Peter Attia MD239 ‒ The science of strength, muscle, and training for longevity | Andy Galpin, Ph.D. (PART I)
EVERY SPOKEN WORD
150 min read · 30,146 words- 0:00 – 0:08
Intro
- PAPeter Attia
[upbeat music] Hey, everyone. Welcome to the Drive podcast. I'm your host, Peter Attia. [upbeat music]
- 0:08 – 7:09
Andy’s path to expertise in exercise
- PAPeter Attia
Well, Andy, uh, you know, it's wonderful to see you, uh, 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. Uh, perhaps there will be an in-person chance the next time.
- AGAndy Galpin
Yeah. Yeah, I'm excited to, to be here this way. It would've been more enjoyable in person, but, uh, we'll make it work.
- PAPeter Attia
You know, I've wanted to speak with you for, for quite a while, and, and I think listeners to this podcast are not, uh, not strangers to the idea of how much of an emphasis I place on exercise. [lips smack] Um, I've said it many times before, I'll continue to reiterate it until the data suggests otherwise, that there's really no more potent tool to improve, uh, longevity, meaning extending the length of life and improving the quality of life and exercise. [inhales] And that includes nutrition, and that includes sleep, and that includes the entire, entire pharmacopeia of medications, supplements, drugs, hormones, et cetera. [inhales] So [clears throat] it's probably for that reason that I would say that exercise makes up a disproportionate amount of the content on our podcast. [lips smack] And of course, within exercise, I tend to divide it really down into these different pillars of, of strength, stability, uh, and, uh, cardio respiratory fitness, which of course then gets further subdivided by the, by the metabolic state and en- energy state of it. And of course, what we're gonna probably talk a lot about today is, is strength, but also all of the things that kinda stem from that, like hypertrophy and, uh, and, and, 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, uh, even, you know, frankly out of high school, college, like, you know, what was your athletic background and what, what made this be something that you have, you know, kind of dedicated all of your time to?
- AGAndy Galpin
Sure. I, I guess initially I need to state a conflict of interest, which is I'm an exercise scientist, so if you wanna start giving more credit to exercise for longevity and wellness, like I cannot be more biased into that lane, [chuckles] um, especially within exercise science strength training. So I've been waiting for 30 years for this to happen in the field. Uh, and so now I get to prove that all my preconceived notions are actually holding true.
- PAPeter Attia
[laughs]
- AGAndy Galpin
And I will refuse to change despite what you said, I will refuse to change despite what the data suggests.
- PAPeter Attia
[laughs]
- AGAndy Galpin
Um, no, for, for really, I grew up in a very small town in southwest Washington. Uh, so I played everything in high school. Uh, c- football, basketball, baseball, track and field, the whole thing. Um, 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, um, Arizona and worked at a facility training professional athletes. I went back and got my master's degree in human movement sciences, which is just a other fancy way of saying kinesiology or exercise science, and then got my PhD in human bioenergetics. Uh, so and in 2011 I got that, came out, um, 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, the condensed version of the academic path. Um, now I think probably more important to your question was college football and then training professional athletes started, uh, at that point as well, and then I started competing in weightlifting, which locally is Olympic weightlifting, that version of it, uh, and then combat sports a lot after that. So I've continued to work with athletes the entire time. I'm still over the last 10 years, you know, running my labs, running our research. Uh, I've s- I've worked with professional athletes, um, in just about every sport with the exception of racing. [chuckles] I have yet to get into Formula 1. Um, but, um, Cy Young winners, MVPs, all pros, you know, the whole, the whole thing, Olympic gold medalists, et cetera. So my, my research actually and my in- interests really come back from the exact same point, and if someone were to return to the very beginning here, which was I was a decent athlete, uh, 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 gonna be an all pro, I was gonna, you know, go to the next level no matter what. That wasn't the case. So when I did things better, I 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 w- know where I got rewarded. So i- if you're not good enough, then it's just like doesn't matter what you do, you're not gonna play at 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, you know, professional level caliber or even Division 1, but I was like, the difference is do you wanna 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 gonna have no chance. And where I'm from, people don't, don't really go to college in general, and they certainly don't play college sports. Um, 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, uh, that often. So that's re- that initial passion came from. Uh, additionally, the, 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 was always better than you. But losing because you didn't prepare was totally unacceptable. Um, we all... Most of the kids I grew up with, we worked on farms or we cleaned stalls, we did something before school. You know, my parents worked in construction, like built things. 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 it's 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, as I'll finish up the, the background is then when I started moving past my athletic career And that's when I f- 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 gonna help them. They don't have funds. And so I, 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 wanna get, help you here in this journey because that's something that's gonna reach my soul of let's give everything we have, have to do something really special that no one's gonna care about besides you and I, and, like, your team and your family." And so that's what drove it initially, um, and that's what really put me in this position, and that's what put me in the position to continue to go and get my master's, to get my PhD was y- you gotta learn more. There's more things going on here. You've gotta find all the answers, you know, that you can. Uh, and if you're doing anything less than that, what are you doing? Uh, you're just giving up. So that's, that's the background of sort of how I got here and, and, uh, what I do now.
- 7:09 – 16:03
Contrasting strength, power, and force production and how they inform us about training for longevity
- PAPeter Attia
Now, you mentioned briefly, um, uh, Olympic lifting. Uh, we've had Lane Norton on the podcast several times. Lane obviously is a, a very successful powerlifter. I think folks are kind of familiar with powerlifting having the three lifts, and it's really about, um, you know, 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, what are the physiologic differences between those two? And, and I'll preface the question for the listener by saying, again, even if you never plan to powerlift or [chuckles] Olympic lift, this is going to be germane to our discussion.
- AGAndy Galpin
Yeah, so this is very... Uh, we... There's actually a, a... Fairly recently we published, uh, 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, uh, 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, not how many times you can do it, not 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. You have 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 it's, that's effectively what it is, right? So it's really an expression of pure strength. It's not really an expression of power at all because the speed component's 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, et cetera. So we're already out the gates, we've confused people because the name of the sport is called powerlifting des- despite the fact that it is not a power exercise, nor is it determined by power. When you move over to Olympic weightlifting, it's the same basic idea. There are now two lifts instead of three, one lift 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 then 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. Right? 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 the clean or the snatch. And so it is an expression of tremendous strength, but there's this, a force or a 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 the powerlifter is just working on powerlifting. So the confusion there is, and this gets worse when we start roping in things like strongman. So str- strongman is fantastic because, again, you think of strength and you think, "That must be the biggest expression of strength," when 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 back to the powerlifters. So now you've already confused powerlifting, weightlifting, and, um, strongman, and none of those three things are actually explaining what they do correctly. Um, we can keep going on with multiple sports here, but this is, this is the gen- the, the core of the problem. The reason you're, I think you're bringing this up is this also explains training adaptations, and it's exactly... It, it's a perfect way to outline to understand what's happening. So if you train like a powerlifter, 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 in more, what we'll say life functional movements, so walking, carrying, uh, lifting objects, uh, and doing it probably multiple times. So the only difference between all those three, and the last part I'll add too, is with Olympic weightlifting, the amount of coordination required, because you're gonna 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, it is, uh, the advantage goes to weightlifters, you know, big time there. You're not gonna see that. Powerlifting is very controlled. It's a very specific foot position, hand position. There's no movement ideally, and it's very, um... It's typically you're minimizing range of motion intentionally because you want to minimize work, right? So 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 gonna win. And that's why they take those funny positions. That's why Lane has both of his feet six miles apart and, and does a... He calls it a deadlift even though it's a fake movement.
- PAPeter Attia
[laughs]
- AGAndy Galpin
I'm just kidding. I mean, s- Lane and I go back many, many years, so, um, he would laugh at that joke, I promise.
