distribution is? That's a question I always put forth to my class as well. I think you can look at papers and get some percentages, but I don't feel super confident doing that, mostly because we have a lot, not that those scientists don't know that, but those are mass extrapolations from small bits of fibers. And one of the things that I'm always interested in is the athlete that's thought to have like some of the greatest endurance capacities or cross-country skiers. And if you were to look at their fiber types, many of them may have a predominance of type one fibers. So the question

is, were they mostly born like that and then they gravitated towards sports that they're good at? Or was there some sort of shift with training? If I had to pick one, it's probably both. But if I had to pick one, I think there's a big genetic component there, probably at baseline and then your response to exercise as well. But it seems to me that most people gravitate towards events that they're pretty good at and they don't do the things that they're not good at. So I think that makes it difficult to study this anyway. But I do think that there's a big genetic component to it. It doesn't mean, again, But I do think that there's a big genetic component to it. It doesn't mean, again, that they don't train hard.

That's always the thing that I get when I have a lot of athletes in my class. It's like, well, we train. It's like there's no question that you guys train extremely hard. But it's also possible that there's something different about you already. So that would be my guess. And you sort of already touched on it a bit, but do we have data to suggest how malleable that is? We all know the extremes, right? We know these sort of mesomorphic specimens that kind of look at weights and get bigger and stronger. And then conversely, we know that sort of wiry person who can't put on muscle no matter what they seemingly do, but

boy, like you get them out there on a, on a bike and you, you, you could never catch them. But when you take someone maybe who's not quite at the extremes, how much can training and over what time period impact fiber type? I think certainly some. I don't think we're going to take someone like myself, who's athletically quite average. I don't think any amount of training was going to make me elite in anything. But I do think that I could improve certain aspects of that for sure. But I don't think it's going to myself move me to up a couple notches. Now, there could be some people who certainly can. I think that this is where there's quite a bit of confusion with

individual response data and things like that. We've published a little bit on this topic about the measurements that we have aren't typically good enough to say, not only did this group increase muscle size more than this group, but this individual increased more than this person, but not quite as much as this person and not quite as much as this person. quite as much as this person and not quite as much as this person. That would require a very, very good instrument. So I think people often take that to mean, so you're saying that there aren't individual responders. I'm not saying that at all. I'm saying that we may not have the ability to appropriately determine who's who. We can say overall, on average, doing this will increase this or that. But I think that just looking around, it seems at least pretty clear to me that there are some people who you

give them a certain response and man, do they look like world beaters a couple months later. So that does tell me something is different about them, but I don't know that we could detect that with a lot of the measurements that we have. Okay. I think the other thing that would be helpful for us to understand before we get into the science of blood flow restriction is to understand what strength is and to understand what hypertrophy is. Do you have a preference with which one we start with? hypertrophy is. Do you have a preference with which one we start with? Either one. Okay. So if we measure the size of my bicep today, we could do it crudely with a tape measure. We could do it more accurately with an MRI or an ultrasound. And you were to prescribe

exercises that we'll talk about. Whether with or without blood flow restriction, we can get into load, we can get into reps, et cetera. We come back and measure. And again, let's just use the gold standard. We'll use an MRI. We'll come back and measure me in six months. And demonstrably, my muscle has gotten bigger. What does that mean? Did I grow more muscle fibers? Did each fiber get bigger? How would you explain to somebody what happened in that cycle of hypertrophy? So there's a couple of different ways that it could happen. You could have an increase in fiber size, which is hypertrophy. So all the muscle cells that you have, maybe not all, but the muscle cell itself has gotten bigger. So that's hypertrophy. The other component would be you have

an increase in the number of cells. That's hyperplasia. In general, we don't think that hyperplasia is playing a big role, at least in adults. And I wouldn't necessarily rule it out, but it doesn't seem like we have a lot of evidence for that. So we always just look at gross changes and assume that it's probably hypertrophy. So when your muscle was to get bigger following exercise, what that would mean is, is that the individual cells inside that bicep have increased in size.

And we typically assume that that's due to increases in overall protein, actinomy myosin and things of that sort. You're obviously going to also have an increase in other components to help support the cell, but that's generally what we mean, an increase in cell size. When you think about like an epithelial cell or something like that, we don't really pay much attention to the size of those cells, right? Like I don't know that anybody, I don't know the dermatologist is looking at somebody's moles when they biopsy them and looking at the individual cells and talking about the size of them.

There we would concern ourselves much more with hyperplasia and certainly metaplasia or dysplasia. Those are the things that really get people concerned. But in this sense, muscles are kind of unique in that they can have not just a non-pathologic, but a healthy change in size. So is it, as you said, do you think it's primarily due to an increase in the amount of actin and myosin within the cell or some other characteristic? Does the actin and myosin complex actually change in size or do you just have more of it? I think that most people would say that because they usually connect it to short-term measures of protein synthesis. So myofibrillar, which is actin and myosin. So synthesizing more and more of those, I think is

the general thought that you have more overall actin and myosin along with other things, of course. And let's talk about strength now. So we can kind of break it down right into kind of mechanical strength and neurologic strength. How do you think about that? So again, let's use the same example of you measure my ability to do a bicep curl. And let's just assume there'll be two measurements. You'll measure my single rep max, so the most that I can do. And then you'll also do a separate test for the most that I can do 10 times or 15 times or something. So you'll measure kind of two different components of strength, maybe absolute extreme and sort of

more of a muscular endurance test. And then you'll have me do a set of prescribed exercises for six months and we'll come back and we'll do that whole thing again. And my one rep max went up by 20% and the amount of weight that I could move 10 times went up 15%. What happened to me mechanically, structurally, neurologically? What explains that change in strength? That's a question that I'm extremely interested in. And I don't know why people get stronger. I think the general thought or how we teach people is the initial change in strength is due to neurological changes. So what does neurologic mean? I think is also up to some debate. But we can think about a signal being sent from the brain through the spinal cord to the alpha motor neuron. So the alpha motor neuron is the nerve that communicates

with the muscle. So there could be changes anywhere in between that. So you have more excitatory input, you have less inhibition, you have lowering of thresholds that makes it easier to fire the type two fibers. There's a lot of different things that could be playing a role there for why someone might get stronger with neural adaptations. So most people are okay with that part. The next part is people will say after about three to four weeks, when the muscle is also getting bigger, that that change in fiber size will also be contributing to a change in string. And that's something that we have recently taken some exception to. And there's been a lot of really good discussions about that part of it. And we'll come back to that, Jeremy, because I've read the studies that

you're referring to. They're super fascinating. And I was actually surprised at how little evidence there was in favor of the dogmatic view. So I look forward to diving into that a little bit more. And you can see why intuitively one would say, well, size must produce strength if size comes from more actin and myosin, which basically means more contractile units. But as we'll see, I think when we talk about some of your more recent work, that's not necessarily settled, is it? Not in my opinion, no. And to be fair, it's not settled one way or the other. But I do think that there's probably a neural component, but I think that there can also be some changes at the local level that might

explain some of those changes in strength. And I think we can discuss that a little bit later as well, but there could be some changes at the myosin head or changes in calcium release and things of that sort. So I don't have any good evidence that that is actually happening, but just some ideas behind why someone might get stronger following exercise. All right. I think that's a pretty solid primer for where we're about to go. So I'll start with the story. I used to swim a lot and, oh God, this might be circa 2010. So call it 10, 11 years ago, I have a friend, Steve Munitonis, who's himself a remarkable swimmer, truly a world-class marathon swimmer. And he was visiting San Diego from where he lived in LA. And he came to join me for a workout at the master's club I swam at. And after the workout,

he brought out these bands. They were called Katsu bands, which we're going to talk about. And he said, okay, Peter, I'm going to put these bands on your thighs, upper thighs, and I'm going to put them on your arms, the upper arm. And I'm going to, you know, compress to a certain level. And he, he had what looked like a blood pressure cuff there that he could sort of calibrate the occlusive pressure. And I want you to swim a 50 yard butterfly all out. Now keep in mind, swimming a 50 yard butterfly all out under any circumstance is quite challenging, but totally doable, right? I mean, you would do a set of 10 50s of butterfly at 90% with 45 seconds in between and be totally fine. And I remember pushing off the wall and before I got to the other wall,

which is 25 yards away to begin turning around to come back, I was like, this is the hardest thing I've ever done. This feels harder than swimming 200 yards of butterfly, which is really hard. So butterfly is one of those strokes where the longest distance it's ever swum is 200 yards. And even people who train to swim the race at 200 yards almost never swim that distance in practice. You're swimming shorter distances perfectly because your form tends to fall apart so badly at 200. And here I was at 25 yards thinking I'm going to die. And by the end of that 50, my body felt like it would normally feel at the end of a 200 yard individual medley or 200 breaststroke, which would be kind of two of the most miserable things you could ever do to yourself. And, you know, that began my kind of curiosity with

this technique. I read a couple of books about it and, you know, unfortunately I kind of just forgot about it. I, you know, once Steve went back up to LA and I didn't have access to the fancy devices, I kind of sort of forgot about it. But recently, it's now become sort of curious to me. So what's the story of Yoshiaka Soto? What was the name of the gentleman who came up with this system? Sato?

