Hypertrophy, Muscle Science, and Eliciting Different Forms Of Stress w/ Dr. Andy Galpin
Dr. Andy Galpin joins us today to talk SCIENCE. He is a Professor of Kinesiology at the Center for Sports Performance at California State University, Fullerton. He has a Ph.D. in Human Bioenergetics and is the founder and director of the Biochemistry and Molecular Exercise Laboratory.
Why do certain types of training programs work better than others? Why do certain people respond to certain types of training better than others?
Andy is a muscle scientist who studies muscle at the single-cell level all the way up to the performance to try to determine what happens in response to high intensity, high power, high velocity, high force exercise acutely and chronically.
He is best known for studying "human thriving". What do we do to not just avoid being sick but how do we optimize? How do we thrive? He spends time examining those that do that so that we really understand what we're shooting for in terms of optimal health and performance.
In this episode, we chat about things like why we think of science the wrong way, why hypertrophy training is so critical for long-term development, the diabetes of dopamine, what happens when we eliminate all stress, and so much more.
I admire his skill for communicating such complex topics in laymen's terms. His new book Unplugged is taking the best seller's list by storm. Make sure you support the message by grabbing a copy and leaving a review on Amazon!
(5:10) - Studying "human thriving"
(10:43) - Why we think of science the wrong way
(13:57) - Satellite cells and their correlation to recovery
(24:53) - Hypertrophy training
(30:24) - Exogenous testosterone
(33:15) - Value of bodybuilding styled training
(39:24) - Using hypertrophy to break plateaus
(43:40) - What happens when you eliminate all stress
(48:53) - Different ways to elicit stress
(57:50) - Diabetes of dopamine
(1:06:41) - Importance of communication skills
Resources we may have talked about:
Skeletal Muscle Hypertrophy with Concurrent Exercise Training
The Body Of Knowledge
How you can connect with Andy:
Hey, this is Dr. Andy Galpin, and you're listening to the airborne mind show.
Hello everyone. This is Misbah Haque. Thank you so much for joining me today and welcome back to the show, whether this is your first, second, 10th, or 30th episode. I appreciate you tuning in your time, your energy, your attention, and your ears mean the world. To me, without you listening, this show would not be where it is today. So once again, thank you. Before we get started, the biggest compliment that you can give is by leaving a review on iTunes, you have no idea how much that helps in terms of rankings, bringing more awareness to the show, and bringing on more interesting guests. So if you could take two or three minutes, not while you're driving, but take two or three minutes, go ahead, leave a review. It would be greatly appreciated. Also be sure to head over to airborne mind.com, where you can check out some free resources and the full show notes there as well.
Today's podcast episode is brought to you by audible.com. If you enjoy books and you are looking for something new to read something that is relevant to problems that you're trying to solve. I made a list for email@example.com for slash reading list. You can see a compilation compile. Did I say that right? Compilation of all the books that previous guests have recommended on the show, and if you decide you want to go for it, you can grab a free audiobook and 30-day free trial there as well. Once again, that is the airborne mind.com forward slash or reading list. So today my guest is Dr. Andy Galpin. He is a professor of kinesiology at the center for sports performance at Cal State Fullerton. He's got a Ph.D. in human bioenergetics and he's the founder and director of the biochemistry and molecular exercise laboratory.
Chances are that you have seen his work before. He is making regular appearances on the barbell shrug podcast. He hosted his own series of podcasts called the body of knowledge. And he's also been on the Joe Rogan Experience, which is a pretty big deal. But yeah, his work has been featured in so many places, you know, on the side he's helped and the many fighters, Olympic athletes, you name it, but at heart, he is a muscle scientist who studies muscle at the single-cell level all the way up to the performance to try to determine what happens in response to high intensity, high power, high velocity, high force exercise, both acutely and chronically. Why do certain types of training programs work better than others? Why do certain people respond to certain types of training better than others? He is kind of best known for studying human thriving, right?