- PAPeter Attia
[chuckles]
- AGAndy Galpin
So that's the basic foundation of, of the difference here. You have a very sport-specific application for powerlifting. Weightlifting is very sport-specific, but it's a much greater range of motion. It has those other components, and strongman is, is kind of addition. I didn't know... I know you didn't ask about strongman, but I-
- PAPeter Attia
No, no, no. But I, I, I-
- AGAndy Galpin
... threw it in there 'cause it kind of rounds the loop out
- PAPeter Attia
... yep, I love that you brought that in. Um- Before I go onto 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. Uh, you wanna throw in a little bit on hypertrophy within the, that trio?
- AGAndy Galpin
Yeah, great. So you can actually add a couple of more scenarios here. Hypertrophy would be more of your bodybuilding, which Layne has also done. Holly, uh, I think you just had Holly on, right?
- PAPeter Attia
Yeah, yeah.
- AGAndy Galpin
So Holly can smash with physique, whether you wanna call it bodybuilding or general physique or any stuff, is simply improving, um, [clicks tongue] 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. Doesn't matter if you're strong or fast or athletic or any of those things. And so there, in fact, this is... It's so interesting, [chuckles] Pete, that you started the conversation like this because this is day one of my strength and conditioning courses of 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. And the last two pieces, just to throw this in there, would be actually if you think about the competitive circuit training sports-
- PAPeter Attia
Like CrossFit, for example
- AGAndy Galpin
... Totally.
- PAPeter Attia
Yep.
- AGAndy Galpin
No offense. I'm just meaning-
- PAPeter Attia
Yeah, yeah
- AGAndy Galpin
... as a sense of they are very strong. They have a lot of muscle, but they're not nearly as strong as powerlifters, you know, like-
- PAPeter Attia
Yep
- AGAndy Galpin
... as a general statement. They're not nearly as strong as World's Strongest Man, but they do a lot more repetitions. And so a World's Strongest Man is gonna win an event doing something like 5 to 15 repetitions, like something, you know, kinda depending. In 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, of number of repetitions. Oh, 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. Uh, 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, um, and asked to do things in a lot of different areas, in a lot of different energy systems and movement patterns and things like that, so it's a really interesting test of, of total physical fitness. And the last one that I like to throw in there is either, is basically track and field, and now you have the truest expression of, of velocity. Uh, 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 and longevity or sport? And if you wanna 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/lose body fat? How do I improve my muscular endurance? And now how do I improve my cardiovascular and 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 at getting faster, peak speed. The best in the world, um, at, at getting able to recover multiple days in a row. Okay, we have, so we have different models o- of that. So that is a nice foundation for all training really.
- PAPeter Attia
Yeah, I l- I love it, and, and there's a matrix brewing right now in my head as you go through that, so we're gonna come and kind of start to fill in some of this matrix as we go. Um,
- 16:03 – 29:34
Muscle energetics: Fuels that provide energy to muscles, and the importance of protein
- PAPeter Attia
[clicks tongue] let's, um, simultaneously go back to the fundamentals, but do so with, um, without any remorse for how rigorous we need to be. [laughs]
- AGAndy Galpin
[laughs] That's the greatest setup ever.
- PAPeter Attia
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? You know, what, what are these, what are these cells that we almost take for granted sometimes?
- AGAndy Galpin
All right, now you're asking me to do, like, a two-semester course-
- PAPeter Attia
[laughs]
- AGAndy Galpin
... in, in, in 20, [laughs] 20 minutes or so.
- PAPeter Attia
[laughs] Well, hey, look, I mean-
- AGAndy Galpin
You-
- PAPeter Attia
... 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.
- AGAndy Galpin
Yeah. All right. Hopefully you're ready for part two, three, four, and five of this sh- uh, podcast. Um, I'll, I'll give you what I can give you, and then we'll come back. Let, let's think about it this way. Um, [clicks tongue] number one, I like to play a little trick. You ever ask people kinda like that Jeopardy! question of what's the biggest organ in your body?
- PAPeter Attia
Mm-hmm.
- AGAndy Galpin
And people generally are going to say skin?
- PAPeter Attia
Yeah, exactly. That's what I would've said actually.
- AGAndy Galpin
Yeah, right. 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 to muscle and none of it to anything else.
- PAPeter Attia
[laughs]
- AGAndy Galpin
So-
- PAPeter Attia
So basically-
- AGAndy Galpin
... you've been warned
- PAPeter Attia
... the brain, the heart, the liver, the lungs are only-
- AGAndy Galpin
Don't give a shit to Peter
- PAPeter Attia
... but they're just there to support the muscles.
- AGAndy Galpin
00%. And if you start talking my worst enemy, the nervous system, I, I'm probably gonna hit end record and go home.
- PAPeter Attia
[laughs]
- AGAndy Galpin
Those neuroscientists just take credit for everything. It's garbage. Hot garbage, right? Give it all to muscle. Um, so you've heard my biases. If you wanna stop listening now, you can. If not, understand that that's where we're going here. And so in general, if you think about it this way, again, muscle is, 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, uh, 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, um, I could go sort of on and on and on about the, the, the physiological, the practical, the general health benefits of, of skeletal muscle.
- PAPeter Attia
And don't be bashful. This is a good time to s- to, to say those things and to expand on them because w- I've said everything you've said, but I think there's more to it. Uh, and I think one of the things you've said-
- AGAndy Galpin
Yeah
- PAPeter Attia
... I, I don't think probably is as appreciated, which is the storage depot for amino acids. Um, because-
- AGAndy Galpin
Yeah
- PAPeter Attia
... we don't really think of it that way, right? We, we sort of... You know, 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 in a mo- You know, if you're working out, it's at least a plausible scenario that amino acids are being broken down... Uh, I meaning 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.
- AGAndy Galpin
Well, it's not even a may. It's like-
- 29:34 – 41:40
The structure and microanatomy of muscle, muscle fibers, and more
- PAPeter Attia
so let's now go back and make sure people understand the structure of a muscle because I wanna talk about different fiber types as well, just to round out some of the physiology. Um, so in an effort to understand the difference between a fast twitch and a low twitch, uh, s- fa- 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.
- AGAndy Galpin
Yeah, sure. So let me go, uh, back just a little bit to understand whole human function movement. Um, I won't go as deep into this one though. I- if you just think about how you actually create movement, it, it really has three core functions. So number one, you have to have some sort of direction or signal, and this is gonna be coming from your nervous system. And so whether this is central or 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 nerves, you get that one. That's it. Don't take anything else in nervous system, right? You get that control. Now, that nerve then has to go into a, a muscle fiber and tell that muscle fiber to contract. Okay. The muscle fiber then is part two. So the cell actually has to contract itself, but that actually doesn't cause ... movement. Uh, muscles are not attached to bone. That's not how it works. So muscle fibers are c- are surrounded by connective tissue. All those connective tissue are bundled together in like a package. So if you imagine buying a bunch of strips of bacon from the butcher, and they would wrap that up in 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, and that's, that's sort of the point. You're transferring force from muscle through connective tissue. That connective tissue comes together, um, 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 f- the front end, we'll leave the neural science 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, it's, it's not plastic. Um, when we look at muscle, it's tremendously plastic, and what I mean by that is it adapts. It changes very quickly, quickly, and rapidly in response to a lot of things. Connective tissue is... doesn't have a blood flow supply, doesn't have energetic demand. It, it's just, it's kind of just there. It's... 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, uh, or negative, uh, is going to be in, 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 biam- 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 myonucleated. And so you probably remember this term from, like, med school or something like that. Um, in fact, I, whenever I talk to biology people about this, they're like, their head is blown 'cause I forget how lost in exercise science I get, both like us nerds. But y- it's, it's very uncommon in nature to see cells that have more than one nucleus, and the nucleus is the, is the, the core of the cell, if you will. It's what holds your DNA. That's what controls, it tells you when to replicate proteins, um, to grow, shrink, die, repair. So the whole control center. So the fact that skeletal muscle has many of them per cell, uh, 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. Um, you can actually... 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.
- PAPeter Attia
Okay.
- AGAndy Galpin
Um, we'll actually pick up, um-
- PAPeter Attia
Let's, we'll find that, and we'll also put that in the show notes.