Sato, yeah. So tell me about this guy and then how he came up with this idea. Yeah. and then how he came up with this idea. Yeah, so some of this is, I'll say, is of legend. But I think the story that he's told is that he was at a Buddhist ceremony, was kind of kneeling. And Sato was also, from what I understand,

interested in bodybuilding, especially in his younger days. So he felt kind of a little bit of numbness or a little bit of sensationness about, or a little bit of sensation that he felt when he was doing heavy squats. So he, he kind of thought that there could be some connection there because he was kneeling and he was restricting blood flow. Okay. Right. That led him to start kind of experimenting with different ways to try and restrict blood flow in his lower body and upper body, etc. I think that there's been some stories that his initial kind of ideas, he actually harmed himself a little bit because he was maybe applying it too tightly.

But I think then he actually had a skiing accident and then applied it to himself and actually rehabbed himself with blood flow restriction and saw some what he thought was some pretty good gains. And I think that he really did probably develop a lot of the methods for at least the initial way we were doing blood flow restriction and kind of made it very popular with studying and research and things of that nature. But yeah, I think he's probably the one who

made it more popular, at least initially, because they started doing research on that in the late 90s, early 2000s, at least in the published literature. So the idea is, is that it mimics something that he had felt before in the gym. And he wanted to see how he could try and do that. And ultimately, he found that you can use very light weights, low loads, but make it feel like you're lifting very, very heavy weights, which is obviously useful, you know, if you have a skiing accident or you don't want to lift heavy weights or you have some sort of injury. Yeah, I had a patient last year who was playing with his kids

and tore his bicep, had a complete tear. So he underwent a surgical repair of that, but we decided to have him use blood flow restriction during the rehab phase so that he could get back to training sooner, obviously under a far less load. Although it's anecdotal, I mean, it was a remarkable recovery that he made, which further kind of piqued my curiosity around this. So this term Katsu is kind of synonymous with blood flow restriction. Is it, and I think it's Japanese for like training with pressure or training with added pressure or something to that effect, correct? Yeah, it means increasing pressure. So it's just a brand. It's the one that's,

it's fair to say is one of the first, but it's just a brand. So we started using, I think a lot of people will use Katsu as just kind of a generic name, but it probably shouldn't be done unless you're using the Katsu apparatus. But yeah, it's a form of blood flow restriction. the Katsu apparatus. But yeah, it's a form of blood flow restriction. So I want to come back to the different types of apparatus, but let's kind of talk through it now, maybe chronologically in terms of the most insights. Like if I was to go back in time to the 1970s and I'm Sato and I'm trying to think about how to test this hypothesis, it seems like hands down, the easiest way to do this would be to use individuals as their own controls and isolate and compress one side and not do for the

other and have them do the same things or do different things and try to isolate the variable. So was that the first experiment that was done? Yeah. The first experiment done on blood flow restriction, at least to my knowledge, on how we think of blood flow restriction. So I always add a lot of caveats because some people will say, well, if you look in the thirties, there were studies done where they applied a cuff, but it wasn't done for the purposes of increasing muscle function. So to my knowledge, with blood flow restriction, how we use it, Shinohara published the first paper in 1998, where they had individuals that all they were looking at was strength,

but they had one leg do a certain exercise with blood flow restriction. The opposite leg did the same exercise without blood flow restriction, and they saw a treatment effect, meaning the limb that underwent blood flow restriction saw a greater change. So that's the first study was looking at a change in actual function with blood flow restriction. It's kind of amazing that that didn't happen until 1998, which is 30 years after Sato began writing about this stuff or at least experimenting with it, right? Yes. The other question for me that's been very difficult to wrap my head around is,

what is the definition of blood flow restriction? If I were to wrap a cuff around my arm and apply no pressure, clearly that's no restriction. If I were to create an occlusive pressure that was twice my systolic blood pressure, almost certainly it would imply not a drop of blood is making its way past. So there's no arterial flow and no venous return. That would obviously blood flow restriction. That would be blood flow restriction. But like everything else, you have a continuum. So how do you think about this? And maybe that's the wrong question. Maybe the better question is in the genesis of kind of the study of this, how was restriction defined? What methods were used and how much variability existed in the studies?

So the idea of blood flow restriction is to reduce blood flow going into the limb, but not completely occlude blood flow. So in other words, we always want blood flow to be going in. So there is a tremendous amount of variability in how the pressure was applied early on. That's improved substantially, an improvement in my opinion at least. The early studies would take a cuff and apply the same pressure to every single person. Independent of their blood pressure. Independent of blood pressure, independent of limb size, independent of the cuff size that you're using. So all of these things are important factors that you can account for by doing this one measurement.

That's how we do it now. But obviously, it's easy to look in the past and throw stones, but there are certainly a lot of variability. So given that the idea is to restrict blood flow, but not occlude it completely during exercise, what we started to do and others have started to do as well is before we do exercise, let's just take the cuff up to the lowest pressure of which there is no flow at all. So if that's a hundred millimeters of mercury means that you no longer have flow going into your limb at all, let's take a percentage of that. So we know that you always have flow during the exercise. Now, do you determine that with Doppler at some distal point to the occlusion? Yes, you can use ultrasound. We use just a handheld Doppler probe that's essentially detecting the pulse. So we can look at it here. We look at it at the ankle.

So before we have anybody do any exercise, we just lie them down. We slowly inflate whatever cuff we're going to use because the cuff size matters. It's gonna totally change the pressure applied. So we slowly inflate it until we don't hear any more flow. And then we take a percentage of that. So if the arterial occlusion pressure, which is the lowest pressure of which there is no flow,

if that's 100 millimeters of mercury, then we'll typically apply anywhere between 40 and 80 millimeters of mercury in our lab at least. Yeah. So two points I want to make, or 1.1 question. The point I want to make that is a very important one that you just made is that this idea of cuff size matters, right? Because the pressure and the force are related by the area that that cuff takes up. So is it safe to say that the wider the cuff, the lower pressure you need to reach occlusion? Yes, that's definitely true. And I think some people interpret that to mean that, does that mean that a wider cuff is better because the pressure is lower? I would say no, because it's pretty much relative. Some would argue that

the wider the cuff is, you might actually attenuate some of the growth beneath the cuff, but certainly the size of the cuff will change the pressure. So as you said, the wider it is, the lower the pressure that you need. But again, as long as you apply whatever cuff that you're going to use to whatever limb you're looking to exercise, taking one measurement can account for everything. So then my question is, when you say 40 to 80%, that is a very wide range. That's like the difference between 40 millimeters of mercury and 80 millimeters of mercury when 100 millimeters of mercury is the occlusive pressure could be the difference between comfort and discomfort as an example, right? Yes. So typically we use 40%. 40, four zero. Yeah. Okay. That's the pressure that we use when all we care about is muscle adaptations. In other

words, increasing muscle size and strength. Now, you can see the same adaptation at 80% with a little bit less work because you're going to fail sooner, but the discomfort is going to be much higher. Now, I think the other component of that is that's muscle adaptation. Now, we have some data, it's very preliminary, but some data that suggests that some of the vascular changes might actually require a higher pressure.

So vascular changes meaning kind of a change in form limb blood flow or form conductance. So that's a gross measurement of basically the vascular network. So there's some indication that maybe you do need higher pressure for that. But that's one study. We did observe it in both the upper and lower body, which gives me a little bit of confidence, but it's one study. But with muscle, I feel pretty confident saying you can use a moderate pressure, 40%, or a high pressure, 80 to 90%, and the adaptation is going to be pretty much the same with respect to muscle size and strength. The discomfort might be, or will be quite different.

Will be much higher with a higher pressure. How much variability is there between an individual's tolerance for discomfort at a fixed occlusive pressure? So I love the idea of using 80% of occlusive pressure because now it's not a given number, it's 80% for that individual. So in theory,

everybody is experiencing the same amount of relative occlusion. But if you took a hundred people and let's even make it more homogeneous. If you took a hundred fit people and you simultaneously applied 80% of occlusive pressure to bilateral upper extremities and just had them sit there. So we'll do the first experiment where nobody does anything. What would the bell curve look like? How tight would it be for the time at which a person cries uncle? And the pressure is 50%? You pick a number. I said 80, but... Okay, 80. I don't know the minute. We have done some discomfort studies applying 40% and just having people sit.

