#239 ‒ The science of strength, muscle, and training for longevity | Andy Galpin, Ph.D. (PART I)

Hey everyone. Welcome to the Drive Podcast. I'm your host Peter Attia. This podcast, my website and my weekly newsletter all focus on the goal of translating the science of longevity into something accessible for everyone. Our goal is to provide the best content in health and wellness, full stop, and we've assembled a great team of analysts to make this happen. If you enjoy this podcast, we've created a membership program that brings you far more in depth content. If you want to take your knowledge of this space to the next level, at the end of this episode I'll explain what those benefits are. Or if you want to learn more now, head over to peterattiamd.com subscribe Now without further delay, here's today's episode. My guest this week is Andy Galpin. Andy is a professor of Kinesiology at California State University, Fullerton, where where his biochemistry and molecular exercise physiology lab researches the acute responses of chronic adaptations of skeletal muscle to high intensity power or force and fatiguing exercise. Andy's research spans adaptations from whole muscle to cellular level changes, which he's applied to his work with professional athletes for more than about 15 years. In this episode we focus our conversation specifically around one of the four pillars of exercise, which is strength. And we focus a lot of the conversation around muscle. Now, at the beginning of this episode, which I really enjoyed, we talk pretty technically, I'm not going to hide that. We get into the anatomy, microanatomy and physiology of the muscle. And I think it's important because I do think that this is a subject matter that I talk about a lot. I think a lot of podcasters talk about this stuff a lot. But I think it's important to really understand some of the details. I mean, something as simple as what does it mean to undergo hypertrophy? What does it mean for a muscle to get bigger? What exactly is getting bigger? What is the difference between power, strength, speed and hypertrophy? And how do those differences phenotypically relate to what's happening at the cellular level or at the functional unit level? So we talk about all those things. We talk about muscles and their energy sources. We talk about the importance of protein on muscle synthesis. We we talk about the various types of muscle fibers, which is actually something where I probably learned more in this discussion on that particular topic than anything else that Andy and I spoke about. We end the conversation looking at a case study of how Andy would create a program for an untrained person who just started to do a few hours of cardio but wanted to spend three days a week Building strength with a focus on building strength for longevity. Now, we did this because that approach was so popular in some of our previous podcasts. I think listeners really like hearing how we take kind of this high fluid science and now bring it back down to how can you apply this to your life? One final point I'll make here is that, as is sort of common with me, I go into these podcasts with a long list of topics I want to explore and sometimes I don't get close to it. And that was certainly the case here, Andy and I barely scratched the surface of what I wanted to cover. So this will be part one of two, because I'll be sitting down again with Andy shortly to do the second part of this. So without further delay, please enjoy my conversation with Andy Galpin. Well, Andy, it's wonderful to see you here on video. We were supposed to do this in person, but we got a good laugh as to why that didn't pan out. But that's okay. Perhaps there will be an in person chance the next time.

Yeah, I'm excited to be here. This way. It would have been more enjoyable in person, but we'll make it work.

I've wanted to speak with you for quite a while and think listeners to this podcast are not strangers to the idea of how much of an emphasis I place on exercise. Said it many times before. I'll continue to reiterate it until the data suggest otherwise, that there's really no more potent tool to improve longevity, meaning extending the length of life and improving the quality of life and exercise. And that includes nutrition, that includes sleep, and that includes the entire pharmacopoeia of medication, supplements, drugs, hormones, et cetera. So it's probably for that reason that I would say that exercise makes up a disproportionate amount of the content on our podcast. And of course, within exercise, I tend to divide it really down into these different pillars of strength, stability and cardiorespiratory fitness, which of course then gets further subdivided by the metabolic state and energy state of it. And of course, what we're going to probably talk a lot about today is strength, but also all of the things that kind of stem from that, like hypertrophy and various things like that, which I think are of huge interest to people. But maybe for folks who don't know you, can you give us a sense of your path, you know, frankly, out of high school, college, like, you know, what was your athletic background and what made this be something that you have dedicated all of your time to?

Sure. I guess initially I need to state a conflict of interest, which is I'm an exercise scientist. So if you want to start giving more credit to exercise for longevity and wellness, like, I cannot be more biased into that lane, especially with an exercise science strength training. So I've been waiting for 30 years for this to happen. The field. So now I get to prove that all my preconceived notions are actually holding true. And I will refuse to change despite what you said. I will refuse to change despite what the data suggests. For really. I grew up in a very small town in southwest Washington. So I played everything in high school. Football, basketball, baseball, track and field, the whole thing. I went to a small school in Oregon where I played college football and got my undergraduate degree in exercise science. And then after that I made some stops in Arizona and worked at a facility training professional athletes, went back and got my master's degree in human movement sciences, which is just another fancy way of saying kinesiology or exercise science, and then got my PhD in human bioenergetics. So in 2011, I got that, came out here to California, and I've been working at Cal State Fullerton ever since. So I've been for a while now the director for the center for Sport Performance there, as well as my lab, which is a biochemistry and molecular exercise physiology lab. So that's the condensed version of the academic path. Probably more important to your question was college football. And then training professional athletes started at that point as well. And then I started competing in weightlifting, which locally is Olympic weightlifting, that version of it, and then combat sports a lot after that. So I've continued to work with athletes the entire time still, over the last 10 years, running my labs, running our research, I've worked with professional athletes in just about every sport with exception of racing. I've yet to get into Formula One, saw young winners, MVPs, all pros, the whole thing, Olympic gold medalists, et cetera. So my research actually and my interests really come back from the exact same point. And if someone returned to the very beginning here, which was I was a decent athlete, but I actually feel like I was in the perfect spot because I wasn't so good that these details didn't matter. I was going to be an all Pro. I was going to go to the next level no matter what, that wasn't the case. So when I did things better, was more effective with training, more effective with recovery, it mattered. I saw differences on the field, right? It was the difference between me being a starter and being not a starter. Or whatever the case is. I also was good enough to know where I got rewarded. So if you're not good enough, then it's just like, doesn't matter what you do, you're not gonna play the next level. So I was in that perfect scenario. And so I was totally obsessed with making sure I gave myself every advantage possible to have some success. I knew I was never going to be professional level caliber or even Division 1, but I was like, the difference is, do you want to play college football or not? That's going to be the difference. So if you can do these things, you might be able to do it. If not, you're going to have no chance. And where I'm from, people don't really go to college in general and they certainly don't play college sports. There's no advanced degrees. And so to me, I was like, wow, you got a chance to do something really special here and do something that no one else you really know has done that often. So that's. That initial passion came from additionally the town I grew up with, my parents and everybody I knew. It is a very working class place. And so losing was always fine, there's always better than you. But losing because you didn't prepare was totally unacceptable. Most of the kids I grew up with, we worked on farms, we cleaned stalls, we did something before school. You know, my parents worked in construction, like building. So that whole idea of like, you fend for yourself and you get what you earn and all that sort of stuff was just something I grew up with. And so moving that into sports and academia was like, if you want a chance like this on you and nobody else. And so do the work or don't do the work. So that's what all pushed me to get here. And then as I'll finish up, the background is then when I started moving past my athletic career and I started finding athletes who wanted to pursue these tremendous goals, like go to the Olympics, but in a sport like women's wrestling, like, no one's going to help them. They don't have funds. And so I just became very interested in these people because I'm like, man, I can help you a lot. No one else cares about you. There's no money on the back end here. There's no fame, there's no social media at the time. I just want to help you here in this journey because that's something that's going to reach my soul of let's give everything we can to do something really special that no one's going to care about besides you and I and your team and your family. And so that's what drove it initially, and that's what really put me in this position. And that's what put me in a position to continue to go get my master's, to get my Ph.D. was, you got to learn more. There's more things going on here. You've got to find all the answers that you can. And if you're doing anything less than that, what are you doing? You're just giving up. That's the background of how I got here and what I do now.

You mentioned briefly Olympic lifting. We've had Lane Norton on the podcast several times. Lane obviously is a very successful powerlifter. I think folks are kind of familiar with powerlifting, having the three lifts, and it's really about these three lifts and what your total is in those three lifts. Can you contrast that a little bit with what Olympic lifting is? And I think, more importantly, what are the physiologic differences between those two? And I'll preface the question for the listener by saying, again, even if you never plan to power lift or Olympic lift, this is going to be germane to our discussion.

There's actually a fairly recently we published the most in depth analysis of muscle composition of Olympic weightlifters. So we can actually come back to that and we can talk more specifically about muscle composition, but in general, as some background, if you think about powerlifting, it's tricky because we're about to run some loops on your brain here. So technically you have force production, which is, in the case of lifting, it is one rep max. So it's the most amount of weight you can lift one time period, not repetitions on how many times you can do it, on how fast you can do it. Just what can you get up in the sport of powerlifting? Like what Lane does it is three exercises, the deadlift, bench and the squat. And it's how much weight can you lift One time you get a couple of tries at it, but that's effectively what it is. So it's really an expression of pure strength. It's not really an expression of power at all because the speed component is very poor. In fact, the deadlift can take as long as you want. It doesn't matter did you get it up or did you not squat, etc. So we're already at the gates, which confused people because the name of the sport is called powerlifting, despite the fact that it is not a power exercise, nor is it determined by power. When you move over To Olympic weight, I think it's the same basic idea. There are now two lifts instead of three. One left being called the snatch and the other one's called the clean and jerk. It's called the clean and jerk because it has two parts. You clean it to your chest and you jerk it over your head. But it's still considered one lift. Name of the game is still one rep max. So whoever can lift the most amount one time is the winner. There's no repetition method to it. The difference is, though, this is now more expression of power, because although it's all about one rep max, it's difficult to lift something over your head as high as possible slowly. So there's a speed component required to the movements to perform, whether it's a clean or the snatch. And so it is an expression of tremendous strength. But there's this velocity component to it. So when you multiply force by velocity, now you've got power. And so technically, the weightlifters, Olympic weightlifters are significantly more powerful than a powerlifter, despite the fact that powerlifters in a sport called powerlifting, so the confusion there is, and this gets worse when we start roping in things like strongman. Strongman is fantastic because again, you think strength and you think that must be the biggest expression of strength. In fact, it's not because strongman is contested over multiple repetitions. So it is an expression of very, very high strength repeated several times. Very, very high strength. But it's not technically a true one rep max that actually goes to the back of the power lifters. So now you've already confused powerlifting, weightlifting and strongman. And none of those three things are actually explaining what they do correctly. We can keep going on with multiple sports here, but this is the core of the problem. The reason you're, I think you're bringing this up is this also explains training adaptations. It's a perfect way to outline, to understand what's happening. So if you train like a power lifter, that's probably represents the best way to get truly strong. If you train like a weightlifter, it represents the best way to get powerful. If you train like a strongman, it represents a fantastic way to get very, very strong and more what we'll say, life, functional movements. So walking, carrying, lifting objects, and doing it probably multiple times. So the only difference between all those three in the last part I'll add to is with Olympic weightlifting, the amount of coordination required, because you're going to take a weight from the ground, throw it over your head, and catch it over your head in a full squat. So when it comes to things like balance and proprioception and eccentric catching, the advantage goes to weightlifters big time there. You're not going to see that powerlifting is very controlled. It's a very specific foot position, hand position. There's no movement. Ideally, it's typically you're minimizing range of motion intentionally because you want to minimize work, working force times distance. And if the game of the game is who can create the most force, you can minimize the distance. You're going to win. That's why they take those funny positions. That's why Lane has both of his feet six miles apart. He calls it a deadlift, even though it's a fake movement. Just kidding. Lane and I go back many, many years, so he would laugh at that joke, I promise. So that's the basic foundation of the difference here. You have a very sports specific application for powerlifting. Weightlifting is very sports specific, but it's a much greater range of motion, has those other components. And Strongman is kind of positioned. I know you didn't ask about Strongman, but I threw that in there because it kind of rounds the loop out.

I love that you brought that in. Before I go on to my next question, let's put one more little bow on that. We've talked a lot about who's the strongest, who's the most powerful, who has the most functional strength. You want to throw in a little bit on hypertrophy within the trio.

Yeah, great. So you can actually add a couple of more scenarios here. Hypertrophy would be more of your bodybuilding, which Lane has also done. Holly, I think you just had Holly on. Right. So Holly can smash with physique. Whether you want to call it bodybuilding or general physique or any stuff is simply improving generally leanness and total muscle mass. And then there's a component of symmetry and shape, things like that that don't really matter for this conversation. So if you add that on top of it, now you're talking about who can optimize muscle size as well as leanness, which is really, really important. With no consideration for function. It doesn't matter if you're strong or fast or athletic or any of those things. It's there. In fact, this is so interesting that you started the conversation like this because this is day one of my strength conditioning courses, the academic semester. I spend the first week actually just on going over these different categories of sport because it does exactly like what you're setting up here. Is it outlines exactly how to train in the last two pieces. Just a throw this in there would be. Actually, if you think about the competitive circuit training sports, CrossFit, for example, totally no offense, I'm just meaning it as a sense of they are very strong, they have a lot of muscle, but they're not nearly as strong as power lifters. As a general statement, they're not nearly as strong as World's Strongest Men, but they do a lot more repetitions. And so a World's Strongest man is going to win an event doing something like five to 15 repetitions. Like something, you know, kind of depending. And CrossFit, you might have to do 90 reps in a given workout, like, way more. And so it's way higher up that scale of number of repetitions. They do some, of course, that are one repetition, but you get the point. It's just like a very crude explanation of what's happening. A lot of function, a lot of different movements, and a lot of workouts repeated in the same day. And so it's a very different test of recovery over three or four days of just brutal onslaught and asked to do things in a lot of different areas and a lot of different energy systems and movement patterns and things like that. So it's a really interesting test of total physical fitness. The last one that I like to throw in there is basically track and field. And now you have the truest expression of velocity. These are the people who are going to be the best at getting you truly fast. And so if you think about this now, what do you need to have as a functional human being for lifespan, longevity, or sport? And if you want to think about this in a spectrum, how do I get absolutely fastest, how do I get the most powerful? How do I get strong? How do I add muscle size, loose body fat, how do I improve my muscular endurance? And now how do I improve my cardiovascular metabolic endurance? This is now occupied in all of those sports. And so we can just look at them as a model for training and saying, the best in the world at getting stronger have been doing this. The best in the world are getting faster peak speed. The best in the world at getting able to recover multiple days in a row. So we have different models of that. So that is a nice foundation for all training.

Really, I love it. And there's a matrix brewing right now in my head as you go through that. So we're going to come and kind of start to fill in some of this matrix as we go. Let's simultaneously go back to the Fundamentals, but do so without any remorse for how rigorous we need to be.

That's the greatest setup ever.

Okay, so let's talk about muscles. What is a muscle? What is the functional unit? How does it generate force? What are the metabolic demands? What makes these cells that are so ubiquitous in our body different from say, the cells in our liver, the cells in our gut, the cells in our brain? What are these cells that we almost take for granted sometimes?

All right, now you're asking me to do like a two semester course in 20 minutes or so.

Look, I mean, I did ask you to do a week in seven minutes, so by that logic we could be here a while. But yeah, let's see what we can do.

All right, hopefully you're ready for part two, three, four and five of this podcast. I'll give you what I can give you and then we'll come back. Let's think about it this way. Number one, I like to play a little trick. You ever ask, kind of like that Jeopardy. Question of what's the biggest organ in your body? And people generally are going to say skin.

Yeah, exactly. That's what I would've said actually.

Well, us again, exercise scientists. And if I didn't give you enough of a bias earlier about being exercise scientist, I'm also a muscle physiologist. So I'm gonna give all the credit in the world, the muscle, and none of it to anything else.

So basically, the brain, the heart, the liver, the lungs don't give a shit, but they're just there to support the muscles 100%.

And if you start talking my worst enemy, the nervous system, I'm probably going to hit end record and go home. Those neuroscientists just take credit for everything. It's garbage. Hot garbage. Give it all the muscle. So you've heard my biases. If you want to stop listening now, you can if not, understand that that's where we're going here in general. If you think about it this way, again, muscle is going to be the largest organ in your body. And you've talked about this a number of times on your show. But it's doing everything from supporting function and so locomotion, getting you throughout the world to being your biggest reserve for amino acids which you need for building any cell, any functional cell in your body. Your brain, your liver, your immune system, all that has to come from somewhere to regulating glucose being your biggest dump and reserve for regulating metabolism, controlling function. I could go on and on and on about the physiological, the practical, the general health benefits. Of skeletal muscle.

