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

00:00:00.000 Hey, everyone. Welcome to the drive podcast. I'm your host, Peter Atiyah. This podcast,

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00:00:41.720 head over to peteratiyahmd.com forward slash subscribe. Now, without further delay,

00:00:47.740 here's today's episode. I guess this week is professor Jeremy Lonecky. Jeremy is an associate

00:00:54.440 professor of exercise science at the University of Mississippi, better known as Ole Miss. He has a

00:01:00.700 PhD in exercise physiology from the University of Oklahoma and a master's in nutrition and exercise

00:01:06.320 from Southeast Missouri State University. He's also a fellow of the American College of Sports Medicine

00:01:13.180 and a member of the American Physiological Society. He's the director of an applied physiology laboratory,

00:01:19.400 and his research focuses on skeletal muscle adaptations to exercise in combination with

00:01:25.080 blood flow restriction. Now, some of you may have seen me recently posting things on Instagram about

00:01:31.540 blood flow restriction. I've been experimenting with it for some time recently. And in this podcast,

00:01:36.860 I even explained the first time I was exposed to it, which was a little over 10 years ago,

00:01:40.280 was actually in a swimming pool. Blood flow restriction is a general term that applies to

00:01:45.580 occluding some portion of the arterial inflow to a muscle. We get into the very nitty-gritty of this

00:01:52.460 during the podcast. And under these conditions, it becomes harder for the muscle to contract. And

00:02:00.380 what it allows an individual to do is exercise with a lower weight than they would normally do

00:02:07.480 unoccluded. Now, as we cover in this episode, there are lots of benefits associated with that.

00:02:11.840 There's also other terms that you may have heard associated with that. The most common

00:02:16.160 term associated with this from a brand perspective is katsu, K-A-A-T-S-U, which is Japanese for

00:02:24.740 basically training with restriction. Anyway, we get into all of that stuff in this episode and more,

00:02:30.760 but perhaps one of the most interesting things that comes out of this discussion, well, at least

00:02:34.820 from an egghead perspective like me, is that blood flow restriction offers a very cool,

00:02:41.720 way to study the relationship between muscle size and muscle strength. And that's a topic we explore

00:02:47.980 very deeply in this episode. We also start this episode off assuming that you know very little

00:02:53.660 about muscles. So we explain the physiology of the sarcomere, the micro anatomy of muscle fibers,

00:03:00.440 the difference between type two and type one fibers. So even if you come into this and you don't know

00:03:05.160 what an actin filament is and a myosin filament is, don't worry about it. We're going to spend quite a

00:03:09.920 bit of time getting you up to speed on that. And of course, if you already have a PhD in exercise

00:03:13.180 physiology and know everything about that stuff and just want to get to the BFR,

00:03:16.880 no problem. Get to that too. So anyway, without further delay, please enjoy my conversation with

00:03:21.760 Jeremy. Hey Jeremy, thanks so much for making time. I've been looking forward to this one for quite a

00:03:31.300 while, both personally and professionally. This is a topic I've wanted to learn a lot more about,

00:03:35.820 something I've been playing with a lot myself, including this morning, particularly painful

00:03:40.220 session this morning of blood flow restriction, which I might be doing wrong. So I'm looking

00:03:44.660 forward to maybe the end of our discussion when we can get into the practical aspects of it. But

00:03:49.360 I want to take a kind of a step back and get a sense about how you became interested in exercise

00:03:53.840 in general. Obviously you've devoted your career to it. So when did that become a passion great

00:03:59.300 enough that you decided it was worth all of your study?

00:04:01.640 Yeah. Thanks for having me on, Peter. I wrestled early on in my life. So I wrestled from probably

00:04:09.420 the age of five through high school, but I wasn't really into training that much. I was into wrestling,

00:04:15.480 but not really lifting weights or any of the conditioning. And my coaches would always tell

00:04:20.060 me that you need to try to get in the gym. You need to stay in the gym, get stronger, get stronger,

00:04:24.680 get stronger. And I didn't really listen up until towards the end of high school. And then I started

00:04:30.920 one of my friends was really into bodybuilding and powerlifting. So I started training with him.

00:04:37.180 I do feel like it probably helped me a little bit in wrestling. And then I kind of got interested in

00:04:43.640 just trying to see how to make a muscle get as big as possible. I started reading, you know,

00:04:48.880 muscle magazines, which is kind of the common story, training in a little bit. Then I focused on

00:04:55.400 exercise science early on in my undergrad. I was just trying to learn how to make a muscle bigger,

00:05:02.200 how to make a muscle stronger. That's all I was trying to get out of every lecture.

00:05:06.760 Towards the middle of, I guess, my undergrad, you have to make a decision about, you know,

00:05:14.000 obviously, what do you want to try and do with your career? And I was dead set on working with

00:05:18.540 athletes. But then I did that and quickly realized that's not what I wanted to do. So they suggested

00:05:24.740 that I instead, maybe you're really interested in research. Why don't you try and do an internship

00:05:29.840 related to that? So I landed at the University of Illinois. And that's where I met Lane and a couple

00:05:36.140 of other people. And that's where I really came across blood flow restriction. And that's where I

00:05:40.960 started to really read a lot about it and then came back and started to really focus all of my time.

00:05:48.080 So that was around 2007, 2008. So just about, you know, reading blood flow restriction and how I

00:05:52.820 might be able to do that. So I started off with wrestling and then kind of got interested in

00:05:57.520 bodybuilding, powerlifting, and then came across blood flow restriction when I was up at Illinois.

00:06:04.020 You mentioned briefly that you did a little bit of work with athletes, which was obviously kind of

00:06:08.680 a logical, at least place to look. But it sounds like you didn't find that to be what you wanted.

00:06:13.180 Why is that?

00:06:13.660 I'm a pretty mediocre athlete, but I always trained extremely hard. And I think I had this mindset that

00:06:21.280 everybody was going to train what I thought training was and how everybody was going to

00:06:26.700 train as hard as I thought they should train. And when I was doing a little practicum work

00:06:31.280 with some of these athletes, I mean, they weren't world-class elite athletes, but they were fairly

00:06:35.080 good collegiate athletes. I didn't get the same vibe that everybody was into training like I was in the

00:06:40.660 training at the time. It doesn't mean they weren't great athletes. They obviously were. It doesn't

00:06:44.440 mean they didn't train hard, but my perception of how they should have been training was not what

00:06:49.520 I thought it was going to be. So I knew I wanted to be in the exercise world, but I quickly learned

00:06:56.300 that I want to do research, but definitely not with animals. So I came back and that's when I got

00:07:01.500 into human research.

00:07:02.380 So where did you do your PhD?

00:07:04.860 University of Oklahoma.

00:07:06.540 And what was the focus of your dissertation?

00:07:10.000 Looking at different methods of applying blood flow restriction. So looking at different exercise

00:07:16.860 loads of 20%, 30%, different pressures. In other words, we were trying to get at this idea of,

00:07:23.840 do you actually need higher pressures? So in my dissertation, we were doing a lot of acute work,

00:07:29.460 which has obviously a lot of limitations with applying it to adaptation, but we were trying

00:07:35.280 to really see kind of a short-term characteristic of what that response would give. Acutely, what does

00:07:41.760 this response give? What does this response give? And then try and kind of pick out two of the more

00:07:47.580 promising ones and then study them head-to-head a little bit later on, which is kind of what we

00:07:51.600 did once I took a job at Ole Miss.

00:07:54.800 I can't wait to talk more about that. And there's no shortage of questions I have for you,

00:07:59.080 but I was thinking about this last night that before we jump into a lot of the questions I

00:08:04.920 have, I think it will be important for people to really understand the ins and outs of muscle.

00:08:11.380 What's the muscle, the structure of a muscle, not the gross anatomy of a muscle, but obviously

00:08:16.300 the microstructure, the physiology of a muscle. So without worrying about going too deep, I think

00:08:22.600 it's okay to do that. Let's talk about a muscle because I don't think we can get into what we're

00:08:29.320 about to talk about if people don't know what a sarcomere is and what actin and myosin are and what

00:08:34.500 the different types of fibers are. So if I were to sort of take a knife and cut down on my bicep and

00:08:41.820 yank it off the tendon and throw it out there as a, you know, a muscle, how would you explain to

00:08:48.320 somebody what's actually going on inside that thing? Yeah, that's a, it's a good question.

00:08:54.400 When we talk about a muscle, so like just your, the whole thing. So it's like a box within a box

00:09:01.460 within a box. The smallest unit of that is, as you said, a sarcomere, which is actin and myosin.

00:09:09.120 And that's the kind of the proteins that we're ultimately synthesizing when we exercise. So we're

00:09:14.680 making more of those. And if you make more of those than you break down, then obviously the

00:09:19.100 muscle will get bigger. So when we actually exercise those actin and myosin interact, and

00:09:26.820 that's how we make a muscle contract. And that's important because when actin and myosin interact

00:09:33.660 and you have muscle contraction, that's where you get a lot of this signaling for ultimate muscle

00:09:39.560 adaptation. So the characteristics of muscle, we have kind of two broad types is how we typically

00:09:47.600 teach it. We have type one, which is more endurance based type two, which is more force based. But in

00:09:54.980 reality, those are probably on a continuum. So when we exercise, we can shift them. We can shift the

00:10:03.260 continuum one way or another, depending upon the type of exercise that you're doing. But in general,

00:10:09.260 when we become more physically active, the overall fiber types shift slower. So they become more

00:10:16.780 oxidative, they become more efficient. That's the general response. So those are the different types

00:10:25.020 of fibers. The actin and myosin, that's the functional unit. They interact to make the muscle

00:10:30.160 contract. Let's explain to people how that works, Jeremy. So you pull out this sort of sarcomere and

00:10:36.100 inside you have these fibers and you've got these Z lines. Explain to people how the actin and myosin

00:10:42.280 actually interact with each other relative to the Z line, what the contraction looks like.

00:10:47.540 And frankly, even one of the more interesting things that I think is a bit counterintuitive the

00:10:52.020 first time people learn it is which part of the interaction between actin and myosin requires ATP.

00:10:57.880 It's a bit counterintuitive when you're first presented with it.

00:11:00.680 Right. So when we decide to exercise, we have a signal that goes from the nerve to the muscle.

00:11:08.120 Basically, we have a release of calcium. And that calcium is going to expose the binding site.

00:11:15.100 So basically, we have these filaments, they slide past each other. That's the general dogma,

00:11:21.500 at least with concentric actions. Eccentric is a little bit more complex. I think they're still

00:11:26.740 trying to figure that out with titan. But just in general, when a muscle contracts, so the myosin is

00:11:33.400 interacting with the actin and it's causing it to pull in. Now, ATP is required to break that bond.

00:11:41.280 So the ATP comes in, it breaks it off, it gets hydrolyzed, which re-cocks it and allows it to be

00:11:48.340 able to reattach, assuming there's more calcium on board. So that's the general basic physiology of

00:11:55.040 muscle contraction. So as long as calcium is there, or as long as the signal is being sent,

00:12:00.180 those sarcomeres, those actin and myosin will keep interacting. So they don't all interact at the

00:12:05.460 same time. Otherwise, you couldn't really sustain exercise. But you have them, you know, in a

00:12:10.320 textbook, we talk about, we have kind of like an image and we have myosin head. But those myosin

00:12:15.340 heads are all the way around that myosin and they're all interacting at different times. So that's

00:12:21.580 how we're able to actually move through kind of a fluid motion. And what's interesting, as you said,

00:12:26.380 is that the ATP is required to actually release the actin myosin complex, which is, we learned in

00:12:34.060 medical school, explains why a corpse is experiencing rigor mortis, right? When a person is dead and they're

00:12:40.500 no longer able to produce ATP, they don't have the ability to release the actin myosin filaments.

00:12:46.520 That's why a body gets stiff, sort of a morbid thought, but it explains physiologically what's

00:12:52.400 happening. So let's now talk a little bit about this difference in fibers, because again, I think

00:12:57.240 most people have probably heard of the idea of a type one and a type two fiber. But as you said,

00:13:03.500 it's probably more complex than that. And there's more of a continuum. I think even by the time I was

00:13:10.280 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

00:13:16.160 a two A, a two AB, a two B. You could argue it's even more complex now. Let's start with the term

00:13:24.960 fast versus slow twitch. I've read conflicting things. So I'm hoping you can clarify this for me.

00:13:30.960 I've read that there's no difference in the twitch speed. They all twitch at the same speed. It's the force

00:13:36.780 of contraction and the speed to fatigue that's being referred to. So the faster twitch muscle

00:13:42.260 has a higher contractile force, but it also fatigues quickly, hence fast twitch. Is there

00:13:48.000 actually a difference in the neurologic signal that's happening there or the speed of contraction

00:13:53.700 for that matter? Yeah, that's a good question. This is not work that I actually do. I have a lot

00:14:00.620 of confusion surrounding this myself and a lot of it reading some of the work by Andy Galpin and some

00:14:06.440 others. A lot of it comes from the old methods are still being used. And the limitations of those

00:14:13.900 is that we don't have, we can't do hybrids. And some people say we should be using these new methods.