Like what do we do to not just avoid being sick, but how do we optimize? How do we thrive? He spends time examining those that do that. So we can really understand what we're shooting for in terms of optimal health and performance. In this episode, we chat about things like why we think of science, the wrong way, why her purchase of retraining is so critical for long-term development, the diabetes of dopamine, what happens when we eliminate all stress and so much more, his book recently came out unplug, which is taking the bestsellers list by storm. He co-wrote that with Brian McKenzie, who will have coming on in a couple of months again. But the best thing that you can do to support his book is, first of all, get it and read it because it's a paradigm-shifting book and head over to Amazon and leave a review.
You have no idea how much that would help spread his message. So if you resonate with some of the things that we talk about regarding unplugged and some of the concepts around it, you want the message to reach more people, make sure you go ahead and do that. I hope you enjoyed this conversation as much as I did. And more importantly, hope you do something with it. Dr. Galvin, welcome to the show. A pleasure to be here, man. Yeah. I'm excited to have you on because I've been following your work for quite some time. And recently I had a chance to attend the talk that you did at Invictus, where he talked about, you know, genetics versus training. And I found some points there. Super interesting. And I just find your, your gift, or actually let's say skillset really fascinating. You're able to take these complex scientific principles and concepts and then bring them down to a level where you can communicate it with the average person and you know, bring it outside of the scientific community and allow coaches, practitioners, and athletes to make use of it as well. So I'm excited to have you on.
Well, I appreciate you saying that you know, that's it's actually a very good microcosm for the talk and in and of itself. So we kind of just went to like inception there. Yeah.
Let us know a little bit about your background and kind of, you know, how you got to where you are today, where some of your time, energy, and attention are focused on at the moment.
Sure. so my, my current job, I'm a professor and the director of what's called the center for sports performance at Cal State Fullerton. And I also run a founder and director of a separate laboratory called the biochemistry and exercise physiology laboratory. So basically what that means is, is, you know, I'm a muscle scientist. So my job is to do research. And we examine and everything from the whole muscle all the way down to the, to the genetic level and everything in between. So we take muscle biopsies and we study human muscle at the single-cell level and all the way up to the performance to try to determine what happens in response to high intensity, high power, high velocity, high force exercise acutely and chronically which is all kind of a fancy way of saying, you know, I'm an athlete.
I played, I played college football. I played every sport. I could get my hands on as a kid. And I always just wanted to know, you know, what are the training questions? You know, what, why do certain types of training programs work better than others? Why some people respond to certain types of training better than others. And so for me, the way to answer that question, because so many people were doing it from what we would call the practical side, which is, you know, coaches on the floor getting these numbers with their athletes. So I wanted to look at it from another perspective, which is okay, well, what are the cellular mechanisms and explanations for why that happens? And then can we actually use that information to help each other? So in other words, if I can identify, Hey, somebody that has more of these certain types of muscle fibers may respond to this type of training.
And I can maybe have that as a theory, and I can send that out to a coach, and then they can actually put that into practice for a few months and come back and say, Nah, it didn't line up in your lab, but it didn't really work in the field. Well, then I know maybe I didn't get the right answer yet. But if it does work, then maybe we fall learned something. So the gist of what I do as a scientist and as a teacher is really to, you know, continue to help understand human performance and do what we call study human thriving. So I'm not interested in disease prevention, although that stuff is clearly important, a lot of people do that. I hit the other end of the spectrum, which is, you know, what do we do, not to just avoid being sick, but how do we optimize? How do we thrive? And let's spend our time examining those that do that so that we really understand what we're, what we're shooting for in terms of optimal health and performance.
Yeah. And I mean, when we look at maybe the last few decades, the shift in our culture as to, you know, the type of training that we're doing and what we're really seeking for in fitness and in performance has kind of slowly started to shift and change. And so would you say that the way that you are studying performance is it's something that really hasn't been done too much in the past, on this level?