- AGAndy Galpin
Okay. Um, I can actually pick up a mu- ind- 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, and you'd be able to see an actual whole muscle cell. Um, they're that large, and in fact, they can be very, very long. So they can be several inches in length.
- PAPeter Attia
A- and l- 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 element's here. This is defined also by a cell membrane, but it's a sort of a longer looking tube as opposed to a sphere. And-
- AGAndy Galpin
I'll... Yeah
- PAPeter Attia
... yeah, just sort of-
- AGAndy Galpin
Yeah. Thank you. Yeah, yeah. Good, good distinction there. I sort of, again, get lost in exercise science here. Um, so yeah, i- if you, if you remember, like, your back to high school biology and you think of a cell as like a circle or an oval, um, this is more... I- it's like that. It's circular, but it's a tube. So it's a very long tube. Uh, the way to think about it is like a ponytail. So if you think about a ponytail, you think about it as one thing, and it's 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 cell, uh, a skeletal muscle cell looks like, which is actually quite different than a cardiac cell. Those are more rectangular, if you will. They're, they're shorter and, and, uh, wider. Um, skeletal muscle fibers are very long, very narrow, but still circular. They still have a cell membrane. They have a bunch of nuclei. Uh, most of the organelle are the same as any other, uh, thing. The, the contractile units we can get to i- in a second, but yeah, that's the basic setup of them.
- PAPeter Attia
And, and just is it... S- give me the typical length of a muscle cell, a skeletal muscle cell.
- AGAndy Galpin
You, you can't really give a typical because depending on, uh... What you'll see with skeletal muscle is structure is function. So if you can 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, and 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 on cross-sectional area-
- PAPeter Attia
Mm-hmm
- AGAndy Galpin
... a diameter length on those. Skeletal muscle, if you look at, like, like, 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, um, theoretically, those fibers could run the whole length.
- PAPeter Attia
A single cell-
- AGAndy Galpin
Correct
- PAPeter Attia
... can run that whole length?
- AGAndy Galpin
Yeah. Even if it runs half that length-
- PAPeter Attia
That's insane
- AGAndy Galpin
... that's extraordinarily long, right? You go back though, and you go to, like, an ocular muscle, then it, it's gonna be minute. It's, it's gonna be extremely small in length. If you go to, um, muscles in, in your digiti, in your fingers, they're gonna be very, very, very, very short. So it's sort of there is no, like, classic range. It could be from millimeters to literally inches in length.
- PAPeter Attia
So what... Uh, so, so presumably the reason that these cells have m- multiple nuclei is, you know, basically to decentralize the actions-
- AGAndy Galpin
Mm-hmm
- PAPeter Attia
... of, uh, cellular construction, right? 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, a m- you know, even a one centimeter long cell, which is enormous, um-
- AGAndy Galpin
Outrageous
- PAPeter Attia
... you, you couldn't simply make all of that work with one nucleus. So the question is, does that mean these nuclei act independently? Like, what's the... where's the central command on this? It seems like a, a remarkable problem.
- AGAndy Galpin
Okay. [laughs] Boy, remarkable problem, remarkable advantage, right? It's the same-
- PAPeter Attia
Yeah
- AGAndy Galpin
... it's the same thing.
- PAPeter Attia
Hard to control, but amazingly adaptive.
- AGAndy Galpin
Exactly. This is exactly right. So if you wanna dive down the entire nucleation question, uh, this gets very, very interesting because a handful of things. We've, we've actually shown in our lab that a lot of, uh, professional athletes have more nuclei per volume. And so this is one of the things that I posit is, is maybe this is why they can adapt so well, might... was why they can handle the volume that they can handle, is they just simply have more of these nuclei, uh, around.
- 41:40 – 51:37
Energy demands of skeletal muscle compared to other tissues in the body
- PAPeter Attia
work. So we've now established that muscle cells are kind of unlike any other cell in the body. Um, [lip smack] how hungry are they for energy?
- AGAndy Galpin
Yeah.
- PAPeter Attia
You know, so for example, when we look at the liver, you know, I always think of the liver as a beautiful organ, maybe not quite as cool as the muscle, but, but it has a special place in my heart, um, because I've always argued that the reason there is no extracorporeal support for the liver is we-
- AGAndy Galpin
Hmm
- PAPeter Attia
... simply can't replicate its complexity, right? So for listeners-
- AGAndy Galpin
Mm-hmm
- PAPeter Attia
... extracorporeal means outside of the body. So dialysis is extracorporeal support for the kidney. Uh, you know, a, a, a, 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, right? 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. I mean, 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, I can sit and talk about the liver with the same level of excitement that you talk about the muscles. Um, and yet here's what's interesting. The liver is not a metabolically greedy organ.
- AGAndy Galpin
No.
- PAPeter Attia
It really doesn't on its own consume much energy. Um, the brain, by contrast, a very complex organ, an incredibly metabolically greedy organ, um, 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've either needed an adaptation strategy away from glucose, uh, or we, we wouldn't have brains as large as we do. Where does the muscle fit into this hierarchy? Where, where is the muscle a high maintenance organ?
- AGAndy Galpin
Yeah. So you know what's cool about the liver is, uh, it, it's, it's kind of like a, a, a professional fighter where, like, you can beat it up-
- PAPeter Attia
Mm-hmm
- AGAndy Galpin
... a lot.
- PAPeter Attia
That's right.
- AGAndy Galpin
You can't do much to the kidneys.
- PAPeter Attia
That's right.
- AGAndy Galpin
They, they just don't have sustainability, right? Um, so I, I have like a secondary love for the liver because it's the closest thing in the body to skeletal muscle in terms of like the fact that it is, it is listening, and it will respond, and it can change. Um, every-
- PAPeter Attia
And as you said, very adaptive, right? I mean, uh, y- y-
- AGAndy Galpin
Super adaptive
- PAPeter Attia
... you'll, you'll appreciate this if you didn't already know it. When we-- when I was in my residency, um, we would do quite a number of, uh, live donor li- liver transplants. So, uh-
- AGAndy Galpin
Yeah
- PAPeter Attia
... this would be an operation where an individual would donate a, a third to a half of their liver to another individual where there was a really good, uh, HLA match. Well, here's what was really interesting. The speed with which 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.
- AGAndy Galpin
Oh, yeah. Totally. That makes sense.
- PAPeter Attia
Yeah. Yeah. So, so basically we c- it just w- you-- there was no amount of food you could give this person to allow them to have enough phosphate backbone to go and ma- you know, for, for the, uh, DNA and RNA and protein synthesis that was going to be necessary to reproduce-
- AGAndy Galpin
That's a lot
- PAPeter Attia
... their liver. So, um, yeah.
- AGAndy Galpin
Yeah.
- PAPeter Attia
You just had to basically be giving them IV phos nonstop because they could ba-
- AGAndy Galpin
It sounds like what we have to do to fibers when we're doing our single fiber experiments. Like you have to bathe them. They just have to have a permanent bath of phosphorus [chuckles] -
- PAPeter Attia
That, that's right
- AGAndy Galpin
... to let it go.
- 51:37 – 57:18
How a muscle contraction works and why it requires ATP
- AGAndy Galpin
where we're at.
- PAPeter Attia
So let's talk about contraction. How does a contraction actually work, and why? Why does a contraction require ATP? What part of the contraction needs it?
- AGAndy Galpin
Yeah. So if we go back, nerve is coming into skeletal muscle, right? 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, 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, right? And so you have a lot of nerves coming in to control a very small number of fibers, and 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 f- low fidelity. You don't need accuracy of hip extension.
- PAPeter Attia
There's basically just one thing. It's contract, not contract. I mean, do it with as much force as possible, but I mean-
- AGAndy Galpin
Or not.
- PAPeter Attia
Yeah, yeah.