00:14:18.920 And I think it all depends on how you're actually identifying the fibers. What are you doing to

00:14:25.060 call it a fast or a slow? How are you ultimately deciding that with your methodology? So I don't

00:14:30.980 honestly know the ins and outs of all those. The general idea, I think, as you said, the type two

00:14:37.580 fibers. So for example, type two X, those typically are bigger. They're typically stronger, but they

00:14:44.060 fatigue much faster. The type two A, it's a little bit more oxidative. They're pretty forceful and you

00:14:51.160 can, they can sustain it for quite some time. So in general, when we exercise, it's thought that type

00:14:57.340 two X usually transitions to type two A. You don't have a whole lot of type two X left over. That's

00:15:03.840 my general understanding. Type one fibers generally a little bit slower and they're not as forceful,

00:15:11.140 but they don't fatigue. It takes a lot to fatigue those fibers. So I think that that's the general

00:15:16.600 characteristics. I think how you go about identifying that, you might get a little bit of different

00:15:21.880 things, but that was the general idea as I understand it, at least.

00:15:25.080 And what accounts for the difference in contractile strength between a type one fiber and say a type

00:15:31.660 two X, take two opposite ends of the spectrum. I mean, sometimes using the extremes is helpful,

00:15:36.860 right? So the type one fiber has lots of mitochondria surrounding the fibrils within the sarcomere.

00:15:43.200 As you said, it is readily able to access glucose and fatty acid oxidatively. Conversely,

00:15:50.720 the type two X fiber, I don't even think it has mitochondria surrounding it. It's purely a

00:15:55.780 glycolytic tool, meaning it's going to basically have to go glucose to lactate. What accounts

00:16:03.060 mechanically for the difference? That's a good question. I think most people would say that

00:16:09.800 perhaps the overall just size difference, whether or not there are other things, how it may interact

00:16:17.000 and the speed of it, that might be different as well. But the big characteristic difference,

00:16:22.880 at least in young people, is that the size of the fiber is just distinctly different.

00:16:27.780 And I think when you look at fiber mechanics outside of the body and you test a type one or test a type

00:16:34.780 two, they will be different. How those interact within the body as a whole, I think is quite a bit

00:16:42.080 different. And that's always been an interest of mine with respect to dynamic strength, moving the

00:16:48.680 whole person, not necessarily saying, well, their fiber is still nice and strong, but what about when

00:16:55.300 the fiber is in the person? What's going on then? So I think there are, I think both of those are very

00:17:00.400 important. I'm not, I don't want to come across like I'm talking down to that type of work. I think

00:17:05.120 it's very important work, but I think they're just different.

00:17:07.960 How genetically set is this? It seems that there's clearly a difference in individual's

00:17:15.300 capacity for work, meaning aerobic work versus explosive strength anaerobic work. But do you

00:17:22.480 have a sense of how genetically diverse the fiber distribution is?

00:17:28.060 That's a question I always put forth to my class as well. I think you can look at papers and get some

00:17:33.600 percentages, but I, I don't feel super confident doing that mostly because we have a lot, not that

00:17:41.440 those scientists don't know that, but those are mass extrapolations from small bits of fibers. And one

00:17:48.820 of the things that I'm always interested in is the athlete that's thought to have like some of the

00:17:54.580 greatest endurance capacities or cross-country skiers. And if you were to look at their fiber types, many of

00:18:01.240 them may have a predominance of type one fibers. So the question is, were they mostly born like that

00:18:07.640 and then they gravitated towards sports that they're good at, or was there some sort of shift with

00:18:13.520 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

00:18:21.220 component there, probably at baseline and then your response to exercise as well. But it seems to me that

00:18:29.400 most people gravitate towards events that they're pretty good at and they don't do the things that

00:18:35.660 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

00:18:42.420 genetic component to it. It doesn't mean again, that they don't train hard or that's always the thing that I get

00:18:50.040 when I have a lot of athletes in my class. It's like, well, we train. It's like, there's no, there's no question

00:18:55.160 that you guys train extremely hard, but it's also possible that there's something different about

00:19:03.200 you already. So that, that would be my, my guess. And you sort of already touched on it a bit, but

00:19:09.020 do we have data to suggest how malleable that is? You know, we all know the extremes, right? Like we

00:19:16.900 know these sort of mesomorphic specimens that kind of look at weights and get bigger and stronger.

00:19:24.060 And then conversely, we know that sort of wiry person who can't put on muscle no matter what

00:19:30.660 they seemingly do, but boy, like you get them out there on a, on a bike and you, you, you can never

00:19:37.540 catch them. But when you take someone maybe who's not quite at the extremes, how much can training

00:19:44.440 and over what time period impact fiber type? I think certainly some, I don't think we're going

00:19:52.560 to take someone like myself who's athletically quite average. I don't think any amount of training was

00:19:59.760 going to make me elite in anything, but I do think that I could improve certain aspects of that for

00:20:06.400 sure. But I, I don't think it's going to myself move me to, you know, up a couple notches. Now there

00:20:15.020 could be some people who certainly can. I think that this is where there's quite a bit of confusion

00:20:21.220 with individual response data and things like that. We've published a little bit on this topic about

00:20:27.520 the measurements that we have aren't typically good enough to say, not only did this group increase

00:20:34.300 muscle size more than this group, but this individual increase more than this person, but

00:20:39.720 not quite as much as this person and not quite as much as this person that would require a very,

00:20:45.440 very good instrument. So I think people often take that to mean, so you're saying that there aren't

00:20:52.220 individual responders. I I'm not saying that at all. I'm saying that we, we may not have the ability

00:20:57.560 to appropriately determine who's who we can say overall on average doing this will increase this

00:21:04.880 or that. But I think that just looking around, it seems at least pretty clear to me that there are

00:21:12.200 some people who you give them a certain response and man, do they look like world beaters a couple

00:21:18.480 months later. So that does tell me something is, is different about them, but I don't know that we

00:21:24.040 could detect that with a lot of the measurements that we have. Okay. I think the other thing that

00:21:29.240 would be helpful for us to understand before we get into the science of blood flow restriction

00:21:35.280 is to understand what strength is and to understand what hypertrophy is. Do you have a preference with

00:21:42.140 which one we start with? Either one. Okay. So if we measure the size of my bicep today,

00:21:50.800 we could do it crudely with a tape measure. We could do it more accurately with an MRI or an

00:21:56.140 ultrasound. And you were to prescribe exercises that we'll talk about whether, whether without

00:22:02.620 blood flow restriction, we can get into load, we can get into reps, et cetera. We come back and

00:22:07.620 measure. And again, let's just use the gold standard. We'll use an MRI. We'll come back and measure me in

00:22:12.740 six months and demonstrably my muscle has gotten bigger. What does that mean? Did I grow more muscle

00:22:21.020 fibers? Did each fiber get bigger? How would you explain to somebody what happened in that cycle

00:22:26.800 of hypertrophy? So there's a couple of different ways that it could happen. You could have an increase

00:22:33.980 in fiber size, which is hypertrophy. So all the muscle cells that you have, maybe not all, but the muscle

00:22:40.420 cell itself has gotten bigger. So that's hypertrophy. The other component would be you have an increase

00:22:46.640 in the number of cells. That's hyperplasia. In general, we don't think that hyperplasia is playing

00:22:54.640 a big role, at least in adults. And I wouldn't necessarily rule it out, but it doesn't seem like

00:23:01.240 we have a lot of evidence for that. So we always just look at gross changes and assume that it's

00:23:06.080 probably hypertrophy. So when your muscle was to get bigger following exercise, what that would mean

00:23:12.100 is that the individual cells inside that bicep have increased in size. And we typically assume that

00:23:20.720 that's due to increases in overall protein, actin and myosin and things of that sort. You're obviously

00:23:26.240 going to also have an increase in other components to help support the cell. But that's generally what we

00:23:34.420 mean, an increase in cell size. When you think about like an epithelial cell or something like that,

00:23:41.740 we don't really pay much attention to the size of those cells, right? Like I don't know that anybody,

00:23:47.900 I don't know the dermatologist is looking at somebody's moles when they biopsy them and looking

00:23:53.500 at the individual cells and talking about the size of them. There we would concern ourselves much more

00:23:59.140 with hyperplasia and certainly metaplasia or dysplasia. Those are the things that really

00:24:04.500 get people concerned. But in this sense, muscles are kind of unique in that they can have not just

00:24:11.800 a non-pathologic, but a healthy change in size. So is it, as you said, do you think it's primarily due

00:24:19.740 to an increase in the amount of actin and myosin within the cell or some other characteristic?

00:24:26.080 Does the actin and myosin complex actually change in size or do you just have more of it?

00:24:33.020 I think that most people would say that, because they usually connect it to short-term

00:24:38.160 measures of protein synthesis. So myofibrillar, which is actin and myosin. So synthesizing more

00:24:44.180 and more of those, I think it's the general thought that you have more overall actin and myosin along

00:24:49.780 with other things, of course. And let's talk about strength now. So we can kind of break it down,

00:24:55.780 into kind of mechanical strength and neurologic strength. How do you think about that? So again,

00:25:03.000 let's use the same example of you measure my ability to do a bicep curl. And let's just assume

00:25:08.640 there'll be two measurements. You'll measure my single rep max, so the most that I can do.

00:25:14.040 And then you'll also do a separate test for the most that I can do 10 times or 15 times or something.

00:25:19.660 So you'll measure kind of two different components of strength, maybe absolute extreme and sort of

00:25:25.420 more of a muscular endurance test. And then you'll have me do a set of prescribed exercises for six

00:25:31.440 months and we'll come back and we'll do that whole thing again. And my one rep max went up by 20%

00:25:37.000 and the amount of weight that I could move 10 times went up 15%. What happened to me mechanically,

00:25:46.700 structurally, neurologically? What explains that change in strength?

00:25:51.340 That's a question that I'm extremely interested in. And I don't know why people get stronger. I think

00:25:59.560 the general thought or how we teach people is the initial change in strength is due to neurological

00:26:09.100 changes. So what does neurologic mean? I think is also up to some debate, but we could think about

00:26:17.420 a signal being sent from the brain through the spinal cord to the alpha motor neuron. So the alpha motor

00:26:23.180 neuron is the nerve that communicates with the muscle. So there could be changes anywhere,

00:26:29.560 in between that. So you have more excitatory input, you have less inhibition, you have lowering of

00:26:36.420 thresholds that makes it easier to fire the type two fibers. There's a lot of different things that

00:26:41.380 could be playing a role there for why someone might get stronger with neural adaptations. So most people

00:26:49.880 are okay with that part. Then the next part is people will say after about three to four weeks, when the

00:26:58.080 muscle is also getting bigger, that that change in fiber size will also be contributing to a change in

00:27:05.900 strength. And that's something that we have recently taken some exception to. And there's been a lot of really

00:27:14.100 good discussions about that part of it.

00:27:16.780 And we'll come back to that, Jeremy, because I've read the studies that you're referring to. They're super

00:27:21.980 fascinating. And I was actually surprised at how little evidence there was in favor of the dogmatic

00:27:30.460 view. So I look forward to diving into that a little bit more. And you can see why intuitively one would

00:27:36.980 say, well, size must produce strength if size comes from more actin and myosin, which basically means more

00:27:44.060 contractile units. But as we'll see, I think when we talk about some of your more recent work, that's not

00:27:50.440 necessarily settled, is it? Not in my opinion, no. And to be fair, it's not settled one way or the

00:27:56.420 other. But I do think that there's probably a neural component. But I think that there can also

00:28:01.940 be some changes at the local level that might explain some of those changes in strength. And I

00:28:08.660 think we can discuss that a little bit later as well. But there could be some changes at the myosin head

00:28:13.780 or changes in calcium release and things of that sort. So I don't have any good evidence that that

00:28:18.900 is actually happening, but just some ideas behind why someone might get stronger following exercise.

00:28:27.360 All right. I think that's a pretty solid primer for where we're about to go. So I'll start with

00:28:33.020 the story. I used to swim a lot. And oh, God, this might be circa 2010. So call it 10, 11 years ago.

00:28:42.420 I have a friend, Steve Munitonis, who's himself a remarkable swimmer, truly a world-class marathon

00:28:50.980 swimmer. And he was visiting San Diego from where he lived in LA. And he came to join me for a workout

00:28:58.800 at the master's club I swam at. And after the workout, he brought out these bands. They were

00:29:06.000 called katsu bands, which we're going to talk about. And he said, okay, Peter, I'm going to put these

00:29:11.140 bands on your thighs, upper thighs, and I'm going to put them on your arms, the upper arm.

00:29:17.100 And I'm going to compress to a certain level. And he had what looked like a blood pressure cuff there

00:29:23.160 that he could sort of calibrate the occlusive pressure. And I want you to swim a 50-yard

00:29:29.700 butterfly all out. Now, keep in mind, swimming a 50-yard butterfly all out under any circumstance

00:29:36.500 is quite challenging, but totally doable, right? I mean, you would do a set of 10 50s of butterfly

00:29:43.320 at 90% with 45 seconds in between and be totally fine. And I remember pushing off the wall.