And don't be bashful. This is a good time to say those things and to expand on them because I've said everything you said, but I think there's more to it and I think one of the things you've said I don't think probably is as appreciated, which is the storage depot for amino acids because we don't really think of it that way. And Lane did a great job talking about this in the podcast, which is we're constantly breaking down and constantly adding new. So there's this pool of turning over amino acids and it's very difficult to study them from a flux perspective. But clearly some of those things getting spun off. You know, if you're working out, it's at least a plausible scenario that amino acids are being, I mean, proteins are being broken down, amino acids being released. They may not be resynthesized right back into that same piece of skeletal muscle. They may be used for another application.

It's not even a Maeve. It's a pretty much guaranteed that that's going to happen. If you kind of think about it this way, I'll give a quick energetic analogy here. I have like a cheesy video I did 10 years ago where I sat in my backyard and shot this and put it on YouTube.

We'll link to it, send it to us and we'll link to it in the show notes.

Yeah, okay. We'll find out somewhere buried in 8 year ago YouTube land or something. So if you think about the very basics of energy, if you were going to be out camping, you're an outdoorsman, right?

Absolutely.

Okay, great. If you're out hunting, which I'm actually even a couple of days from my hunting trip. So this is front of mind is why this analogy comes up. You know, you may need to create a fire. You have a handful of options and the very first one being if you had a match. Right. A match is very easy to light and if anyone lights a match on fire, it's going to give you instantaneous energy, the fire, and it's going to last some amount of seconds before it burns out. I don't know what Those seconds are.5 seconds, 10, 12, doesn't matter. So some short amount of seconds, worst case scenario, you need energy. Great. The downside is you have limited supply of them. They're kind of finicky and you better hope they don't get wet and they're just not reliable. At best case, if none of that happens, you're still going to get some amount of seconds. If you need the energy right now though, that's where you start. In terms of your tissue, that's going to be ATP. That's going to be your phosphocreatine energy system. So the stoichiometry is one to one there you break down one fossil creatine. You're going to get one mole of ATP out of that. That's great. That's stored internally in your muscle. So that's already right there. In fact, it's generally loaded right up on the myosin head or close to it. And so it can contract tissue. And we can come back to what all that stuff means.

We'll talk about actin myosin in a minute. Cause I want people to actually know what this physically looks like. But let's go back to the energetics.

Great. So that's your little energy boost system. Now if you had a little bit more forward thinking, you would say, okay, let me use that mask to then actually just light a newspaper. If you had newspaper or something like that. And if you're in the woods, papers, same thing. You get fairly quick light, not as fast as a match. And it would give you some few minutes of energy. It doesn't matter what these numbers are. It's just conceptual stuff here. And that's great. That's going to be carbohydrate. So carbohydrate is stored both in the cell as well as outside the cell in three major areas. But in the cell it's going to give you a lot more energy. That is the most direct fast. Stoichiometry is a little bit better, but not much actually. And so you're going to get a couple of moles of ATP per molecule of carbohydrate. It's better, but it's like you're sort of splitting hairs here a little bit. If that gets low, you can now pull glucose out of the blood. And for a little bit of terminology here, glycogen in the tissue is what it's called. Glycogen in liver is what it's called. If we put that in the blood, that's called glucose, blood sugar. Roughly talking the same things here. So we can pull that out of the blood and then we can actually, if that gets low, we can pull that out of the liver. So that's the basic like energy pathway. And the liver then functions as kind of your backup storage system for glucose to make sure that you can regulate blood glucose while you're changing concentrations of glycogen in tissue. That's really what it's doing. Because you don't want, obviously, as you've talked about a million times, a bunch of instability and blood glucose. That's a bad thing. It's one of the four things that your body will regulate almost over almost anything else. In addition to ph and blood pressure, et cetera and electrolyte concentrations, they don't like to mess with those things at all. Everything else will move around those things to keep those stable. If we're in the tissue now and we've got past our newspaper, the next thing, it would be a giant piece of wood. If you had firewood or something like that. Lighting firewood in the wild is very difficult to do. It doesn't happen in seconds. You need to know what you're doing. But it's going to give you exponentially more fire length. I mean, you could put a log on a fire and that could literally be on going the next morning when you wake up and give you hours. Think about that as fat. Now, I like this whole analogy is if you know a little bit about the chemistry of fat versus carbohydrate, they're both big long chains of carbon. Just like a paper is actually made of wood. It's sort of just a separate piece of the same thing. So you get a small six carbon chain from glucose, you can get any number of lengths of chains of fat.18 carbon fatty acid chain, you can put three of those on a backbone of glycerol and you've gotten yourself 50 carbon molecules per triglyceride, something like that. Stoichiometry gets better here. You're going to get something like 3 or 400 ATP per molecule of fat. And that's where things get actually better. Okay. The fat is actually coming mostly though from outside of the muscle. So energy from fat mobilization comes throughout the body somewhat evenly. Glucose comes mostly from the intra muscle itself and then a little bit from the backup supplies if it gets low. Phosphocreatine comes directly from the muscle. All that energetic background to say when you start moving, you start trying to create exercise. Where's the last piece we forgot here? Oh, that's protein. So protein actually in this analogy would be functioning more like a piece of metal. So if you had metal in the woods and you needed a fire and you had absolutely nothing else, you can in theory melt metal with a fire. You're going to get some. But it is a very, very low end proposition. If you absolutely have to do it, you can do it to survive. But if that's your fueling strategy. You're in a big, big problem because you're going to run out of metal very quickly in the woods. You're out of it. It's also the only thing you have to create shelter and stability and to fend for food and everything else. And so it is a plausible way to provide energy. It's just a terrible one. It's mostly there for you to reconstruct new tools. And so if you're in the woods and you have metal and you need to make a knife, you can fashion that. Okay, now we need to melt that thing down and make a roof. We could fashion that. Now we need to melt that back down and make a shovel. It's meant to be kind of broken back down, recreated in the same and different forms of the same basic item. And so that's really what we're looking at. The ability to play back and forth with carbohydrate and fat as different fuel system. That's really. We don't have time to get to that today. It's not really the best thing. But the ability and the need and the point of protein in tissue, it is not fuel, although it can be for what I explained, it's really, that is taking it and saying we need it mostly for this task right now. We did it mostly for skeletal muscle, we need it mostly for immune system, we need it mostly for these other functions. And so one of the ways to quickly lose muscle is to put yourself in a compromised position. Because it's going to say, if we're choosing between keeping that 24 inch bicep or clearing up something we need, immunologically, it's going to go towards that. This is also why we see protein redistribution across muscle. Like say you spend a bunch of times on your bicep and your biceps get really, really big and then you don't train your calf and let's just say your protein intake is insufficient, you'll start redistributing proteins from the calf up to the bicep to actually enable that growth. And so you're thinking you're getting bigger, but you're really just taking it from other places if protein intake itself is not sufficient. And so it really is a cornerstone. And if you look at the research, you're going to see this very clearly as something. If you ever wonder why some of these people are just like so diligent about protein intake and why this has become such a big deal is it's the raw material. You really can't get Anywhere else. And you can get carbohydrates and fat and you can go through that whole thing in a lot of ways. You can't fake protein, though. It's just very challenging to do so. And the last little piece I'll say there is, why this is so important to me is you can't fake muscle, most specifically without the protein. And when we start losing muscle now, we enter a whole cascade of problems from physical performance. Your interest is more of like aging and longevity. That whole cascade becomes a problem. And then we can certainly talk about the specific changes in muscle and pass some of the details you've actually covered before. Yeah, those are things like it just becomes a really big deal. So it just doesn't make any sense to skimp on that one as a place to go.

Yeah, it's worth repeating when you look at people across their lifetimes and you evaluate for muscle mass and you divide people up and categorize them by the amount of muscle mass they have. And we should talk about this because of course, my interpretation of the data is that once you normalize for strength, strength wins. But it's sort of easier to measure muscle mass. You know, all you need to do is put somebody in a DEXA and you sort of can figure out their almi. And so we tend to look at survival curves based on almi, which for the listener just means the amount of lean muscle you have in your arms and legs normalized to your height. Appendicular lean mass index. There's no ambiguity about the fact that more muscle means a longer life. It's as clear as high VO2 max means a longer life. So let's now go back and make sure people understand the structure of a muscle, because I want to talk about different fiber types as well, just to round out some of the physiology. So in an effort to understand the difference between fast twitch and a slow twitch muscle fiber, which has a metabolic difference, I'm curious as to what the structural difference is and maybe just kind of explaining how myofibrils work and things like that.

Let me go back just a little bit to understand whole human function movement. I won't go as deep into this one, though. If you just think about how you actually create movement, it really has three core functions. So number one, you have to have some sort of direction or signal. And this is going to be coming from your nervous system. And so whether this is central peripheral, whether this is autonomic, whether this is a controlled somatic action response, it doesn't really matter for this Conversation, the nerve has to tell it what to do. So if nerves, you get that one. That's it. Don't take anything else. Nervous system, you get that control. Now that nerve then has to go into a muscle fiber until the muscle fiber to contract. The muscle fiber then is part two. So the cell actually has to contract itself, but that actually doesn't cause movement. Muscles are not attached to bone. That's not how it works. So muscle fibers are surrounded by connective tissue. All those connective tissue are bundled together in a package. So if you imagine buying a bunch of strips of bacon from the butcher and they would wrap that up and kind of Saran wrap together, that's actually kind of what a muscle looks like. So you've got that saran wrap connecting it. So if you pulled on one piece of bacon, you'd notice the whole package moves. That's sort of the point. You're transferring force from muscle through connective tissue. That connective tissue comes together into a tendon, and that tendon then attaches to bone. And so the third part for human movement is actually connective tissue. And so you have to have a signal, you have to have a muscle contract that has to make connective tissue pull on a bone. That actually is what generates human movement. Well, if you look at the front end, we'll leave the neuroscience to other people. You look at the connective tissue, and it's very difficult to understand what's happening there for a number of reasons. But mostly it's not plastic. When we look at muscle, it's tremendously plastic. And what I mean by that is it adapts. It changes very quickly and rapidly in response to a lot of things. Connective tissue doesn't have a blood flow supply, doesn't have energetic demand. It's kind of just there. There's more to that story, but we'll just kind of leave it like that. The core of the issue of adaptations, whether they are pro or negative, is going to be in skeletal muscle. And so here's what that actually looks like. A nerve will come down and actually attach and innervate to a whole host of muscle fibers. And so you can imagine skeletal muscle fibers are some of the largest cells in all of biology by diameter. They're tremendous in humans. In fact, what's actually very interesting about humans that makes us special is our muscle fibers are what's called multinucleated. And so you probably remember this term from like med school or something like that. In fact, whenever I talk to biology people about this that, like their head is blown because I forget how lost in exercise science I get. It's very uncommon in nature to see cells that have more than one nucleus. And the nucleus is the core of the cell, if you will. It's what holds your DNA. It tells you when to replicate, proteins, to grow, shrink, die, repair. So the whole control center. So the fact that skeletal muscle has many of them per cell. In fact, it's not a few, it's not two or three. It is thousands per cell. So skeletal muscle can be extraordinarily large. I have a video of this somewhere. I can't remember actually. There might have been a picture in a men's health thing we did. There's a video somewhere.

We'll find that and we'll also put that in the show notes.

Okay. I can actually pick up a single muscle fiber from a human with tweezers and you can see it with your naked eye. So we could hold this. In fact, I could do it right now. If I had one. I could hold it in front of the camera. You'd be able to see an actual whole muscle cell. They're that large. In fact, they can be very, very long. So they can be several inches in length.

Let's help folks understand what defines a cell, because normally outside of the muscle, we kind of define a cell by a cell membrane has a single nucleus. I mean, we kind of know what the constitutive elements here. This is defined also by a cell membrane, but it's a sort of a longer looking tube as opposed to a sphere.

Good distinction there. I sort of again get lost in exercise science. If you remember, like back to high school biology. And you think of a cell as like a circle or an oval. It's like that, it's circular, but it's a tube. So it's a very long tube. The way to think about it is like a ponytail. So if you think about a ponytail, you think about it as one thing. It is a ponytail, but it's made up of a whole bunch of long tube individual hairs, and they all wrap together to make a ponytail. That's what a skeletal muscle cell looks like, which is actually quite different than a cardiac cell. Those are more rectangular, if you will. They're shorter and wider. Skeletal muscle fibers are very long, very narrow, but still circular. They still have a cell membrane, they have a bunch of nuclei. Most of the organelle are the same as any other thing. The contractile units we can get to in a second. But yeah, that's the basic setup of them.

Give me the typical Length of a muscle cell, a skeletal muscle cell, you.

Can'T really give a typical because depending on what you'll see with skeletal muscle is structure, is function. So if you contrast this to cardiac tissue. So cardiac tissue is actually quite interesting because it is what we call the ultimate slow twitch fiber. And so all of cardiac tissue is slow twitch. In fact, the slow twitch are even more slow twitch than the skeletal and they tend to be fairly uniform. So you could give specific numbers and cross sectional area, a diameter length on those skeletal muscle. If you look at your sartorius, which is that kind of muscle that goes from that pointy part of the front of your hip down to the inside middle of your knee, theoretically those fibers could run the whole length.

A single cell.

Correct.

Can run that whole length, yeah.

Even if it runs half that length, that's extraordinarily long. You go back though, and you go to like an ocular muscle, it's going to be minute, it's going to be extremely small. And length, if you go to muscles in your digiti, your fingers, they're going to be very, very, very, very short. There is no like classic range. It could be from millimeters to literally inches in length.

So presumably the reason that these cells have multiple nuclei is basically to decentralize the actions of cellular construction. So you've got DNA making RNA in the proximity of that nucleus coming out onto the Golgi making protein. And if you had, for example, even a 1cm long cell, which is enormous, outrageous, you couldn't simply make all of that work with one nucleus. So the question is, does that mean these nuclei act independently? Where's the central command on this? It seems like a remarkable problem.

Remarkable problem, remarkable advantage. It's the same thing here.

Hard to control, but amazingly adaptive.

Exactly. This is exactly right. So if you want to dive down the entire nucleation question, this gets very, very interesting because we've actually shown in our lab that a lot of professional athletes have more nuclei per volume. And so this is one of the things that I posit is maybe this is why they can adapt so well. That's why they can handle the volume that they can handle, is they just simply have more of these nuclei around.

And you believe that that is how much genetic and how much adaptation to training.

Boy, I would love to give you an answer there. There's going to be a component to both. We actually know numerous lifestyle factors that influence these things. But the more recent data are showing this. In general, we have thought that nuclei have a couple of things so one, it's not just nuclei count that matters, which is what we previously thought. The shape matters. There's like spheres, there's ovals, there are all kinds. And it looks like the shape determines the function, the location determines the function. And so it looks like there are subtypes of nuclei that surround, for example, the mitochondria. And they're going to be very specific to mitochondrial repair. And then there's other types that are more specific, the periphery that'll do cell wall damage. And then there are some actually that are regulating injury specifically. This is what it looks like right now. And so there are subtypes. And this is very, very recent understanding, and this is probably why some folks recover, respond to injury more than others is they just simply have more of the subtype. Now to your question, nature versus nurture. What's challenging about that is the measurement fidelity here is difficult and the tech is moving quickly. But it's sort of like every couple of years when the microscopes get better, we sort of realize that all the three previous years are now invalidated. And so there's just a lot of movement back and forth. And in fact, if you look at this related to cell growth, in other words, hypertrophy, there seems to be tremendous confusion about the role of these things in growth or not. So there used to be a thing that we referred to as a mile, nuclear domain limitation. So in other words, a cell would only grow, so this would be your fiber. It would only hypertrophy or grow in diameter to the extent at which the nuclei could control it. And so in order to gain more growth, you actually have to get more satellite cells to come nuclei. And then when you detrain, that cell goes back down in diameter, but you preserve the mononuclear number. And so then, now retraining is easier than it was the first time.