- AGAndy Galpin
Yeah, like-
- PAPeter Attia
Yeah
- AGAndy Galpin
... but, and so you're gonna have hundreds-
- PAPeter Attia
But that, but 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 to... And, and of course you have multiple interocular muscles, so it's, you know, you have-
- AGAndy Galpin
A lot, yeah
- PAPeter Attia
... 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. Um-
- AGAndy Galpin
Yep
- PAPeter Attia
... yeah.
- AGAndy Galpin
If you contrast that to, like, your, 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, it's not even close, right?
- PAPeter Attia
Wow.
- AGAndy Galpin
Like, I need to be very precise with my fingertips.
- PAPeter Attia
Yeah.
- AGAndy Galpin
But my eyes are on a whole new level of precision of where we have to be. Um, so-
- PAPeter Attia
Yeah. I think-
- AGAndy Galpin
... if there's one to one or one to two in the eyes, it, it could be thousands per motor unit in the glutes. On, off.
- PAPeter Attia
Yeah.
- AGAndy Galpin
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.
- PAPeter Attia
[laughs] God, that's so, that's so fantastic. Okay.
- AGAndy Galpin
Yeah.
- PAPeter Attia
Continue. So nerve comes in.
- AGAndy Galpin
So nerve comes in and does that. Now, here's a couple of other layers. Um, without going too far into nerve, you're familiar, I'm sure, with SAID principle. So you have specific adaptation for imposed demand. There's another principle in here called Henneman's size principle. So Alvin Henneman's one of my favorite scientists and, and 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.
- PAPeter Attia
P- let's make sure people understand what that means in terms of what's an action potential? How, how does a nerve actually deliver its signal?
- AGAndy Galpin
Yeah. So it's, it's... We have this fun interplay between chemistry, electricity, and chemistry. That, that's exactly how contraction works, right? So you have to go from an ele- electrical signal to a chemical signal, back to electrical signal. So what happens is you've got, uh, sodium and potassium c- and chloride are your main players, right? And chloride is a negative charge. Uh, potassium, of course, is positive and, and sodium is positive. Um, 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. Kevorkian, right? You give a giant bolus of potassium to somebody, and they're just gonna slowly stop-- their heart's gonna slowly stop contracting. Why? Because the amount of potassium intracellular is gonna become fairly equivalent to the amount of extracellular potassium. And so the, the change in, uh, gradient electrically between the outside of the cell and inside of the cell becomes neutral. And so no action potential is what this, this thing's called. No, 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 thirty millivolts intracellular. You know, 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 positives moves, more negatives have moved, and so you get the idea. And boom, we hit this flip of this switch, and this is what we call all or none. And so 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. And so the analogy we'll use here in, in our undergraduate classes is it's a light switch. So once you hit that certain threshold of millivolt, the muscle fiber contracts as hard as it possibly can. There is no way-- there's no dimmer switch here. You can't go eighty percent, eighty-five, fifty. It's one hundred percent once you get to that action potential, right? You actually see the, the millivolts just rocket back up, and there's this whole cascade of, um, 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. So 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 attraction or... It's not actually how it works, but it's gonna feel like that. Um, what actually-- 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-
- PAPeter Attia
Hmm
- 57:18 – 1:07:56
Muscle fibers: modulation between fiber types with movement and changes in fibers with training and aging
- AGAndy Galpin
getting a muscle-
- PAPeter Attia
And by the way, just so folks understand-
- AGAndy Galpin
Sure
- PAPeter Attia
... uh, 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. Again, whether you're talking about-
- AGAndy Galpin
Yeah, at the muscle level.
- PAPeter Attia
Yeah, at, at the level of the muscle.
- AGAndy Galpin
Yep. So this is the next part. This is why we had to bring up Henneman size principle. So within these motor units, you have, um, 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. So all your-- i-if you had, let's just say we had two motor units. Um, one of those motor units is slow twitch, and one of those motor units is gonna be fast twitch fibers that interface. So if we had five fibers in that motor unit or five hundred, it doesn't really sort of matter right now. We have a couple of factors actually coming on. But they're gonna 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 gonna contract at full speed. So the only way we actually change how much force we're creating in 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 grabbed 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 wanna 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. Because there's no way to re- 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-
- PAPeter Attia
Performance
- AGAndy Galpin
... uh, power.
- PAPeter Attia
Yeah, yeah. So, so-
- AGAndy Galpin
Car's actually bigger. You get the idea.
- PAPeter Attia
Yeah, yeah. So let's use that example when you're talking, just going back really quickly to the athlete. So, um, how quickly is that response modulated when I want to deadlift something?
- AGAndy Galpin
Yeah. So you, you can ac- you can see this in real life. You can actually see this. I have a video of a deadlift, actually, of a friend of mine doing this where, um, it-- so the initial step that's gonna happen here are you're gonna activate slow twitch, uh, s- sorry, lower threshold motor units, which are gonna be almost exclusively slow-twitch fibers. The only way that we really know to increase that is through force production demands. And this is gonna-- like, we're gonna come back to this when we get to fiber type stuff eventually for aging, um, and some of the stuff that came out even this week that you, you may have not seen yet. But, um, the challenge with fast-twitch 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 s- and the, 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's some more than a few papers showing a hypertrophic effect of slo- slow-twitch fibers-
- PAPeter Attia
Hmm
- AGAndy Galpin
... with 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 So it, it just appears to be very easy with any level of activity to maintain and preserve health of slow-twitch fibers. But because fast-twitch fibers require force production, and you generally don't get high force production in 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's being, like, not used." And so that, 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 un- uh, uh, 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 own 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 are 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, um, and unregulated movements. And so when we see this, uh, fiber type grouping thing occur with aging, it's almost exclusively a problem of fast-twitch fibers and not loss of slow-twitch fibers. And so that also explains lack of fidelity as well as potentially some problems with fine, uh, unit movements.
- PAPeter Attia
And what is the heterogeneity of fast and slow-twitch mixtures within different areas? So presumably the eye is all slow-twitch. It's not partic- uh, it doesn't particularly require much force, and it, you know, s-
- AGAndy Galpin
It doesn't require much force, but it r- it does require a lot of speed.
- PAPeter Attia
Yeah. Interesting.
- AGAndy Galpin
So you need to be able to dart back and forth quickly. So I actually don't know the-
- PAPeter Attia
Okay. But let's-- Okay.
- AGAndy Galpin
Here, here's my guess
- PAPeter Attia
So let's, let's look at a big skeletal muscle, like the lats or the glutes.
- AGAndy Galpin
Yeah.
- PAPeter Attia
Is there, is there-- Yeah.
- AGAndy Galpin
So we have two things you have to pay attention to here is we have a, a, a huge amount of person-to-person variation.
- PAPeter Attia
Okay.
- AGAndy Galpin
So you, you and I-
- PAPeter Attia
Within what bracket, though? Give me a sense of... Like, presumably everybody has at least 20% of each. I'm making that up, but is there...
- AGAndy Galpin
Yeah. So let me do the second part, and we'll come back to that first part.
- PAPeter Attia
Okay.
- 1:07:56 – 1:18:36
Andy’s study of twins demonstrating the difference in muscle fibers between a trained and untrained individual
- AGAndy Galpin
this is what our twin study did. Rather than biopsy them-
- PAPeter Attia
Yeah
- AGAndy Galpin
... five years old, um-
- PAPeter Attia
You biopsy them as adult twins
- AGAndy Galpin
... we, we got lucky.
- PAPeter Attia
Yeah.
- AGAndy Galpin
We got monozygous twins. Right
- PAPeter Attia
Who presumably had enough differences in what they were doing that you could see a signal if there was-
- AGAndy Galpin
Th- about 35 years difference of training.
- PAPeter Attia
And what did you see?
- AGAndy Galpin
So, and i- if we compare this now to... I can go back and tell [laughs] that story. You've been in labs, you, you'll appreciate this. Um, one of our graduate students who'd been in our lab for probably three or more years was sitting next to my colleague, Jimmy Bagley, and they're pulling muscle fibers, right? And 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. And he's like, "Oh yeah, like monozygous?" I'm like, "Yeah." So monozygous means their DNA is exact, so not just brothers that got born-
- PAPeter Attia
Yeah
- AGAndy Galpin
... at the same time, so you have genetic replication. So we have that category locked. And, and then Jimmy was sort of like, "Oh, cool. Do they exercise?" And she's like, "Oh yeah, well, like..." I think, I can't remember which one. He was like, "Well, my dad doesn't exercise, but my uncle has been competing in Ironmans for 35 years."