00:29:53.580 And before I got to the other wall, which is 25 yards away to begin turning around to come back,

00:29:59.620 I was like, this is the hardest thing I've ever done. This feels harder than swimming 200 yards of

00:30:06.860 butterfly, which is really hard. So butterfly is one of those strokes where the longest distance

00:30:12.800 it's ever swum is 200 yards. And even people who train to swim the race at 200 yards almost never

00:30:18.920 swim that distance in practice. You're swimming shorter distances perfectly because your form tends

00:30:24.160 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

00:30:34.420 that 50, my body felt like it would normally feel at the end of a 200-yard individual medley or 200

00:30:43.180 breaststroke, which would be kind of two of the most miserable things you could ever do to yourself.

00:30:47.260 And, you know, that began my kind of curiosity with this technique. I read a couple of books about

00:30:56.560 it. And, you know, unfortunately, I kind of just forgot about it. I, you know, once Steve went back

00:31:01.300 up to LA and I didn't have access to the fancy devices, I kind of sort of forgot about it. But

00:31:07.020 recently it's now become sort of curious to me. So what's the story of Yoshiaka Soda? What was the name

00:31:14.400 of the gentleman who came up with this system? Sato? Sato, yeah. So tell me about this guy and then

00:31:20.500 how he came up with this idea. Yeah. So some of this is, I'll say, is of legend. But I think the

00:31:29.620 story that he's told is that he was at a Buddhist ceremony, was kind of kneeling. And Sato was also,

00:31:37.040 from what I understand, interested in bodybuilding, especially in his younger days. So he felt kind of

00:31:43.520 a little bit of numbness or a little bit of sensation that he felt when he was doing heavy

00:31:48.500 squats. So he kind of thought that there could be some connection there. Because he was kneeling and

00:31:54.480 he was restricting blood flow. Okay. Right. That led him to start kind of experimenting with different

00:32:00.440 ways to try and restrict blood flow in his lower body, upper body, et cetera. I think that

00:32:06.440 there's been some stories that his initial kind of ideas, he actually harmed himself a little bit

00:32:13.020 because he was maybe applying it too tightly. But I think then he actually had a skiing accident and

00:32:18.660 then applied it to himself and actually rehabbed himself with blood flow restriction and saw some,

00:32:23.860 what he thought was some pretty good kind of gains. And I think that he really did probably develop a lot

00:32:31.060 of the methods for at least the initial way we were doing blood flow restriction and kind of made it,

00:32:36.820 you know, very popular with studying and research and things of that nature. But yeah, I think

00:32:43.380 he's probably the one who made it more popular, at least initially, because they started doing research

00:32:52.940 on that in the late nineties, early two thousands, at least in the published literature. So the idea

00:32:59.520 is, is that it mimics something that he had felt before in the gym and he wanted to see how he could

00:33:04.680 try and do that. And ultimately he found that you can use very light weights, low loads, but make it

00:33:10.600 feel like you're lifting very, very heavy weights, which is obviously useful. You know, if you have a

00:33:14.880 skiing accident or you don't want to lift heavy weights or you'd have some sort of injury.

00:33:18.660 Yeah. I had a patient last year who was playing with his kids and tore his bicep, had a complete

00:33:26.160 tear. So he underwent a surgical repair of that, but we decided to have him use blood flow restriction

00:33:33.160 during the rehab phase so that he could get back to training sooner, obviously under a far less load.

00:33:40.780 And although it's anecdotal, I mean, it was a remarkable recovery that he made,

00:33:44.860 which further kind of piqued my curiosity around this. So this term katsu is kind of synonymous

00:33:51.820 with blood flow restriction. Is it, and I think it's Japanese for like training with pressure or

00:33:57.700 training with added pressure or something to that effect, correct? Yeah. It means increasing

00:34:01.860 pressure. So it's just a brand. It's the one that's, it's fair to say is one of the first,

00:34:08.740 but it's just a brand. So we started using, I think a lot of people will use katsu as

00:34:15.540 just kind of a generic name, but it probably shouldn't be done unless you're using the katsu

00:34:20.360 apparatus. But yeah, it's just, it's a form of blood flow restriction.

00:34:25.400 So I want to come back to the different types of apparatus, but let's kind of talk through it now,

00:34:30.080 maybe chronologically in terms of the most insights. Like if I, if I was to go back in time

00:34:35.300 to the 1970s and I'm Sato and I'm trying to think about how to test this hypothesis,

00:34:41.600 it seems like hands down, the easiest way to do this would be to use individuals as their own

00:34:48.400 controls and isolate and compress one side and not do for the other and have them do the same things

00:34:58.400 or do different things and try to isolate the variable. So was that the first experiment that was

00:35:03.360 done? Yeah. The, the first experiment done on blood flow restriction, at least to my knowledge

00:35:10.460 on how we think of blood flow restriction. So I always add a lot of caveats because some people

00:35:17.900 will say, well, if you look in the thirties, there were studies done where they applied a cuff,

00:35:22.660 but it wasn't done for the purposes of increasing muscle function. So to my knowledge with blood flow

00:35:30.720 restriction, how we use it, Shinohara published the first paper in 1998, where they had individuals

00:35:37.540 that all they were looking at was strength, but they had one leg do a certain exercise with blood

00:35:44.720 flow restriction. The opposite leg did the same exercise without blood flow restriction. And they

00:35:51.480 saw a treatment effect, meaning the limb that underwent blood flow restriction saw a greater change. So

00:35:57.940 that's the, the first study was looking at a change in actual function with blood flow restriction.

00:36:03.960 It's kind of amazing that that didn't happen until 1998, which is 30 years after Sato began

00:36:10.040 writing about this stuff, or at least experimenting with it, right? Yes. The other question for me,

00:36:16.140 that's been very difficult to wrap my head around is what is the definition of blood flow restriction?

00:36:22.380 If I were to wrap a cuff around my arm and apply no pressure, clearly that's no restriction.

00:36:29.900 If I were to create an occlusive pressure that was twice my systolic blood pressure,

00:36:38.180 almost certainly it would imply not a drop of blood is making its way past. So there's no arterial flow

00:36:45.400 and no venous return. That would obviously blood flow restriction. That would be blood flow restriction.

00:36:52.300 But like everything else, you have a continuum. So how do you think about this? And maybe that's

00:36:59.240 the wrong question. Maybe the better question is in the, in the genesis of kind of the study of this,

00:37:05.720 how was restriction defined? What methods were used and how much variability existed in the studies?

00:37:13.060 So the idea of blood flow restriction is to reduce blood flow going into the limb, but not completely

00:37:21.120 occlude blood flow. So in other words, we always want blood flow to be going in. So there is a

00:37:27.900 tremendous amount of variability in how the pressure was applied early on. That's improved substantially

00:37:35.160 at improvement in my opinion, at least the early studies would take a cuff and apply the same pressure

00:37:41.820 to every single person. Independent of their blood pressure, independent of blood pressure,

00:37:47.200 independent of limb size, independent of the cuff size that you're using. So all of these things

00:37:53.820 are important factors that you can account for by doing this one measurement. That's how we do it now.

00:37:59.900 But obviously it's easy to look in the past and throw stones, but there were certainly a lot of

00:38:05.860 variability. So given that the idea is to restrict blood flow, but not occlude it completely during

00:38:14.500 exercise, what we started to do and others have started to do as well is before we do exercise, let's just

00:38:23.060 take the cuff up to the lowest pressure of which there is no flow at all. So if that's 100 millimeters of

00:38:29.860 mercury means that you no longer have flow going into your limb at all, let's take a percentage of

00:38:35.200 that. So we know that you always have flow during the exercise. Now, do you determine that with Doppler

00:38:42.120 at some distal point to the occlusion? Yes, you can use ultrasound. We use just a handheld Doppler probe

00:38:50.140 that's essentially detecting the pulse. So we can look at it here. We look at it at the ankle.

00:38:56.000 So before we have anybody do any exercise, we just lie them down. We slowly inflate whatever cuff we're going

00:39:04.920 to use because the cuff size matters. It's going to totally change the pressure applied. So we slowly inflate

00:39:13.580 it until we don't hear any more flow. And then we take a percentage of that. So if the arterial occlusion

00:39:20.540 pressure, which is the lowest pressure of which there is no flow, if that's 100 millimeters or

00:39:25.980 mercury, then we'll typically apply anywhere between 40 and 80 millimeters of mercury in our lab at

00:39:32.740 least. Yeah. So two points I want to make, or one point, one question. The point I want to make that

00:39:38.240 is a very important one that you just made is that this idea of cuff size matters, right? Because

00:39:43.560 the pressure and the force are related by the area that that cuff takes up. So is it safe to say

00:39:50.820 that the wider the cuff, the lower pressure you need to reach occlusion?

00:39:57.400 Yes, that's definitely true. And I think some people interpret that to mean that, does that mean

00:40:04.140 that a wider cuff is better because the pressure is lower? I would say no, because it's pretty much

00:40:09.680 relative. Some would argue that the wider the cuff is, you might actually attenuate some of the growth

00:40:15.740 beneath the cuff, but certainly the size of the cuff will change the pressure. So as you said,

00:40:21.900 the wider it is, the lower the pressure that you need. But again, as long as you apply whatever cuff

00:40:29.240 that you're going to use to whatever limb you're looking to exercise, taking one measurement can account

00:40:34.440 for everything. So then my question is, when you say 40 to 80%, that is a very wide range. That's like

00:40:44.760 the difference between 40 millimeters of mercury and 80 millimeters of mercury when 100 millimeters

00:40:49.760 of mercury is the occlusive pressure could be the difference between comfort and discomfort as an

00:40:55.380 example, right? Yes. So typically we use 40%. 40, 4-0. Yeah. Okay. That's the pressure that we use

00:41:05.280 when all we care about is muscle adaptations. In other words, increasing muscle size and strength.

00:41:11.560 Now you can see the same adaptation at 80% with a little bit less work because you're going to fail

00:41:19.160 sooner, but the discomfort is going to be much higher. Now, I think the other component of that

00:41:27.860 is that's muscle adaptation. Now we have some data, it's very preliminary, but some data that suggests that

00:41:36.360 some of the vascular changes might actually require a higher pressure. So vascular changes meaning

00:41:43.580 kind of a change in form limb blood flow or form conductance. So that's a gross measurement of

00:41:51.260 basically the vascular network. So there's some indication that maybe you do need higher pressure

00:41:57.680 for that. But that's one study. We did observe it in both the upper and lower body, which gives me a

00:42:03.660 little bit of confidence, but it's one study. But with muscle, I feel pretty confident saying

00:42:09.440 you can use a moderate pressure, 40%, or a high pressure, 80 to 90%. And the adaptation is going

00:42:18.420 to be pretty much the same with respect to muscle size and strength. The discomfort might be, or will

00:42:25.200 be quite different. We'll be much higher with a higher pressure. How much variability is there between

00:42:31.160 an individual's tolerance for discomfort at a fixed occlusive pressure? So I love the idea of using

00:42:38.140 80% of occlusive pressure because now it's not a given number. It's 80% for that individual. So in theory,

00:42:45.200 everybody is experiencing the same amount of relative occlusion. But if you took a hundred people

00:42:52.340 and let's even make it more homogeneous. If you took a hundred fit people and you simultaneously

00:43:00.740 applied 80% of occlusive pressure to bilateral upper extremities and just had them sit there,

00:43:09.040 so we'll do the first experiment where nobody does anything, what would the bell curve look like? How

00:43:13.980 tight would it be for the time at which a person cries uncle? And the pressure is 50%?

00:43:20.120 You pick a number. I said 80, but- Okay, 80. I don't know the minute. We have done some discomfort

00:43:26.520 studies applying 40% and just having people sit. Yeah. So at 40%, what's the answer?

00:43:31.640 It's pretty low. We stopped it at four minutes. We didn't have anybody who couldn't do it.

00:43:38.420 But you are going to have some people who do experience that as more discomfort than other

00:43:43.280 people. But it becomes much greater when you obviously combine it with muscle contraction.

00:43:48.260 But yeah, you're right. So when we say a 40% AOP, that doesn't necessarily mean a 40% reduction in

00:43:57.020 blood flow either. Those are two separate things. So when we apply 40% of AOP, the reduction in blood

00:44:03.980 flow might be different depending on how big the muscle is, a variety of other things. And the

00:44:08.940 discomfort associated with that will also vary depending on the person. There's some people

00:44:14.260 who we have who, they perceive almost everything as extreme discomfort. Whereas we have people on

00:44:20.900 the opposite side as well. But in general, we see, I can't think of the actual numerical value, but

00:44:27.240 we have 40% is right here. And then with 80%, it shifts, meaning that the average is certainly higher.

00:44:34.220 But there are certain people who, the discomfort they feel at 40 is not different than it is at 80

00:44:40.740 because they already rated it so high. So I mean, that's the limitation of the scale. But yeah,

00:44:46.080 you're right. What is the approximate blood flow restriction that occurs at 40% AOP? How much of

00:44:53.180 the blood flow, arterial flow is being limited and how much venous pooling is occurring?