Yeah. So at 40%, what's the answer? It's pretty low. We stopped it at four minutes. We didn't have anybody who couldn't do it. But you are going to have some people who do experience that as more discomforting than other people. But it becomes much greater when you obviously combine it with muscle contraction. But yeah, you're right. So when we say 40% AOP, that doesn't necessarily mean a 40% reduction in blood flow either. Those are two separate things. So when we apply 40% of AOP, the reduction in blood flow might be different depending on how big the muscle is, a variety of other things.

And the discomfort associated with that will also vary depending on the person. There's some people who we have who they perceive almost everything as extreme discomfort, whereas we have people on the opposite side as well. But in general, we see, I can't think of the actual numerical value, but we have 40% is right here. And then with 80%, it shifts, meaning that the average is certainly higher. But there are certain people who, you know, the discomfort they feel at 40 is not different than it is at 80 because they already rated it so high. So, I mean, that's the limitation of the scale, but yeah, you're right. What is the approximate blood flow restriction that occurs at 40% AOP? How much of the blood flow, arterial flow is being limited and how much venous pooling

is occurring? I don't know the actual percent drop off the top of my head. It isn't 40%. On average, it's a little bit less than that, depending upon the position and depending on what you're doing. But yeah, in general, I think during the rest period, you probably do have venous occlusion because it doesn't take, it's not thought to take a lot of pressure to collapse a vein. So during the exercise, you're obviously pumping it back out with the muscle pump. But I would say at a, at say at most of the pressures that we apply, at least at rest, there is venous pulling occurring. Yeah.

Today, I finished my workout with a set of leg press. So did 30 reps, rest 30 seconds, 15 reps, rest 30 seconds, 15, rest 30 seconds, 15. And I'm not sure what hurt worse, just the 30 seconds in between or the actual last two sets, the 15 reps on the last two sets. I mean, the whole thing was just so wildly uncomfortable. Again, I'm flying by the seat of my pants, not doing this based on occlusive pressure. So I don't know how far off I am. It's something I'm looking forward to diving deeper into. I think you've already convinced me I should be more scientific in my approach because I'm sort of white knuckling it and putting these things on and screaming for dear life. So I'm in pain kind of before the, I'm sort of very uncomfortable before I start.

And even after that first set of 30, I'm questioning my sanity. So who knows, maybe I'm applying too much. It would seem that the directionally, would you have a nomogram of occlusive pressure versus expected number of reps at a percentage of one rep max? Yeah, that's also tough. I think most of the loading that we use is 30%. And to be honest, if we have somebody who's stronger, they're not getting 30, 15, 15, 15. There's no question they're going to be at failure. Most of the time when we actually do experiments, we just have people exercise four sets

to as many repetitions as you can. That way we can at least hold that constant so we can control for effort. But I do think that you can use the number of repetitions as a weak surrogate of blood flow restriction. So I would say that if you're using 20 or 30%, you should be getting close to 30 repetitions. No, no, for the first set.

So, and then close to 15, you may get 12, but if you can't get 30 on the first one or get close to that, the load is probably too high or the wraps are too tight. I would say that if you're in pain before you're starting, it's too tight. I would say that if you're in pain before you're starting, it's too tight. And we've done a lot of work on practical restriction as well. I would say that practical meaning where we don't really know how much pressure is being applied. We're applying a knee

wrap. That's what I refer to as practical blood flow restriction. I think if you are rehabbing or you're in a clinical setting or you're working in that, I think you really need to know the pressure that you're applying. I think if you're a healthy person in the gym who wants to use blood flow restriction, I don't think it's all that important to know the pressure. Assuming you have the discussion that we're having now where I know the load is low. I apply the wraps. I'm in pain. Well, then the wraps are too tight.

So I loosen them up. Then I can get close to 30 reps and then close to 15 on the last three sets. Now on the last one, depending on how strong you are, you might fail pretty quick in that fourth set. That's okay. But I do agree with you that I think that you can use goal repetitions as a way to have some idea at the level of restriction that's being applied. So when you're at 40% occlusive pressure, what would be the kind of maximum period of time you would let a subject stay under that pressure, both in terms of the combined lift recovery period? under that pressure, both in terms of the combined lift recovery period? Yeah, I think if they're just starting out, I think it one, it depends on are they resistance training? Or are they doing kind of low intensity aerobic exercise? If it's low intensity aerobic

exercise, you can probably keep it on for 30 or 40 minutes, because it doesn't feel that discomforting, because you're you're exercising at a low intensity. The cuffs are not all that tight. You're not building up a tremendous amount of metabolites, probably why you're not also getting a tremendous amount of adaptation. But with resistance exercise, I think if you're just starting out, it's hard to have a minute, I think maybe seven, eight, nine minutes, 10 minutes or so. I would say one exercise is a good place to start. We've done it early on. We did multiple exercises for people who are untrained and that's pretty tough, but I would say, you know, start off with four sets of an exercise and then take

the cuffs off or take the wrap off. And then you might be able to eventually work up to a couple, but I wouldn't with resistance training. I don't think that you should leave it on continuously for probably more than a few exercises, but if you've never done it, I wouldn't go beyond one just so you can start to kind of see what it feels like. And so if 40 to 80% of occlusive pressure is the technical way to do it, what other metric do you, would people use if they don't have access to a Doppler? For example, if somebody knew their blood pressure, I can see why that would not necessarily be... I can see why systolic blood pressure would not be the same as occlusive

pressure. Is it a reasonable proxy? Not always. It really depends upon... If the size of the cup that you're using is very similar in size, then you could do that and base the pressure as a percentage of your systolic pressure. I think the average gym goer, I think one of the things that you could do is apply the wrap as a percentage of your resting limb size. So there's some data that's used that. One of the ways that we've tried to work with is condition people to feel what 40% is supposed to feel like.

So you would have to have the device one day. So we're doing this because there are some places that are applying this to clinical populations where they have only a small amount of time with the patient and then they send them home to do exercises. The idea being is that you could be with the patient, have them feel what 40% is supposed to feel like, and then say, when you get home, try to mimic this pressure. So we've had some success with that. We are able to get people to, on average, rate around 40%, but the individual level

is anywhere between 20% and 60% of AOP. So it's not terrible, but it's not very good yet. So it's not terrible, but it's not very good yet. One of the things that led us to that is that initially I was on a paper a long time ago that said you should rate the pressure based on seven out of 10, because that can make sure that the pressure will be sub-occlusive. And that's overall pretty much true. The issue is, is that you have a tremendously wide range and it's not reliable, meaning that on day one,

you might say seven out of 10 is 90% AOP. The next day, it might be 10%. So we don't really recommend that scale anymore. We're interested in this idea of conditioning and or using a percentage of a resting circumference and or what we talked about earlier, we use repetitions as kind of a goal. The cups I have are super cheapo cups. I feel like I want to invest in sort of nice ones, but the one thing they have on them is numbers. So I've got a sense of like on arms, I need to be between seven and eight and on legs between 11 and 12. And sometimes I just overcook it. And after the first set, I have to loosen them if I want to have any hope of completing the exercises. And then going back to weight, 20 to 40% of one rep max is about the place you like people to be.

Yeah, I generally prefer lower, meaning around 20 or 30%. There are some people who creep up to 40. And so I just think that the real utility of using blood flow restriction is the fact that you can use it with very low loads. So that's the benefit. We've tried to combine it with high loads in different aspects. And other people have run training studies with it,

but it's not additive. So it doesn't add anything more to high load training. And it's probably because high load normal exercise is a maximal stimulus. So it's hard to maximize something that's probably already pretty much maximal in a given training session. So that's why I'm like, if you want to lift with heavy weights, then just do that. I think the utility of using blood flow restriction is with

that you can use lower loads. Any playing with the speed, either concentrically or eccentrically? And does that matter? The slower you go, the less repetitions you're obviously going to be able to do. I don't think that it probably matters overall too much, especially for growth. The pace that we typically use is about one second up, one second down. So relatively quick pace. Some people use a second and a half. So if you use a second to a second and a half, it's usually a nice controlled movement. We haven't messed with too much in the lab,

but I don't think it would matter too much. I think it would alter how much work you were able to do and the load that you'd be able to use more than anything. Do you think that ultimately time under tension is all that's going to matter? So if you do it slower, but you get fewer reps, it's still okay if you have the same time under tension? Yeah, for the most part. Because when we think about a muscle growing, at least when I think about a muscle growing, where it requires a muscle to be activated

for a sufficient duration of time for all those signaling pathways to be turned on. So from my perspective, there's a lot of different ways for that to occur. You know, you can use really, really heavy weights, you know, repeatedly, and that will do it. Or you can use low loads, or you can use very slow pace as well. I think all of those are kind of doing similar things. You're recruiting these more and more and more fibers, activating them and signaling them to grow. So yeah, I think it would be very similar. And how much rest are you prescribing? I did 30 seconds today. Sometimes I do like a super set where I'll do one muscle, another muscle, another muscle,