I mean, this is unbelievable. But this is the old adage of muscle memory, quote, unquote. It's easier to regain muscle you once had than to put on muscle you never had. And I've never heard a molecular explanation for that, but that's a very plausible mechanism.

Now, it looks like that's not correct, though.

You retain the nuclei, it looks like that's not correct. Interesting.

It's very back and forth is the way I'll say it. So something is there. The story I just outlined to you, like, it makes intuitive sense. I got really hot on it for a number of years, and then it was like some more challenging data came out. And it was like, well, we don't think so. I'm just going to have to say, like, tbd. This is like a. Every week another paper comes out and it's just like, okay, now we're back on it, and now we're back off. And now we realize there's subtypes of my nuclear. And they're like, oh, shit, okay.

It will lend itself, obviously, to a longitudinal type study. I mean, in an ideal world, you would take relatively young, presumably pliable, athletes in their teens and study them over time under different training demands. Obviously, the dream case is doing it with identical twins, which we've done.

So I could just totally interrupt you. We can go to that twin study if you want.

Let's put a pin in it, because I want to come back to making sure people still understand how these things work. So we've now established that muscle cells are kind of unlike any other cell in the body. How hungry are they for energy? So, for example, when we look at the liver, I always think of the liver as a beautiful organ. Maybe not quite as cool as the muscle, but it has a special place in my heart. Because I've always argued that the reason there is no extracorporeal support for the liver is we simply can't replicate its complexity. For listeners, extracorporeal means outside of the body. So dialysis is extracorporeal support for the kidney. A VAD or an ECMO is extracorporeal support for the heart or heart and lungs combined. A ventilator, extracorporeal support for lungs. We can't do that for a liver. If a patient tragically overdoses on Tylenol in an attempt to take their life, and they reach a point of irreversibly damaging the liver, you can't put them on liver support until they get a transplant. That patient will be dead in about two days if they don't get a transplant. And I think it comes down to a lot of the stuff you already talked about. Glucose homeostasis, one of the most important bits of homeostasis in the body, is controlled with a level of precision I can't fathom. I can sit and talk about the liver with the same level of excitement that you talk about the muscles. And yet, here's what's interesting. The liver is not a metabolically greedy organ. No, it really doesn't, on its own, consume much energy. The brain, by contrast, a very complex organ, an incredibly metabolically greedy organ, which is probably why we need the liver to support the brain. Without the liver being so good at maintaining glucose, homeostasis our brain would have either needed an adaptation strategy away from glucose, where we wouldn't have brains as large as we do. Where does the muscle fit into this hierarchy? Where is the muscle? A high maintenance organ.

What's cool about the liver? It's kind of like a professional fighter where you can beat it up a lot.

That's right.

You can't do much to the kidneys. They just don't have sustainability. I have a secondary love for the liver because it's the closest thing in the body to skeletal muscle in terms of the fact that it is listening and it will respond and it can change.

And as you said, very adaptive, super adaptive. You'll appreciate this if you didn't already know it. When I was in my residency, we would do quite a number of live donor liver transplants. So this would be an operation where an individual would donate a third to a half of their liver to another individual where there was a really good HLA match. Well, here's what was really interesting. The speed with which the that portion of their liver would regenerate was so staggering that if you didn't anticipate it with inhumane doses of intravenous phosphorus, they would have an enormous metabolic crisis.

Oh yeah, totally. That makes sense.

There was no amount of food you could give this person to allow them to have enough phosphate backbone for the DNA and RNA and protein synthesis that was going to be necessary to reproduce their liver. So you just had to basically be giving them IV phos nonstop.

It sounds like what we have to do with fibers when we're doing our single fiber experiments. You have to bathe them. You just have to have a permanent path of phosphorus. They won't go anywhere.

That's right. And they could regenerate a third of their liver in two weeks. It's simply staggering. And now, of course, the caveat for the person listening is this only works when the architecture of the liver is preserved. So once you cross into the path of cirrhosis and inflammation, it's over. So unfortunately, that person whose liver has been so beat up, for example, status post nafld Nash or alcoholic liver disease, you get to a point where it no longer has that capacity to regenerate.

You know, the kind of, the nice part about the story is though, if you fix it before that, you have a good chance.

Absolutely.

So you can mess up for a long time, but if you do take that action before you hit that level, I shouldn't even say it this way, but you can almost get back to scratch. You can get A lot of regeneration there and a lot of recovery.

You're right. And the kidneys being so sensitive to blood pressure, so sensitive to the damage of high glucose, the lungs being so sensitive to smoking and things like that. I just think the liver is an unsung hero of the body.

It's the thing that keeps you like. It's the bonk. Those from endurance towards when the liver is finished, it doesn't matter how much mental strength you have, it is a wrap. You are going down. If you get hit in the liver, if you watch any sports, you get hit in the liver instantaneously, you're crippled. Doesn't matter. You could be mentally, you're there, but your body will seize and shut you down.

Isn't that what happened to Oscar De La Hoya against Bernard Hopkins? Do you remember that fight?

I don't remember that fight, but I've seen it 500 times. I work a lot with UFC fighters and a number of. I've actually headline fight this weekend for one of my guys. So, yeah, I've seen it in those sports a ton. I've seen a little toe, just the tip of a toe, click the liver and world champions just get locked up and fall ground. It does not like being aggravated like that, but it will handle a beating for the most part. You can beat it up pretty good. And if you see like any blood chemistry stuff and if you're looking at alt AST stuff and you're like, ah, you're pretty. It'll come back pretty quick if you take the right steps. The kidney is the one you see when you're like, oh, we're not coming back from this one.

All right.

So going back to muscle, it's tremendously responsive to everything you're doing and it's listening. So your question of how energetically demanding it is, There's a couple of things to say about this. People will talk a lot about, hey, if you add more muscle mass, that's going to elevate your basal metabolic rate so you'll burn more calories just sitting there. That is true, but it's not to a level that you actually think it's probably. I think the numbers are something like.

30 calories with how much increase in.

Muscle mass per pound?

Per pound. Okay.

I think it's like something like that. It's not actually level. And you can make the argument, well, after three or four years, that is that extra five or ten pounds. Okay, sure. But it's not like I feel like some people think it's going to go from their basal metabolic rate is going to go from 1500 calories a day to 2,500 because they put on five pounds of muscle. That's just way outside the realm of what's going to happen. There are many reasons you probably want to put some muscle on, but like adding the metabolic. And that's because the question is how energetically demanding are they actually? Think about it the opposite. Skeletal muscle is pretty lazy. It wants to be as efficient as possible. Because if you think about functionality of physiology, you want your brain running full course as often as you possibly can. You want continual interception of what's happening in your outside world, as well as introspection going on, it's also making decisions, et cetera. Skeletal muscle is simply like a backup system. It's thinking more about. It was like, what do you need done, boss? You need something done to elevate your function. We're on it. If not, we're going to sit down and shut up and wait to be sort of told a little bit. And so what that means is if you need energy now, muscle will jump to action. It'll get you going. We see this from everything, from meat. It's like if you have this energetic need to burn 200 calories, your photos are tapping, you'll start doing sort of all these things that skeletal muscle going.

Tell folks what neat is.

This is non exercise energy. So it's energy you're burning that's not physical activity or exercise or the energy needed to survive, to breathe, to digest, to go through basic stuff. So it is the other 10 or so percent of energy throughout the day that accounts for people losing weight or not losing weight or gaining weight, that fluxes pretty well, depending on your metabolic health, depending on your total size, depending on your other stuff. So if you ever see those people who are like, man, they just can't sit still, those are like colloquially the people that probably have a pretty high knee, so they're just burning energy kind of sitting here. Other people are more stoic physically, are going to have sort of a lower thing. This is also one of the things that explains how people can maintain the same amount of physical training, like exercise performance, as well as health at tremendously different levels of calorie intakes, because we can adjust neat very quickly. And your body is. It's kind of like a last bit of polish, last bit of paint, like, what do we need to do here?

There's huge buffer in there where you can massive increase decreaseness.

Yeah. Depending on what you need to do. So we can kind of change our metabolic set point, if you will, to keep you at the same body size, irrelevant of going up and down in calories. And I'm sure you guys cover that a thousand times with Lane.

So let's talk about contraction. How does a contraction actually work? And why does a contraction require a ATP? What part of the contraction needs it?

If we go back, nerve is coming into skeletal muscle, and it would in some instances, like the eye, actually, we have what's called a motor unit. So we have a motor unit across all these things. So motor unit is the nerve that's coming in as well as all of these single fibers that that nerve is innervating. So what that means is in the eye, for example, you have motor units as small as almost one to one, which means there's a single motor unit coming in and activating a single muscle fiber that gives you extraordinary control of dexterity. And so you have a lot of nerves coming in to control a very small number of fibers. That makes you have real high precision with exactly where you're controlling. You contrast that to muscles like the glutes. You need a lot of strength, force production of the glutes, but very low fidelity. You don't need accuracy of hip extension in terms of.

There's basically just one thing. It's contract, not contract. I mean, do it with as much force as possible or not.

And so you're going to have hundreds.

That's basically the only dimension you have to regulate is what is the force and speed of contraction. Whereas with the eye, which is a great example, I'm glad you made that contrast. Our eyes have insane fidelity. And of course, you have multiple interocular muscles a lot. You have all of these muscles above, below, on the side of the eyes. And the amount of tuning that has to happen to allow humans to be able to do what we do so well, which is very subtly pick things up with our eyes.

If you contrast that to, like your fingers, which we need to have, it's the second highest level of fidelity we have to have. The eyes are still an order of magnitude higher in terms of fidelity and accuracy of movement. It's not even close. I need to be very precise with my fingertips, but my eyes are on a whole new level of precision of where we have to be. So if there's one to one or one to two in the eyes, it could be thousands per motor unit in the glutes. On, off, on 50%, 20%. So you can stand erect while having some sort of like 20 level of glute contraction to full hip extension, vertical jump, explosion, squat, deadlift, whatever the case.

That's so fantastic. Okay, continue. So nerve comes in.

So nerve comes in and does that. Now here's a couple of other layers without going too far into nerve. You're familiar, I'm sure, with said principle, so you have specific adaptation for post demand. There's another principle in here called Henneman size principle. So Eldwin Henneman's one of my favorite scientists. His principle basically says there's low threshold and high threshold motor units. And what that means is there are some motor units that are very easy to get turned on and some that you have to just aggravate the shit out of them to get them to turn on.

Let's make sure people understand what that means in terms of what's an action potential. How does a nerve actually deliver its signal?

We have this fun interplay between chemistry, electricity and chemistry. That's exactly how contraction works. So you have to go from electrical signal to a chemical signal, back to electro signal. So what happens is you've got sodium and potassium and chloride are your main players. And chloride is a negative charge. Potassium, of course, is positive and sodium is positive. The fun way to look up this and pay attention to this, if you ever forget here is. Peter, you're probably more familiar with this than I am, but look at patient assisted suicide with Dr. Morgan. You give a giant bolus of potassium to somebody and they're just going to slowly stop. Their heart's going to slowly stop contracting. Why? Because the amount of potassium intracellular is going to become fairly equivalent to the amount of extracellular potassium. And so the change in gradient electrically between the outside of the cell inside of the cell becomes neutral. And so no action potential occurs. And so what you need to have happen is a change in electrical volt from outside the cell to inside the cell. And typically we're talking like negative 30 millivolts intracell and there's, it's kind of a number. And once enough of the sodium potassium start moving in the correct directions, then the electricity changes because our positive is moved more negative. Get the idea? Boom, we hit this split, this switch, and this is what we call all or none. Skeletal muscle fibers can't contract at different levels of force. What I mean is once you flick them on, they go on fully. And that's the only way they can contract. The analogy we use here in our undergraduate class is the light switch. So once you hit that certain threshold of millivolt, the muscle fiber contracts as hard as it possibly can, there is no weight, there's no dimmer switch here. You can't go 80%, 85, 50. It's a hundred percent. Once you get to that action potential, you actually see the millivolts just rocket back up and there's this whole cascade of recovery. This is what your sodium potassium pumps are doing to try to reset that gradient, put them back in the right direction so you can have another contraction again. This is actually what explains tetany. If you contract that fiber multiple times in a row before it gets back to reset, then it just feels like it's in an isometric contraction, or it's not actually how it works, but it's going to feel like that. Totally off the topic, but what actually happens is you have so many muscle fibers and they're contracting and relaxing at such a fast rate to your muscle, it feels like the whole thing's just locked up. But they're actually flicking on, flicking off.

And by the way, just so folks understand, explain to folks how despite an all or none action potential and an all or none contraction of a single fiber, you can still get variable degrees of strength at the level of the muscle.

So this is the next part. This is why we had to bring up Penman's size principle. So within these motor units, you have sizes. Now, what's interesting is most of the time, in normal situations, all the muscle fibers in that motor unit are of the same fiber type. Let's say we had two motor units. One of those motor units is slow twitch, and one of those motor units is going to be fast twitch fibers at interface. So if we had five fibers in that motor unit, or 500, it doesn't really sort of matter right now. We have a couple of factors actually coming on, but they're going to be of all like type, generally within that same motor unit. So the only way that we relegate force production is this. We have to know that all five of those muscle fibers, once they get turned on, are going to contract at full speed. So the only way we actually change how much force we're creating a whole muscle is by altering how many of these motor units get turned on. So the size principle tells us we're going to turn on the low threshold units first. And so if you go to do what you just did, so you reached over and grab a glass of water, it's probably best we don't turn on our high threshold, high force production. Generally larger, not always, but generally larger motor units that have generally faster fibers that Are generally bigger number one or two reasons why you don't want to do that. Number one is we produce unnecessary force. So instead of slowly touching that glass to your lips, you'd smash them off your face. You can't go down. So if that motor unit can produce five pounds of force and you need two pounds of force, there is no way to go backwards. So you always start at the smallest unit possible and turn on more motor units. If more force production is required. Secondarily, it just burns energy. So fast twitch muscle fibers are more metabolically demanding than slow twitch muscle fibers. And so you're going to waste gas doing that. This is exactly why your car starts off in first gear, second, et cetera, et cetera. We lose efficiency as we go up, but we gain performance.

So let's use that example when you're talking just going back really quickly to the athlete. So how quickly is that response modulated? When I want to deadlift something, you.

Can see this in real life. I have a video of a deadlift actually from a friend of mine doing this where. So the initial stuff that's going to happen here. Are you going to activate slow touch, sorry, lower threshold motor units, which are going to be almost as close to slow to fibers. The only way that we really know to increase that is through force production demands. Like we're going to come back this when we get to fiber type stuff eventually for aging. And some of the stuff that came out even this week you may have not seen yet. The challenge with fast stretch muscle fibers is they're only then based on this logic activated under high threshold demands, which are high force demands, you can do anything to activate and the data will show this. On aging, you see virtually no reduction in slow twitch fibers. With aging, you see no reduction in size. In fact, there is some reduction. More than a few papers showing a hypertrophic effect of slow fibers of aging. There is no loss in velo. There's no loss in specific tension, which is like force per unit of size. There's no loss of power. It just appears to be very easy with any level of activity to maintain and preserve health of sulfate fibers. But because fast stretch fibers require force production and you generally don't get high force production and activities of daily living, then those fibers go unutilized for long stretches of time. Eventually they go away. And so what we see happen is this really interesting thing called fiber type grouping where the nerve will basically say, okay, that fiber is being not used. That whole motor unit will decay and the fibers will be preserved. The other neighboring motor units will actually grow new extensions, activate some of the previously gone motor units, and then convert those fibers into whatever fiber type happens in that previous motor unit. So in general, what we see happening here is slow twitch fibers start absorbing or slow twitch motor units start absorbing fast twitch fibers and bringing them to their motor unit. And so we see these large patches of single fiber types throughout the muscle. And so the last part of that puzzle is in a motor unit, those fibers are connected by the same neuron and they're the same fiber type, but they're not laying next to each other. You don't want them in the same spot. They're sort of dispersed throughout the muscle. And so that gives you smoothness of contraction. And so one of the things that happens is if you start punching, like the entire right side of your bicep is one motor unit. The entire left side is when you contract that motor unit alone, you get super spastic, out of control and you get twitchy and unregulated movements. When we see this fiber type grouping thing occur with aging, it's almost exclusively a problem of fast twitch fibers, not loss of slow twitch fibers. And so that also explains lack of fidelity as well as potentially some problems with fine unit movements.