00:44:57.580 I don't know the actual percent drop off the top of my head. It isn't 40%. It's on average is a little

00:45:04.140 bit less than that, depending upon the position, depending on what you're doing. But yeah, in

00:45:10.200 general, I think during the rest period, you probably do have venous occlusion because it

00:45:14.820 doesn't take, it's not thought to take a lot of pressure to collapse a vein. So during the exercise,

00:45:21.260 you're obviously pumping it back out with the muscle pump. But I would say at most of the pressures

00:45:27.320 that we apply, at least at rest, there is venous pulling occurring. Yeah. Today I finished my workout

00:45:33.700 with a set of leg press. So did 30 reps, rest 30 seconds, 15 reps, rest 30 seconds, 15. And I'm not

00:45:45.900 sure what hurt worse, just the 30 seconds in between or the actual last two sets, the 15 reps on the last

00:45:55.140 two sets. I mean, the whole thing was just so wildly uncomfortable. Again, I'm flying by the seat of my

00:46:00.320 pants, not doing this based on occlusive pressure. So I don't know how far off I am. It's something I'm

00:46:08.160 looking forward to diving deeper into. I think you've already convinced me I should be more scientific

00:46:12.380 in my approach because I'm sort of white knuckling it and putting these things on and screaming for dear

00:46:19.140 life. So I'm in pain kind of before the, I'm sort of very uncomfortable before I start. And even after

00:46:26.520 that first set of 30, I'm questioning my sanity. So who knows, maybe I'm applying too much. It would

00:46:32.820 seem that the directionally, would you have a nomogram of occlusive pressure versus expected

00:46:39.860 number of reps at a percentage of one rep max? Yeah. That's also tough. I think most of the loading

00:46:48.860 that we use is 30%. And to be honest, if we have somebody who's stronger, they're not getting

00:46:55.500 30, 15, 15, 15. There's no, there's no question they're going to be at failure. Most of the time

00:47:01.720 when we actually do experiments, we just have people exercise four sets to as many as repetitions as you

00:47:07.220 can. That way we can at least hold that constant so we can control for effort. But I do think that you

00:47:14.440 can use the number of repetitions as a weak surrogate of blood flow restriction. So I would

00:47:20.980 say that if you're using 20 or 30%, you should be getting close to 30 repetitions. No, no, for the

00:47:30.040 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

00:47:36.460 close to that, the load is probably too high or the wraps are too tight. I would say that if you're in

00:47:42.800 pain before you're starting, it's too tight. And we've done a lot of work on practical restriction

00:47:49.720 as well. I would say that practical meaning where we don't really know how much pressure is being

00:47:54.580 applied. We're applying a knee wrap. That's what I refer to as, as practical blood flow restriction.

00:48:00.020 I think if you are rehabbing or you're in a clinical setting, are you working in that? I think

00:48:05.220 you really need to know the pressure that you're applying. I think if you're a healthy person in the

00:48:11.400 gym who wants to use blood flow restriction, I don't think it's all that important to know the

00:48:16.520 pressure. Assuming you have the discussion that we're having now where I know the load is low.

00:48:22.160 I apply the wraps. I'm in pain. Well, then the wraps are too tight. So I loosen them up.

00:48:28.820 Then I can get close to 30 reps and then close to 15 on the last three sets. Now on the last one,

00:48:35.640 depending on how strong you are, you might fail pretty quick in that fourth set. That's okay.

00:48:42.160 But I do agree with you that I think that you can use goal repetitions as a way to

00:48:47.700 have some idea as at the level of restriction that's being applied.

00:48:52.360 So when you're at 40% occlusive pressure, what would be the kind of maximum period of time you

00:48:58.820 would let a subject stay under that pressure, both in terms of the combined lift recovery period?

00:49:03.960 Yeah. I think if they're just starting out, I think one, it depends on are they resistance training

00:49:10.140 or are they doing kind of low intensity aerobic exercise? If it's low intensity aerobic exercise,

00:49:15.680 you can probably keep it on for 30 or 40 minutes because it doesn't feel that discomforting because

00:49:22.760 you're exercising at a low intensity. The cuffs are not all that tight. You're not building up a

00:49:28.080 tremendous amount of metabolites, probably why you're not also getting a tremendous amount of adaptation.

00:49:32.640 But with resistance exercise, I think if you're just starting out, it's hard to have a minute.

00:49:39.600 I think maybe seven, eight, nine minutes, 10 minutes or so. I would say one exercise is a good place to start.

00:49:47.500 We've done it early on. We did multiple exercises for people who are untrained and that's pretty tough.

00:49:53.300 But I would say, you know, start off with four sets of an exercise and then take the cuffs off or take

00:49:59.880 the wrap off. And then you might be able to eventually work up to a couple. But I wouldn't

00:50:05.000 with resistance training, I don't think that you should leave it on continuously for probably more

00:50:10.280 than a few exercises. But if you've never done it, I wouldn't go beyond one just so you can start to

00:50:15.440 kind of see what it feels like. And so if 40 to 80 percent of occlusive pressure is the technical way

00:50:21.480 to do it, what other metric do you, would people use if they don't have access to a Doppler? For example,

00:50:29.740 if somebody knew their blood pressure, I can see why that would not necessarily be, I can see why

00:50:35.540 systolic blood pressure would not be the same as occlusive pressure. Is it a reasonable proxy?

00:50:40.280 Not always. It really depends upon if the size of the cuff that you're using is very similar in size,

00:50:47.860 then you could you could do that and base the pressure as a percentage of your systolic pressure.

00:50:54.700 I think the average gym goer, I think one of the things that you could do is apply the wrap as a

00:51:01.200 percentage of your resting limb size. So there's some data that's done that's used that. One of the ways

00:51:08.460 that we've tried to work with is condition people to feel what 40 percent supposed to feel like.

00:51:16.080 So you would have to have the device one day. So we're doing this because there are some places that

00:51:22.140 are applying this to clinical populations, where they have only a small amount of time with the

00:51:29.840 patient, and then they send them home to do exercises. The idea being is that you could be with

00:51:36.220 the patient, have them feel what 40 percent supposed to feel like, and then say, when you get home,

00:51:42.240 try to mimic this pressure. So we've had some success with that. We are able to get people to,

00:51:51.160 on average, rate around 40 percent, but the individual level is anywhere between 20 and 60 percent

00:51:58.500 of AOP. So it's not terrible, but it's not very good yet. One of the things that led us to that

00:52:07.640 is that initially, I was on a paper a long time ago that said you should rate the pressure based on

00:52:14.840 7 out of 10, because that can make sure that the pressure will be sub-occlusive. And that's overall

00:52:21.920 pretty much true. The issue is that you have a tremendously wide range, and it's not reliable,

00:52:29.760 meaning that on day one, you might say 7 out of 10 is 90 percent AOP. The next day, it might be 10 percent.

00:52:38.080 So we don't really recommend that scale anymore. We're interested in this idea of conditioning and or

00:52:43.760 using a percentage of a resting circumference, and or what we talked about earlier, we use repetitions

00:52:51.100 is kind of a goal. The cups I have are super cheapo cups. I feel like I want to invest in

00:52:56.480 sort of nice ones, but the one thing they have on them is numbers. So I've got a sense of like

00:53:02.460 on arms, I need to be between 7 and 8, and on legs between 11 and 12. And sometimes I just overcook it.

00:53:13.280 And after the first set, I have to loosen them if I want to have any hope of completing the exercises.

00:53:19.020 And then going back to weight, 20 to 40 percent of one rep max is about the place you like people to

00:53:26.920 be. Yeah, I generally prefer lower, meaning around 20 or 30 percent. There are some people who creep

00:53:33.700 up to 40. And so I just think that the real utility of using blood flow restriction is the fact that

00:53:40.960 you can use it with very low loads. So that's the benefit. We've tried to combine it with high loads.

00:53:48.540 In different aspects, and other people have run training studies with it, but it's not additive.

00:53:54.000 So it doesn't add anything more to high load training. And it's probably because high load

00:53:59.680 normal exercise is a maximal stimulus. So it's hard to maximize something that's probably already

00:54:05.720 pretty much maximal in a given training session. So that's why I'm like, if you want to lift with

00:54:11.620 heavy weights, didn't just do that. I think the utility of using blood flow restriction is with

00:54:17.380 that you can use lower loads. Any playing with the speed, either concentrically or eccentrically?

00:54:24.640 And does that matter?

00:54:25.760 The slower you go, the less repetitions you're obviously going to be able to do.

00:54:30.520 I don't think that it probably matters overall too much, especially for growth. The pace that we

00:54:37.260 typically use is about one second up, one second down. So a relatively quick pace. Some people use

00:54:43.160 a second and a half. So if you use a second to a second and a half, it's usually a nice controlled

00:54:49.620 movement. We haven't messed with too much in the lab, but I don't think it would matter too much.

00:54:56.380 I think it would alter how much work you were able to do and the load that you'd be able to use

00:55:00.580 more than anything.

00:55:02.260 Do you think that ultimately time under tension is all that's going to matter? So if you do it slower,

00:55:07.680 but you get fewer reps, it's still okay if you have the same time under tension?

00:55:12.100 Yeah, for the most part. Because when we think about a muscle growing, at least when I think about

00:55:16.060 a muscle growing, where it requires a muscle to be activated for a sufficient duration of time for

00:55:23.280 all those signaling pathways to be turned on. So from my perspective, there's a lot of different

00:55:28.920 ways for that to occur. You can use really, really heavy weights repeatedly, and that will do it. Or

00:55:35.400 you can use low loads, or you can use very slow pace as well. I think all of those are kind of doing

00:55:42.920 similar things. You're recruiting these more and more and more fibers, activating them, and signaling

00:55:49.400 them to grow. So yeah, I think it would be very similar.

00:55:53.480 And how much rest are you prescribing? I did 30 seconds today. Sometimes I do like a superset where

00:55:59.960 I'll do one muscle, another muscle, another muscle, and just go back and forth with two different muscles

00:56:04.540 and not take a passive rest. What do you think about those approaches?

00:56:09.160 In general, we use about 30 seconds. That's the standard one that we use in our lab.

00:56:15.840 When I've experimented in the gym, I think that supersetting works really well, especially if you

00:56:22.660 are working out of muscle that's not necessarily directly under blood flow restriction.

00:56:29.140 So for example, the chest, there is some idea that just doing a standard bench press exercise

00:56:36.140 with blood flow restriction around the arms would augment the size of the chest. There's some data

00:56:42.380 that indicates that. To me, I think a lot of that is driven by the fact that the muscles distal to the

00:56:49.740 cuff, the triceps are fatiguing, and the chest is picking up the load. So in the gym, I like to

00:56:55.300 experiment with that. So do some chest and then superset with some tricep extension or something like

00:57:01.020 that. But we haven't studied that in the lab, but those are things that I've messed around with in

00:57:05.600 the past.

00:57:06.600 Well, it's interesting. I've never thought to do something like a bench press with it,

00:57:11.780 frankly, mostly out of fear. But I guess if you adjust the weight low enough, it shouldn't really

00:57:17.360 be that much of an issue. I mean, once I did deadlifts restricted, I wasn't sure if it was a

00:57:23.280 great idea. I mean, it was very lightweight. It was probably like 135 pounds. So it was not the type of

00:57:28.780 weight I felt like I could ever hurt myself with. But I was like, okay, well, let's do 30 reps here

00:57:33.300 of 135-pound deadlift under restriction. Truthfully, I thought it was pretty freaking cool. I think in the

00:57:40.920 end, I didn't keep doing it because I was like, well, look, I don't want to develop bad habits

00:57:44.160 deadlifting under such fatigue. What's your thought on doing complex multi-joint movements?

00:57:52.920 Yeah, there is data looking at bench press, squat, and they have seen some benefits. I generally

00:58:02.720 agree with you. I think that you can do those, assuming that you're using lightweight. I tend

00:58:09.440 to prefer kind of isolation movements, especially if the goal is growth. But you could do them. I think

00:58:16.800 that you'd have varying success depending on the movement. The deadlift, I mean, if it's a Romanian

00:58:22.960 type deadlift, maybe I could see that having maybe some sort of benefit. But I think I'd have a similar

00:58:29.880 thought as you. It's like, am I going to change my mechanics somehow and then put myself at risk and

00:58:35.300 then really require blood flow restriction in order to train because I'm hurt? So yeah, you can do

00:58:42.840 compounds that there's certainly evidence that suggests that it can help with the squat, help

00:58:47.700 with the barbell bench press. We tend to use isolation movements and for research purposes,

00:58:53.400 obviously. But I tend to feel that a little bit better and I feel a little bit safer doing those

00:58:59.980 types of exercises. Let's talk about risks because I know that when people think about blood flow

00:59:05.600 restriction, I've had people ask me, are you worried about rhabdo? Are you worried about nerve damage?

00:59:11.940 Basically, what are the risks of this and what's the safety profile?