and just go back and forth with two different muscles and not take a passive rest. What do you think about those approaches? In general, we use about 30 seconds. That's the standard one that we use in our lab. When I've experimented in the gym, I think that supersetting works really well, especially if you are working out of muscle that's not necessarily directly under blood flow restriction. So for example, the chest, there is some idea that just doing a standard bench press exercise with blood flow restriction around the arms would augment the size of the chest. There's some data that indicates that. augment the size of the chest. There's some data that indicates that. To me, I think a lot of that is driven by the fact that the muscles distal to the cuff, the triceps are fatiguing and the chest

is picking up the load. So in the gym, I like to experiment with that. So do some chest and then superset with some tricep extension or something like that. But we haven't studied that in the lab, but those are things that I've messed around with in the past. Well, it's interesting. I've never thought to do something like a bench press with it, frankly, mostly out of fear. But I guess if you adjust the weight low enough, it shouldn't really be that much of an issue. I mean, once I did deadlifts restricted, I wasn't sure if it was a great idea. I mean, it was very lightweight. It was probably like 135 pounds. So it was not the type of weight I felt like I could ever hurt myself with. But I was like, okay, well, let's do 30 reps here of 135 pound deadlift under

restriction. Truthfully, I thought it was pretty freaking cool. I think in the end, I didn't keep doing it because I was like, well, look, I don't want to develop bad habits deadlifting under such fatigue. What's your thought on doing complex multi-joint movements? Yeah, there is data looking at bench press, squat, and they have seen some benefits. I generally agree with you. I think that you can do those, assuming that you're using lightweight. I tend to prefer kind of isolation movements, especially if the goal is growth. But you could do them. I think that you'd have

varying success depending on the movement. The deadlift, I mean, if it's a Romanian-type deadlift, maybe I could see that having maybe some sort of benefit. But I think I'd have a similar thought as you. It's like, am I going to change my mechanics somehow and then put myself at risk and then really require blood flow restriction in order to train because I'm hurt? So yeah, you can do compounds that there's certainly evidence that suggests that it can help with the squat help with the barbell bench press we tend to use isolation movements and for research purposes obviously but i i tend to feel that a little bit better and i feel a little bit safer doing those type of exercises let's talk about risks because i know

that when people think about blood flow restriction, I've had people ask me, are you worried about rhabdo? Are you worried about nerve damage? Basically, what are the risks of this and what's the safety profile? Sure. So I think that's a completely reasonable kind of response when you're telling people that, hey, I'm restricting blood flow. And I think you should might consider it. I think the first response that I would hope a person would say is, what's the safety of that? I think a couple things. One, it helps to understand that this is a very acute response. In other words, we're restricting blood flow for minutes, not for hours.

So I think that that's important. I think the safety profile overall is comparable to that of high-load exercise or traditional exercise. There are two concerns that people generally bring up. First is blood clotting. Second is muscle damage. In other words, does it increase the risk of blood clots? Does it increase the risk of muscle damage? And I think those are the way I stated that is how it should probably be stated. So anytime we exercise

or anytime we wake up and live, as you know, there's a risk. There's always a risk for something to occur. In my mind, the question, the important question is not, is there a risk? But when we add blood flow restriction, does it increase the risk? And it doesn't appear to, at least at the group level and mostly healthy individuals. So it doesn't increase the risk of blood clots. And that has been looked at in some clinical populations as well, which is good. It doesn't increase the risk of muscle damage. You will get sore, but when we look at the fiber, it appears to be intact. So it doesn't appear to be some structural damages at all. Have there been studies where they've measured CK levels and contrasted them with and without restriction? And does there

appear to be more breakdown, at least measured by CK? No, generally when they look at most of those, there's not a whole lot of difference between the same exercise without blood flow restriction. There's certainly soreness that I feel confident about, but not necessarily structural damage. Another one that's been kind of brought up is the blood pressure response to this exercise. So proximal to the cuff is blood pressure going up centrally in the heart, the aorta, the brain. Yeah. And compared to the same exercise without it, it usually is higher, but it's usually comparable to that. If not a little bit lower than high load exercise. So I think the key component of that is of course, it's probably going to be higher. You're

restricting blood flow, but how high does it get and how quickly does it return back to baseline? So I think that those are kind of two important components. Now, when we've compared it to high load exercise, it's usually pretty similar. And it usually comes back down to baseline within five minutes that those are healthy individuals. Now there was a paper written on it suggesting that that's great, but there are certain populations where they may hyper respond to that. And I think that's a good point. So I do think that it might be something to consider. You know, if you have some sort of clinical ailment, you might want to, you know, if you might be hypersensitive

to that reflex, that might be something to really think about. In myself, when I think about doing unrestricted heavy movements, so five to eight reps of deadlifts or something where I'm really going for it, that feels like I have a much higher blood pressure than the blood pressure I feel like I'm under doing blood flow restriction. Even though there's a much greater discomfort with the blood flow restriction. I never really get the feeling like my head's going to pop off my shoulders, which I commonly feel when I'm doing a heavy deadlift. Yeah, I agree. And I think that's a lot of the intramuscular pressure all over, you know, a systemic kind of restriction.

Well, yeah, because I think when you're really lifting heavily, the intra-abdominal pressure is what allows you to do it. And, you know, that's actually compressing the aorta. So it'd be interesting if you really think about where the pressure matters the most. But I would say that overall, it does appear to be very safe. You know, that's something that we're, we've been interested in for a long time. appear to be very safe. That's something that we've been interested in for a long time. I do think that as with anything, when you give a drug in a large clinical trial, you start to see some side effects that you've never seen before. So my guess is that when it becomes more and more and more popular, we will find there will be certain rare events that we've never seen before.

There will be certain rare events that we've never seen before, but I think in the actual studies that have been done, we see it to be overall relatively safe. It doesn't increase the risk at least, assuming it's done appropriately. Has the following experiment ever been done where you take, well, in an ideal world, I guess you would take the same subject, right? So you have them do the exact same exercises for the same number of reps. So you take, let's say 30% of one rep max and do the 30, 15, 15, 15, but one of the arms is occluded. The other is not. So the one that's not is not hurting at all. That should be pretty easy to do that in the unoccluded side, correct?

Correct. So you're exercising one arm under blood flow restriction and the other arm is not? Correct. But you're using the same weight, the same reps, the same rest, everything. Yes. Shinohara, for example, same workload. One had blood flow restriction, the other one didn't. That was within subject. Those studies have been done. I think the criticism on within subject studies is with respect to strength, not necessarily muscle growth, because some people think that, not some people, I mean, it is an observable fact that when you train one side, but not the other, the other arm oftentimes can increase in strength. But I'm not sure that that happens when both limbs train. I think the limb actually responds to the local, what it's

been trained to do. So I don't know that it's that big of a limitation with strength, but yeah, those studies have been done. And what are they finding typically when they're under the same load? One side is restricted. One side is not. Is the restricted side still making gains in strength and or size? Yeah. Generally, the blood flow restriction will be better than a work-matched control, even if it's the same person, with the caveat that it's not to failure. And that's the difficult thing if you're using 30%, because 30%, for some people, you'll be reaching failure almost on four sets in the non-included arm. So I think that should be stated. I think when we have one limb trained to failure, the other limb

trained with blood flow restriction to failure, we've done those studies lots. The adaptation is usually pretty similar, but the volume, the exercise volume needed is much lower with the blood flow restriction limb. That's what I was sort of going to get at, which is, is blood flow restriction mostly just a tool to increase or decrease the time to failure and therefore act as a more efficient means to fatigue the various fibers? Yes. I think that's fair to say with a couple of potential things to consider. Blood flow restriction by itself. So just the application of restriction and deflation and some ACL reconstruction post-surgery environment has shown to have some sort of benefit. So that suggests to me that there could be something to the restriction of blood flow.