Yeah, no. Yeah, exactly. Right. we have the luxury now, or we had the luxury in our past, basically focusing all of our, what we'll call exercise on the sake of sports performance. So in other words, you know, when we exercise in the 1970s, it was because we were trying to get better at sport ABC or Dwell, now we've, we've evolved or devolved. And we're about to really cross the threshold where the reason we do exercise is completely different. There are some that are still there for the sake of sports performance, but the vast majority of exercise research or exercise science is really focused on reclaiming basic human physiology through exercise, right. Which is a fancy way, I guess, of saying it's, it's there to help us overcome the negative things that we have had in our life as a result of technology and abundance, and like becoming generally physically far easier.
We really still have this huge gap in science from the performance side of it, with anything besides your very standard 30 minutes or 45 minutes of steady-state, you know, what we'll call cardio jogging, things like that. The other of the spectrum is your very classic hypertrophic, three sets of 10 leg extensions, you know, the last decade or so in large part because of Marty Gibala and his team high-intensity intervals have started to jump in and that's fantastic, but this is something I noticed at the very, very beginning of my college career, that there are so many other types of train and there's so many integrations and iterations of this. Like we don't have any research on any of these combination training modes, which is actually far more realistic to any athlete. And this is far before CrossFit ever did it, I mean, I didn't know, a single athlete in the 1980s that only lifted three sets of 10 or only did intervals or did accommodate no one has done that. I mean, decades, if not longer. So yeah, you're right, man. We just have a huge gap in terms of understanding anything from the performance side of science, outside of the very standard. And, and there's a good reason for that. Very, very, very good reason. So I don't blame them, but the hole is there, nonetheless. Yeah.
Something that stuck out to me that you mentioned in your talk, and I've repeated this a couple of times when Irene came onto the show and Calvin came on the show and you said that our understanding is limited by the technology that we have to measure it. Right. It's, it's one of those things like we need to remain open-minded really in all aspects because certain things we may have believed that was deemed impossible, such as that hyperplasia concept that you talked about now that we have that technology to measure it. We've, you've clearly shown that it is possible. And that just leaves us to think like, what else is there out there that we haven't tapped into yet solely because the technology isn't available to measure.
Yeah. I mean, you can pick your, your example, whatever you want, especially any of you at home that has an exercise science degree or an undergraduate degree next visit or something like that. I mean, pick, pick the thing that you got taught in school that was the absolute truth, or this never happens. This always happens. And you can basically trace a direct line between improvements and technology and changing of that understanding. So pick your poison. It really doesn't matter. It's very, very clear lactate is another very popular one, right? So for decades, we thought this is actually what causes fatigue. Then as we improve our ability to accurately and improve the fidelity of the measurements, we realize that not only is that not right, but it's completely wrong, it's the exact opposite. And then you have really innovative people like George Brooks come along and start saying actually when we start integrating our applying lactate directly to people after traumatic brain injury, they get far better.
And the brain actually selects lactate over glucose, a lot of the time preferentially. So, we couldn't get to those understandings though in 1920s AB Hill couldn't figure that stuff out because he didn't have the chemistry to be able to titrate these things out. So we, I mean, I actually I'll go back to that wonderful book I'm blanking on the author's name, but sapiens that's made a lot of ways. He makes a very good point in that book about the word ignoramus, which has basically Latin for, we don't know and in his argument. And I tend to agree with him that the single purpose that the scientific revolution occurred is because of the fact that we finally acknowledged ignoramus, which is a way of saying we acknowledge that we don't know things because what's the point of doing research if you know it.
Yeah. So we have to keep in mind that science does not work. People, people have to think of science, the exact wrong way. People think of science as proof and idiots, actually by definition the exact opposite. It doesn't prove anything. It does reduce uncertainty. But we are always hamstrung by our inability to measure things at the deepest level possible. And that's getting better of course, but it'd be pretty foolish for you to think, you know, everyone in the history mankind was wrong and we're the generation, we're the smart ones that got it all figured out. So yeah, we, we constantly see this and you can go back as far as you want, where we believe something for decades or a hundred years until we got the more accurate technology and realize we were totally wrong or partially wrong or wrong at some level.