00:59:17.200 Sure. So I think that's a completely reasonable kind of response when you're telling people that,

00:59:26.780 hey, I'm restricting blood flow and I think you might consider it. I think the first response that

00:59:32.620 I would hope a person would say is, what's the safety of that? I think a couple things. One,

00:59:39.080 it helps to understand that this is a very acute response. In other words, we're restricting blood

00:59:46.480 flow for minutes, not for hours. So I think that that's important. I think the safety profile overall

00:59:54.700 is comparable to that of high load exercise or traditional exercise. There are two concerns that

01:00:00.820 people generally bring up. First is blood clotting. Second is muscle damage. In other words, does it

01:00:09.100 increase the risk of blood clots? Does it increase the risk of muscle damage? And I think those are

01:00:15.000 the way I stated that is how it should probably be stated. So anytime we exercise or anytime we wake up

01:00:22.140 and live, as you know, there's a risk. There's always a risk for something to occur. In my mind,

01:00:28.680 the question, the important question is not, is there a risk? But when we add blood flow restriction,

01:00:35.800 does it increase the risk? And it doesn't appear to, at least at the group level and mostly healthy

01:00:43.820 individuals. So it doesn't increase the risk of blood clots. And that has been looked at in some

01:00:49.280 clinical populations as well, which is good. It doesn't increase the risk of muscle damage. You will

01:00:55.700 get sore, but when we look at the fiber, it appears to be intact. So it doesn't appear to be some

01:01:02.800 structural damages at all. Have there been studies where they've measured CK levels and contrasted them

01:01:09.740 with and without restriction? And does there appear to be more breakdown, at least measured by CK?

01:01:14.720 No. Generally, when they look at most of those, there's not a whole lot of difference between

01:01:18.980 the same exercise without blood flow restriction. There's certainly soreness that I feel confident

01:01:24.720 about, but not necessarily structural damage. Another one that's been kind of brought up is

01:01:31.400 the blood pressure response to this exercise. So proximal to the cuff is blood pressure going

01:01:38.420 up centrally in the heart, the aorta, the brain. Yeah. And compared to the same exercise without it,

01:01:44.860 it usually is higher, but it's usually comparable to that. It's not a little bit lower than high

01:01:50.820 load exercise. So I think the key component of that is, of course, it's probably going to be higher.

01:01:57.280 You're restricting blood flow, but how high does it get and how quickly does it return back to baseline?

01:02:03.460 So I think that those are kind of two important components. Now, when we've compared it to high

01:02:08.920 load exercise, it's usually pretty similar and it usually comes back down to baseline within five minutes.

01:02:14.300 Those are healthy individuals. Now, there was a paper written on it suggesting that

01:02:19.220 that's great, but there are certain populations where they may hyper-respond to that. And I think

01:02:26.940 that's a good point. So I do think that it might be something to consider. If you have some sort of

01:02:33.840 clinical ailment, you might want to, if you might be hypersensitive to that reflex, that might be

01:02:40.280 something to really think about. In myself, when I think about doing unrestricted heavy movements,

01:02:47.420 so five to eight reps of deadlifts or something where I'm really going for it, that feels like I

01:02:56.820 have a much higher blood pressure than the blood pressure I feel like I'm under doing blood flow

01:03:02.360 restriction. Even though there's a much greater discomfort with the blood flow restriction,

01:03:07.280 I never really get the feeling like my head's going to pop off my shoulders, which I commonly

01:03:12.360 feel when I'm doing a heavy deadlift. Yeah, I agree. And I think that's a lot of the intramuscular

01:03:18.260 pressure all over, you know, a systemic kind of restriction. Well, yeah, because I think when

01:03:24.260 you're really lifting heavily, the intra-abdominal pressure is what allows you to do it. And, you know,

01:03:30.660 that's actually compressing the aorta. So it'd be interesting if you really think about where the

01:03:35.660 pressure matters the most. But I would say that overall, it does appear to be very safe.

01:03:41.660 You know, that's something that we're we've been interested in for a long time. I do think that

01:03:46.420 as with anything, when you give a drug in a large clinical trial, you start to see

01:03:51.580 some side effects that you've never seen before. So my guess is, is that when it becomes more and more

01:03:58.680 popular, we will find there will be certain rare events that we've never seen before. But I think

01:04:05.400 in the actual studies that have been done, we see it to be overall, relatively safe. It doesn't

01:04:11.280 increase the risk, at least, assuming it's done appropriately.

01:04:15.520 Has the following experiment ever been done where you take, well, in an ideal world, I guess you'd take

01:04:21.900 the same subject, right? So you have them do the exact same exercises for the same number of reps.

01:04:29.680 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,

01:04:37.700 the other is not. So the one that's not is not hurting at all. That should be pretty easy to do

01:04:44.980 that in the unoccluded side, correct? Correct. So you're exercising one arm under blood flow

01:04:50.340 restriction, the other arm is not? Correct. But you're using the same weight, the same reps, the

01:04:54.660 same rest, everything. Yes. Shinohara, for example, same workload. One had blood flow restriction,

01:05:01.940 the other one didn't. That was within subject. Those studies have been done. I think the criticism

01:05:07.020 on within subject studies is with respect to strength, not necessarily muscle growth.

01:05:13.360 Because some people think that, not some people, I mean, it is an observable fact that when you train

01:05:19.220 one side, but not the other, the other arm oftentimes can increase in strength. But I'm

01:05:25.120 not sure that that happens when both limbs train. I think the limb actually responds to the local,

01:05:32.920 what it's been trained to do. So I don't know that it's that big of a limitation with strength,

01:05:38.240 but yeah, those studies have been done. And what are they finding typically when they're under the same

01:05:43.220 load? One side is restricted, one side is not. Is the restricted side still making gains in strength

01:05:48.600 and or size? Yeah. Generally, the blood flow restriction will be better than a work matched

01:05:54.680 control, even if it's the same person. With the caveat that it's not to failure. And that's the

01:06:01.540 difficult thing if you're using 30%. Because 30%, for some people, you'll be reaching failure almost on

01:06:08.960 four sets in the non-included arm. So I think that should be stated. I think when we have

01:06:15.740 one limb trained to failure, the other limb trained with blood flow restriction to failure,

01:06:21.220 we've done those studies lots. The adaptation is usually pretty similar, but the volume,

01:06:26.620 the exercise volume needed is much lower with the blood flow restriction limb.

01:06:31.800 That's what I was sort of going to get at, which is, is blood flow restriction mostly just a tool to

01:06:39.980 increase or decrease the time to failure and therefore act as a more efficient means to fatigue the various

01:06:50.580 fibers. Yes. I think that's fair to say with a couple of potential things to consider. Blood flow restriction

01:07:00.380 by itself. So just the application of restriction and deflation and some ACL reconstruction, post-surgery

01:07:09.020 environment has shown to have some sort of benefit. So that suggests to me that there could be something

01:07:16.800 to the restriction of blood flow. Same thing when we have people walk very slowly. In other words,

01:07:22.960 they're not really walking to failure or even close to failure, but there does appear to be

01:07:28.620 some adaptation. It's not close to what you see with resistance exercise, but there's something

01:07:34.800 that's a little bit more there. So I think with resistance exercise, that might be a very fair

01:07:40.880 statement to say that you're just causing the muscle to have to activate more of the muscle sooner and

01:07:47.600 fatigue sooner than a non-occluded condition. I think that's fair, but to say that that's the only thing,

01:07:55.120 the only benefit of blood flow restriction, I don't know that we can say, especially considering

01:08:01.160 the vascular response I talked about earlier, that the vascular network, the blood flow,

01:08:08.640 the resting blood flow to the forearm or calf, it does appear to respond with a higher pressure,

01:08:15.200 but not a lower pressure, despite that both of them are doing a tremendous amount of work.

01:08:18.920 So I think it might be fair to say with muscle with respect to resistance exercise, but

01:08:23.580 I have some remaining questions before I would go all in.

01:08:28.760 So let's get back to something that we touched on earlier. We'll get to it in more depth,

01:08:34.020 which is the relationship between strength and hypertrophy. It's very clear that they're

01:08:39.240 correlated. It's not clear which way the arrow of causation runs, if there is a causal relationship

01:08:48.560 between them. What's the conventional thinking on this? The conventional wisdom or the conventional

01:08:55.040 thinking is that once muscle growth is there, that it's probably contributing to changes in strength.

01:09:02.700 That's the textbook definition. Neural first, followed by large contributions from muscle hypertrophy.

01:09:11.540 And doing a lot of research in the low load realm, as we've done, I started to really see that

01:09:18.340 maybe that's actually not the case because we almost always see muscle growth, which is similar to or

01:09:28.180 equivalent to that of high load exercise. But the strength, assuming that we're not practicing the

01:09:33.920 test repeatedly, is almost always less. And in my mind, I had a hard time coming up with a lot of

01:09:42.880 excuses. I did for several years. But at some point, in talking with my students, we just started to ask the

01:09:51.980 question about, well, where did this story come from, about muscle growth playing a role? And why do we even

01:09:59.020 think it in the first place? Because I'm trying really, really hard to make excuses for why we aren't seeing it.

01:10:04.940 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

01:10:11.740 really becomes difficult for people to have this conversation because everybody has learned the

01:10:18.140 same thing that I learned. It's neural, then hypertrophy, neural, then hypertrophy. And they have a hard time

01:10:24.720 taking a step back and going, okay, but were those studies ever able to actually make that claim?

01:10:32.540 Yeah. So where did that hypothesis come from? What is the evidence in support of the null hypothesis?

01:10:37.480 I think if you were to get a bunch of people together, and we measured muscle size, and we

01:10:43.860 measured strength, on average, people who are bigger will be stronger. People who are smaller

01:10:51.340 will be weaker. That's true. And we've seen that. We've documented that ourselves. But that's not an

01:10:58.980 effect of exercise because we see the same relationships in people who have never exercised

01:11:05.440 in their life. You're saying that the correlation or association between strength and size is equally

01:11:11.640 strong in the untrained as it is the trained? Correct. The question that we're discussing is

01:11:17.840 when a person begins to exercise and then they get stronger, is that due to changes in muscle size?

01:11:26.840 And that's where I have the question. I don't question whether or not they're related. I completely agree

01:11:32.600 that they are. But when we exercise, does a change in one result in a change in the other? So it

01:11:40.140 obviously makes a lot of sense that it could. For all the reasons that we said earlier, we're increasing

01:11:46.160 actinamized, we're increasing this protein. Why would they not then produce greater strength? But there's

01:11:53.820 numerous times in the literature where we have shown greater changes in muscle size, but strength doesn't

01:12:01.280 even change. So that leads me to believe that there could be quite a bit of disconnect with respect to

01:12:09.460 muscle growth and the change in strength. Now, you wrote a paper basically trying to

01:12:15.360 go back to the root of this dogma. I think you basically found that there were sort of three papers

01:12:23.760 that formulated this viewpoint. Two of them, I think, were from the 70s. And then one was kind of a review

01:12:29.340 paper of one of those papers. Am I remembering this correctly?

01:12:33.380 Yeah. So the one that's commonly cited is Mauritania DeVries or DeVry. And they had five

01:12:41.300 individuals. One arm lifted weights. The other arm did not lift weights. And they were basically

01:12:51.000 inferring muscle growth off changes in service EMG. So they did measure arm circumference, but that wasn't

01:12:58.660 the variable they were using to quantify growth. They were looking at changes in the slope of this

01:13:04.540 integrated EMG. So if they saw a change in the slope, they inferred that to mean muscle growth.

01:13:11.780 If they didn't see a change in that slope, then they said that was neural.

01:13:15.820 Can you explain to me how that works? I don't know enough about EMG to understand that inference.

01:13:21.300 At least in my opinion, you cannot infer growth off a change in EMG.

01:13:24.820 But what they were doing is, is that let's say, let's pick a variety of weights. So let's say 10

01:13:31.900 pounds, 20 pounds, 30 pounds and up. So what is the EMG amplitude? So, but EMG amplitude is

01:13:39.740 essentially an estimate of muscle action potential. So how much signal do you get when you lift 10

01:13:45.000 pounds at baseline versus 20, 30, 40? Then they would do that every couple of weeks.

01:13:51.400 So if they lifted 10 pounds and the, basically the amplitude was a little bit less,

01:13:57.600 they would infer that that was being picked up by muscle growth.

01:14:01.880 So the amplitude they're using to assess the neurologic signal. And over time, they're saying

01:14:09.760 if the neurologic signal is going down and the effort is the same, hypertrophy makes up the

01:14:16.660 difference. Or for example, yeah, I got it.

01:14:19.480 One of the points that we're always trying to make is that guarantees that at some point hypertrophy

01:14:28.520 is going to be a mechanism. You're not actually testing a mechanism. You're just assuming that

01:14:33.560 at some point it will be a mechanism. So that was the same thing with Ikai and Fukunaga, which is the

01:14:38.400 other study. So they actually did measure muscle size. And to my knowledge, that's actually the first

01:14:44.420 study to actually document changes in muscle size in response to resistance exercise. So what I would

01:14:51.360 call a landmark paper. I really enjoy the paper. But what they infer is, is that if muscle growth

01:14:57.940 changes, then it must be playing a role. And if it doesn't change and they got stronger, then it must

01:15:05.800 be neural. And that's kind of the, where we've been at ever since. In other words, that when we run a

01:15:11.940 training study, if you get stronger, but we don't document a change in muscle size, it's neural.

01:15:18.020 If you get stronger and we measure changes in muscle size, well, then it was neural and hypertrophy.