What is the heterogeneity of fast and slow twitch mixtures within different areas? So presumably the eye is all slow twitch. It doesn't particularly require much force.

It doesn't require much force, but it does require a lot of speed. So you need to be able to dart back and forth quickly. So I actually don't know the.

Let's look at a big skeletal muscle like the lats or the glutes.

So we have two things you have to pay attention to here is we have a huge amount of person to person variation.

Within what bracket though? Give me a sense of. Presumably everybody has at least 20% of each. I'm making that up. But is there.

Let me do the second part. We'll come back to that first part. So there's actually, as you're alluding to a second ago, there's also tremendous difference between muscle to muscle. And so some muscles, if we look at it like, if we compare my soleus to your soleus, you might be 90% slow twitch in your soleus, I might be 70. And that would be a large variation in that muscle. If you look at animal models, cell culture to any murine, like you're going to see a hundred percent slow twitch in a soleus.

And the reason is because we walk the soleus has got to be a majority slow twitch muscle fiber. We just spend too much time ambulatory to risk any inefficiency in that system.

100%. If you look at the shank in general, you've got two primary muscles of movement there, the soleus being the smaller one. They both attach to the bottom of your foot. That's your Achilles planteris, right? So goes through there. If you were to take your foot and your toe and like point it towards your face and you were to flex your calf, that one that pops up, that has that kind of U shape. If you have a nice calf anyways, that big one that pops up to the middle, that's your gastroc, the one that kind of sits behind. It's underneath the very bottom where your calf stuff kind of ends and it goes into that long piece that's the soleus. And the gastrocs is almost the opposite. It is almost exclusively fast twitch, but not nearly as exclusive as your soleuses. So the soleus is what we call postural or anti gravity for the exact stuff you mentioned. It needs to stay up and it needs to be on. In fact, you can actually have a soleus contracted for hours and be totally, totally fine. And you won't even realize it. For the most part, it's actually good metabolically, but you would not realize it if you contracted your gastroc for more than a few seconds. We were probably going to feel the burn like pretty quickly. So the variation in something like a Soleus could be that. I think probably if you saw somebody who's 30% fast twitch in the soleus, that's a very, very high number. I wouldn't be surprised if I saw somebody 95 though, if you contrast that to a muscle like the vl. So the vast lateralis, the quad, the outside quad muscle, as you know. But for the audience now, the variation gets extraordinarily large. So in general, the VL is like what we typically say is 50, 50 fast switch flow. And the record, it gets far more complicated than fast switch slow twitch. But we're just kind of keeping it at that level for now. We have shown actually in our lab a couple of things. So one, we biopsied a whole bunch of people who are Olympians, world caliber, national caliber, in our lab, men and women. And some of those individuals are 80 plus percent, 85% fast switch.

And by the way, just did you also do vm? And why is there a difference between vl, VM and intermediate?

Just due to access, generally access and safety A lot more potential things to hit in the medial, nothing out the outside. I nick anything. We have problems.

You could be up to 80% fast twitch on your VL if you're. And by the way, is that true across all sports? Like if you had the Tour de France champion, would you expect him to, even though he's the best of the best and his VL is a monstrosity, would you expect him to have that high a fast twitch?

So in some of the folks we've biopsied in the more endurance space, they are as high as 90% slow twitch in the VL. It's basically 0 to 0. You can run the whole gamut of composition in the vo.

So, and we're back to the same question, which is if you had a time machine and you could go back and biopsy them as five year olds, we really don't know what they looked like then.

Well, this is what our twin study did. Rather than biopsy them at 5 years old, we got lucky.

You biopsy them as adults, as twins.

We got models like as twins who.

Presumably had enough differences in what they were doing that you could see a.

Signal if There was about 35 years difference of training.

And what did you see?

If we compare this, now that I can go back and tell them, at least you've been in labs, you'll appreciate this. One of our graduate students had been in our lab for probably three or more years, was sitting next to my colleague Jimmy Bagley, and they're pulling muscle fibers, sort of like the things that come up when you're staring under a microscope, pulling out individual muscle fibers with tweezers for hundreds of hours on time. Like your brain goes into weird spots. And so she was sort of just telling him, oh yeah, like my dad's a twin or whatever. Oh cool, whatever. Oh yeah, like monozygous. I'm like, yeah. So monozygous means their DNA is. Exactly. So not just brothers that got born at the same time. So you have genetic replication. So we have that category lock. And Jimmy was sort of like, oh cool, did they exercise? And she's like, oh yeah, well, like I think, I can't remember which one. He's like, well, my dad doesn't exercise, but my uncle has been competing in Ironman's for 35 years. And Jamie was like, what?

It's a dream experiment.

Wait, wait, so let me get this straight. You have identical twin parents, father. One of them has been 30 plus years of documented endurance exercise. The other, what's he do? She's like, no, he's never exercised in high school. And we're like, and you've been in my lab for three years and this.

Is the first we're hearing about this.

You're fired, you're not graduating. So we were able to pull them into the lab and bring them in. And so he was one of these classic endurance nerds. Every workout had been documented for 30 years. He's got 50 journals written down. So we knew the caloric expenditure, we knew the miles. We just had everything. Half marathons, marathons.

And phenotypically, how different did they look?

Almost identical.

Even with all the training, they still looked. I mean, I'm saying not in the face, of course, but just muscularly. How did they appear phenotypically?

No, I know what you're saying. They were almost identical. The only exception was the non exercising twin was a little bit less lean. I think he had, I can't remember exactly, but something like three or four more kilos of body fat, maybe less.

Isn't that kind of amazing too?

Do you know what their muscle looked like, though?

It really speaks to the hereditary nature. Well, yeah, yeah. So I want to come back to that because that's what's important. But at the surface, think about that. You have these two guys that are genetically identical. Presumably both looked good. And one is by all intents and purposes a fanatic around exercise. The other is a couch potato. But on the outside, they look relatively equivalent. Tells you a couple of things. One body habitus is remarkably hereditary. I mean, it is, I believe, more hereditary than. It's certainly on par with height and eye color in terms of how hereditary it is. The second is what you're about to tell us, I suspect, which is that the outside is but a fraction of the story.

So here's what we did. I got super excited and I was basically like, I'm going to take every measure possible. This is DEXA scans, this is vertical jump. VO2 max blood chemistry, muscle biopsies, psychological evaluations. With an IQ test. We just did everything we could possibly do. The total amount of lean mass.

By the way, you'd created just a random IRB to do this? Like what?

Oh, yeah. I mean, like we took time to design the study, put an IRB through the whole sort of thing.

How long did it take? Just so people understand the pace at which science moves from the microscope discussion until you've got these guys in your.

Lab, maybe eight months.

Oh, wow, that's really fast. You already had the funding, I assume?

Yeah, I Didn't care. Like, I'm paying For this regardless, 100%. Like, in fact, I literally did pay for their plane flights out of my pocket. I didn't want to deal with the stuff. I was like, just book the flights right now. We got to schedule the work. Put it on my credit card. I don't care. I'm not missing this chance.

So what did you see?

What's interesting was that body composition lies the untrained person again. Five, six pounds, more fat mass, something like that. Maybe three kilos was too high. I can't remember. So I'm like, oh, that's interesting.

On Dexa, what was the difference in muscle mass?

Like a hundred grams? I think the number was 71.

You're at the detection way beyond. So they're essentially identical.

They were almost identical. Totally in muscle mass right now. Interesting. The endurance guy did not lift at all. No strength training whatsoever. Strictly running, cycling. Swung like a very classic.

Can you imagine just the Godankin experiment of triplets where you had a third guy here that only lifted weights? Can you just imagine?

I can't imagine. Like, this was like an hour of her thesis defense.

Oh, God.

This was that question right there.

Okay. All right.

We actually did another study in Stockholm, Sweden, with lifelong skiers. I won't get too derailed here, but these are people who are world champions in the 1940s and 50s and cross country skiing, Olympic gold medalists, and didn't stop competing. Now they're in the age of 85 plus, up to 92 years old, and we're still competitive skiers. And compare them to age matched healthy folks over here in America. So I've spent a little bit of time in this, like, aging athlete thing.

I actually wrote a little bit about that cohort in my book.

Oh, really?

The skiers?

Yeah, yeah, that's us.

It's insane what they were capable of.

I can tell you a lot more behind the scenes on that one.

I'd love to. Yeah, let's come back to it.

Walking into the hospital across the street and just like jumping off the curb. Cause there was ice and you're like, oh, you're in 90 and you just decided to jump that curb for fun, like when no one was watching you. Because we could, like see them from the window coming in. I'm just like. Just so. Just like one guy finishing a VO2 max, sitting on the chair, taking like two breaths and going. I didn't understand the test. Let me try it again. And trying to get back on the mic. This is like 12 seconds after VO2 max and a whole bunch of other stuff like that was incredible. So back to the twin studies, that was identical in general. You could categorize some things. So I'll kind of make this a little bit shorter. If you looked at muscle quality. So this is echo intensity on an ultrasound, this is vertical jump, this is leg extension strength. It was either identical or it favored the non exercising twin. Everything else that you would classically associate as an exercise adaptation favored the exerciser. Blood lipid panel, blood pressure, body composition, certainly VO2 max was significantly higher. Resting heart rate, like all the classic textbook endurance exercise, as A, B and C, it stacked up exactly as you'd think. The neutral stuff, total muscle mass, that was basically on point. And then blood glucose was favored for the exerciser, like all that stuff you would predict.

But just to make sure I understand, the non exerciser was stronger, stronger, better.

Jumper, higher quality muscle.

Go into the higher quality again to make sure I understand that. Beyond the metric driven stuff, is that a subjective assessment of muscle quality?

No, no, no, no. You can actually measure this via an ultrasound. And so this is like a measure of. It's called echo intensity. It's a measure of. It's akin to measuring how much intramuscular fat is inside the actual tissue. That's what echo intensities kind of basically tell you.

So you're saying the exercising guy had more intramuscular lipid.

Right.

Just to play devil's advocate, isn't that an adaptation to his endurance training where he wants to have more intramuscular lipid because he wants to have more logs near the fire? He's burning those logs totally.

And you wouldn't have to dig hard to find support for that.

And I think that's different from the intramuscular lipid we see in the diabetic, for example, or in the insulin resistant.

There's a level when you cross, when there's no exercise there, then there's a different reason that that happens.

But still, what's interesting to me is that the strength metrics also favored the non exerciser.

It was all favored to neutral. Either some of the metrics were similar or not statistically different, but they hedged towards a non exerciser. So you could say at best they were neutral to favoring the non exerciser is, I think the most fair way, but there's not a metric there that favored the exerciser on that side of the house. So what is your biopsy related?

Yeah, let's talk about the biopsy.

It gets very different. So I'll give you the quick version. There's a more interesting version. The non exerciser was almost identical to what you'd see in the literature and what we've done a ton of times where you have something like you're fairly mixed in terms of phenotype, so you've got some percentage of fast twitch, some percentage of slow twitch. But in fact he had about, if I remember correctly, something like 20% of his fibers are in what we call this hybrid format. And so I sort of alluded this earlier. There's fast switch fibers or slow twitch fibers, but the story goes much deeper. That's not really how the whole thing plays out. So these hybrid fibers are a single individual cell. So one muscle fiber that co expresses fast and slow twitch and in fact it'll express that in different areas throughout the length of the fiber. So it'll be exclusively fast twitch in one portion, fast and slow in another portion, and exclusively slow twitch in another portion of et cetera.

Let's make sure people understand what the difference is between a fast and a slow twitch fiber. I want to come right back to where we are, but I just want to make sure we haven't lost that.

In general, there's a lot of ways to describe it, but the easiest way is to describe it by the name. So fast twitch means that the twitch or the speed of contraction is higher. These fibers can contract and squeeze together through the mechanisms. We haven't got to yet. We'll get there myosin actin at a much faster rate. Having said that, the fast twitch fibers tend to be larger, though not always and certainly not in endurance training individuals and definitely not with aging. They almost always are more glycolytically driven. And so they're going to have more of the enzymes responsible for anaerobic glycolysis. They're going to have more glucose in the cell. They're going to have less intramuscular triglycerides that generally have more phosphor creatine. Slow twitch fibers are fatigue resistant, which means these are the ones that can contract kind of all day long because they don't use as much glucose. So they do use quite a bit still, they are much better at using fat as a fuel. They tend to have more and larger mitochondria. The downside is they don't contract with as much velocity in general. So that's the functional, that's why we call them twitch.

And just to be clear, the force difference between them, it doesn't matter, it's just velocity. Or is there a force difference as well?

So a couple of things. In large part, force production for muscle fibers is determined mostly by size, cross sectional area. So getting the fiber bigger is the play to get it faster. Having said that, power is markedly different.

Because power is based on velocity as well.

Times the multiply the force by the velocity. So if you use this metric that we'll use in single fiber experiments called specific tension, which is sort of like relative strength, you take the size portion out of the equation, what you're going to see is a true slow twitch. So these are also called type 1 fibers. If you compare those to a type 2A, so that's a fast twitch muscle fiber, you're going to see something like 5 to 6x power between these two. So it's not a small.

When you normalize for size, when you normalize for cross sectional diameter.

If you go to the 2x fibers, which is a special class of fast switch fibers, now you're talking 20x that power.

And that is mostly explained by more metabolic apparatus. What's enabling the speed? No, why does the 2x fiber go faster?

In fact, the way that we differentiate muscle fibers in the laboratory is we measure what's called the myosin heavy chain to kind of actually come back to microanatomy here. So the way the muscle fibers work is this is all in a 3D sequence. So you can imagine that cylinder. I'm going to explain it to you in 2D just so you understand. But this is actually occurring in 3D. And so what happens is you've got two of these microfilaments called actin and myosin. What happens is they're overlapped so they're not touching each other. And you've got myosin kind of laying in the middle and it's this big thick tube and it's got these heads that flick off the top of it. Now these heads reach up and they extend again in 3D. But if, just think about it, 2D, they reach up and grab on what's called actin. The idea when you contract the muscle is the myosin will reach up and they're going to reach out outward. So if you're watching this video, you're seeing my hands kind of reach up and away from my body, like I'm stretching my arms, like I'm doing a big T, if you will. And my hands would then grab onto the actin. And then if I were to squeeze my hands and bring my hands closer to my face, the myosin is actually then pulling the actin closer together. So what actually happens in real life is those start stacking on top of each other. And that's why when you squeeze your bicep, it actually glows larger vertically because those muscle fibers are stacking on top of each other, and that's actually elevating in size. What determines force production versus velocity is what we call cross bridges. The amount of time that these myosin heads grab onto actin, that little place of connection is called a cross bridge. The more those cross bridges you have, the more effectively you can pull the actin closer to each other. The more effectively do that, the faster the contraction, the more forceful the contraction is going to be. So primary thing explaining force production is the amount of cross bridges. So the thicker your myosin, the more likely you are to grab actin, the faster, the stronger the hold, if you will. So the better connection your hand has to that thing it's grabbing onto, rather than you can imagine, like a couple of fingertips on it and trying to pull something closer to you versus having your whole hand wrapped around it, a strap on it, chalk on it, you're gonna be able to rip that thing down quickly. Now, there are six actin that surround in a circle each myosin in human skeletal muscle. So again, picture that 3D structure. So you can imagine if I'm standing up in a room and I'm myosin and six people are forming a circle around me, like they're gonna jump me or celebrate me or whatever. That's what it looks like. And my arms can sort of reach out, and no matter where my arms are, there's gonna be somebody that I can grab.

And you only have two arms still in this, you only have two myosin filaments.

You have a ton. So you have one myosin film.

I'm sorry, you only have two heads, or how many heads do you have?

Bajillions.

Okay. So you have billions of heads to grab onto six potential targets. So you're always going to grab a.

Target, you're going to grab one. Right now, you can't increase the amount of those actin that are around you. But we do see that in other animals. So this is one of the reasons that explains why, like, fruit flies, spiders, and things like that can contract with so much more force relative to humans, is they might have 8 or 10 or 12 or 20 myosin or actin per myosin.