Same thing when we have people walk very slowly. In other words, they're not really walking to failure or even close to failure, but there does appear to be some adaptation. It's not close to what you see with resistance exercise, but there's something that's a little bit more there. So I think with resistance exercise, that might be a very fair statement to say that you're just causing the muscle to have to activate more of the muscle sooner and fatigue sooner than a non-occluded condition i think that's fair but to say that that's the only thing the only benefit of blood flow nutrition i i don't know that we can say especially considering the vascular response i talked about earlier, that the vascular network, the blood flow, the resting blood flow to the forearm or calf, it does appear to respond with

a higher pressure, but not a lower pressure, despite that both of them are doing a tremendous amount of work. So I think it might be fair to say with muscle with respect to resistance exercise, but I have some remaining questions before I would go all in. So let's get back to something that we touched on earlier. We'll get to it in more depth, which is the relationship between strength and hypertrophy. It's very clear that they're correlated. It's not clear which way the arrow of causation runs, if there is a causal relationship between them. What's the conventional thinking on this? The conventional wisdom or the conventional thinking is that once muscle growth is there, that it's probably contributing to changes in

strength. That's the textbook definition. Neural first, followed by large contributions from muscle hypertrophy. And doing a lot of research in the low load realm, as we've done, I started to really see that maybe that's actually not the case because we almost always see muscle growth, which is similar to or equivalent to that of high load exercise. But the strength, assuming that we're not practicing the test repeatedly, is almost always less. And in my mind, I had a hard time coming up with a lot of excuses. coming up with a lot of excuses. I did for several years, but at some point in talking with my students, we just started to ask the question about, well, where did this story come from about muscle growth playing a role? And why do we even think it in the first place? Because I'm trying really, really hard to make excuses for why we aren't seeing it.

But maybe we should go back to the beginning and see why did we ever think it in the first place? And that's where I think it really becomes difficult for people to have this conversation because everybody has learned the same thing that I learned. It's neural, then hypertrophy, neural, then hypertrophy. And they have a hard time taking a step back and going, okay, but were those studies ever able to actually make that claim? Yeah. So where did that hypothesis come from? What is the evidence in support of the null hypothesis? I think if you

were to get a bunch of people together, and we measured muscle size and we measured strength, bunch of people together, and we measured muscle size, and we measured strength. On average, people who are bigger will be stronger. People who are smaller will be weaker. That's true. And we've seen that. We've documented that ourselves. But that's not an effect of exercise because we see the same relationships in people who have never exercised in their life. You're saying that the correlation or association between strength and size is equally strong in the untrained as it is the trained? Correct. The question that we're discussing is when a person begins to exercise and then they get stronger, is that due to changes in muscle size? And that's where I have the

question. I don't question whether or not they're related. I completely agree that they are. But when we exercise, does a change in one result in a change in the other? So it obviously makes a lot of sense that it could. For all the reasons that we said earlier, we're increasing actinomies, we're increasing this protein. Why would they not then produce greater strength? But there's numerous times in the literature where we have shown greater changes in muscle size,

but strength doesn't even change. So that leads me to believe that there could be quite a bit of disconnect with respect to muscle growth and the change in strength. Now, you wrote a paper basically trying to go back to the root of this dogma. I think you basically found that there were sort of three papers that formulated this viewpoint. Two of them, I think, were from the 70s. And then one was kind of a review paper of one of those papers. Am I remembering this correctly?

Yeah. So the one that's commonly cited is Mauritania de Vries or de Vry. And they had five individuals, one arm lifted weights, the other arm did not lift weights. And they were basically inferring muscle growth off changes in surface EMG. So they did measure arm circumference, but that wasn't the variable they were using to quantify growth. They were looking at changes in the slope of this integrated EMG. So if they saw a change in the slope, they inferred that to mean muscle growth. If they didn't see a change in that slope, then they said that was neural. Can you explain to me how that works? I don't know enough about EMG to understand that inference. At least in my opinion, you cannot infer growth off a change in EMG. But what they

were doing is that, let's say, let's pick a variety of weights. So let's say 10 pounds, 20 pounds, 30 pounds and up. So what is the EMG amplitude? So, but EMG amplitude is essentially an estimate of muscle action potential. So how much signal do you get when you lift 10 pounds at baseline versus 20, 30, 40? Then they would do that every couple of weeks. So if they lifted 10 pounds and the, basically the amplitude was a little bit less, they would infer that that was being picked up by muscle growth. Uh, so the amplitude they're using to assess the neurologic signal. And over time, they're saying if the neurologic signal is going down and the effort is the same, hypertrophy makes up the difference. Or for example, yeah, I got it.

One of the points that we're always trying to make is that guarantees that at some point hypertrophy is going to be a mechanism. You're not actually testing a mechanism. You're just assuming that at some point it will be a mechanism. So that was the same thing with Ikai and Fukunaga, which is the other study. So they actually did measure muscle size.

And to my knowledge, that's actually the first study to actually document changes in muscle size. And to my knowledge, that's actually the first study to actually document changes in muscle size in response to resistance exercise. So what I would call a landmark paper, I really enjoy the paper. But what they infer is, is that if muscle growth changes, then it must be playing a role. And if it doesn't change, and they got stronger, then it must be neural. And that's kind of where we've been at ever since. In other words, that when we run a training study, if you get stronger, but we don't document a change in muscle size, it's neural. If you get stronger

and we measure changes in muscle size, well, then it was neural and hypertrophy. So to me, I don't think we can make that claim because you're just assuming that the ability to document it means it's actually doing something with respect to strength. I would like to see a little bit more rigor in that. I understand why people would think it. I get all of that. That makes sense to me as well. But my question is, is that does it actually? And we've approached this through a variety of different ways, but I think it does help to think about this historically. Where did this come from? And it really does seemingly come from those two studies. And then Digby Sale had a very, come from those two studies. And then Digby Sale had a very, really great paper reviewing kind of all the work that had been done, where he suggested that most training studies are only

documenting a certain aspect of an actual person's training age. So they're never going to be able to actually answer this question because the studies are too short. But I don't know that that's fair to say because more time to freeze is eight weeks, which is the same duration as a lot of other studies that have basically contradicted it. So yeah, you're right. Those are the three papers that are commonly cited for this neural first followed by hypertrophy. Even outside of BFR, which seems to provide a very elegant tool to test the hypothesis, as you've explained, and we'll get into in a little bit more detail, it seems that you could do other experiments to test this even without blood flow restriction.

For example, couldn't you have somebody do workouts where they only do one to five reps of exercises and they're basically always functioning. And each of those is to failure, right? So if you're doing one rep, it's a one rep max. If you're doing two reps, it's 95% of one rep max. If it's three reps, it's probably 90%. If it's five reps, it's probably 85% of one rep max. So you cycle through those workouts where you increase strength. In fact, I'll put a very practical example to this. I know specifically athletes who train this way and they train with a trap bar and they do not do the eccentric motion. So they lift the weight up

and drop it, lift the weight up and drop it. And they're never going above five reps. So they're really trying to maximize strength, which comes more from the concentric movement. And they're trying to minimize any hypertrophy because they're athletes for whom strength to weight is the most important ratio. So it's very typical workout for runners. So they'll dramatically increase their strength without adding size. And then you could compare that to the opposite type of workout where you do more of a bodybuilding workout. You're probably never going below eight reps and you'll get bigger. And I could imagine a scenario where you don't even get as strong as that other person. I mean, wouldn't that demonstrate how uncoupled these two metrics can be? Yes, I agree with you. And we've done this

several times now. We've tried to address this question via study design, doing something very similar to what you said, where we have one group that's training, just doing the one RM test. That's it. they come in they work up to about five total reps and then they go home because we're trying to maximize the strength signal but not get growth because essentially to answer this question we have to know if the muscle did get bigger and stronger what would strength look like if muscle growth had not occurred? So when we look at the traditional training group, we have them doing about eight to 12 reps. And this is a very simple

movement, the bicep curl. In that group, we see muscle growth and we see a change in strength. Now, what a majority of articles would do is say, given that muscle growth is there, that muscle growth must be contributing to strength. In our mind, we have to say, well, what would strength look like if growth hadn't been there? And when we look at the other group that was just doing 1RMs, the strength is the same. Now, it's not greater, but it is the same. now it's not greater but it is the same i i do think that the more complex the movement becomes the the greater that separation starts to happen so we were doing a barbell bench press my guess is is that the group doing one rm or close to a one rm would be far better than an eight to twelve

but it's just the fact that the movement is very, very simple. So similar to what you said, in our mind, this does provide some method of trying to address this because we see a group with no growth compared to a group with growth, but the strength is the same, suggesting that that change in muscle size is not necessary for a change in strength, nor does it appear to be contributing given that the strength is the same. Now, there are limitations with that. One of the big ones is that in order to get that differential in growth, we had to apply slightly different exercise patterns. So one group was doing eight to 12, still a high load, but not 100%, where we had another group

training at 100%. So some suggested that, well, that's not really that fair of a comparison. There's more things that are different than just the muscle growth. And that's true. And they suggested that instead, that we should follow that up with some mediation analysis, where we look at how much of this change relative to a control is driven by muscle size within each group individually. And when we did that, we did not see any mediation, meaning that none of the change in strength could be explained by that change in muscle size in either one of the groups.

Explain that more for me. I'm not sure I follow how you would determine that. So there are some statistical kind of approaches where you can do some causal mediation. some statistical kind of approaches where you can do some causal mediation. In other words, you can look at the relationship between, let's say we have these two exercise groups. So instead of looking at them head to head, let's look at them individually compared to a group that's not doing any exercise at all. That way we can kind of really control for the random error across time. So measurement noise, random biological variability, et cetera. Essentially what mediation is doing is saying, okay, we have this group here. How much strength did they gain? So they got stronger. So that's a direct relationship.