01:15:26.100 So to me, I don't think we can make that claim because you're just assuming that the ability to

01:15:32.660 document it means it's actually doing something with respect to strength. I would like to see a little

01:15:38.540 bit more rigor in that. I understand why people would think it. I get all of that. And that makes

01:15:44.740 sense to me as well. But my question is, is that does it actually, and we've approached this through

01:15:51.920 a variety of different ways, but I think it does help to think about this historically. Where did this

01:15:57.820 come from? And it really does seemingly come from those two studies. And then Digby Sale had a very,

01:16:04.780 really great paper reviewing kind of all the work that had been done where he suggested that most

01:16:12.160 training studies are only documenting a certain aspect of an actual person's training age. So they're

01:16:19.620 never going to be able to actually answer this question because the studies are too short. But I don't

01:16:25.380 know that that's fair to say because more time to breeze is eight weeks, which is the same duration as a lot

01:16:31.180 of other studies that have basically contradicted it. So yeah, you're right. Those are the three

01:16:36.840 papers that are commonly cited for this neural first followed by hypertrophy.

01:16:43.360 Even outside of BFR, which seems to provide a very elegant tool to test the hypothesis,

01:16:47.760 as you've explained, and we'll get into in a little bit more detail, it seems that you could do other

01:16:52.860 experiments to test this even without blood flow restriction. For example, couldn't you have somebody do

01:17:00.160 workouts where they only do one to five reps of exercises and they're basically always functioning

01:17:08.320 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

01:17:13.500 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

01:17:19.240 85% of one rep max. So you cycle through those workouts where you increase strength. In fact, I'll put a

01:17:27.700 very practical example to this. I know specifically athletes who train this way and they train with

01:17:34.080 a trap bar and they do not do the eccentric motion. So they lift the weight up and drop it,

01:17:42.580 lift the weight up and drop it. And they're never going above five reps. So they're really trying to

01:17:47.500 maximize strength, which comes more from the concentric movement. And they're trying to minimize

01:17:53.740 any hypertrophy because they're athletes for whom strength to weight is the most important ratio. So

01:17:59.940 it's very typical workout for runners. So they'll dramatically increase their strength without adding

01:18:06.460 size. And then you could compare that to the opposite type of workout where you do more of a bodybuilding

01:18:13.860 workout. You're probably never going below eight reps and you'll get bigger. And I could imagine a

01:18:20.140 scenario where you don't even get as strong as that other person. I mean, wouldn't that demonstrate

01:18:24.860 how uncoupled these two metrics can be? Yes, I agree with you. And we've done this several times now.

01:18:33.280 We've tried to address this question via study design, doing something very similar to what you said,

01:18:39.580 where we have one group that's training, just doing the one RM test. That's it. They come in,

01:18:45.820 they work up to about five total reps and then they go home because we're trying to maximize the

01:18:51.740 strength signal, but not get growth. Because essentially to answer this question, we have to

01:18:56.860 know if the muscle did get bigger and stronger, what would strength look like if muscle growth had not

01:19:04.720 occurred? So when we look at the traditional training group, we have them doing about eight to 12 reps.

01:19:10.580 And this is a very simple movement, the bicep curl. In that group, we see muscle growth and we see a

01:19:18.060 change in strength. Now, what a majority of articles would do is say, given that muscle growth is there,

01:19:25.920 that muscle growth must be contributing to strength. In our mind, we have to say, well, what would strength

01:19:32.900 look like if growth hadn't been there? And when we look at the other group that was just doing one RMs,

01:19:38.460 the strength is the same. Now it's not greater, but it is the same. I do think that the more

01:19:46.100 complex the movement becomes, the greater that separation starts to happen. So we were doing

01:19:51.860 a barbell bench press. My guess is, is that the group doing one RM or close to a one RM would be far

01:19:58.660 better than an eight to 12. But it's just the fact that the movement is very, very simple.

01:20:03.280 So similar to what you said, in our mind, this does provide some method of trying to address this

01:20:12.200 because we see a group with no growth compared to a group with growth, but the strength is the same,

01:20:19.520 suggesting that that change in muscle size is not necessary for a change in strength,

01:20:26.040 nor does it appear to be contributing, given that the strength is the same. Now, there are limitations

01:20:33.680 with that. One of the big ones is that in order to get that differential in growth, we had to apply

01:20:42.980 slightly different exercise patterns. So one group was doing eight to 12, still a high load, but not

01:20:50.200 a hundred percent, where we had another group training at a hundred percent. So some suggested

01:20:56.080 that, well, that's not really that fair of a comparison. There's more things that are different

01:21:02.180 than just the muscle growth. And that's, that's true. And they suggested that instead that we should

01:21:10.020 follow that up with some mediation analysis, where we look at how much of this change relative to a

01:21:17.120 control is driven by muscle size within each group individually. And when we did that,

01:21:23.320 we did not see any mediation, meaning that none of the change in strength could be explained

01:21:29.540 by that change in muscle size in either one of the groups.

01:21:33.920 Explain that more for me. I'm not sure I follow how you would determine that.

01:21:38.000 So there are some statistical kind of approaches where you can do some causal mediation. In other words,

01:21:46.020 you can look at the relationship between, let's say we have these two exercise groups.

01:21:51.900 So instead of looking at them head to head, let's look at them individually compared to a group

01:21:56.540 that's not doing any exercise at all. That way we can kind of really control for the random error

01:22:01.900 across time. So measurement noise, random biological variability, et cetera.

01:22:07.800 Essentially what mediation is doing is saying, okay, we have this group here.

01:22:11.920 How much strength did they gain?

01:22:15.760 So they got stronger. So that's a direct relationship.

01:22:19.200 So when this group exercises, they got stronger.

01:22:23.080 Now mediation says, okay, let's add in a variable here to see if we can remove this relationship either

01:22:29.800 partially or completely.

01:22:31.620 So if we add in muscle growth to the model, and then this group no longer correlates with strength,

01:22:39.680 then we'll know that that relationship is completely driven by this other variable.

01:22:44.720 Now we wouldn't expect for it to be completely, but we would expect for it partially.

01:22:49.820 But we didn't see that in either one of the groups.

01:22:52.900 Is the contrapositive then that it's not at all coupled?

01:22:57.060 Because if you were to ask me what my intuition is, which is worth maybe a warm bucket of hamster

01:23:03.240 vomit, my intuition would be there is an association, but it's not 100% causal.

01:23:11.140 So the R squared might be 0.5, not 0.99.

01:23:16.900 So in other words, I would not guess that there is no association.

01:23:20.900 I certainly wouldn't guess a negative association,

01:23:23.400 but I wouldn't guess that it's one-to-one causal.

01:23:26.960 Can the mediation tease that out?

01:23:29.240 Yes, because it would be a partial mediation in that sense.

01:23:32.900 And you did not see a partial mediation?

01:23:35.020 No, we didn't see any effect at all.

01:23:37.240 Now, there are other potential reasons.

01:23:39.440 I mean, we have to think about random error across time with our measurement and things of that.

01:23:44.100 I don't think that any of the work that we have done so far can conclusively say that it plays no role.

01:23:51.440 But I do think that we're having an accumulating amount of evidence that's suggesting that

01:23:58.380 if it does play a role, it is so small that we aren't able to ever detect it.

01:24:05.420 So I am not sure that muscle growth in response to exercise is a mechanism.

01:24:11.940 I've seen no experimental evidence that suggests that that's the case.

01:24:16.260 Now, for a practical, pragmatic person, what would that mean for them?

01:24:22.240 Well, I think what it could mean is, is that if you are interested in maximal strength,

01:24:28.020 in getting as strong as possible, you probably don't care whether it's a mechanism or not.

01:24:33.460 You just want to know, how do I get strong?

01:24:35.360 I think we can learn a couple of things from some of these experiments.

01:24:40.260 One, that there's a huge specificity component, meaning that if you want to be a very good squatter,

01:24:47.660 a very good deadlifter, and being very good squatter or being a very good deadlifter means

01:24:52.100 you're able to lift as heavy as possible one time, then that means you should be training

01:24:57.220 at least a good portion of the time at or close to that one RM.

01:25:01.900 Now, if you really believe that growth might be playing some role, what that might mean

01:25:10.960 for you is to say, well, if it is playing a role, it might be pretty small.

01:25:15.220 So maybe I can allocate less overall time to it, which would be good for most strength

01:25:20.920 athletes because that's typically what requires a lot of recovery because you're doing a lot

01:25:25.980 of volume to make a muscle grow.

01:25:27.500 So I become more skeptical of muscle growth as a mechanism every year that goes by.

01:25:34.440 We're still doing more experiments to try and address this, but there certainly is no

01:25:39.620 evidence right now that suggests that it is a mechanism.

01:25:42.460 We have a lot of evidence that suggests that it isn't, but I do think it would be premature

01:25:47.320 to say, well, we've completely ruled it out.

01:25:50.280 I don't think that's fair to say at all.

01:25:52.220 So what are some other explanations?

01:25:53.520 I mean, I guess nobody's disputing the neurologic component to this.

01:25:57.620 Is one hypothesis that that is the entirety of it?

01:26:01.180 Or do you think that there is another mechanism that isn't fully clear?

01:26:05.440 Yes.

01:26:05.960 I think some people would say that some people are of the opinion that the exercise induced

01:26:11.020 changes are probably predominantly neural.

01:26:14.060 I'm not there yet.

01:26:15.500 I think that there could be some local changes at the muscle and that might be able to explain

01:26:23.680 why some groups get stronger.

01:26:26.200 That's not just neural.

01:26:27.840 In other words, maybe the muscle at the local level is actually getting better at responding

01:26:35.120 to forceful contractions.

01:26:36.700 So maybe it's, you know, how it deals with calcium or how the myosin head binds.

01:26:40.740 Maybe there's some alterations there qualitatively that aren't due to muscle size, but I don't

01:26:47.680 know what those would be necessarily.

01:26:49.440 I can only offer potential reasons.

01:26:52.680 And I think that's usually the argument that's brought up mostly against our point is, well,

01:26:58.300 if muscle growth is not a mechanism, then what exactly is it?

01:27:01.780 And I don't think that that's a fair argument, honestly, because I don't know that you have

01:27:08.000 to know for sure what something is to say, we don't have a lot of evidence for this.

01:27:12.220 And there's a lot of evidence against this, but that's just my kind of thinking.

01:27:17.320 But I do think that there probably is a huge neural component, but I don't know that there

01:27:23.800 isn't something going on at the local level that is independent of a change in muscle size,

01:27:29.340 but it is still muscular, perhaps.

01:27:32.980 So how common is BFR with athletes today?

01:27:38.620 I think it's becoming more and more common.

01:27:42.360 I know at Ole Miss, for example, as well as a lot of other Division I schools in the athletic

01:27:47.580 department, I would say a large portion of them do have blood flow restriction devices.

01:27:52.380 So they are using it for rehab.

01:27:54.220 And I know that I've seen players on ESPN and the NBA, NFL using blood flow restriction

01:28:02.460 as well.

01:28:03.540 For rehab exclusively, or do you see them using it when they're not injured as well?

01:28:07.840 I think there's a couple of NBA players just looking at some of the stories where they were

01:28:11.720 using it, not for rehab, but just as an everyday kind of way to train where they were able to

01:28:18.060 recover just a little bit faster.

01:28:19.460 And they don't have to have a, as they've aged, you know, they want to make sure that

01:28:23.860 they're ready to play on the actual court instead of just spending all their time recovering

01:28:28.460 from their workout.

01:28:29.560 So I think that they perceive this as one option to use where they're able to get some kind

01:28:36.500 of workout in, but maybe recover quite a bit faster than they might doing normal exercise.

01:28:42.020 Is the speed of the recovery a function of less trauma to the muscle during the workout?

01:28:47.440 Or why, why is their recovery quicker?

01:28:50.640 I don't know that we know that, but I, it does appear that when they are injured and

01:28:58.000 they're working out with blood flow restriction, they're able to usually to get a little bit

01:29:03.800 more out of that compared to high load exercise, or at least very similar to that, but they have

01:29:07.820 less pain during the movement.

01:29:10.060 So maybe they're able to get a little bit more out of the rehabilitation than they normally

01:29:13.540 are because maybe they're, before they're inhibited to a greater degree with, by pain,

01:29:20.060 that's reduced a little bit through the application of blood flow restriction.

01:29:23.440 But I don't really know, to be honest.

01:29:28.000 If let's take an extreme, a bodybuilder, right?

01:29:32.080 Where they're not being judged at all on strength.

01:29:34.360 I mean, I have yet to see a bodybuilder who's not very strong, but presumably due to the, just

01:29:39.560 the overwhelming amount of volume in their training.

01:29:42.360 But, you know, I even talked about this with Lane on the podcast when he was explaining

01:29:47.160 how, look, at the end of the day, the volume is what's going to matter.

01:29:49.760 And, you know, you can do that with isolated movements.

01:29:52.160 You can do that with compound movements, but you just need to get lots and lots and lots

01:29:58.540 of volume across these kind of ranges.

01:30:01.420 So if the goal is purely hypertrophy, which at least during part of the bodybuilder, but the

01:30:06.800 bodybuilder cycle is the case, how would they utilize BFR?

01:30:10.940 First of all, would it be a valuable tool above traditional training?

01:30:14.220 And if so, what would be the optimal way to use it?