And ants, which we always think of as, like, for their size, being insanely strong, they'll do that. So evolution's tool to make things stronger is give more actin. Because you already have an infinite number of myosin heads. The more things I can give you to grab onto, the stronger you are.

The stronger you're gonna be.

You realize there's somebody out there using CRISPR right now trying to figure out how to double the number of these things in humans. Right?

So I'm not going to say this officially. All I'm going to say is, well, officially the world knows about the bear muscle studies that we've worked on. So there have been bare tissue come through. And under my microscope put it that way, bare tissue is actually quite unique. So they actually have a. So humans have that 2A and they.

Have that 2X which is formerly 2B. Right.

Incorrectly identified as 2B. That's correct. Most other animals do actually have, in fact 2B. And the 2B is even faster than the 2X. And bears have a lot of them. So this is one of the other reasons why they simply have a fiber type that is much faster than any of the fastest ones. We have cheetahs, other cats like that have like 20 to 60% of these 2B fibers, just extraordinarily high amounts, which allows them to go super fast.

And in those, do they have more actin targets?

I think cats are pretty close to 6 to 1. We could fact check that one, but I'm pretty sure that part of it tends to be fairly similar mammals. It's when you get to the insects and things like that, I think where that number jumps off. But my comparative physiology is not the sharpest. So don't trust me there.

That's a great description of the micro anatomy. And I want to remember.

Let me finish the speed thing. Cause this is what.

Okay, yeah, yeah, yeah.

So what determines the speed? So on those little myosin, where it kind of connects to the actin, it's called the myosin head. Now, part of that is a bunch of stuff that you guys don't need to know about, but a part of that is it's called the heavy chain. So there's a light chain portion and a heavy chain on the tip there. The way that we get a muscle to contract is ATP. So what happens is the myosin are kind of loosely connected to the actin at all times. But in order for it to grab and pull, you need a strong connection. And for that connection to happen and for that to be able to pull it together, it requires energy. So, pardon the somewhat crude analogy, but the way that it kind of works is if you imagine cocking a pistol. So in order to actually cock the pistol versus fire the trigger, the squeezing the trigger, it takes a lot less energy than cocking it back. If you've ever cocked a thing like actually you have to pull pretty hard. So the energy that we need actually for muscle contraction is not the pulling together, that's actually almost passive. It is the cocking back part that takes energy. And so that energy comes from ATP. So on the little tip of that myosin head is an enzyme called ATPase. As you know, you hear ace, you think kinase, like you think something enzyme that's going to work. That's the molecule that hydrolyzes ATP splits ATP rather. So to make that simple. So what you have to do is actually invest in ATP that gives you energy, use that energy to cock that myosin back into place. And now it's kind of sitting there. But it can't bind strongly until calcium comes into the picture. It gets released from the sarcoplasmic reticulum. That has to come to the equation. It has to cause this conformational change in actin and move these T tubules or that comes from T tubules and move some other things around. Once those things get moved around by the calcium, the myosin is like, oh, boom. It connects something and then it just almost subconsciously snaps as hard as it possibly can. And that's why you can't regulate force production, is like it's just gonna catch and snap. In order for that to go back, you actually have to invest more in ATP. This is also side note, what explains rigor mortis. So this happens, it gets contracted, you don't have the energy to then pull it back in. So then you stay in this locked skeletal muscle contraction position. So now the speed at which you can do that, that ATPase thing, that's what determines single muscle fiber contractile speed. That's also that myosin heavy chain is what we measure in the lab. And that's how we determine fast switch versus slow twitch. So if you were to use a technique that we use called gel electrophoresis, basically you put a gel between two pieces of glass and you just pour gel in there and it gets like solidified just like hair gel, like a little bit thicker. And then you put each individual muscle fiber in its own vertical lane. And then you put a little bit of positive charge on the top end, a little bit of negative charge in the bottom end, or inverse doesn't matter. And Then you actually put a little bit of chemical bath around the muscle fiber that has a charge. You turn the electricity on positive, goes to negative, et cetera. And so those fibers run down vertically through the gel. We hit stop at a certain time point and the smaller ones have gone further because smaller molecular will go through the gel faster. And so we stop, we develop it like you would develop a picture, like old school photography stuff. Literally the same silver nitrate sector that you use. And we can see the ones that have gone further down are slow twitch. The ones that want to say up higher are fast twitch. And of course, we use molecular weight markers to confirm all that, but that's effectively what we're looking at. So what that means is the myosin heavy chain molecular weight determines fiber type and that regulates its twitch ability. The more of those and the faster those heavy chains work, the faster ATPase can operate, the faster the whole thing can contract, the faster the muscle fiber contracts. And there you go. And that's why muscle fiber type is not predicated on size. It is specific to either metabolic abilities in the olden days or now, more specifically twitch velocity.

So I guess all of this now brings us back to a better position in which we can understand the biopsy studies in these identical twins.

If you look at the fiber profile of the untrained twin, it lines up very close to what you'd see in a textbook. So it was around 50% slow twitch and about 30% of these fast twitch 2a form, but then about 20 or so percent in this hybrid format, 2a or 2x2a. So here's one of the things that's interesting when you get into the 2x conversation. There are clearly humans have the ability to express 2x. It's just extraordinarily rare. And so what tends to happen is this. If you find somebody that has what we call pure 2x fibers. So these are single fibers that are expressing only 2x. A couple of things have happened. Number one, they've probably had that muscle fiber de innervated for decades. That's really the only time we see it. In fact, if you look at spinal cord injury folks who had a de innervated thing for decades, they're as high as 50 or 60% of their total fiber type being 2x. And so this seems to be the default strategy of if you don't activate or utilize a muscle, it eventually is going to fall to 2x. Why we have absolutely no idea. I could guess that we don't seem to know. We see it sometimes in older folks.

But Even then, sorry, 2x is the hybrid, single fiber hybrid.

2X is a pure fiber type. It is the ultra fast, okay? It is the one. So any hybrid is going to be called something like. There is a 1, 2A hybrid, there's a 2, a 2X hybrid, and there's even a triple hybrid one, 2, a 2X. It has all three fiber types in the same cell. Those are fairly uncommon. A1, 2A hybrid and A2, A2X hybrid are very, very common. A pure 2X by itself though is extraordinarily rare. In fact, we've done hundreds of thousands of individual fibers in my lab and have probably seen in total 20 or 30 pure 2x fibers. You're talking generally something like 0.1% of fibers, something like that are pure. Now if you dive in literature here, you're going to get confused very quickly because a lot of people don't use detailed enough laboratory methodologies to differentiate these. And so they're going to say, oh, there's all kinds of 2x fibers. They're really not. They're very clearly two a 2x fibers. They just didn't run high fidelity enough to actually differentiate between hybrids. And so you'll pick up two A2X fibers as having some portion of 2X. And so it's a difference between does that fiber contain 2x versus is that a purely 2x5, which is sort of a semantic difference. But in all world it's a big deal if you find somebody with a high percentage of 2x fibers. Something odd is going on. The only exception here is there's no data really on truly fast people. We have a lot on powerful people. We have a lot on kayakers and bodybuilders and weightlifters. But as we discussed at the beginning, that's actually not truly meaning.

We don't have data on sprinters.

No.

Why?

Great question. It's hard to get these folks in the lab. I guess people haven't been interested in it. It's not a thing. We just don't have them. The only thing we have is there's a case study done, a guy who, I think he still owns a world record. It's not hard to figure out his name, though I can't technically say it. 110 meter hurdles, I think, and 60 meter hurdles at the time had the world record of both. I think still has one of them. He's the only one I know. I was a graduate student at the time, so I didn't run the study, but I Certainly had my hands on the fibers plenty of times. And he has something like 24% pure 2x fibers. I'd like to see that replicated.

So the untrained guy was 50% slow, 30% 2A, 20% hybrid. AX2A 2X, 2A 2X. Yep. And then what was the trained cardio?

Only trained about 95% pure slow twitch.

So right there you have the explanation for why he was weaker. He just couldn't generate the force.

It's a couple of things. So it answers a handful. Number one, do they change? We know this demonstrably.

This is highly malleable.

Yeah, not even close. We actually know that there's data on nutrition, there's nutritional aspects that will alter fiber type composition. Anything that's going to go activate PGC1 Alpha and that whole cascade is going to activate, increase sort of tribal site. This is going to happen. There's actually a study came out very recently on resveratrol. Doing it not in humans, but like a very reasonable dose. Five grams of resveratrol, I think in cattle, just like not that much at all for a 2000 pound animal. Cause significant changes in fiber type profile, and there's a whole host of nutritional interventions. The question of, okay, does it change the physical activity? It's been answered so many times for so many decades now. It's just like very clear. And in our case, okay, how much, how much can I really change? An important amount? Well, I don't know what these people's default is, because one could argue the untrained guy was actually in an adaptation state.

Yeah, he had a higher state. He deviated away from his potential.

Right. Because one thing that seems to be very clear is these two A2X fibers are generally associated with poor health. And so we see this concentration go up with any kind of physical activity.

Or space flight, whereas a 2x by.

Itself 2x is basically irrelevant because they just don't exist. If you have them, it's generally bad news. So you don't want to train into them. So the ideal scenario here is two A will seem to be the place you want to turn into. If you do any sort of physical training, those hybrids tend to go down, especially two A2Xs, they kind of go away. And so I'm not surprised that the trained individual had none of them. And I'm also not surprised at the untrained ones. So it lined up pretty textbook. So the magnitude of change is meaningful. It's a case study, all that, but.

It matters what's Your hypothesis, if you had a third brother, a triplet, who was a weightlifter or a powerlifter, the.

Distinction I actually don't think would matter a ton. You're going to get the same answer. I would not be surprised if that third was 70% past twitch 2A and 30% type 1. Yeah. With probably very few hybrids, if they're trained now, the one distinction is the two A2X fibers tend to be a little more responsive to a little bit of workload. You have to hit sufficient audience to really get them to go all the way away. But it's not that much. So if you're just like kind of like a laissez faire lifter, you'll still have some there. But if you're training seriously, those things are going to go away. So I don't really think, given enough time and exposure, I don't really think that there's a limit to the plasticity among fiber types even within a normal human condition. Now this was 35 years.

Do we have a sense about the window in which you are maximally susceptible to it? So if someone listening to this is 50 years old and they've kind of been sedentary a lot of their lives, but because they listen to this podcast, they've now got the motivation to become big time exercisers, how much can they bend the arc of their fiber curve?

So fiber type is actually really quite cool because it doesn't seem to matter what age you are. So training studies in 70 year olds, we see dramatic changes in fiber type in six weeks, eight weeks certainly. And the magnitude of change doesn't seem to differentiate. In fact, the way that you want to think about this is it's kind of like an asymptote. The less trained you are, the faster things, faster the initial adaptation, the closer to your edge. So if you're a weightlifter, in fact, we saw this differentiated so with our world caliber lifters compared to national caliber lifters. The world caliber lifters had been lifting at a very high level for like eight or so years, but the national caliber had been lifting more like four years. They were close to fiber type, but the national calibers had more faster fibers. So what this tells you is initial changes happened very quickly, but getting from that last few percentage up took years for that second group. But we will see this again four to six weeks. To see a demonstrable change in fiber type composition is. And it doesn't seem to matter with age. In fact, as you age, it probably gets easier because your level of untrained is so high, if that situation is there.

One other thing I want to ask you about on the microanatomy side, Andy, is you sort of have talked about it indirectly, but if a person hasn't maybe caught it, can you just explain how hypertrophy fits into this? So when a person wants to have bigger muscles, what's happening at the cellular level with their muscle fibers?

So there's an interesting discussion here. The easy answer is, when we generally say hypertrophy, what we're referring to is diameter or cross sectional area. And so if you remember, if you think about the muscle fibers being that cylinder, the width of the cylinder just expands. And so that circle gets larger is the way to think about it.

And a crude analogy is getting fatter means each adipocyte is getting bigger. It's taking on and storing more triglyceride.

Yep, exactly. So from a skeletal muscle perspective, the diameter gets larger. There's actually interesting work. We actually have some tissue on its way to Auburn right now. Because one of the things that's been interesting, it's like a bro science thing for years of sarcoplasmic hypertrophy versus contractile hypertrophy. And so what this is really positing is, is the change really coming from fluid retention basically, or is it actually enhanced of the contractile tissue, which in this case would be actinomycin? Seems to have some initial work there. That's a little bit of both. And it happens the different phases of training.

Is the question, do different types of training increase sarcoplasmic versus contractile hypertrophy? Or is the broader question, hey, is a bodybuilder a bodybuilder? Because their sarcoplasmic reticulum is huge, but their contractile units are not that much bigger than the average person. I want to make sure I understand the question.

So it's close. Not the sarcoplasmic reticulum. It's what we call sarcoplasmic hypertrophy. So this would just be an increase in diameter with additional fluid. So it is close to what you're saying. So in other words, does this thing even exist, in other words, or is all increases in muscle size through strength training? Assuming it's like a normal positive adaptation, not some sort of weird thing, Is it actually happening because myos and actin are getting thicker? Remember, you can't add act.

I got it. Okay, wait. That's amazing. We don't know the answer to that question yet.

We don't. More data have started Coming out. But even a few years ago, the idea that sarcoplasmic hypertrophy was a thing was thought of as like garbage row science.

Meaning the idea, the assumed belief was anytime muscles got bigger, they were getting bigger in the contractile units.

Correct.

But by the way, I'm not shocked that that was the default hypothesis. I'm shocked that it wasn't definitively known.

It was a technology issue. It was an assay problem, like figuring out how to actually measure this. When you take a muscle fiber out.

Of a human, even with an electron microscopy, you couldn't do this.

That's not the problem. It's the standardization of fluids that's the issue here.

When you sample the tissue, it's how do you lock the fluid into place?

Basically, correct. How do you take this cell out of a living human, get it into.

Some petri dish and preserve its fluid architecture without contaminating it? I got it. And you couldn't do that with like liquid nitrogen immediately, that flash freezes.

So if you get crystals in there, you actually lyse, you screw the whole thing.

Got it. Just because I'm such a freaking nerd, I can't stand it. How did you guys solve this problem?

Well, I didn't solve it, first of all. Mike Roberts out of Auburn has produced a lot of really interesting work in this area. His labs is extraordinary. But they just figured out they were able to kind of take an assay from a colleague of his, figure out how to preserve it. And liquid nitrogen is actually fine. But then from there you have to thought correctly and you have to do it. So he troubleshot this whole thing for a couple years.

You accept the crystals that'll blow up the size because of course the.

If you freeze them correctly.

Yeah, it's how you thought.

Chemistry is hard like this. So it gets very detailed. But Mike could give you a better.

And I hope there's some high school college kid listening to this, who's studying chemistry, who's realizing just how cool and interconnected all of these worlds are. Chemistry, biology, physics, they're just so linked.

I always joke that, like there's only one thing in this world, there's only one science. It's just math. As much as I hate math, the chemistry is math, energy is math, biomechanics is math. It's that math and reductionism, but that's it. Those are two things. So to go back, what the question is, here's where the exercise scientist comes in. Why is it a bodybuilder can have more muscle, yet they're not stronger than a strongman or a weightlifter. Like, how does this actually happen? And this is where this whole thing comes about. Like, how is it that my hypertrophy can exceed your hypertrophy, but somehow your strength? And the easy, like, sophomore answer is all neurological adaptations. Okay, fine, sure. But, like, there's nothing happening intracellularly. Well, I don't think that's correct. And in fact, it doesn't look to be the case. And so there is some sort of combination, because here's the juxtaposition. There's a thing called lattice spacing, which is there's an optimal distance between that myosin and actin. In other words, if I was trying to produce a powerful contraction, but I was buttered up next to each other, I can't actually squeeze that hard because there's nowhere to go. If I'm too extended, then I actually can't.

So that's the same idea as preload in a heart.

100% preload is going to determine stroke, volume, everything incoming in. So this spacing, if you're going to start adding contractile units one way or the other, you have to preserve spacing somehow. The idea is it will exceed. It will expand hypertrophically only to the.

But if it actually compromises your going back to math, I promise you there's a mathematical optimization for the exact strike distance between actin and myosin to not be overextended or underextended and to have that perfect preload for maximum contraction.