So when this group exercises, they got stronger. Now mediation says, okay, let's add in a variable here to see if we can remove this relationship either partially or completely. So if we add in muscle growth to the model, and then this group no longer correlates with strength, then we'll know that that relationship is completely driven by this other variable. Now, we wouldn't expect for it to be completely, but we would expect for it partially. But we didn't see that in either one of the groups. Is the contrapositive then that it's not at all coupled? Because if you were to ask me what my intuition is, which is worth maybe a warm bucket of hamster vomit, my intuition would be there is an association, but it's not 100% causal. So the R squared might be 0.5, not 0.99. So in other words, I would not guess that there is no association. I certainly wouldn't guess a negative association,

but I wouldn't guess that it's one-to-one causal. Can the mediation tease that out? Yes, because it would be a partial mediation in that sense. And you did not see a partial mediation? No, we didn't see any effect at all. Now, there are other potential reasons. I mean, we have to think about random error across time with our measurement and things of that. I don't think that any of the work that we have done so far can conclusively say that it plays no role. But I do think that we're having an accumulating amount of evidence that's suggesting that if it does play a role, it is so small that we aren't able to ever detect it. So I am not sure that muscle growth

in response to exercise is a mechanism. I've seen no experimental evidence that suggests that that's the case. Now, for a practical, pragmatic person, what would that mean for them? Well, I think what it could mean is, is that if you are interested in maximal strength, in getting as strong as possible, you probably don't care whether it's a mechanism or not. You just wanna know, how do I get strong? I think we can learn a couple things from some of these experiments.

One, that there's a huge specificity component, meaning that if you want to be a very good squatter or a very good deadlifter, and being very good squatter or being a very good deadlifter means you're able to lift as heavy as possible one time, then that means you should be training at least a good portion of the time at or close to that one RM. at or close to that one RM. Now, if you really believe that growth might be playing some role, what that might mean for you is to say, well, if it is playing a role, it might be pretty small. So maybe I can allocate less overall time to it, which would be good for most strength athletes, because that's typically what requires a lot of recovery because you're doing a lot of volume to make a muscle grow. So I become more skeptical of muscle growth as a mechanism every year that goes by. We're still doing more experiments to try and address this, but there certainly is no evidence right now that suggests that it is a mechanism. We have a lot of evidence that suggests that it isn't, but I do think it would be premature to say, well, we've completely ruled it out. I don't

think that's fair to say at all. So what are some other explanations? I mean, I guess nobody's disputing the neurologic component to this. Is one hypothesis that that is the entirety of it, or do you think that there is another mechanism that isn't fully clear? the entirety of it? Or do you think that there is another mechanism that isn't fully clear? Yes. I think some people would say that some people are of the opinion that the exercise induced changes are probably predominantly neural. I'm not there yet. I think that there could be some local changes at the muscle and that might be able to explain why some groups get stronger. That's not just neural. In other words, maybe the muscle at the local level is actually getting better at responding

to forceful contractions. So maybe it's, you know, how it deals with calcium or how the myosin head binds. Maybe there's some alterations there qualitatively that aren't due to muscle size, but I don't know what those would be necessarily. I can only offer potential reasons. And I think that's usually the argument that's brought up mostly against our point is, well, if muscle growth is not a mechanism, then what exactly is it? And I don't think that that's a fair argument, honestly, because I don't know that you have to know for sure what something is to say, we don't have a lot of evidence for this. And there's a lot of evidence against this,

but that's just my kind of thinking. But I do think that there probably is a huge neural component, but I don't know that there isn't something going on at the local level that is independent of a change in muscle size, but it is still muscular perhaps. So how common is BFR with athletes today? I think it's becoming more and more common. I know at Ole Miss, for example, as well as a lot of other division one schools in the athletic department, I would say a large portion of them do have blood flow devices. So they are using it for rehab. And I know that I've seen players on ESPN and the NBA, NFL using blood flow restriction as well. For rehab exclusively, or do you see them using it when they're not injured as well?

I think there's a couple NBA players just looking at some of the stories where they were using it not for rehab, but just as an everyday kind of way to train where they were able to recover just a little bit faster. And they don't have to have a, as they've aged, you know, they want to make sure that they're ready to play on the actual court instead of just spending all their time recovering from their workout. So I think that they, they perceive this as one option to use where they're able to get some kind of workout in, but maybe recover quite a bit faster than they might doing normal exercise. Is the speed of the recovery, a function of less trauma to the

muscle during the workout or why is their recovery quicker? I don't know that we know that, but I, it does appear that when they are injured and they're working out with blood flow restriction, they're able to usually to get a little bit more out of that compared to high load exercise or at least very similar to that but they have less pain during the movement so maybe they're able to get a little bit more out of the rehabilitation than they normally are because maybe they're before they're inhibited to a greater degree with by pain that's reduced a little bit through the application of blood flow restriction but i don don't really know, to be honest. Let's take an extreme, a bodybuilder, right?

Where they're not being judged at all on strength. I mean, I have yet to see a bodybuilder who's not very strong, but presumably due to just the overwhelming amount of volume in their training. But I even talked about this with Lane on the podcast. And he was explaining how, look, at the end of the day, the volume is what's going to matter. And, you know, you can do that with isolated movements. You can do that with compound movements, but you just need to get lots and lots and lots of volume across these kind of ranges. So if the goal is purely hypertrophy, which at least during part of the bodybuilder cycle is the case, how would they utilize BFR? First of all, would it be a valuable

tool above traditional training? And if so, what would be the optimal way to use it? Yeah, I think it could be. It could be a tool if that's how they choose to use it. I think for muscle growth, I think I agree with Lane that it really comes down to personal preference because even without blood flow restriction, we've seen from 30% up to 80% or even higher can produce the same amount of muscle growth. So I think that allows you to have some level of preference on based on how you feel that day or what you enjoy. There are days where if you have a heavy day, for example, and you're going to the gym, but you don't feel good or you're not psychologically have it. And it could be potentially dangerous for

you to use a heavy weight because you're not focused. Then maybe that's a time where you might be able to implement some blood flow restriction because you can use light weights. It doesn't require as much focus. And you could probably see a lot of the same response, at least with growth. Another component could be is that it just helps with some variety. I don't think that variety is necessary per se for muscle growth to be optimal. But I think if you're training for an extended period of time across your life, things can get pretty boring if you're just doing the same thing all the time. So it could be a way to try and spice it up a little bit.

And then obviously, if you're hurt, it could be a great tool to use because there is a lot of or becoming to be more and more evidence that it's helpful in the rehabilitation world. So I think there's a variety of ways that it can be used. But I do think that it's probably important to note that if a person's not comfortable with it, they don't have to do blood flow restriction in order to optimize how much muscle that they can grow. But it is a tool that could be potentially quite effective for them. Yeah. Actually, the example you gave is exactly what happened today, which was today's main set for me was a five by five deadlift. So obviously that's a heavy-ish day. And I took five sets to warm up to get to the starting weight. That first set of five,

I was like, yeah, I'm struggling. Second set, still struggling. Third set, struggled more. Fourth set, I was like, boy. And I'm supposed to be escalating the weight. And on the fifth set, two reps in, I thought, this is the day you hurt yourself because I'm going to break my form to get number three, four, and five. So I actually just stopped. And that's why I went and did the leg press with blood flow restriction, which was a very light weight. I mean, I don't even remember how many pounds it was, but it was the type of weight that if I wasn't restricted, I could have done a hundred reps, I'm sure. So, but it was a great way to mix up the training and that's the kind of stuff I'm interested in exploring. I also kind of think of this as a tool for people who maybe don't have some of the

technique to do heavier lifts much in the same way. I've sort of thought of the super slow lifting protocols as reasonable protocols for people who just don't have the desire to train at higher volume and frequency and, or don't have the technical chops. Now that said, I've always felt that the problem with super slow training is unless it's done to failure, which is upsettingly painful if you've tried those workouts, it's probably not nearly as beneficial as traditional training. The sort of super slow advocates will say it's on par with traditional training, right? You could do 20 minutes once or twice a week and have the benefits of six hours per week. I'm not sure that that's true even from a hypertrophy standpoint, but if it is true, it's probably limited to the few people who truly can fail. And I don't know

if you've ever tried these super slow workouts, but it's very difficult to truly fail. I think it's very hard for, I think, most people. Yeah. A long time ago, but I never did much with it. There was somebody that I worked with in my PhD who was very interested in it for a while, but yeah, I was never really a fan for sure. How come? For the same reason or? I never felt like I was going to get very strong from doing something like that. I'm just moving so slow and the weight is usually so light that I don't know how much that would be transferring over to something that I was interested in at the time, which was to get as strong as possible. It's definitely hard. There's no question, but I didn't enjoy that form of