01:30:17.260 Yeah, I think it could be.

01:30:18.620 It could be a tool if that's how they choose to use it.

01:30:22.080 I think for muscle growth, I think I agree with Lane that it really comes down to personal

01:30:27.720 preference because even without blood flow restriction, we've seen from 30% up to, you

01:30:34.540 know, 80% or even higher can produce the same amount of muscle growth.

01:30:38.160 So I think that allows you to have some level of preference on based on how you feel that

01:30:43.740 day or what you enjoy.

01:30:46.080 There are days where if you have a heavy day, for example, and you're going into the gym,

01:30:52.600 but you don't feel good or you're not psychologically have it.

01:30:55.500 And it could be potentially dangerous for you to use a heavy weight because you're not focused.

01:31:02.060 Then maybe that's a time where you might be able to implement some blood flow restriction

01:31:05.540 because you can use light weights.

01:31:07.700 It doesn't require as much focus.

01:31:10.080 And you could probably see a lot of the same response, at least with growth.

01:31:15.460 Another component could be is that it just helps with some variety.

01:31:19.500 I don't think that variety is necessary per se for muscle growth to be optimal.

01:31:25.680 But I think if you're training for an extended period of time across your life,

01:31:29.340 things can get pretty boring if you're just doing the same thing all the time.

01:31:33.700 So it could be a way to try and spice it up a little bit.

01:31:38.080 And then obviously, if you're hurt, I mean, it could be a great tool to use because there

01:31:42.320 is a lot of or becoming to be more and more evidence that it's helpful in the rehabilitation

01:31:48.480 world.

01:31:49.440 So I think there's a variety of ways that it can be used.

01:31:51.660 But I do think that it's probably important to note that if a person's not comfortable

01:31:56.960 with it, they don't have to do blood flow restriction in order to optimize how much muscle

01:32:02.920 that they can grow.

01:32:04.880 But it is a tool that could be potentially quite effective for them.

01:32:09.740 Yeah.

01:32:09.960 Actually, the example you gave is exactly what happened today, which was today's main set

01:32:14.360 for me was five by five deadlift.

01:32:17.120 So obviously, that's, you know, a heavy-ish day.

01:32:21.460 And I took five sets to warm up to get to the starting weight.

01:32:26.220 That first set of five, I was like, yeah, this, I just, I'm struggling.

01:32:30.780 Second set, still struggling.

01:32:33.160 Third set, struggled more.

01:32:34.940 Fourth set, I was like, boy.

01:32:37.000 And I'm supposed to be escalating the weight.

01:32:38.620 And on the fifth set, two reps in, I thought, this is the day you hurt yourself because I'm

01:32:45.500 going to break my form to get number three, four, and five.

01:32:48.480 So I actually just stopped.

01:32:49.900 And that's why I went and did the leg press with blood flow restriction, which was a very

01:32:55.460 lightweight.

01:32:56.320 I mean, I don't even remember how many pounds it was, but it was the type of weight that

01:33:00.060 if I wasn't restricted would have, you know, I could have done a hundred reps, I'm sure.

01:33:03.880 So, but it was a great way to mix up the training and that's the kind of stuff I'm interested

01:33:08.740 in exploring.

01:33:09.940 I also kind of think of this as a tool for people who maybe don't have some of the technique

01:33:17.820 to do heavier lifts, much in the same way I've sort of thought of the super slow lifting

01:33:24.460 protocols as reasonable protocols for people who just don't have the desire to train at

01:33:31.900 higher volume and frequency and, or don't have the technical chops.

01:33:36.920 Now that said, I've always felt that the problem with super slow training is unless it's done

01:33:43.060 to failure, which is upsettingly painful.

01:33:46.560 If you've tried those workouts, it's probably not nearly as beneficial as traditional training.

01:33:53.680 You know, the, the, the sort of super slow advocates will say it's on par with traditional

01:33:59.800 training, right?

01:34:02.140 You could do 20 minutes once or twice a week and have the benefits of six hours per week.

01:34:05.800 I'm not sure that that's true, even from a hypertrophy standpoint, but if it is true,

01:34:10.900 it's probably limited to the few people who truly can fail.

01:34:15.460 And I don't know if you've ever tried these super slow workouts, but it's very difficult to

01:34:21.820 truly fail.

01:34:22.840 I think it's, it's very hard for, I think most people.

01:34:26.280 Yeah.

01:34:26.620 A long time ago, but I, I never did much with it.

01:34:30.020 There was somebody in my, that I worked with in my PhD who was very interested in it for

01:34:35.060 a while, but yeah, I was never really a fan for sure.

01:34:39.400 How come for the same reason or.

01:34:41.600 I never felt like I was going to get very strong from doing something like that.

01:34:44.720 I'm just moving so slow and the weight is usually so light that I don't know how much that would

01:34:51.620 be transferring over to something that I was interested in at the time, which was to get

01:34:55.800 as strong as possible.

01:34:57.680 It's definitely hard.

01:34:58.840 There's no question, but I didn't enjoy that form of training.

01:35:03.800 So it's safe to say that the one place, I think you really talked about this already,

01:35:07.280 but I just want to make sure we put a dot on it.

01:35:09.220 The one place where it's unambiguous that you need to be doing a traditional lift without

01:35:14.320 restriction is if you're training for maximum strength of that lift, which again, I don't

01:35:21.540 think most people are doing maximum strength bicep curls.

01:35:24.460 I don't think that's, but, but when you start to talk about a bench press, a squat, a deadlift,

01:35:28.300 a leg press for that matter, if you're, if you care so much, there's probably no substitute

01:35:34.080 for being in that 80% to a hundred percent one RM.

01:35:39.120 Is that kind of a safe takeaway?

01:35:42.080 Yeah.

01:35:42.680 And if you do blood flow restricted exercise with low loads, assuming it's not extremely low,

01:35:49.040 like if you're around 20 or 30%, you will get stronger, but it will be to a much smaller degree

01:35:55.460 than you would with traditional exercise.

01:35:57.200 I completely agree.

01:35:58.900 And I'll just add to, we get this a lot where it's like, well, you're doing bicep curls in your

01:36:03.880 study is like, because we're using bicep curl.

01:36:06.620 It's a research model to answer a particular question.

01:36:10.060 We're not personally training people.

01:36:11.940 So I think sometimes people lose the reason why certain things are done.

01:36:18.160 Sometimes people will look at low load literature with blood flow restriction or even low load

01:36:23.440 literature without blood flow restriction and say, yeah, but look at this study.

01:36:27.320 They found very similar changes in strength as high load exercise.

01:36:30.100 And some of those studies do exist, but the majority of those that do find that effect.

01:36:36.840 If you look at the methods, what they're doing is the low load BFR group is doing the one

01:36:42.660 RM every two weeks or every three weeks.

01:36:45.660 And they're doing it in effect to try and reset the load so they can assume that they're progressing.

01:36:54.260 But what they end up doing is practicing lifting a heavy weight.

01:36:58.280 So you're not actually studying low loads of BFR.

01:37:01.660 You're studying low loads with BFR plus one RM training.

01:37:05.920 And I think that that's a very important point.

01:37:09.780 And we actually reviewed this.

01:37:12.120 We published a paper on this topic where we show that when you only look at the studies

01:37:17.780 with low loads that don't practice doing the one RM test repeatedly, almost all of them

01:37:24.260 lose the high load exercise.

01:37:27.220 Just again, illustrating the point that it's about lifting heavy weight is the best way to

01:37:33.360 get better at lifting heavy weight.

01:37:35.280 It doesn't mean that you won't get stronger lifting lighter weight, but you won't be as

01:37:40.100 strong as you were.

01:37:41.440 Let me summarize what you just said, because I think in terms of big picture, there are

01:37:46.300 really two areas where BFR shines.

01:37:50.780 One of them is in an individual who for some reason can't lift heavy weight, but still needs

01:37:57.880 to get stronger and potentially bigger.

01:37:59.840 And the obvious example is the person who's recovering from an injury.

01:38:04.340 And then potentially the person who just has a concern about lifting heavy weight, either

01:38:09.800 from a technical standpoint or injury avoidance or things like that.

01:38:13.860 The second place where BFR seems to really stand out is in hypertrophy.

01:38:18.380 Most of these studies are demonstrating slightly superior hypertrophy response despite less total

01:38:29.060 volume and certainly lower load.

01:38:31.400 It's at least as good in hypertrophy and in some cases better as my reading of the literature.

01:38:36.100 If you have a low load with BFR compared to a work-matched low load group without BFR,

01:38:42.400 hypertrophy is better almost always.

01:38:44.400 And to make them equal, you will just have to go more on the, you'll have to go to a

01:38:50.880 greater degree of reps on the unrestricted side to failure, basically.

01:38:56.180 Yep.

01:38:56.820 And therefore it takes more time.

01:38:58.480 Correct.

01:38:58.900 To get the same effect.

01:38:59.860 So it's a more efficient way potentially to generate hypertrophy.

01:39:03.160 It's probably more accurate than what I said earlier.

01:39:05.040 Now, the vascular adaptations, again, I keep putting that caveat in because it's always

01:39:11.020 in my mind because I really expected that to be the same across the board as well.

01:39:16.740 Meaning that as long as you're doing a lot of repetitions, it shouldn't matter whether

01:39:20.060 there's BFR or not.

01:39:21.680 That's not what we found.

01:39:23.280 Now, whether or not that can be repeated, I'm not sure.

01:39:27.420 Hopefully we can do that in the future.

01:39:28.800 But because my thinking for a long time was similar to what you were saying earlier.

01:39:34.660 It doesn't really matter whether there's BFR or not.

01:39:37.240 If you do enough, it'll be very similar.

01:39:39.400 The workload will just be less.

01:39:41.160 And I think that, again, it's true for muscle, but I don't know if that's true for every single

01:39:44.940 variable.

01:39:46.440 Let's talk about the mechanism by which this is happening.

01:39:48.940 My assumption, which I don't know if it's right or wrong, is that at least one of the

01:39:56.520 reasons that BFR can produce so much hypertrophy at such low load is in response to the metabolic

01:40:05.640 challenge that's posed.

01:40:07.380 And so one of the things I was doing quite a bit was testing lactate levels with and without

01:40:12.800 BFR.

01:40:13.440 It's very easy to demonstrate that when you occlude your arm, for example, well, distal

01:40:20.060 to that occlusion, lactate is going through the roof because you're exercising that arm

01:40:24.600 and you're not letting the lactate clear out of circulation.

01:40:27.400 So I'm pinpricking my finger and getting very, very high lactate levels.

01:40:33.000 And so that's obviously a metabolic byproduct of any time you're exercising and then especially

01:40:39.880 when you're doing this type of exercise.

01:40:41.860 And so, yeah, I could demonstrate that I had a higher level of lactate doing blood flow

01:40:48.580 restriction than not, even when I was lifting slightly more weight and doing something traditional.

01:40:54.880 Do we think that that matters in this equation?

01:40:57.320 Do we think that that's partially driving this?

01:40:59.980 And that's just one of the metabolites that we can measure easily.

01:41:02.620 There's plenty that we can't.

01:41:04.460 Yes, I would agree.

01:41:06.060 I think that there's kind of two schools of thought.

01:41:08.140 One is that the pooling of these metabolites in and of themselves is turning on some of

01:41:15.260 these anabolic signaling pathways, meaning just the fact that you're pooling lactate around

01:41:20.380 the fibers, that that's able to activate growth.

01:41:24.700 I used to be interested in that idea.

01:41:27.260 We tried to test this using a couple of different ways.

01:41:30.620 We didn't find an advantage to doing that.

01:41:34.880 So we kind of started to say, well, maybe there's nothing to metabolize in and of themselves,

01:41:40.600 but maybe it's what they're causing the muscle to do.

01:41:45.160 So in other words, maybe the way we think about it now is, is that as you said, you're exercising

01:41:50.620 with blood flow restriction.

01:41:52.000 The metabolites are being trapped.

01:41:53.700 What we think is, is that they're augmenting muscle activation.

01:41:57.840 So they're causing the muscle to have to work a lot harder than it normally would because

01:42:04.000 you're pulling this lactate around it and you might fatigue some of these cross bridges.

01:42:09.620 So we have to recruit more and more and more and more fibers.

01:42:14.320 So that's where we think the benefit of metabolites is, is that they're basically inducing fatigue,

01:42:20.580 which then leads to further muscle activation.

01:42:23.700 And muscle activation for a sufficient duration of time is, is the name of the game, at least

01:42:30.840 in my opinion, for making a muscle grow.

01:42:33.420 So one of the, the big kind of questions always is, are the mechanisms themselves different

01:42:41.720 from traditional exercise?

01:42:43.980 If I do high load exercise, is that going to be a different mechanism than when I do low

01:42:50.320 load exercise with blood flow restriction?

01:42:51.940 And I don't think so.

01:42:54.620 And I'll tell you why.

01:42:56.720 I think that the mechanism involved in activation is different.

01:43:03.080 But once the fiber is activated, all the signaling pathways, from what I understand, are going

01:43:09.460 to be very similar.

01:43:10.340 So when we lift a heavy weight, it requires a tremendous muscle activation to even lift

01:43:18.560 one rep.