A hundred percent.

And if your hypertrophy train. I'm. This is. Now I'm totally making this up, but if your hypertrophy training interfered with that and compromised it, you might gain size at the expense of potential strength.

Right? Or if that high perchrophy was coming simply from excessive fluid and not actually contracting, then you would actually have a larger muscle. When I say fluid retention, I'm not talking about, like, acute fluid retention. I'm not saying, like, you're bloated today. You've waterloaded. I mean, there's enhanced fluid in a homeostatic balance inside the tissue because diameter has gotten larger, but it wasn't met with an equal amount of increase in contract volumes. So if that number gets off.

Yeah, I think another physiologic point that's worth explaining to people is how much. People are familiar with the idea that 2/3 to 70% of our weight. I stood on the scale this morning. That number on the scale, 2/3 to 70% of it is H2O. And then people say, okay, well, how can that be? Because I get that my blood plasma is water. That can't be where it all is. No. Most of it is in the cells of our body. And the muscle is, of course, no exception, given that it's such a ubiquitous cell.

Totally. And in fact, given that it occupies the vast majority of mass in your body and given the fact that in order for it to store its primary unit of energy, it needs to bring water with it, being glucose, that's going to pull that thing.

And just tell folks how that differs from, again, going back to bodybuilding. I love following Jay Cutler on Instagram because I was just such a fan of his as a bodybuilder. And he's just one of these guys who, in retirement is still training hard, paying attention to his nutrition. It was an interesting video. So he went into like, In N Out Burger and he was like, it's my cheat day today, I'm going into In N Out Burger. And he places this monster order. What caught me was how much. He said, no salt, no salt, no salt, no salt. So he was like, two burgers here, fries here, but no salt, no salt, no salt, no salt. Clearly this guy knows something about the effect of salt sodium on fluid retention. That's a different fluid than what we're talking about now.

Yes and no. In the sense of like, he probably has an either direct or indirect understanding of if you smash down 7 grams of salt right now, bad things are about to happen in a lot of areas. Like, more specifically, if you just look at, we're getting maybe after. But if you look at hydration and dealing with the athletes that I deal with, a weight cut is a huge deal. Managing a, a 15 or more pound reduction water over a course of 48 hours and then putting that back in. If you don't understand being hypo osmotic or hyperosmotic or ISO osmotic, like, you're going to cause a whole host of problems, from kidney issues to diarrhea to bloating to all kinds of problems. So you have to actually understand what you put back in them has to be the same thing as what's intracellular.

Or there's going to be a huge shift.

You're not going to drive fluid into tissue. And you get into situations where guys are peeing and girls are severely dehydrated, they're peeing, yet they put very little fluid actually back into tissue because blood volume got so large, it expanded so quickly, they have a sense to excrete because total volume gets too high, quote unquote. But they didn't actually balance electrolytes. And so nothing goes intracellular, which is where you're trying to get it to outside of organs. Once your organs have functional organs, rather, as ever.

And are there any rules of thumb on that? We were talking before the podcast started how had food poisoning and in a span of like two days, I lost seven pounds. And my weight is about the most stable metric in my life. Like, it just doesn't fluctuate a pound. So to lose seven pounds in two days, basically due to the fluid losses of being sick and having to go to the bathroom about every seven minutes, coupled with not really wanting to eat during that period of time, what is your best guess as to. I mean, let's just posit that much of that £7, six and a half of it is water. What's the ideal strategy to replenish that in terms of hyper hypo or ISO osmotic? If I'm going to try to replenish.

That in the form of liquid handful of things. Number one, you need to go slowly. So you got to make sure that you don't get excessive.

So I don't want a pound for four liters worth of four grams of sodium in the first six hours. I'm feeling better.

Yep. So number one, you want to shoot for something like the neighborhood of 110% to 125% of fluid weight. Cause you're going to lose some to your own. It's going to happen. So let's say you lost seven. My brain is like, okay, we're going to go to eight and a half, nine pounds, something like that. You want to round this and call this a gallon? Okay, we're at a gallon. All right, we're going to bring that in over the course of three hours. Maybe four or two gallons.

Right?

Well, four liters in a gallon. Ish. Little overchange. Two point.

So a couple gallons?

Yeah, I mean a gallon is four liters. A liter is a kilo. So you're talking four kilos.

You could do that over two days?

No, like three hours.

Oh, you could?

Oh, yeah.

Once your GI system settles down. So you would have fighters that would. I guess they have to. If they're going from a weigh into competition, they've got to bring that in for sure.

Last week, guy in Abu Dhabi weighed in 136 pounds. There's 152 pounds within probably five hours.

And what was the osmolarity of with no Urine, No.

Diarrhea? No. Gi, none of those things.

What was the osmolarity of the fluid he took in?

So it depends. The guy going through it this week as well, we actually measure that. So we actually will measure, run a basic sweat test and you can figure out sodium concentrations and then the amount that they get back is actually dependent upon them. So that number can fluctuate depending on if they're a high salt, low salt sort of sweater. It also depends on how much salt we've had to pull out the week of or, or not. Obviously if we don't pull out salt five or six days away or like anything bananas like that. But if you have 7 to 8% of your body fat you have to lose, or, sorry, 7 to 8% of body fluid, of your body weight and fluid you have to lose. We're going to take some salt out for a couple days just to get.

Us down there and salt out. Tell me how many grams per day they're down to in sodium.

Zero. You're gonna get down to zero on those last couple days. So you're gonna get down to like a classic example is we might have them at like two and a half grams, kind of like fight week per day. It's like not unreasonable. But the day before water cut day, it's zero. It's as much as like you're boiling chicken to get as much possible stuff out of there. You're eating as much as close to zero as we possibly can for that 24 hour period. If you have to go there, ideally you don't have to go that low, but sometimes you have to.

That's a bigger impact than cutting calories, which you don't really want to do at that point.

Calories are irrelevant at that point. It is simply physical weight of food. And this is a fluid manipulation here. If we can keep them at like a gram for that last day, like cool. But a lot of the times you're staring down the barrel of an 8 to 15 pound water cut on a day, you just need every advantage possible.

Wait, wait, wait. I'm sorry, 8 to 15 pounds of water you can cut in a day?

Yeah, for sure.

In a guy that starts out as little as like 160 pounds. If you, if you're trying to get 160 to 147, you're doing that in a day.

You can, it's not ideal, but you can for sure. You could do that in half a day.

Okay, let's make it ideal. Would two days be ideal to do that.

So ideally in this situations, you come into fight week in the proper situation. So you need to come into fight week hydrated on normal or like even maybe slightly higher salt normal or higher carbohydrate. You need to come in healthy, you need to come in recovered, not overtrained, all that stuff. Like you have to play a whole bunch of games here. Monday through sort of Thursday, you're going to start getting as much of this off passively as you possibly can. And so you're going to typically keep carbohydrate very low, 50 or less grams, sort of depending on what they're doing. And you're going to deplete glycogen. That alone is going to start helping you pull some water. So you're going to passively do it. You can play games with fiber. And so you have these low residue diets the last couple of days. And so you can make sure you're not holding on to food in your gut that can buy you a couple of kilos, depending, a kilo, depending on the size of the person. And so ideally, for example, if you came in Monday of fight week at 170lbs, hopefully we can kind of get you down to like164,165 by Thursday.

Just passive stuff.

Yeah. And now you're talking like we've got nine to do over 24 hours. Well, you're going to float a couple throughout the day, just urinating and stuff because you're being very hydrated. You're going to float one or so overnight this because of that. So really there goes three right there. So now you're talking like we got to do six or seven of like active water dropping in that situation. So that really is a 15 pound week. But it's not that bad.

Those six come just from taking that is the sodium, complete sodium restriction.

You're going to have to add in some sort of sweating component. So you're going to have to do so sauna or cardio, something like that. The ideal situation is you do need a little bit of physical activity maybe to burn any last little bit of glycogen without getting too terrible feeling. And then from there see a lot of what's called a mummy wrap. So you basically lay down and you put a bunch of blankets on yourself. It's like very easy to regulate blood pressure and make sure you're okay, you're not at risk of passing out. You'll sweat like a pretty good amount like that.

And then weigh in is Friday morning.

9 o' clock in the morning, usually a lot of times if we actually do this best, you don't do much of that the night before. You wake up the next morning and you're say four pounds over. And you can actually sweat out four pounds pretty easy in a sauna. 20, 30 minutes, 20 minutes in a sauna, 10 minutes long down.

And then fight is Saturday night. So you've got 18 hours plus to put it back on.

More like 30, 36, because they're going to weigh in at 9 o' clock in the morning Friday and, and typically if we do this again, correct, all these scenarios don't always play out, by the way. It's making me get quite chaotic. You would ideally be back to your normal Monday weight within four to five hours after that weigh in. So you're only touching that final scale number for a very short amount of time. You're kind of faking the scale so you're back to that normal fight night by the next morning, like you're certainly well back normal. Now. The only difference, the only thing here is recovery. Muscle glycogen in 36 hours is close enough. If you do this correctly, you can get pretty good weight. You can actually get body weight back, no problem. The difficult part is getting brain fluid back. I'm not totally convinced that gets all the way back in 36 hours. So that's the like little bit of a challenge that you have, but there's just no way around that.

So is there an advantage to be made for a fighter who I'm just making up the weight of 147, but just pick a weight to live train and show up at 150 instead of 160, so that, okay, the drawback is he's going to be in the ring at less weight, but the advantage is he went through less metabolic fluid shift in the two days prior and maybe he's actually just physiologically better.

So there's actually a good amount of research on that of looking at exactly what happens then doing performance testing pre and post. It's not that bad actually from a performance perspective, as long as you stay within certain reins. If you get excessive, then yeah, there's been a number of folks follow the ufc. Look at Frankie Edgar. He's won multiple world championships, significantly undersized. So that works. In general though, it starts to become challenging because in the sport of mma, the weight classes are so large. In boxing, you've got a weight class every four to seven pounds. So if a guy is really six pounds heavier than you, is it that big a deal in boxing? No. If a guy is 15 pounds heavier in a grappling sport and you'll see this, like, he held me against the cage. I couldn't. She just held me down. She didn't even beat. Ideal situation is nobody cuts weight. Ideal situation is that's all gone. But how do you ever do that? Because somebody will be like, well, I'll take that advantage. So ideally, if you do it right and you can come into fight week at 6% over fight weight, it should be no problem. Performance wise, you should get there. Other than like the pain in the ass it is to deal with. You start getting to 8% fight week. Okay, it's 10% fight week. Like, it's going to be really, really challenging.

All right, let's bring this all back. We've gone probably a lot deeper into the physiology, the anatomy, the microanatomy of the muscle, but I think it's worthwhile. I think this was an investment that was worth making because now it becomes a lot easier to talk about some of the things that are effectively the application of this. And I really want to kind of go back to how we started talking about this, which was through the lens of different types of athletes that are effectively the beacon of excellence in anything that has to do with muscle. So we talked about a powerlifter. Powerlifter, despite the bad nomenclature, is ostensibly the strongest athlete at the all out max, one rep, don't care how long it takes movement. You then go to that weightlifter who's also doing a one rep. But boy, he or she is also got to be incredibly coordinated and therefore by definition, because of the nature of the movement, incredibly explicit, explosive. But it's just one rep. The strongman, he's throwing boulders and having to pick them up and throw them again and again, again, insane amount of strength. But you're not just relying on one energy system. You've got to also have a little bit of endurance, both muscularly, cardiovascularly. The CrossFit athlete, also very strong, also agile, mobile, has the explosivity, but not basically isn't as good at anything as those first three, but has something that none of them have, which is a greater degree of endurance. I think we looped in the bodybuilder, which aesthetically looks like better than all of them, has bigger muscles than all of them, but has to meet no other requirement. And then I think, I like that you brought in finally the sprinter, which is the pure, you could argue the highest ratio of power to weight and locomotion optimized. Okay, I will never be half as good as any of those six. And most people listening to this don't need to be, but we probably want bits of each of them in us, right? So let's now talk about hypothetical ways to train. And I did this with Lane, and people really liked this approach, so maybe we'll try to do the same thing. Let's go through some hypothetical case studies, right? So person comes to you and says, andy, I want you to design a training program for me. Here's what I look like now. Here's what my goals are. And the goal is a no holds barred approach to what they need to do. In other words, unless I specify it as part of the problem, don't hold back. So we'll start with the easy one, which is the untrained individual who comes to you and says, okay, I bought it. I'm all in on this. I'm willing to go to the gym. You know, Peter's already got me doing a couple hours a week of zone two on the bike, but I don't even know how to approach this strength training thing. I'm willing to put three hours a week in the gym. I want to get bigger. I had a DEXA scan, and it really showed that my ALMI was about the 40th percentile. And looking at the literature, I think being at or above the 75th percentile for lean mass is a better place to be. So that's where I'd like to be in a year, two years, three years. But I also want it to matter, you know, I want to be stronger. I want to be able to do stuff when I get older. I don't just want to get bigger. I want to be able to never enter a competition. I'm not here to enter the strongman competition. But, like, I never want to hurt. I want to be able to chop wood in my backyard. I want to be able to carry stuff around. I want to be able to travel with a backpack on any other questions you have for me before you design my program?

Andy, how many days per week did.

You say I could be up to going into the gym? Like, three days a week, an hour at a time.

Three days total. Okay, cool. So you've basically described every one of our executive clients and our Rapid health optimization program, so I can nail this one. Obviously, most of my career with professional athletes, but we deal with this problem all the time at Rapid. Here's what I would say. You've already got zone two stuff knocked out that's steady state. Here's what you need to pay attention to. You described muscle was insufficient, so we got it in our brain. We're automatically thinking we've got to put on muscle mass. You also said they're untrained though. And one of the things you're going to see quite clearly.

Oh, sorry, I sort of left out. I was active in high school and college. It's not like I've never done anything. But, you know, I've been working really hard at my job, started a family and so for the last 10 years, my only exercise has been activities of daily living, which include sometimes hiking and playing with my kids. I haven't been in the gym.

Perfect. You still described everybody in rapid health optimization. No problem. So I'm just going to walk you through. I'm going to break the fourth dimensional wall here. All right, we need hypertrophy. This is the base and foundation of everything. You're going to get stronger by doing hypertrophy at this stage of your training. Like we talked earlier, those are not always coupled. You can get stronger without getting more muscle mass very clearly. And you can get really a lot of muscle without optimizing strength. We talked about that. At the end of those spectrums, you're at this end of the spectrum, the opposite. Those are going to be basically linked at this phase in your training. So we don't have to do both. You can do one and get both adaptations at the same time.

Because I'm so low on the curve, anything is going to give me a bit of.

In fact, we can get that from not even lifting weights. Because in fact, of our training studies, you'll see that equal adaptations in muscle size hypertrophy from even steady state cycling initially for six to eight weeks, you'll see equal. All of our concurrent training models and studies show the same thing. Like not only is there not an interference effect at this stage, it's a complimentary. In fact, a study came out more recently showing six weeks of endurance exercise, steady state cycling prior to hypertrophy actually enhanced end result muscle growth. So spending time initially getting physically fit before trying to add muscle mass for someone like this, it's a very fruitful investment.

So the fact that I've been doing my zone 2 for 2 months actually has you pretty happy?

Super happy. Okay. I'm also thinking, all right, you mentioned longevity physical function as we move down. You also mentioned, you said three years from now or something, which tells me your mind is really thinking about long term investment here.

That's right. Peter has Me committed to this is not about looking good in my bathing suit in six weeks. I'm not in a rush.