- PAPeter Attia
Mm. [laughs]
- AGAndy Galpin
And Jimmy was like, "What?"
- PAPeter Attia
[laughs] It's a dream experiment.
- AGAndy Galpin
Like, "Wait, wait."
- PAPeter Attia
Yeah.
- AGAndy Galpin
"So, so let me get this straight. [laughs] You have identical twin parents or 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 since high school."
- PAPeter Attia
[laughs]
- AGAndy Galpin
And we're like, "And you've been in my lab for three years."
- PAPeter Attia
And this is the first we're hearing about this.
- AGAndy Galpin
[laughs] This is the first we're hearing about this. Like, you're, you're fired. You're, you're not graduating. Um, so we were able to pull them into 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, [laughs] we knew their miles. We just had everything.
- PAPeter Attia
And phenotypically-
- AGAndy Galpin
Had marathons and ironathons
- PAPeter Attia
... how different did they look?
- AGAndy Galpin
All this stuff. Id- ident... Almost identical.
- PAPeter Attia
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 phenoty- phenotypically?
- AGAndy Galpin
No, I know what you're saying.
- PAPeter Attia
Yeah.
- 1:18:36 – 1:31:15
Microanatomy of fast-twitch and slow-twitch muscle fibers
- AGAndy Galpin
portion, et cetera.
- PAPeter Attia
Let's, let's make sure people understand what the difference is between a fast and a slow twitch fiber. Let's-
- AGAndy Galpin
Yep
- PAPeter Attia
... and we'll come... I wanna come right back-
- AGAndy Galpin
So-
- PAPeter Attia
... to where we are, but I just wanna make sure we haven't lost that thread.
- AGAndy Galpin
Yeah. In general, there's a lot of ways to describe it, but, um, the, the easiest way is to describe it by the name. So fast twitch means that the twitch or the speed of contraction is higher. And so those, these fibers can contract and, and squeeze together with... through the mechanisms we haven't got to yet, we'll get there, uh, myosin actin, um, 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, um, and definitely not with aging. Um, that they tend to be almost, they almost always are more glycolytically driven and so they're gonna have more of the enzymes responsible for anaerobic glycolysis- Um, they're going to have more glucose in the cell, um, they're gonna have less intramuscular triglycerides, and they're going to be having... they generally have more phosphocreatine. Slow-twitch fibers are fatigue-resistant, which means these are the ones that they can contract kind of all day long because they don't use as much glucose, though they do use quite a bit still. They are much better at using fat as a fuel. They are, uh... they tend to have more and larger mitochondria, and, um, the downside is they don't contract with as much velocity, uh, in general. So that's the, the functional. That's why we call them twitch.
- PAPeter Attia
And, and just to be clear, the force difference between them is n- n- it doesn't matter. It's just velocity, or is there a force difference as well?
- AGAndy Galpin
So the... Yeah, no. Well, so a couple of things. Um, in, in large part, force production for muscle fibers is determined mostly by size, cross-sectional area.
- PAPeter Attia
Hmm.
- AGAndy Galpin
So getting the fiber bigger is the play to get it faster. Having said that, power is markedly different. And so if you're talking about-
- PAPeter Attia
Because power is based on velocity as well.
- AGAndy Galpin
That's... Yeah. You times the... multiply the force, um, by the velocity. So if you use this metric that we'll use in single fiber experiments, um, called specific tension, which is sort of like s- relative strength, so you, you take the size portion out of the equation, um, what you're gonna see is a true slow twitch, so these are also called type 1 fibers. Um, if you compare those to a type 2A, so that's a fast-twitch muscle fiber, um, you're gonna see something like five to six x power between these two. So it's not a small amount.
- PAPeter Attia
When you normalize for size.
- AGAndy Galpin
Yeah.
- PAPeter Attia
When you normalize for cross-sectional area.
- AGAndy Galpin
If you go, if you go to the 2x fibers, which is a special class of fast-twitch fibers, now you're talking 20x that power curve.
- PAPeter Attia
And that is mostly explained by more metabolic apparatus?
- AGAndy Galpin
See-
- PAPeter Attia
What's enabling-
- AGAndy Galpin
No
- PAPeter Attia
... the speed? Why does the 2x fiber go faster?
- AGAndy Galpin
Yeah. It's all... has to... In fact, the way that we differentiate muscle fibers in a laboratory is we measure what's called the myosin heavy chain. And so if... to, to kind of actually come back to microanatomy here. So the way the muscle fibers work is this is all in a, a 3D sequence, right? So you can imagine that cylinder. I'm gonna 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. All right? Now, what happens is they're overlapped, so they're not touching each other, and you've got myosin, um, 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. Right? Now, these heads reach up, and they extend, again, in 3D, but if... just think about it in 2D. They reach up and grab on what's called actin. All right? And so the idea when you contract the muscle is the myosin will reach up, and they're gonna reach out sort of 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, that's... 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 the size. And so what determines force production versus velocity is what we call cross-bridges. So the amount of time that these myosin heads grab onto actin, that little place of connection is called a cross-bridge. The more of those cross-bridges you have, the more effectively you can pull the actin closer to each other. The f- the more effectively you do that, the faster the contraction, the more forceful the contraction's 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, and, like, 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. And 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.
- PAPeter Attia
And you only have two arms still in this? You only have two myosin filaments?
- AGAndy Galpin
No, you have a ton.
- PAPeter Attia
Okay. Okay.
- AGAndy Galpin
You, uh... so you have one myosin filament.
- PAPeter Attia
I'm sorry. You only have, um, t- uh, two heads, or how many heads do you have?
- AGAndy Galpin
D- d- bajillions.
- PAPeter Attia
Okay, so you have billions of heads to grab onto six potential targets. So you're always gonna grab-
- 1:31:15 – 1:40:49
Factors that determine one’s makeup of muscle fibers and how adaptable they are with training
- PAPeter Attia
So I guess all of this now brings us back to a better position in, in, in which we can understand the biopsy studies in these identical twins.
- AGAndy Galpin
So if you, if you look at the fiber profile of the untrained twin, it, it lines up very close to what you'd see in a textbook, right? So it's around 50% slow-twitch And about 30% of these fast-twitch 2A form, but then about 20 or so percent is hybrid form
- PAPeter Attia
2- 2A or 2X?
- AGAndy Galpin
2A.
- PAPeter Attia
Oh, okay.
- AGAndy Galpin
So here's one of the things that's interesting. When you get into the 2X conversation, um, there are clearly... humans have the ability to express 2X. It's just extraordinarily rare.
- PAPeter Attia
Mm.
- AGAndy Galpin
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. They've... Number one, they've probably had that muscle fiber denervated for decades. That's really the only time we see it. In fact, if you look at spinal cord injury folks who've, you know, had a denervated 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 gonna fall to 2X. Why? We have absolutely no idea. I could guess, but we don't seem to know. We see it sometimes in older folks, but even then-
- PAPeter Attia
And again, 2X... Sorry, 2X is the hybrid, single, single fiber hybrid?
- AGAndy Galpin
2- 2X is a pure fiber type. It is the ultra fast.
- PAPeter Attia
Oh, okay. Okay.
- AGAndy Galpin
It is the one. So any hybrid is gonna be called something like, there is a 1-2A hybrid, there's a 2A-2X hybrid, and there's even a triple hybrid, 1-2A-2X. It has all three fiber types-
- PAPeter Attia
Mm
- AGAndy Galpin
... in the same cell. Those are, those are fairly uncommon. A 1-2A hybrid and a 2A-2X hybrid are very, very common. A pure 2X by itself, though, is extraordinarily rare.