training. So it's safe to say that the one place, I think you really talked about this already, but I just want to make sure we put a dot on it. The one place where it's unambiguous that you need to be doing a traditional lift without restriction is if you're training for maximum strength of that lift, which again, I don't think most people are doing maximum strength bicep curls. I don't think that's, but when you start to talk about a bench press, a squat, a deadlift, a leg press for that matter, if you care so much, there's probably no substitute for being in that 80% to 100% one RM. Is that kind of a safe takeaway? Yeah. And if you do blood flow restricted exercise with low loads,

assuming it's not extremely low, like if you're around 20 or 30%, you will get stronger, but it will be to a much smaller degree than you would with traditional exercise. I completely agree. And I'll just add too, we get this a lot where it's like, well, you're doing bicep curls in your study. It's like, because we're using bicep curl, it's a research model to answer a particular question. We're not personal training people. So I think sometimes people lose the reason why certain things are done. Sometimes people will look at low load literature with blood flow restriction or even low load literature without blood flow restriction and say, yeah, but look at this study. They found very similar changes in strength as high load exercise. And some of those studies do exist, but the majority of those that do find that

effect, if you look at the methods, what they're doing is the low load BFR group is doing the 1RM every two weeks or every three weeks. And they're doing it in an effect to try and reset the load so they can assume that they're progressing. But what they end up doing is practicing lifting a heavy weight. So you're not actually studying low loads of BFR. You're studying low loads with BFR plus 1RM training. And I think that that's a very important point. And we actually reviewed this. We published a paper on this topic where we show that when you only look at the studies with low loads that don't practice doing a 1RM test repeatedly, almost all of them lose the high load exercise.

Just again, illustrating the point that it's about lifting heavy weight is the best way to get better at lifting heavy weight. It doesn't mean that you won't get stronger lifting lighter weight, but you won't be as strong as you were. Let me summarize what you just said, because I think in terms of big picture, there were really two areas where BFR shines. One of them is in an individual who for some reason can't lift heavy weight, but still needs to get stronger and potentially bigger. And the obvious example is the person who's recovering from an injury. And then potentially the person who just has a concern about lifting heavy weight, either from a technical standpoint or injury avoidance or things like that.

The second place where BFR seems to really stand out is in hypertrophy. Most of these studies are demonstrating slightly superior hypertrophy response despite less total volume and certainly lower load. It's at least as good in hypertrophy and in some cases better as my reading of the literature. If you have a low load with BFR compared to a work-matched low load group without BFR, hypertrophy is better almost always. And to make them equal, you will just have to go more on the, on the, you'll have to go to a greater degree of reps on the unrestricted side to failure basically. Yep. And therefore it takes more time to get the same effect. So, so it's a more efficient way potentially to generate hypertrophy is probably more accurate than what I said earlier.

Now, the vascular adaptations, again, I keep putting that caveat in because it's always in my mind because I really expected that to be the same across the board as well. Meaning that as long as you're doing a lot of repetitions, it shouldn't matter whether there's BFR or not. That's not what we found. Now, whether or not that can be repeated, I'm not sure. Hopefully we can do that in the future. But because my thinking for a long time was similar to what you were saying earlier. It doesn't really matter whether there's BFR or not.

If you do enough, it'll be very similar. The workload will just be less. And I think that, again, is true for muscle, but I don't know if that's true for every single variable. Let's talk about the mechanism by which this is happening. My assumption, which I don't know if it's right or wrong, is that at least one of the reasons that BFR can produce so much hypertrophy at such low load is in response to the metabolic challenge that's posed. And so one of the things I was doing quite a bit was testing lactate levels with and without BFR. It's very easy to demonstrate that when you occlude your arm, for example, well, distal to that occlusion, lactate is going through the roof because you're exercising that arm and you're not letting the lactate clear out of circulation. So I'm pinpricking my finger and getting very,

very high lactate levels. And so that's obviously a metabolic by-product of anytime you're exercising. And then especially when you're doing this type of exercise. And so, yeah, I could demonstrate that I had a higher level of lactate doing blood flow restriction than not, even when I was lifting slightly more weight and doing something traditional. Do we think that that matters in this equation? Do we think that that's partially driving this? And that's just one of the metabolites that we can measure easily. There's plenty that we can't. Yes, I would agree. I think that there's kind of two schools of thought. One is that the pulling of these metabolites in and of themselves is turning on some of these anabolic signaling pathways, meaning just the fact that you're pulling lactate

around the fibers, that that's able to activate growth. I used to be interested in that idea. We tried to test this using a couple of different ways. We didn't find an advantage to doing that. So we kind of started to say, well, maybe there's nothing to metabolize in and of themselves, but maybe it's what they're causing the muscle to do. So in other words, maybe the way we think about it now is, is that as you said, you're exercising with blood flow restriction, the metabolites are being trapped. What we think is, is that they're augmenting muscle activation. So they're causing the muscle to have to work a lot harder than it normally would,

because you're pulling this lactate around it and you might fatigue some of these cross bridges. So we have to recruit more and more and more and more fibers. So that's where we think the benefit of metabolites is, is that they're basically inducing fatigue, which then leads to further muscle activation and muscle activation for a sufficient duration of time is the name of the game, at least in my opinion, for making a muscle grow. So one of the big kind of questions always is, are the mechanisms themselves different from traditional exercise? If I do high load exercise, is that going to be a different mechanism than when I do low load exercise with blood flow restriction?

And I don't think so. And I'll tell you why. I think that the mechanism involved in activation is different. But once the fiber is activated, all the signaling pathways, from what I understand, are going to be very similar. So when we lift a heavy weight, it requires a tremendous muscle activation to even lift one rep. If you are trying to do a bicep curl and you're only activating a small portion of your fibers and you're trying to lift 70 pounds of your one RM is a hundred pounds. That's an enormous bicep curl. I was about to say, I really feel pretty pathetic here. Yep.

But go ahead. So choose any lift in order to lift that heavy weight. You need to activate a large portion of your musculature. Otherwise the weight isn't going to move compared to low loads where you don't need to activate a large portion of your musculature. Otherwise, the weight isn't going to move compared to low loads where you don't need to activate the same amount of muscle fibers initially because the weight is extremely low. So when we exercise with low lows in BFR, we're activating only a small amount initially, but those metabolites, as you discussed, only a small amount initially, but those metabolites, as you discussed, start to become trapped and we activate more fibers, more fibers, more fibers, and more fibers. And then by the end,

we've activated a similar amount of fibers as we did with high load exercise. By the way, is there an order in that? So if your one RM bicep curl is a hundred pounds, so with no blood flow restriction, you pick up 80 pounds and bang out, I don't know, 10 reps, eight reps. Compare that with if you picked up 40 pounds and banged out 40 reps. What is happening from a fiber fatigue standpoint under those two scenarios? In general, we have what we call the Hinneman size principle, where you recruit type one motor units first, and then as you require, based on the exercise, you recruit type two in addition to type one. So when you lift a heavy weight, you're getting to the type twos

very quickly because you need them. Whereas with lower weight, you probably are taking a little bit of time, but then you are eventually getting to those type two motor units. So if the person in my example fails at eight reps with 80 pounds and 40 reps with 40 pounds. It's just that the 40 reps took a lot longer to burn through the type one fibers and then the type two A's and the two A B's. And then finally at the very end, the two X failed. Whereas when he did the same exercise, you know, 20 minutes later at 80 pounds and failed at eight reps. He did the same sequence, but he just got to the two X much sooner. Is that what you're saying? Yeah. And the reason why I say that is if you look at, if you pull out fibers following training, type one and type two fibers

have both been shown to grow in both high-load exercise as well as low-load exercise with and without blood flow restriction. So they both respond. Some people have suggested that type one might grow a little bit more with low-load training, but I'm not convinced on that yet. I think that it's probably very similar to high-load exercise, although I see the thinking.