So one of the things that you'll see very specifically with aging is a loss of physical function. And that's more geared for power. In fact, the rate of. You've probably covered this before. Rate of loss of muscle mass as you age is something like a half to 1% per year. Loss of muscle strength is double to triple that. Loss of muscle power is triple that. And so what are you seeing? You see a very precipitous drop in muscle power. And why is that happening? A little bit of loss of speed. Aha. So preserving, in fact, you can do this. You can go look at the world records of all sports across age groups. So if you look at like track and field, what's the world record in the a hundred meter dash and what's the world record for the 30 to this? What's the world record for the 40 to 50 year old range? 50 to 60. And what you'll see is strength sports like powerlifting. The world record through age doesn't go down that much. The world record in speed and jumping sports just falls off a cliff. So it's preserving speed. In addition, my friend Greg Grosicki just published a paper this week in Journal of Physiology, a blue ribbon journal in our field. It's the highest you get. This was actually looking specifically at single fiber contractile function changes with aging. The data here are extraordinarily clear. Have been a long. You see very little loss of function in slow touch fibers through aging, regardless of exercise or not. I sort of mentioned this earlier, but you see a dramatic reduction in fast twitch fibers and you actually don't see a drop of power. And so there's nothing internal to the muscle fiber that's going down. So another way to say this is if you take an individual muscle, it's the fiber loss that's the problem, it's the fiber size. The atrophy of fast twitch fibers is the almost exclusively the problem with aging and muscle. You have got to maintain fast twitch fiber size. Now there are some loss of total fibers, but that is actually very difficult to find scientifically. Counting total amount of fibers in a live human muscle is extraordinarily difficult. Really what we're after here is anytime I'm thinking longevity, I'm thinking primarily absolute force and power has to be preserved. And this is a fastric fiber atrophy issue. This is a target. So these are the things spinning in my head. So how is this three day a week combination interlock, just to make sure.

We translate that, Andy, because I think that was so important what you just said. You're basically looking. I'm 50 and you're looking down the barrel of my life saying you want to live another 40 years and you want to be functioning. The most important thing I can do for you in the gym is not focus on the things that you're gonna get for free. It's focus on the things that are declining so rapidly. And I will, as a corollary to that, get a bunch of that other stuff for free. But I have to focus on the atrophy of your fast twitch muscle fibers because it's already happening and we need to stave that off. And we need to put in the gym systems to support the reversal of that process. Because if I just ignore that, I might as well be that highly exercised twin guy who's doing all his cardio, but at the end of the day he can't jump off the curb. He's going to be this hypercardio athlete who's still a decrepit person in the last decade of their life.

To make it even better or worse, those fibers require specific types of training. Unless you specifically do that, you just don't have any chance of a those tissues. The other tissues aren't as like hypertrophy. Hypertrophy is pretty non specific in terms of your training application. But if you want to make sure that you're targeting fast twitch fibers like this requires very specific protocols or like you have no chance faster. Slow touch fibers are going to get activated with any activity of daily living. They're going to get activated with any amount of physical extra, whether you're doing intervals, zone two, zone six, it doesn't matter. Zone 28. Pick whatever you want. Sochets are good. It's the fast twitch fibers that require intention. And that's why I make such a big deal of it, because you can't accidentally get those. It's sort of like what we say in fighting is you can sometimes accidentally knock somebody out. There are fluke punches. There are no accidental submissions. There's no fluke arm bars. Like you have to know what you're doing there or not. So coming back to our avatar, by.

The way, I love that line because I often say that to especially my female patients who are completely untrained, borderlining on cachectic, afraid of lifting weights. They just want to do yoga all day. And when I say, look, we have a problem here, you're osteopenic and you're so weak. I am worried for your life. And they say, I just don't want to lift weights because I just don't want to get too big. And it's like, I have good news for you. The myth of accidental muscle has been fully debunked.

Fully.

Me and every other guy out there can tell you we're waiting for it to happen. It hasn't happened. The odds that you're going to wake up and think, God damn it, I'm too muscular, it just won't happen.

The vast majority of us sitting around hoping and praying and devoting most of our waking hours and non waking hours to this goal that you think might accidentally happen. You're good. You're totally safe here. All right, so we know we have to preserve pastor muscle fibers for the long term. We know we have to take care of VO2 max. This is another. I'm sure you covered this in depth. Important thing for longevity. All right. But we got some constraints we also have to be considerate of. I have not trained in 10 years. I'm going to get very sore very quickly. And if I become too sore that it dissuades further training. Now I'm going to lose you. I bought in, but that shit was too hard. I was so sore I couldn't even walk. Blah, blah, blah, blah, blah. I think in your show with Holly, she talked about making sure you start with a very low volume, way lower volume than you think. We have time. We just need to move. I'm going to be very cautious of eccentric movements. They will generate more soreness than relative. And the last part, before I give you some direct answers, is we want to start building movement patterns that we're going to need over time. And so this is an investment. We can get all that done by doing the same sort of training where we're practicing movement patterns. We're getting that stuff grooves so we don't pick up injuries later. We're not getting excessively sore. We're building some muscle mass because we're going to get that anyways and we don't need that. So if this was a six month program, because you can't write the same program for the next 50 years, what's the first six months? I guess if that's your question, zone two is out of the way. I would probably stick to fairly similar to what Holly said initially, which was, okay, something like one to three working sets of probably four exercises a day, something like that. We want to spread those across upper, lower, and kind of some different movement patterns. And we want to practice the compound movements. I'm not going to isolated single joint movements yet. Let's learn how to do a goblet squat. Okay. This is a squat. You're going to hold the dumbbell sort of in front of your chest. Great. We're going to learn to do a hip extension. We're going to learn to do a basic overhead press or some bent rows, things like that. And I'm going to spend 30 minutes on those things. I don't even really care about tracking progression at this point. We're going to track, get to get the movement pattern down. Right. Did you brace as our spine in the proper position? Are you breathing through your nose and through proper positions? Is your neck in the right spot? Great. All this foundational stuff that feels like not a big deal at all right now because it shouldn't be. But we're making sure boxes are checked so that when we start progressing load later, that neck doesn't start getting irritated and we're just being in that position.

Okay. So we're basically completely optimizing movement patterns. We're making sure we don't hurt ourselves. We're learning new skills. We're learning skills of exercise. Let's now go to the next six months. So I come back to you, Andy, and I say, you know, this has been great. Like, this is not as difficult as I thought it was gonna be. I've kind of enjoyed going to the gym. And honestly, like, I even see a little more definition in my arms and my legs and I'm a little hungrier, so I've been eating a little bit more. I haven't lost any weight or anything, but my pants fit a little bit better. I'd like to take this up a notch. I can't commit more time though, Andy. Three 60 minute spots is all I can get because I still got to get my kids from school and work is just as demanding as ever. But how do I increase the desire to be even bigger and even stronger and even more functional?

So now we have to start investing that 60 minutes in those three workouts into different sections per workout. So we need to start doing something to start addressing power and speed. I'm going to give that the first 10 to 15 minutes though. We don't need to go nuts now, but we need to introduce those movement patterns and those velocities and those tissue tolerances we call it. So your ability to land and absorb, it's not creation of power, but it's the back end how did I stop that movement? How do I land from it? We're going to continue to invest in the muscle growth. Now we can start pushing the pace a little bit and then we're actually at the end start investing in either muscular endurance and or interval stuff. So if we're still continuing to do zone two, that's great. But we haven't worked on getting heart rate up, coming back down, and regulating that whole piece. So what's that look like? The first 10 or so minutes of all three workouts per week, we're going to do something in basic movement patterns. So let's imagine a box jump. We'll do a box jump. We're going to jump from the ground and land on a box that's say 18 inches in the air. We're going to practice that movement pattern. I want you landing on the box, not on the ground. That reduces the eccentric landing because you're going to be absorbing way less. So you're not going to get out of sore, but you're going to have to pop a little bit. You have to jump to get up there. And we're bracing that movement pattern. I want to probably do something.

How are you determining that height, Andy? 18 inches seems really high to me. How do I know if I shouldn't be 12 to start? What level of fatigue? How many times would I do this so that I can gauge how high it needs to be?

There should be no fatigue. This is simply about high. This is load tolerance, then low tolerance, and it's introducing power. Okay, so you're going to start learning how to move fast, but you're going to do it in a safe thing where you're not going to pull a hamstring.

And just to be clear, Andy, I don't need to compete in sports. I don't play basketball anymore. Are you sure you need me doing this? Because all I'm trying to do is I just want to be able to pick up my grandkids in 30 years or 20 years.

Yeah, a hundred percent. So in order to pick up your grandkids, you need to not be in the hospital. You need to be not living in an assisted living home. Do you know what puts people in an assisted living home? Falling and breaking a hip. The connection between morbidity, mortality with a hip break is extraordinary after the age of 60. It's not even 90. It is 60ish. Large reason people fall is they actually don't have foot speed. What do you mean? If you catch yourself, your toe on the corner or you slip you have to have the foot speed to be able to put your other foot or that foot back out in front of you in the proper position. Then you have to have the eccentric strength to stop that fall. And so I need foot speed to get there and then I need eccentric strength to brace the fall so you don't land and break your hip. That's what's going to keep you playing with your kids when you're 60, capiche?

Yeah. Even though I don't want to be a quote unquote explosive athlete, I still have to kind of train like one in some part.

And I'm asking for 10 minutes of your workout.

Okay.

So I want to keep you there. You can imagine the. I can continue to give you examples and analogies, but this is. If you want to go for a hike again and you trip or you need to be able to get up and do a little scramble, your 10 year old grandkid is going to want to go up that rock. You got to have a little pop to get up there too. You want to be able to pull yourself like all these things. That's what's going to keep you from going. No, you know, I'll just sit down here and wait. You go ahead and go.

Yeah, exactly. I had a patient once say something that I love. I asked him kind of what were his goals for aging and he said to always be able to go to my kids and grandkids. And he meant it both micro and macro, meaning I never want to be in the position where I can't get on an airplane and travel and go wherever they are. And I never want to not be able to go physically in the moment to where they are. I thought it was just a very elegant explanation.

The second part's brilliant.

That's so good because that's the example there. I'll wait here versus no, I'm going to come with you up that little rock.

It's the water slide. It's. God, I don't want to climb up those stairs. It's seven of them, but it's all the little stuff. I have two little kids, so I'm very in the world of what a four year old will do.

So what are some other things that we would do in that first 10 to 15 minutes? So I love the idea of the box jump with landing on top. So you don't have that huge, massive deceleration. What about bounds, skips, things like that would all be in there.

Yep. Medicine ball throws are great. Medicine ball slams are great. Medicine ball tosses up in the air, high as you can go, as far as you can go behind you. These are reinforcing movement patterns you built the previous six months. Proper hip extension versus low back extension, et cetera. It is also doing what we call triple extension. So you're simultaneously explosively extending the hip, knee and ankle. And this is a very important human movement pattern. You can do that without jumping and landing by throwing a medicine ball, tossing it. If you go to plyometrics, you have to be a little bit careful here. Plyometrics are totally safe for all ages as long as you account for volume. You just can't do too many of them at too high of an intensity. In this case the eccentric load. So jump rope, a five minute jump rope is just plyometrics. When you go single leg to single leg, you start increasing risk. So if you're to jump from your right leg and land on your right leg alone risk. But two leg to two leg is very easy. For Pete's sake, you can play hopscotch. Hopscotch is just two legged. Plyometric to single leg to back forward progression, lateral. It's a wonderful little exercise.

Isn't it interesting when you go to a playground and watch kids play to realize the they're not being told to do this, just the inherent ability that they have to be explosive. And as you said, how that deteriorates with age. You just can't imagine watching a group of 40 year olds sitting around just deciding let's go play this fun game where we jump around. I mean you do that if you're playing a sport. You do that if it's part of your pre programmed workout. But it's not the equivalent of neat.

There's no spontaneous.

Yeah, it's not spontaneous.

Last one I love is actually don't get thrown off by this word, but I love sprinting. Just give me 70%. You would be surprised of like whoa, it feels like great slash, terrible. But if you can get on like a woodway or a control situation like that and you can just do some like 70% spritz. Just getting through the motion kind of a tempo is what you. If you're a runner, like you'd call it that type of stuff for very short distances. I'm talking like 15 seconds. Just kind of stride it out. Okay, slowly come back down. Wait a minute or two. Fully recover here. Okay, ready? Roll back into it. Two, three, four seconds and then give me pick it up for five seconds. Six seconds. Okay, slowly back down. Just getting used to handling Movement and being an athlete and moving and not being everything is locked into a position where it's structured and secure and all that stuff. So I really, really like movement, athletic movement and multiple planes. Four people. The last example I'll give you is just back to like high school and middle school sports. We're going to play 10 minutes of basketball, go to the court, we're going to shoot, drive it up and down. We're going to play racquetball as our warmup today. We're going to play badminton. You get over there, I get over here. Like two and two. Badminton. You can do a lot of little different things that are going to be multiplanear. It's going to be speed, agility, quickness at this point. So you're going to get change of direction. All this stuff is the foundation piece you need to get to when we actually do some speed agility drills next year or wherever we're going to get to, which is going to be part of your plan. So those are all a bunch of examples. I would recommend doing a different one each day of those three. So it's Mondays, we're going to do med ball stuff. Cool. Wednesdays, it's going to be pickleball. And then Fridays we're going to do some jump stuff and some medicine ball, horizontal throws, whatever the case is. Or it can be jump rope, it's going to be hopscotch, things like that. I'm not against bounding broad jumps. I typically want to start here, two on two. So two leg, leave two leg land. To this person, they don't have to be forward. They can be lateral jumps, they can be combinations, they can be all kinds of things. You honestly be surprised. Like, I don't want to say this too loud in case somebody hears, but that stuff's actually kind of fun. It's pretty fun. You're going to get a lot of giggles. You're like, I haven't jumped like this. Like, they're going to feel weird and it's going to be way different than what they're thinking. The sync training thing is you'll get some giggles. So that would be my intro to every single bit.

That's your opener. That's 10 to 15 minutes.

Now we're hot. Now we're ready. Now we're going to move into strength training. And so what I would still do is keep the same structure, total body on all three days. Because here's what's also going to happen once a month. You're going to miss one of those Days for more, your kid's going to get sick. I got too busy at work. Blah, blah, blah, blah, blah. If you do body part splits, you'll.

Start missing big things.

You're going to miss chunks. So I like in these situations, these people, I want whole body every day. You're going to recover just fine. I would do a different rep range. So I would do something like Monday, it's going to be, say, three to four sets of five to seven reps. You're going to be able to go heavier. You're going to have a minute and a half rest between each one.

What RPE do you do there? Seven to eight, Just for folks listening. At the end of that, you're finishing with maybe two reps left in the tank.

Yep. Like for the working set for Wednesday, let's go 15 to 20 reps percent. So now you're actually going to have less. You're probably going to drive less soreness because you're activating probably less. You're going to get more of a pump. You can actually like, push the repetitions and you can work harder and probably get a little bit less sore. And you'll feel more of an acute satisfaction for a lot of people. Right. Like you feel the feeling in your risk has gone down a little bit. Then the third day you could go really wild and you could do something like isometrics, where you're just holding positions. Very good for joint, very good for connective tissue, and very good for just doing something different. All three of these are equally effective for hypertrophy. Your gains in muscle size are going to be identical across the board. And now you've introduced three different elements.

Let's talk a little bit about isometric. I'm now going to deviate from my patient back to being Peter and interviewing. We didn't talk about it, but everybody's probably heard of an isometric. It's force generation or muscle contraction without movement. Big part of my recovery from shoulder surgery. I had a labral repair a while ago and this was the first thing I was permitted to do was begin humeral extension and flexion without movement. And, you know, interestingly, I hadn't really spent much time doing isometrics outside of that. With a few exceptions. There were some dedicated. A lot of isometric deadlifts I was using as a precursor to deadlifting. Just a great way to warm up. But I don't think I was actually aware that isometric training could generate or elicit the same hypertrophy response as isotonic or movement based Contraction. Why is that the case? How does one know where to be in the range? So, for example, if I do a bicep curl, I can get every range of the bicep, but do I know if there's an isometric benefit to being here versus here versus here?

So are you 10% flexion? 30% flexion, 110% flexion. I have so much to say on this one. Are we good for two and a half? Three? We go another three hours.

I will say this, we're clearly going to do a part two of this podcast.