- PAPeter Attia
Mm.
- AGAndy Galpin
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 2X. Now, if, if you dive in the literature here, you're gonna get confused very quickly, because a lot of people don't use detailed enough laboratory methodologies to differentiate these.
- PAPeter Attia
Mm.
- AGAndy Galpin
And so they're gonna say, "Oh, there's all kinds of 2X fibers." They're really not. They're very clearly 2A-2X fibers. They just didn't run high fidelity enough to actually differentiate between hybrids, and so you'll pick up 2A-2X fibers as having some portion of 2X. And so it's a difference between does that fiber contain 2X versus is it a purely 2X fiber? Which is sort of a semantic difference, but in our world it's a, it's a big deal. Um, if you find somebody with a high percentage of 2X fibers, um, something odd is, 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-
- PAPeter Attia
Meaning we don't have data on sprinters?
- AGAndy Galpin
No.
- PAPeter Attia
Why?
- AGAndy Galpin
Great question. It- it, it's hard to get these folks in the lab, I guess. Um, people haven't been interested in it. It's not a thing. We just don't have them. The only thing we have is-
- PAPeter Attia
[laughs] People coming to you
- AGAndy Galpin
... uh, there is a case study. There's a case study done on a, um, a guy who's... I think he still owns a world record. Um, it's not hard to figure out his name, but I can't technically say it. Um, 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. Um, he's the only one I know, and I actually, uh, 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. Um, and he had something like 24% pure 2X fibers. Um...
- PAPeter Attia
So what did the-
- AGAndy Galpin
I'd like to see that replicated
- PAPeter Attia
So, so, so go... So, so the untrained guy was 50% slow, 30% 2A, 20% hybrid AX?
- AGAndy Galpin
Uh-huh.
- PAPeter Attia
Okay.
- AGAndy Galpin
2A-2X.
- 1:40:49 – 1:49:59
Hypertrophy and what happens at the cellular level when a muscle grows
- AGAndy Galpin
Um-
- PAPeter Attia
One other thing I wanna ask you-
- AGAndy Galpin
Yeah
- PAPeter Attia
... about on the microanatomy side, Andy, is, uh, explain... You, you sort of have talked about it indirectly, but I... if, 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?
- AGAndy Galpin
Right. So there's an interesting, um, discussion here. The, 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 fiber as being that cylinder, the width of the cylinder just expands.
- PAPeter Attia
Mm-hmm.
- AGAndy Galpin
And so that circle gets larger is the way to think about it. Um-
- PAPeter Attia
J- And, and a-
- AGAndy Galpin
Now-
- PAPeter Attia
... and a crude analogy is getting fatter means each adipocyte is getting bigger. It's taking on and storing more triglyceride.
- AGAndy Galpin
Yep. Yep, exactly. So from a skeletal muscle perspective, it, it... the diameter gets larger. Um, there's actually interesting work. We actually have some tissue on its way to Auburn right now. 'Cause 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 an a- uh, actin and myosin. Um, seems to have some initial work there that's a little bit of both, and it happens at different phases of training. Um, so-
- PAPeter Attia
S- Sorry
- AGAndy Galpin
... the way to think about this-
- PAPeter Attia
Is, is, is the question do different types of training increase sarcoplasmic versus contractile hypertrophy, or is the broader question, you know, 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'm, I'm not sure I... I wanna make sure I understand the question.
- AGAndy Galpin
Yeah. So it's close, not the sarcoplasmic reticulum. It's what we call sarcoplasmic hypertrophy.
- PAPeter Attia
Okay.
- AGAndy Galpin
So this would just be an increase in diameter with additional fluid intake. So it is close to what you're saying.
- PAPeter Attia
Okay.
- AGAndy Galpin
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 that's-
- PAPeter Attia
Yeah, yeah
- AGAndy Galpin
... sort of weird thing. Is it actually happening because myosin and actin are getting thicker?
- PAPeter Attia
I see. I got it. Okay.
- AGAndy Galpin
I mean, you can't add ac-
- PAPeter Attia
Wait, that's amazing. We don't know the answer to that question yet?
- AGAndy Galpin
We don't. More data have started coming out.
- PAPeter Attia
Wow.
- AGAndy Galpin
But even a few years ago, the, the idea that sarcoplasmic hypertrophy was a thing was thought of as like garbage bro science.
- PAPeter Attia
Meaning the idea, the, the, the sort of assumed belief was anytime muscles got bigger, they were getting bigger in the contractile units?
- AGAndy Galpin
Correct.
- PAPeter Attia
Well, by the way, I'm not-
- 1:49:59 – 2:01:48
How athletes quickly cut water weight and the rehydration process
- AGAndy Galpin
look at... We're getting sort of maybe off track, but like if you look at hydration and, and dealing with the athletes that I deal with, a weight cut is a huge deal, right? Like managing, um, 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 hypoosmotic or hyperosmotic or isoosmotic, like you're gonna 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-
- PAPeter Attia
There's gonna be a huge shift
- AGAndy Galpin
... you're not going to drive fluid-
- PAPeter Attia
Yeah
- AGAndy Galpin
... you're not gonna drive fluid into tissue. And, and you get into situations where guys are peeing or girls are severely dehydrated, they're peeing, yet they put very little fluid actually back into tissue because blood volume got so large and expanded so quickly they have a, 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, um, functional organs rather.
- PAPeter Attia
And are there any rules of thumb on that? So, you know, we were talking before the podcast started how, you know, I had food poisoning, um-
- AGAndy Galpin
Yeah
- PAPeter Attia
... and in a span of like two days I lost seven pounds, and my weight is about the most stable metric in my... Like it just doesn't fluctuate a pound. So to lose seven pounds in two days, uh, 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-
- AGAndy Galpin
Sure
- PAPeter Attia
... um, what is your best guess as to how much... I mean, let's just posit that much of that seven pounds, six and a half of it, is water. What's the ideal strategy to replenish that in terms of, um, hyper, hypo, uh, or, or isoosmotic if I'm gonna try to replenish that in, in, in the form of liquid?
- AGAndy Galpin
Yep. Handful of things. Number one, you need to go slowly.
- PAPeter Attia
Yeah.
- AGAndy Galpin
Right? So you gotta make sure that you don't get excessive.
- PAPeter Attia
So I don't wanna pound four liters of worth of four grams of sodium in the first-
- AGAndy Galpin
Correct
- PAPeter Attia
... six w- six hours. I'm feeling better.
- AGAndy Galpin
Yep. So number one, you, you wanna shoot for something like the neighborhood of 110% to 125% of fluid w- wa- weight. Like that's... 'Cause you're going to lose something urine. It's gonna happen. So let's say you lost seven, like my, my brain is like, okay, we're gonna go to eight and a half, nine pounds, like something like that. Like you wanna round this and call this a gallon.
- PAPeter Attia
Mm-hmm.
- AGAndy Galpin
Okay, like we're at a gallon. All right. We're gonna bring that in over the course of three hours.
- PAPeter Attia
Or two gallons, right?
- AGAndy Galpin
Maybe four.
- PAPeter Attia
Is that... I've lost my train. Is a pound a quarter gallon?
- AGAndy Galpin
Well, four liters in a gallon-
- PAPeter Attia
Yeah
- AGAndy Galpin
... ish.
- PAPeter Attia
Yeah, yeah.
- AGAndy Galpin
A little over, change-
- PAPeter Attia
Okay
- AGAndy Galpin
... two point, you know, times a kilo
- PAPeter Attia
... so, so cou- couple gallons, right?