But both of them will grow in response to both types of exercise. In general, at the extreme level, is a bodybuilder's hypertrophy more explained by type one or type two fibers, or are they both massive relative to anybody else? I would say probably the increase in both,, there's not one thing I can point to that would suggest that for me. But I think that in response to training, my guess is that both of them would increase. I think you might be able to make an argument that people who might, again, go back to our argument earlier, who start lifting weights and realize, man, I'm actually able to grow quite a bit. Maybe they already had more type two fibers to begin with, which is

something is more responsive to loading. So maybe you can make that argument. But I think in response to when a bodybuilder exercises, I would probably guess that both of them are going to grow both types of fibers. You mentioned very briefly passive BFR. What's the application for that? Is that in a highly injured person? Yeah. And again, there's only a small number of studies that have shown this. That could be for a variety of reasons. One, it could be because those are hard to do, where you have somebody who had ACL surgery, and then we apply blood flow restriction to their limb. We inflate and then we deflate for a period of time, a couple times a day. And that's been shown to slow muscle loss. But there's only a few studies that have

shown that. Now, again, you don't see growth. You only see a slowing of loss. Attenuation of loss, which is a big, big deal when people undergo surgery. I'm very interested in whether or not that's true. One of the things that gives me a little bit of pause is that there's not more of those studies. So in my mind, I always wonder, is that because those are, again, hard to do? Or is it because those studies do exist, but they didn't see anything and they didn't publish it? So I'm cautiously optimistic that that could be useful. But I do

think that as soon as a person can exercise, you know, and we kind of published a paper on this idea a long time ago, kind of what we view as a progression of blood flow restriction. In other words, someone who wants to, who can't do anything, how do we get them back to doing something? So we start off with, if they can't even walk, we apply this restriction to slow down muscle loss. Once they can maybe walk on a treadmill or walk very slowly, but they can't lift weights, we start to transition them to that phase where they're able to increase muscle size and strength just a little bit. And if nothing else, maintain what they have. But then once they can transition to resistance exercise, I think that's where they're going to see the biggest bang for their buck. And then they can go to high-load exercise if they choose.

But I do feel like that's a very potentially useful progression to this technique. This is such an important question. It's a real shame this isn't being studied. Like if I were czar for a day and I was in charge of where research dollars would be spent, I would be putting, because I don't think it would take that much money by the way, but I would absolutely prioritize this question when you consider the extent of muscle loss that occurs in sedentary individuals following elective surgery, emergent surgery, and injuries. So those are three very big buckets of people, disproportionately, by the way, affected in the elderly, where the effects are devastating. I'm sure you're familiar with

the literature of you take somebody in their seventh decade of life and you train them very hard for a year. They'll put on X pounds of muscle and then put them in a hospital bed for 10 days. They will lose all of it. They will lose every ounce that they spent a year diligently gaining. lose every ounce that they spent a year diligently gaining. To think that there could be a tool that could slow that, and we don't know the answer definitively, strikes me as just unbelievable, unwise decision that's been made. So I would hope somebody who has the authority over where those dollars go is listening to this and realizing that the morbidity and mortality associated with muscle loss, especially in the elderly, is so significant. And one of the things we talk about a lot with our patients is once you get to be 70 and certainly 80 years old, you're kind of one

fall away from the end of your life, even if you don't die directly, right? So there's the catastrophic fall where you hit your head, you have a cerebral hemorrhage and you die. That's not the majority of them. The real fall you are away from the end of your life is the injury that basically never permits you to get back on your feet. Because even when you recover from the direct injury, maybe a broken hip, which is common, you never get back the strength and stamina you once had. I just think BFR should be explored much more in this population. That should be standard of care if indeed it is effective in both the passive and then the, as you described, the progression, right? So passive, low end aerobic, low load resistance, right? So passive, low end aerobic, low load resistance. And ultimately, if you can get back to high load resistance, great. Right. So if you had unlimited resources right now, what experiment

would you want to do? What are the burning questions that if Francis Collins called you tomorrow and said, Jeremy, I've got this extra a hundred million bucks. We've got to get rid of it. What can you do? That's a good question. I would do something with blood flow restriction, of course, but my interest right now is related to trying to figure out why people get stronger. And I think I can always tie that back into blood flow restriction and be able to do things of that sort. But I'm interested in what that means and what a change in strength from resistance training, what that means for overall function of a person. So when I get stronger with resistance training, does that actually carry over to improvements

in my walking ability and things of that sort? So those are some things that I'm interested in. With blood flow restriction, I'd obviously do kind of what you just stated. I'd have to probably connect with our med school in order to do a study like that. But I would be interested in the application of blood flow restriction by itself. I think that that is something that I've been interested in for a long time. Again, I think it'd have to be not something we could do right out of my lab. We'd have to work with something we could do right out of my lab. We'd

have to work with a hospital, of course, but I'd be interested in that. And I'd be interested in doing it on a large scale because all of those studies that currently exist are extremely small sample size. So for, for, of course, for a variety of reasons, but I'd want to start answering a lot of these questions with large sample sizes. That would be kind of my dream studies. Whatever it would be, whether it's strength, whether it's this, bigger studies, longer studies, I think that $100 million, I could do a lot for sure. Well, amazingly, that's a fraction of a penny compared to the amount of research that goes into the fraction of dollars that goes into biomedical research, but that's not necessarily

always allocated wisely. Nevertheless, this has been a super interesting discussion. Again, you can tell personally, I just want to understand this for myself, for my patients. And ultimately, I think this is a very important topic for anybody who's interested in any aspect of that continuum we discussed. So Jeremy, thank you very much. And I'm really so glad that Lane connected us. I'm sorry I didn't have a little extra alcohol. I know Lane mentioned you always like to have a drink when we start a talk and I should have thought to have sent out a nice bottle of tequila for you. Or is it scotch? What did Lane say is your favorite? It's scotch, 100'll, I'll forgive you. You know, maybe we can do it again and we can maybe have scotch next time. Perfect. A single malt, I assume. Of course. Yes. Yeah.

Do you drink it neat or do you add like the one spoon of water to it? I drink it neat generally. Okay. I have a friend from residency, so I don't, I'm personally not a huge scotch guy. I love tequila and Japanese whiskey, but I love talking to people who love scotch and can walk me through the ins and outs of it. But this friend of mine, obviously a single malt guy, would import water from Scotland from a very specific lake. And he explained to me why the scotch would get a little better and it would open up a little bit more and be a little less anesthetizing to the tongue. If you would add just this one spoon of lukewarm water to it. I don't remember the exact reason, but it somehow had to do with diluting it just a little bit to prevent some of the anesthetic effect. But you, you're a neat guy, which I, I like tequila

neat and Japanese whiskey neat as well. Yeah, I'm not quite on that level of drinking where I'm importing specific water, but I do appreciate a good drink for sure. I find it interesting, by the way, you know, on the topic of sort of genetics, I really do think people just genetically can like the taste of scotch or not. taste of scotch or not. And I don't possess the gene, I think, because I've sampled very fancy scotches and I've never found it palatable. But I don't doubt for a moment that you or someone who does finds just as much enjoyment in the actual taste of it that I would, for example, in some of these other things I like. It's interesting because my students make fun of me for this, but I can't drink beer unless it's like a fruity type of beer. So they, they've obviously mocked me for that, but I can't drink beer, but I can drink hard liquor for sure all day. But the, the beer stuff I can't do unless

it tastes like apple pie or something else, then I'm all, I'm on board, but just standard beer can't do it. I'm with you. I think standard beer is about on par with urine in terms of palatability. So I never understood how Budweiser stays in business. Yeah. I can't do really any of that. All right, Jeremy. Well, thanks so much. This was a super interesting discussion. I really appreciate it. Thanks for having me on, Peter. Thank you for listening to this week's episode of The Drive. If you're interested in diving deeper into any topics we discuss, we've created a membership program that allows us to bring you more in-depth exclusive content without relying

on paid ads. It's our goal to ensure members get back much more than the price of the subscription. Now to that end, membership benefits include a bunch of things. One, totally kick-ass comprehensive podcast show notes that detail every topic, paper, person, thing we discuss on each episode. The word on the street is nobody's show notes rival these. Monthly AMA episodes or ask me anything episodes, hearing these episodes completely. Access to our private podcast feed that allows you to hear everything without having to listen to spiels like this. The Qualies, which are a super short podcast that we release every Tuesday through Friday, highlighting the best questions, topics, and tactics discussed on previous episodes of The Drive. This is a great way to catch up

on previous episodes without having to go back and necessarily listen to everyone. Steep discounts on products that I believe in, but for which I'm not getting paid to endorse and a whole bunch of other benefits that we continue to trickle in as time goes on. If you want to learn more and access these member only benefits, you can head over to peteratiamd.com forward slash subscribe. You can find me on Twitter, Instagram, and Facebook, all with the ID PeterAttiaMD. You can also leave us a review on Apple Podcasts or whatever podcast player you listen on. This podcast is for general informational purposes only and does not constitute the practice of medicine, nursing, or other professional healthcare services, including the giving of medical advice.

No doctor-patient relationship is formed. The use of this information and the materials linked to this podcast is at the user's own risk. The content on this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice from any medical condition they have, and they should seek the assistance of their healthcare professionals for any such conditions. Finally, I take conflicts of interest very seriously. For all of my disclosures and the companies I invest in or advise, please visit peterottiamd.com forward slash about,

where I keep an up-to-date and active list of such companies. Thank you.