There's a whole show on this area because of this. So you actually sort of invertedly asked, well, what's actually driving muscle hypertrophy? It's not the workout per se, it's the stimuli. So then what are those stimuli? That's a whole conversation. And the reason hypertrophy is training wise in terms of what reps to do, what type of exercise I consider to be the least scientific. Interesting is because it takes the least precision, because the mechanisms are so spread across different areas. You can go from A, B or C, you don't have to have all three. You can also have A and B, or you can have anc, or you're going to get there. The muscle is very much listening to that signal. It's not so much for other things. And so it's very easy to kind of land accidentally in hypertrophy range. As long as a couple of things happen, as long as sufficient overload occurs, you're going to get there. So this overload can happen over time. It doesn't even matter how you achieve the overload. More volume, more reps per set, more weight, extra range of motion. All these things are different strategies for progression. And if that happens, you're going to be in a pretty good spot, barring the mechanism session is we're just going to get so far down the road here we're never going to come back and answer your patient question. But that's one thing to think about. So isometrics, the short answer is they're going to be activating a number of those same mechanisms. So you're going to cause the same amount hypertrophy. Where do I be in that range of motion? Well, there's no answer there. This is the primary downside of isometric.

This is where you'll mix it up, presumably.

Certainly mix it up. In general, muscles respond best to being at the highest stretch. So if you can have that thing at the highest level of extension generally, but it kind of depends on the muscle you're putting more. In fact, you can actually take a muscle fiber and hang it vertically and hang a weight at the end of it and it will grow. So being stretched that long is a very strong signal to grow. And so when you generally train a muscle over a large range of motion, you're putting the muscle on a larger stretch. And so that signal alone activates that whole anabolic cascade for hypertrophy. So my default if you're going to do an isometric is to do it closer to the end range of motion, where it feels the most tight, if you will, not the finish position. But it very much depends on what you're after. Because the thing that gets tricky here is many muscles are single joint. And so if you look at the soleus, as we talked about earlier, that crosses the ankle joint only. But if you look at things like the gastroc, it crosses the knee and ankle joint. So putting the soleus in the right position is only dependent upon the ankle. Putting the gastroc in the right position is dependent upon the ankle and the knee. And so if the knee is flexed, you're never going to get the gastroc to contract properly. You can't get a full contraction of the gastroc and a reflex knee. You have to have an extended knee and extended ankle because it's going to just get short on one end of that spectrum. And same thing happens with the biceps muscles.

So translation, a seated calf raise only works the soleus. A standing calf raise works both gastroc and soleus.

Correct the same thing with like a tricep push down versus an overhead tricep extension behind neck. Now you're talking. The triceps muscles across the shoulder joint are now going to be put on stretch when you go behind the neck and bada bing, bada bing.

So that's why I recently saw a study that looked at tricep extension in flexed versus extended humeral position. And the difference in muscle mass was significant when the arm was up, when the humerus was flexed.

Right. We see this in the hamstrings. We see this at the glutes. Muscles like to be put on stretch. Well, they don't like it, but you're going to get.

They respond to it. Yes. Get the better compensation.

Now, that changes in a situation like what you were dealing with. Because the example I use oftentimes, like, imagine somebody who's kind of get like a nagging elbow pain. You're like, man, every time I do a lot of bicep curls and stuff My elbow just gets me. Okay, great. Can we actually train the biceps without aggravating the elbow? Hard to do, because no matter which brachioradialis biceps break, they're all going to cross the elbow joint. What if that's a nagging shoulder problem? Aha. Well, now if we do like a preacher curl, which is when your arm is out in front of you, you're shortening the biceps part that cross the shoulder joint, and you can still work across the elbow joint, and it will not aggravate your shoulder. If you were to do an incline curl where your shoulder and arm is behind you, you're putting it on stretch across the shoulder joint. Now, those bicep curls are going to aggravate your shoulder, theoretically. So, going back to isometric question, it depends on your specific surgery and whoever you're obviously talented therapist or whoever was running that had you on, I'm sure they were putting you in a position to get a little bit of activation in the joint that they wanted, but not actually aggravate and let the thing recover. So the angle you pick is dependent upon a number of factors. It could be sports specific. So if you take the case of like a power lifter, you may just want to train in your final position of your squat and get very used to being strong there. Going extra depth is only just going to make you worse as a lifter because you're now traveling further distance and you got to do more work. So there's no easy answer. That's one of the reasons why we generally frown on isometrics is they just take a lot of intention, where if I generally just say, do a normal full range squat, then you don't have to guess.

But if you had an athlete who said, look, even at this stage, I'm really willing to do a little bit of isometric, let's say using the squat as an example, you're going to load the bar in a low position, they're going to stand under a weight that is much heavier than they could ever lift and basically push up against the bar. I mean, how are you doing an isometric squat, for example?

Do this in a number of ways. So you can do a bench, you can do squat, you can do anything. So typically what we'll do is you'll put the barbell in the rack. And so you can imagine like a.

Squat rack, and you raise the arms of the rack.

Yep. And you have safety pins that run horizontal, perpendicular to the ground. So instead of putting the bar on top of those, you put the bar below them. And so you just lift up against the rack and nothing moves. And so you can set your position, whether you're putting it behind your neck for a squat, whether you're putting a bench below it, and you just push up on those. We actually have these built in the lab. And on the bottom is a force plate. And those allows us to do an exercise or movement called.

So that's how you can tell how heavy they're pushing.

Right. And so we can measure force produced into the ground at various positions.

Does isometric offer any other advantage over safety?

Yeah, there's a ton of advantage to it. The advantage is you have less degrees of freedom, less moving parts. So if I get you in a position, say in a squat, and your spine looks good, and everything looks good, there's a very low likelihood you're going to get out of position. The back squat is extraordinarily complicated. There's a lot of moving parts. We have degrees of freedom at the ankle, knee, hip, low back ribs, shoulder, neck. In an isometric, nothing moves. All we have to deal with is compression. Sometimes compression is aggravating, axial loading being specific. But axial loading is also fantastic for momentum density. So the reason I threw isometrics in for our client, kind of working back to is you were talking about. You mentioned that as one of the problems. It's like, okay, great. We know we can smash actually on these people with very low risk and get a lot of stimuli there and not have to worry about getting in position at different parts. And we have this thing called the strength curve. When you do a typical isotonic movement, like a normal lift of a normal dumbbell or something, you're only going to be challenged in the areas in the range of motion where you're the weakest. So if you look at our study on lifting with bands like heavy bands from a deadlift, you're going to lift at the very, very bottom, and you're going to have very low load. In fact, you could have as much as a 40% reduction in load at the bottom. But when you come up, up, and you start crossing the knee joint and you start gaining mechanical advantage, it becomes extraordinarily easy. But the bands start getting heavier. And so the actual tenacity that happens throughout the entire thing is fairly equal, if not, well, certainly greater at the top. So you can train that whole area of the strength curve with things like this is why people use bands and chains and things like that, is to be able to produce more resistance in areas where they're stronger and they're not being held back by the weakest position that they're in. To wrap that up, then you can actually then train that. So then you can go into that weakest position and do an isometric in that weak position without having to put a whole bunch of load on your body. Like you would need to get in.

Their spots, getting to and from it.

Right. So it's nice because with people like this, you could put her in like an RDL position, like a hinge position, which is a kind of a complicated movement and just be like grab and pull and nothing moves. And they can pull as freely and as hard as they want. It's very difficult for people with a low training age to truly express maximum force output on a free range motion because there's too many variables. I'm in the right position. Is my back safe? Am I losing my balance? If I just say grab this part, pull on this part as hard as you possibly can, and nothing's going to move, People can just go nuts.

So walk me through how you do that. For an rdl, for example, Example, you're going to do kettlebell, dumbbell, barbell, rdl, barbell. Okay.

Set the barbell in the squat rack, put it underneath and set the height of those safety pins to whatever height feels comfortable for you. And so you'll then get in there and do that RDL and you'll pull up against that bar and nothing will move and your back will feel comfortable. Wherever that range of motion is for you, your glutes can be there, your feet can be in the right position. We get total foot, big toe activation, get that whole arc.

You're doing this two foot down.

You do one legged, you would most likely start this thing two footed. Just to develop for this person in this goal, we're trying to let them express peak force output and feeling comfortable.

And how long do they need to stay in that isometric position?

3 seconds to. Some of the times we with our athletes will go up to five minute asymmetric holds.

Up to what?

Five minutes. You can do like we'll do rear for elevated split squat, home hold, isometric hold for up to five minutes, which presents a tremendous neurological challenge.

I'm generally up for things that are ridiculous. I don't know that I could do it isometric hold for five minutes.

You've ever done like super high volume lunges or split squats? Like hundreds, Things like that? Yeah, yeah.

I did a four minute set of split squats the other day.

Yeah. Okay, so just get in that position. Rear foot elevated just a little bit and just hold it for two minutes to see. It's a fun task. You'll enjoy it.

No, I'm sure I will. Where are you creating the resistance for them? You're just, again, same thing, bar over shoulder.

In that particular scenario, you don't need any time will be your resistance.

Oh, in other words, it's isometric only in that you're just holding a position.

Correct. It's just like doing a wall squat. It's like a better version of a wall squat, if you will. So you can go for a long time to kind of come back here, racing here. That's what we'd have those three separate days.

Yeah. This is interesting, Andy, because I never. So I can really see now how you could create a full day of isometrics if you wanted to go down that rabbit hole. It's easy. That one of those days is purely isometric.

In this situation, too, even holding, you could hold a plank. That is an isometric exercise. Right. It's the one that people love. Holding a hip extension position and just making sure you can actually continue to have your glutes on, utilize. You mentioned the squat earlier. So you can do this in a couple of ways. You can actually go all the way down and truly hold that bottom position. That is challenging, though, if people don't have the right positioning. If you do, it's a or you can close. It's a great way to build it. So I wouldn't be opposed to that if they're close and doing 30 seconds. But here's the difference. I would cap that as failure. Not when they quit or get fatigued, but when they break position.

This is one of the tests we do with our patients, and the Excellent grade is two minutes in a full 90 degree squat.

Why do you stop at 90?

No, better than 90. Lower than 90. So parallel thigh parallel squat.

Sorry, my size parallel.

That's just the standard we've picked. But the failure, as you said, you know, the goal is two minutes. Can you go two minutes and you fail? Not when you give up. You fail when you basically shoot your butt out, lunge forward, make a compensatory movement that is beyond that. We use that as a great test of strength without having to put people at risk.

You could easily generate that day. You can also do. So one of the things we haven't talked about yet is it's important that you're moving in multiple planes. There's three major planes of movement, which is frontal, sagittal, and transverse, which Basically means you need to be moving like up and down like a squat or you need to be moving things away to you and towards you like a bench press. You also need to be moving things laterally so like a lateral lunge as well as twisting and rotation. And so you want to pick a few things in these areas. The other thing you want to keep in mind is single leg versus either split stance or unilateral. And so there's no perfect number you have to hit here, but you would want to select something across those three days where you're not doing everything is two foot supported. So you mentioned one footed rdos. You could do step ups. You can do split squats, you can do rear fit elevated split squats. There's a single leg press, single leg extension. There's just a lot of ways you can do that. So you'd want to keep kind of an eye on that going. Like, all right, is everything. I'm using barbell and everything I'm using to. Okay, maybe that's not ideal. So maybe I'm going to use a kettlebell over here because I can actually do this movement over here with a rotation and a press. Okay, great. But now I'm going to pick dumbbell for this movement and this movement over here, I'll use a machine. Lovely. Great. And now you're in a really nice position where you're not getting held back so much by technical demands. This person is only six months in a training. You don't want their whole day being learning how to do a movement and then boom, that 60 minutes goes up. But you also don't want to be like, well, these are too hard. So let's just stay on machines the whole time. It's not a long term investment, so we want to invest a little bit in growth. 20%, 60% isn't what you need to be here. 20% long term development, 20 other percent is fun. That's how we generally think about the 60, 20, 20 split. So that's how we split it. So the last piece here to wrap this thing up is I would finish every session with something that either gets close to a max heart rate or is a personal pain point.

I always close off with Katsu and there's some intense pain, but my last thing is always two minutes of BFR on the air bike, which combines two beautiful personal pieces of pain.

What's the thing that they love to hate? What's the area that they want to grow? They hate their triceps. Okay, great, we're going to Finish the session with a tricep blast. We're just going to smash it. They did some feel like, yep, okay, I got the thing done. One thing people hate is when they're not listened to. And when they come in, they're like, I want to get my glutes in to get stronger or whatever. And you just like they're working them, but they're not real. You want them to walk out.

It's the double down. Concentrate on.

It's one little session. It could be whatever. We used to do this on Saturdays with the NFL players because Saturdays were mostly a recovery regeneration day, which means they would never show up. And so it was like, hey, Saturdays are a gun show. We're doing nothing but biceps and triceps. Be like, all right, who showed up to you pick one, you pick one, you pick one, you pick a tricep. Like everyone got to pick one. And we just do these ridiculous made up circuits. And then they would all just get super pumped in their arms and it was like, all right, now go do your 45 minutes, go see your PT, go see your athletic trainer. Like people are people. Give them a little bit of what they want. And just make sure in one of those days we touch high heart rate one way or the other.

And when you touch high heart rate, a classic way that one might do this would be a Tabata type exercise where it's basically four, four minutes of intense work. What are some ways that you might recommend getting high heart rate in there? Do you want to do it with jumping? Do you want to do it on a bike, on a rowing machine? What do you like to use?

We typically want to keep away from eccentrics. This is where CrossFit is done very poorly. It's like you're putting your in a position of fatigue in very risky situations at a lot of times. So something that's for this individual. Again, let me clarify that comment was regarding this individual. Probably not a great thing for other individuals. It's fantastic. You should totally do it. Air bikes are fine, rowers are fine here. If you really want to, you can actually do specific breath hold manipulation. So if you just alter breathing. So this is CO2 tolerance. CO2 can get very, very high. You can deal with the suck without doing any physical work. This is all the stuff we've done at xpt Live in the pool. You can do a lot of stuff with weights underwater and just changing what you're doing with ventilation. And you can get to a level of pain very quickly that requires very little physical Trauma. There are lots of ways we can play that. Simple examples would be do a 10 second sprint on the bike and then go into a breath hold. You want to see your heart rate shoot up incredibly fast. And then you're going to come back out of that and you got 30 seconds, but you're going to go nasal only, recovery breath.

How long breath hold, by the way?

Well, you're going to see, but the goal is maximum.

Okay. In other words, go 10 seconds all out, breath hold until failure. 30 second recovery, nasal only. How many rounds of that?

Let's see if you can get three.

Okay.

One might be the answer though. You might go like, I'm not even close to ready to do this again. Two might be there. You can also do that inhale hold prior to the sprint. So you can do an inhale, hold, breath in hold, and then hit that sprint. I mean, there's just a ton of ways you can get to playing with CO2 tolerance if that's part of the equation. And again, you'll see your heart rate get up to damn near maximum. That doesn't require much physical work. So if you need to spare joints, you need to spare soreness, you can do spare energy, but you want to get that stimulus thing. There's lots of tricks that way you can play.

So, Andy and listeners, I think we have some really bad news and some really good news. The really bad news is we've probably been talking for three hours and we.

Got one case study done.

Yeah, we've got one case study done and we haven't talked about a ton of physiology that I had in my 10 pages of notes here. What's really sad is I had 10 pages of single space notes that I wanted to talk about. And we got into the first. I'm not being facetious, we got into the first half of the first page, at which point I threw it over and totally rerouted everything we were going to talk about based on your answer. And we have nine and a half pages of notes, plus a whole bunch of questions that we didn't get to here. So the bad news is there's zero chance we're going to finish this podcast now. The good news is I hope you will come back and we can do this again relatively soon so that listeners can have a part two of this discussion, you know, hopefully within a month or two months of part one. Is that something you're. I'm going to put you on the spot and ask you this. You're willing to give us another episode here?

I think we can. I'll talk to my people, your people.

Talk to my people, and then we'll figure it out. Yeah. Andy, this has been super interesting. Literally will be putting a few of these things into practice tomorrow for me in the gym. If I'm putting things into practice that are in just the purview of the guy who's never exercised, I can't wait to get into more. My phenotype, which is, hey, I do exercise, but how do I take it to the next level?

There's a lot of interesting things we can do when we get to that. Fun conversation about everything from like if you want to see behind the veil of professional athletes, you want to see what they really do for sleep, you want to see what they really do for nutrition, you want to see what they really do for training. We can go down that route too.

Well, Andy, this has been amazing. Thank you very much for your time, your expertise and I'll see you again in hopefully a month or two.

Sounds good man. Thank you.

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Sam.