- 2:01:48 – 2:04:21
Different types of athletes
- PAPeter Attia
All right. Let's bring this all back, 'cause I, I, I know... I'm guessing, you know, that, that 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 wanna kinda go back to- Um, 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 power lifter. Power lifter, 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 explosive, but it's just one rep. The strongman, um, he's, you know, throwing boulders and having to pick them up and throw them again and again, again, insane amount of strength, but you, 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, you know, athlete, also very strong, also agile, mobile, has the explosivity, but not, you know, 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, you know, 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 know, 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. I think there's six, right? One, two... Yeah, there's six of them. Um, and most people listening to this don't need to be, but we probably want bits of each of them in us, right? [lip smack] So let's now talk
- 2:04:21 – 2:09:10
Training advice for a hypothetical client who’s untrained and wants to add muscle and functional strength for longevity
- PAPeter Attia
about hypothetical ways to train, and let's-- I did this with Lane, and people really liked this approach. Um, 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, [clears throat] 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, don't, don't [chuckles] -- unless I specify it as part of the problem, don't hold back, you know? All right. So we'll start with the easy one, which is [clears throat] the untrained individual, um, who comes to you and says, "Okay, I bought it. You know, I'm, I'm all in on this. Um, I'm willing to, to go to the gym. You know, Peter's alwe- 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, [clears throat] I don't know, put three hours a week in the gym. I want to get bigger 'cause I, you know, I had a DEXA scan, and it really showed that my ALMI was about the 40th percentile. And I really, you know... 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, in a year, two years, three years. Um, but I also want it to matter. You know, I wanna be stronger. I wanna be able to do stuff when I get older. I don't just want to get bigger. I wanna be able to, um, never enter a competition. I'm not here to enter the strongman competition, but, like, I never wanna hurt. I wanna be able to chop wood in my backyard. I wanna be able to carry stuff around. I wanna be able to travel with a backpack on," blah, blah, blah. Any, any other questions you have for me before you design my program, Andy?
- AGAndy Galpin
How many days per week did you say?
- PAPeter Attia
Um, I, I could be up to d- going into the gym, like, three days a week, an hour at a time.
- AGAndy Galpin
Three days total. Okay, cool. So you've basically described every one of our executive clients in our Rapid Health Optimization program. So, [chuckles] like, so I can nail this one. Um, ob- obviously, spent most of my career with professional athletes, but we, we deal with this problem all the time in Rapid. So here, here's what I would say. You've already got zone two stuff-
- PAPeter Attia
Yep. We do. I'm t- I'm doing the-
- AGAndy Galpin
... locked down. That's steady state.
- PAPeter Attia
Yep.
- AGAndy Galpin
Great. Copy that. Um, here's what you need to pay attention to. You described muscle as insufficient, so we gotta... in our brain, we're automatically thinking, "We've gotta put on muscle mass." You also said they're untrained, though, and one of the things you're gonna see quite clearly-
- PAPeter Attia
Oh, sorry. I, I, I sort of left out. Um, like I, I was active in high school and college. Like I... 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 the last 10 years, my only exercise has been, um, [lip smack] like activities of daily living, which includes sometimes hiking and playing with my kids. But yes, I have, I haven't been in the gym. I haven't been in the gym in, in a decade.
- AGAndy Galpin
Yeah. Perfect. Yep. You still describe everybody-
- PAPeter Attia
Okay
- AGAndy Galpin
... in Rapid Health Optimization, right? No problem. So the way that I'm just gonna walk you through sort of... I'm gonna break the fourth dimensional wall here. My brain immediately thinking, "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, but 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 n- 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. We can do one and get both adaptations at the same time.
- PAPeter Attia
Because I'm so low on the curve, anything is going to give me a bit of both.
- AGAndy Galpin
In fact, we can get that from not even lifting weights Because in fact, in, in our training studies you'll see that you'll see equal adaptations in muscle size hypertrophy from even steady state cycling.
- PAPeter Attia
Mm.
- AGAndy Galpin
Initially.
- PAPeter Attia
[laughs] Right.
- AGAndy Galpin
S- For six to eight weeks you'll see equal, um, all of our concurrent training models and studies will show the same thing. Like, not only is there not interference, an interference effect at this stage, it's a complementary. 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.
- PAPeter Attia
Hm.
- AGAndy Galpin
So spending time initially getting physically fit before trying to add muscle mass for someone like this, it's, it's a very fruitful investment.
- PAPeter Attia
Great. So the fact that I've been doing my zone two for two months actually has you pretty happy.
- AGAndy Galpin
Super happy.
- PAPeter Attia
Okay.
- AGAndy Galpin
Okay.
- 2:09:10 – 2:15:51
Changes in muscle and muscular function that occur with aging
- AGAndy Galpin
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.
- PAPeter Attia
That, that's right. Peter has me committed to, you know-
- AGAndy Galpin
Yeah
- PAPeter Attia
... this is not about looking good in my bathing suit in six weeks. I'm not in a rush.
- AGAndy Galpin
Copy that.
- PAPeter Attia
Yep.
- AGAndy Galpin
Right. 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. Uh, 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?
- PAPeter Attia
Speed.
- AGAndy Galpin
A little bit of loss of speed. Aha. So preserving... In fact, you, 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 100 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 power lifting, the world record through age doesn't go down that much. The world record in speed and jumping sports just falls off a cliff.
- PAPeter Attia
Yeah.
- AGAndy Galpin
So it's preserving speed. In addition, uh, my friend Greg Grossecki just published a paper this week in, uh, Journal of Physiology, a, a, a blue ribbon journal in our field, right? It's as high as you get. And this was actually looking specifically at single fiber contractile function changes with aging. And the data here are extraordinarily clear, have been a long run. You see very little loss of function in slow twitch 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, um, a drop of power, and so there's nothing internal to the muscle fiber that's going down. So one other way to say this is if you take an individual muscle fiber-
- PAPeter Attia
It's the fiber loss that's the problem
- AGAndy Galpin
... it's the fiber size. The atrophy of fast twitch fibers is the almost exclusively the problem with aging and muscle.
- PAPeter Attia
Hm.
- AGAndy Galpin
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 fiber, fibers in a live human muscle is extraordinarily difficult. So what, really what we're after here is anytime I'm thinking longevity, I'm thinking primarily absolute force and power, um, has to be preserved, and it's... This is a fast twitch fiber atrophy issue. Um, th- this is a target. So these are the things spinning in my head. So how is this three-day a week combination gonna look? Okay.
- PAPeter Attia
And sorry, just to make-
- AGAndy Galpin
Last week-
- PAPeter Attia
... just to make sure we translate that, Andy, 'cause I think that was so, uh, important what you just said. You're basically looking, I'm 50, and you're looking down the barrel of my life saying, "You wanna live another 40 years, and you wanna 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, 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. 'Cause if I just ignore that, you know, I might as well be that highly exercised twin guy who's, you know, doing all his cardio, but at the end of the day, he can't jump off the curb. He can't, you know... He's gonna be this, the hyper cardio athlete who's still a decrepit person in the last decade of their life.
- AGAndy Galpin
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 at those tissues. The other tissues aren't as, uh... Like hypertrophy. Hypertrophy is pretty nonspecific in terms of your training application. But if you wanna make sure that you're targeting fast twitch fibers, like this, this requires very specific protocols or, or like you have no chance. Fast tw- slow twitch fibers are going to get activated with any activity of daily living. They're gonna get activated with any amount of physical training-
- PAPeter Attia
Yeah
- AGAndy Galpin
... whether you're doing intervals, zone two, zone six, it doesn't matter, right? Zone 28, pick whatever you want, slow twitch are good. It's the fast twitch fibers that require intention, and that's why I-
- PAPeter Attia
Yeah
- AGAndy Galpin
... I make such a big deal of it because you can't accidentally get those.
- PAPeter Attia
Yep, that's right.
- AGAndy Galpin
It's sort of like what we say in fighting is like you can sometimes accidentally knock somebody out. There are fluke punches. There are no accidental submissions though. Like, there's no fluke arm bars.
- PAPeter Attia
Mm-hmm.
- AGAndy Galpin
Like, [laughs] like you have to know what you're doing there or not.
- PAPeter Attia
Yep.