01:43:19.060 If you are trying to do a bicep curl and you're only activating a small portion of your fibers

01:43:24.980 and you're trying to lift 70 pounds, if your one RM is a hundred pounds, that's an enormous

01:43:30.480 bicep curl.

01:43:31.260 So I was about to say, I really feel pretty pathetic here.

01:43:34.340 Yep.

01:43:34.640 But go ahead.

01:43:35.880 So choose any lift.

01:43:38.240 In order to lift that heavy weight, you need to activate a large portion of your musculature.

01:43:44.340 Otherwise the weight isn't going to move.

01:43:46.140 Compared to low loads, where you don't need to activate the same amount of muscle fibers

01:43:51.000 initially because the weight is extremely low.

01:43:54.820 So when we exercise with low loads and BFR, we're activating only a small amount initially.

01:44:01.820 But those metabolites, as you discussed, start to become trapped and we activate more fibers,

01:44:07.440 more fibers, more fibers, and more fibers.

01:44:09.980 And then by the end, we've activated a similar amount of fibers as we did with high load exercise.

01:44:15.880 By the way, is there an order in that?

01:44:17.660 So if your one RM bicep curl is a hundred pounds.

01:44:21.620 So with no blood flow restriction, you pick up 80 pounds and bang out, I don't know, 10 reps,

01:44:31.260 eight reps.

01:44:31.860 Compare that with if you picked up 40 pounds and banged out 40 reps, what is happening from

01:44:43.460 a fiber fatigue standpoint under those two scenarios?

01:44:47.620 In general, we have what we call the Henneman size principle, where you recruit type one motor

01:44:53.700 units first.

01:44:55.040 And then as you require, based on the exercise, you recruit type two in addition to type one.

01:45:02.440 So when you lift a heavy weight, you're getting to the type twos very quickly because you need

01:45:07.720 them.

01:45:08.460 Whereas with lower weight, you probably are taking a little bit of time, but then you are

01:45:13.880 eventually getting to those type two motor units.

01:45:16.080 So if the person in my example fails at eight reps with 80 pounds and 40 reps with 40 pounds,

01:45:24.540 it's just that the 40 reps took a lot longer to burn through the type one fibers.

01:45:30.140 And then the type two A's and the two A B's.

01:45:34.400 And then finally at the very end, the two X failed.

01:45:37.820 Whereas when he did the same exercise, you know, 20 minutes later at 80 pounds and failed

01:45:44.380 at eight reps, he did the same sequence, but he just got to the two X much sooner.

01:45:49.820 Is that what you're saying?

01:45:51.140 Yeah.

01:45:51.640 Yeah.

01:45:52.140 And the reason why I say that is if you look at, if you pull out fibers following training,

01:45:57.860 type one and type two fibers have both been shown to grow in both high load exercise as

01:46:03.940 well as low load exercise with and without blood flow restriction.

01:46:07.440 So they both respond.

01:46:09.240 Some people have suggested that type one might grow a little bit more with low load training,

01:46:15.500 but I, I'm not convinced on that yet.

01:46:18.440 I think that it's probably very similar to high load exercise, although I see the thinking,

01:46:22.420 but both of them will grow in response to both types of exercise.

01:46:27.440 In general, at the extreme level, is a bodybuilder's hypertrophy more explained by type one or type

01:46:34.920 two fibers, or are they both massive relative to anybody else?

01:46:39.140 I would say probably the increase in both, although I don't, I'm not, there's not one thing I can

01:46:45.840 point to that would suggest that for me, but I, I think that in response to training, my guess

01:46:53.540 is that both of them would increase.

01:46:55.240 I think you might be able to make an argument that people who might, again, go back to our

01:47:00.760 argument earlier, who start lifting weights and realize, man, I'm actually able to grow quite a

01:47:06.460 bit. Maybe they already had more type two fibers to begin with, which is something is more responsive

01:47:13.140 to loading. So maybe you can make that argument, but I think in response to exercise, when a bodybuilder

01:47:19.520 exercises, I would probably guess that both of them are going to grow both types of fibers.

01:47:24.380 You mentioned very briefly, passive BFR. What's the application for that? Is that in a highly

01:47:30.560 injured person?

01:47:32.100 Yeah. And again, there's only a small number of studies that have shown this. That could be for

01:47:37.940 a variety of reasons. One, it could be because those are hard to do, where you have somebody who

01:47:43.520 had ACL surgery, and then we apply blood flow restriction to their limb. We inflate and then we

01:47:50.120 deflate for a period of time, a couple of times a day. And that's been shown to slow muscle loss.

01:47:54.560 But there's only a few studies that have shown that. Now, again, you don't see growth. You only

01:48:00.480 see a slowing of loss.

01:48:02.280 Attenuation of loss, which is a big, big deal when people undergo surgery.

01:48:06.960 I'm very interested in whether or not that's true. One of the things that gives me a little bit of pause

01:48:12.380 is that there's not more of those studies. So in my mind, I always wonder, is that because

01:48:19.360 those are, again, hard to do? Or is it because those studies do exist, but they didn't see anything

01:48:25.860 and they didn't publish it? So I'm cautiously optimistic that that could be useful. But I do

01:48:33.360 think that as soon as a person can exercise, you know, and we kind of published a paper on this idea

01:48:39.860 a long time ago, kind of what we view as a progression of blood flow restriction. In other

01:48:45.240 words, someone who wants to, who can't do anything, how do we get them back to doing something?

01:48:50.400 So we start off with, if they can't even walk, we apply this restriction to slow down muscle loss.

01:48:57.060 Once they can maybe walk on a treadmill or walk very slowly, but they can't lift weights,

01:49:02.200 we start to transition them to that phase where they're able to increase muscle size

01:49:05.820 and strength just a little bit. And if nothing else, maintain what they have. But then once they

01:49:11.120 can transition to resistance exercise, I think that's where they're going to see the biggest

01:49:17.400 bang for their buck. And then they can go to highlight exercise if they choose. But I do feel

01:49:23.440 like that's a very potential useful progression to this technique. This is such an important question.

01:49:29.480 It's a real shame. This isn't being studied. Like if I were czar for a day and I was in charge of

01:49:35.120 where research dollars would be spent, I would be putting, because I don't think it would take that

01:49:40.820 much money by the way, but I would absolutely prioritize this question. When you consider

01:49:45.560 the extent of muscle loss that occurs in sedentary individuals following elective surgery,

01:49:53.780 emergent surgery and injuries. So those are three very big buckets of people disproportionately,

01:49:59.800 by the way, affected in the elderly where the effects are devastating. I'm sure you're familiar

01:50:04.840 with the literature of, you know, you take somebody in their seventh decade of life and you train them

01:50:10.180 very hard for a year. They'll put on X pounds of muscle and then put them in a hospital bed for 10

01:50:17.700 days. They will lose all of it. They will lose every ounce that they spent a year diligently gaining.

01:50:23.300 To think that there could be a tool that could slow that and we don't know the answer definitively

01:50:30.560 strikes me as just unbelievable, unwise decision that's been made. So I would hope somebody who has

01:50:38.140 the authority over where those dollars go is listening to this and realizing that the morbidity

01:50:43.040 and mortality associated with muscle loss, especially in the elderly, is so significant. And one of the

01:50:50.100 things we talk about a lot with our patients is once you get to be 70 and certainly 80 years old,

01:50:55.560 you're kind of one fall away from the end of your life, even if you don't die directly, right? So

01:51:01.200 there's the catastrophic fall where you hit your head, you have a cerebral hemorrhage and you die.

01:51:06.440 That's not the majority of them. The real fall you are away from your, the end of your life

01:51:12.460 is the injury that basically never permits you to get back on your feet. Because even when you recover

01:51:20.180 from the direct injury, maybe a broken hip, which is common, you never get back the strength and

01:51:26.500 stamina you once had. I just think BFR should be explored much more in this population. That should

01:51:32.720 be standard of care if indeed it is effective in both the passive and then the, as you described,

01:51:39.280 the progression, right? So passive, low end aerobic, low load resistance, and ultimately if you can get

01:51:45.900 back to high load resistance, great. Right. So if you had unlimited resources right now, what,

01:51:51.660 what experiment would you want to do? What's the, what are the burning questions that if

01:51:55.680 Francis Collins called you tomorrow and said, Jeremy, I've got this extra a hundred million bucks,

01:52:00.480 we just, we've got to get rid of it. What can you do? Huh? That's a good question. I would do

01:52:06.360 something with blood flow restriction, of course, but my interest right now is related to trying to

01:52:11.200 figure out why people get stronger. And I think I can always tie that back into blood flow restriction

01:52:16.860 and be able to do things of that sort. But I'm interested in what that means and what a change

01:52:24.240 in strength from resistance training, what that means for overall function of a person. So when I get

01:52:31.360 stronger with resistance training, does that actually carry over to improvements in my walking

01:52:37.360 ability and things of that sort? So those are some things that I'm interested in with blood flow

01:52:42.860 restriction. I'd obviously do kind of what you just stated. I'd have to probably connect with our med

01:52:48.320 school in order to do a study like that, but I, I would be interested in the application of blood

01:52:54.660 flow restriction by itself. I think that that is something that I've been interested in for a long time.

01:53:00.700 Again, I think it'd have to be not something we could do right out of my lab. We'd have to work

01:53:05.740 with a hospital, of course, but I'd be interested in that. And I'd be interested in doing it on a large

01:53:11.840 scale because all of those studies that currently exist are extremely small sample size. So for,

01:53:18.700 of course, for a variety of reasons, but I'd want to start answering a lot of these questions with

01:53:24.520 large sample sizes. That would be kind of my, my dream studies, whatever it would be,

01:53:29.880 whether it's strength, whether it's this bigger studies, longer studies. I think that a hundred

01:53:35.820 million dollars, I could do a lot for sure. Well, amazingly, that's a fraction of a penny

01:53:42.440 compared to the amount of research that goes into the fraction of dollars that goes into biomedical

01:53:46.720 research, but that's not necessarily always allocated wisely. Nevertheless, this has been a

01:53:51.340 super interesting discussion. Again, you can tell personally, I just want to understand this

01:53:54.540 for myself, for my patients. And ultimately I think this is a very important topic for,

01:54:00.100 for anybody who's interested in any aspect of that continuum we discussed. So Jeremy,

01:54:04.600 thank you very much. And I'm really so glad that Lane connected us. I'm sorry. I didn't have

01:54:08.920 a little extra alcohol. I know Lane mentioned you always like to have a drink when we start to talk.

01:54:13.580 And I should have thought to have sent out a nice bottle of tequila for you. Or is it scotch? What did

01:54:18.680 Lane say is your favorite? It's, it's scotch 100%. So, you know, I'll forgive you, you know, maybe we

01:54:24.300 can do it again and we can maybe have scotch next time. Perfect. A single malt, I assume. Of course.

01:54:30.740 Yes. Yeah. Do you drink it neat or do you add like the one spoon of water to it? I drink it neat

01:54:36.660 generally. Okay. I have a friend from residency. So I don't, I'm personally not a huge scotch guy. I love

01:54:42.420 tequila and Japanese whiskey, but I love talking to people who love scotch and can walk me through

01:54:50.100 the ins and outs of it. But this friend of mine, obviously a single malt guy would import water

01:54:55.700 from Scotland from a very specific lake. And he explained to me why you could, the scotch would

01:55:01.360 get a little better and it would open up a little bit more and be a little less anesthetizing to the

01:55:05.520 tongue. If you would add just this one spoon of lukewarm water to it. I don't remember the

01:55:12.400 exact reason, but it somehow had to do with diluting it just a little bit to prevent some

01:55:18.100 of the anesthetic effect. But you're a neat guy, which I like tequila neat and Japanese whiskey neat

01:55:24.500 as well. So. Yeah. I'm not quite on that level of drinking where I'm importing specific water,

01:55:30.500 but I do appreciate a good drink for sure. I find it interesting, by the way, you know,

01:55:35.600 on the topic of sort of genetics, I really do think people just genetically can like the taste of

01:55:40.620 scotch or not. And I don't possess the gene, I think, because I've, I've sampled very fancy

01:55:47.700 scotches and I've never found it palatable, but I don't doubt for a moment that you or someone who

01:55:53.380 does finds just as much enjoyment in the, in the actual taste of it that I would, for example,

01:55:58.640 in some of these other things I like. It's interesting because my students make fun of me for

01:56:02.720 this, but I can't drink beer unless it's like a fruity type of beer. So they, they obviously mock me for

01:56:10.000 that, but I can't drink beer, but I can drink hard liquor for sure all day. But the, the beer stuff I

01:56:17.600 can't do unless it tastes like apple pie or something else, then I'm all about, I'm on board, but just

01:56:24.340 standard beer can't do it. I'm with you. I think standard beer is about on par with urine in terms

01:56:31.640 of palatability. So, uh, I've never understood how Budweiser stays in business, but, uh, yeah,

01:56:36.200 I can't do really any of that. All right, Jeremy. Well, thanks so much. This was,

01:56:41.640 this was a super interesting discussion. I really appreciate it. Thanks for having me on Peter.

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The Peter Attia Drive - October 11, 2021

#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

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