- AGAndy Galpin
So coming back to our, our avatar-
- PAPeter Attia
By the way, I love that line because I often say that to especially my female patients who are completely untrained, borderlining on cachectic, um, afraid of lifting weights. You know, they just wanna do yoga all day, and when I say, "Look, we have a problem here. You're osteopenic, um-
- 2:15:51 – 2:30:51
Training plan for the hypothetical client
- AGAndy Galpin
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 gonna 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. Right? I think in your show with Holly, she talked about making sure you start with a very low volume, like, like way lower volume than you think.
- PAPeter Attia
Yep.
- AGAndy Galpin
We have time. Like, we just need to move. I'm gonna be very cautious of eccentric movements because they will, um, 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, where we're practicing movement patterns, we're getting that stuff grooved so we don't pick up injuries later. We're not getting excessively sore. We're building some muscle mass 'cause we're gonna get that anyways, and we don't need to there. So if this was a six-month program, because you can't write the same program for the next 50 years, right? What's the first six months, I guess is... if that's your question.
- PAPeter Attia
Yep.
- AGAndy Galpin
All right. Zone two's out of the way. Um, I would probably stick to fairly similar, uh, to what Holly said initially, which was, okay, something like one to three s- working sets of probably four exercises a day, something like that. Um, we wanna spread those across upper, lower, and kinda some different movement patterns, and we wanna practice the compound movements. I'm not going to isolated single joint movements yet. I'm going to let's learn how to do a goblet squat. Okay, this is a squat. You're gonna hold the dumbbell sort of in front of your chest. Great. We're gonna learn to do a hip extension. We're gonna learn to do a basic overhead press or some bent rows, things like that, and I'm gonna spend 30 minutes on those things. I don't even really care about tracking progression at this point. We're gonna track, um, did you... Did you get the movement pattern down right? Did you brace? Is our, is our spine in the ri- proper position? Are you breathing through, um, 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, 'cause 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, right? We're just being in that position. We're gonna do that, right?
- PAPeter Attia
Okay, so we're basically completely optimizing movement patterns. We're making sure we don't hurt ourselves. Um, we're learning new skills, right? We're learning skills of exercise.
- AGAndy Galpin
Yep.
- PAPeter Attia
Let's now go to the next six months. So I come back to you, Andy, and I say, um, "You know, this has been great. Like, this is not as difficult as I thought it was gonna be. I, I really... 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. Um, I'm, I'm... I'd like to take this up a notch. Uh, I can't commit more time though, Andy, so I'm really kinda, you know, three 60-minute spots is all I can get 'cause I still gotta, you know, get my kids from school, and, and work is just as demanding as ever. Um, but how do I in- increase the desire to be even bigger and even stronger and even more functional?"
- AGAndy Galpin
Great. 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. Um, I'm gonna 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, that, that, that tissue tolerance, we call it. So your ability to land and absorb. It's not creation of power, but it's the back end. How do I stop that movement? How do I land from it? We're gonna continue to invest in, in the muscle growth, but now we can start pushing the pace a little bit, and then we're gonna 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, of all three workouts per week, we're gonna do something in basic movement patterns. So let's imagine a box jump Right? We'll do a box jump. We're gonna s- jump from the ground and land on a box that's, say, 18 inches in the air, right? We're gonna practice that movement pattern. I want you landing on the box, not on the ground. That reduces the eccentric landing 'cause you're gonna be absorbing way less, so you're not gonna get as sore, but you're gonna have to pop a little bit. You're gonna have to jump to get up there, and we're bracing that movement pattern. I'm gonna probably do something like-
- PAPeter Attia
How are you determining that height, Andy? 18 inches seems really high to me. Uh, how, how do I know if I shouldn't be 12 to start? What, what level of fatigue? How many times would I do this so that I can gauge-
- AGAndy Galpin
Yep
- PAPeter Attia
... how high it needs to be?
- AGAndy Galpin
There should be no fatigue. This is simply about high-
- PAPeter Attia
This is load tolerance
- AGAndy Galpin
... power production.
- PAPeter Attia
This is load tolerance then?
- AGAndy Galpin
Load tolerance, and it's, it's introducing power.
- PAPeter Attia
Okay.
- AGAndy Galpin
So you're gonna start learning how to move fast, but you're gonna do it in a, a safe thing where you're not gonna pull a hamstring.
- PAPeter Attia
And, and just to be clear, Andy, I, you know, I, I, I don't, I don't need to compete in sports. I don't play basketball anymore. I'm not... Are you sure you need me doing this? 'Cause all I'm trying to do is I just wanna be able to pick up my grandkids in 30 years or 20 years.
- AGAndy Galpin
Yeah, 100%.
- PAPeter Attia
Okay.
- AGAndy Galpin
So in order to pick up your grandkids, you need to not be in the hospital, right? You need to be not living in an assisted living home. Do you know what puts people in assisted living home? Falling and breaking a hip. The connection between morbidity and mortality with a hip break is extraordinary after the age of 60. It's not even 90. It is 60-ish. Um, reason, 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 gonna keep you playing with your kids when you're 60.
- PAPeter Attia
Got it. So even though-
- AGAndy Galpin
Capisce?
- PAPeter Attia
Yeah. So I... It's not... Even though I don't wanna be a, a, a quote-unquote explosive athlete, I still have to kinda train like one.
- AGAndy Galpin
In some part.
- PAPeter Attia
Yeah.
- AGAndy Galpin
And I'm asking for 10 minutes of your workout.
- PAPeter Attia
Okay.
- 2:30:51 – 2:38:27
What drives muscle hypertrophy?
- AGAndy Galpin
elements.
- PAPeter Attia
Let's talk a little bit about isometric. I'm, I'm now gonna deviate from my patient into back to being Peter, uh, and interviewing. Um, [lip smack] we didn't talk about it, but everybody's probably heard of an isometric. It's force generation, uh, or muscle contraction without movement. Big part of my recovery from shoulder surgery, I had a labral repair, uh, you know, a while ago, and this was the first thing I was permitted to do, um, was-
- AGAndy Galpin
Oh, yeah
- PAPeter Attia
... begin, uh, you know, humeral extension and flexion without movement. And, um, 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 sort of warm up. Um-
- AGAndy Galpin
Mm-hmm
- PAPeter Attia
... 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. Um, w- why is that the case? Uh, 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?
- AGAndy Galpin
Yeah. So are you 10% flexion, 30% flexion-
- PAPeter Attia
Yeah
- AGAndy Galpin
... 110% flexion? Where at? I have so much to say on this one. Um, are we good for two and a half, three? We good another three hours?
- PAPeter Attia
[laughs]
- AGAndy Galpin
We good? Uh, there's a whole-
- PAPeter Attia
I will say this. We're, we're clearly gonna do a part two of this podcast, so we'll, we'll, yeah, thank, yeah.
- AGAndy Galpin
[laughs] There, there's a whole, a, a whole show on this area, um, because, because of this. So you actually sort of inadvertently asked what's actually driving muscle hypertrophy And is it not, it's not the workout per se, it's the stimuli, right? 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 and interesting, is because it takes the least precision. Because the mechanisms are so spread across different areas that it's sort of like 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 A and C, or b- Y- you're gonna get there. Um, the muscle is very much listening to that signal. It's not so much for other things. And so it, 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, like 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. Like all these things are different strategies for progression, and if that happens, you're going to be in a pretty good spot. [lip smacks] Um, so like barring the, the mechanism discussion is we're just gonna get like so far down the road here we're never gonna come back and answer your, your patient que- question. Um, but that's, that's one thing to think about. So isometrics, the s- the short answer is they're, they're going to be activating a number of those same mechanisms, so you're going to cause the same amount of hypertrophy. Where do I be in that range of motion? Well, there's no answer there. This is the primary downside of isometrics.
- PAPeter Attia
This is where you mix it up, presumably?
- AGAndy Galpin
You certainly mix it up. In general, muscles respond best to being at the highest stretch. So if you can have that thing at the, the highest level of extension t- generally, but it kinda depends on the muscle, um, you're going to generate the... You, you're putting more... In fact, y- 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, uh, 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 of, of, um, where it feels the most tight, if you will, not the, not the finish position.
Episode duration: 2:55:14
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