All right. Now I would love to dig into one of the concepts that you touched on in your talk which was about my own nuclei and satellite cells. Right. And having these more, more, my nuclei and satellite cells would equal bigger muscles. And they, there was a co-relation there to recovery as well. Right. Could you dig into that a little bit?
Sure. The way that it basically works is you have to realize that all of your individual muscles are actually comprised of millions, if not more, probably more of individual muscle fibers or muscle cells. So the way that a muscle function is it's the collective expression of those individual parts. So if you dive down into those individual parts, what you find is they are in fact regulated by thousands, if not millions of little organelle called the nuclei. So if you remember from your middle school or high school biology class, they are the part of the cell that controls regulation tells it to grow, shrink, die repair, et cetera. It also is what holds your DNA. So it's really the master regulator of any cell type. And so it's no different than human muscle or microfibers as we call it. So one of the things that we have started to examine and that was, will be the collective, we, myself filling a very small part, but a lot of researchers around the world for a long time have been studying how many of these nuclear you have cause most folks don't realize that human muscle fibers are some of, if not the largest cells by volume in all of biology.
Hmm. I mean, they're huge. I, you can see this, there's a video I did for a TV show. While I've got it, I think it's up on my YouTube page, but it's up on YouTube somewhere where you can see just with the naked eye, I take a bunch of muscle fibers that I took from a biopsy. So those from somebody's quad, and I can pick up one individual muscle fiber with just a set of tweezers with my naked eye. And you could see it on that camera, on the end of the tweezer. So there, they're huge, huge, huge, huge, huge cells, which means that again, very on like any other cells in biology, human fibrous are what are called multinucleate. So most cells and biology have one cell one nucleus. Well, because we're so large, we have to have thousands, if not millions of nuclei per cell, and the easy analogy there.
If you ran a company and you had three employees have one nucleus, right? You could have one boss or one manager, but as you expand and you open up another office across the country and you open up another one and another country, and as you get larger and larger and larger, if you still only have that one manager, it's very, very difficult when a doorknob breaks at one of your offices in Guatemala. And if you have to be there to be the one to approve it, it's very, very difficult. So it's easier for you to expand and grow and shrink and repair and increase the rate of turnover, right. Which is a way of saying when there's slight damage, can you fix it and repair it really quickly? The only way to do that is to increase the amount of these managers of these mononuclear you have.
So that's one of the major focuses in this area of science is what's the role exactly. Of these nuclei. And one of the things that we're fairly sure of is that STEM cells that are late dormant around the cell when the need comes to add more, they can actually kind of, for lack of a better term, go into the fiber, turn into a nucleus, so you can increase the nuclear count and therefore it can enhance your control of the muscle. Again, the easy example is to think, why is it that your friend recovers faster from this exact same workout, even though you both sleep the same, you get the same hormones, nutrition, et cetera. Well, potentially that person has more nuclei in their fibers. And so it's just easier for them to tell the fiber exactly what to do in terms of repair.
And my friend, Kevin Mirik just published a really nice paper. I think I threw it up on my Instagram a few days ago. But a really nice paper when he examined this in a very interesting model. Now it was a rat, I think and it's not perfect, but it does provide us some detailed mechanism of the exact relationship between these satellite cells and how they turn into the nuclei. And in fact, his work has actually made me start to question and I'll probably have to now go back on some of the things I said on podcasts, like just a year ago. Cause I think I was wrong on some of this stuff and this happens all the time because Kevin does such nice work. So you know, Kevin's actually would be a fantastic guest for the show if he's actually done a tremendous amount in the whole idea of concurrent training and love to bring him on.
At some point, there were a lot of myths in that area that adding a robotic exercise actually compromises or kills your gain. So he's got a very nice publication. If you're interested, it's fairly easy to read actually Mirik M U R a C H as well as Bagley Jimmy Bagley, B a G L E Y, their paper on the con what's scientifically called concurrent training. It's very, very nice. But nonetheless, I mean that's kind of what we're identifying is the relationship between these things and the fact that counterintuitively a lot of really high-levelallows athletes actually have very small muscle fibers, and that allow them to have more nuclei that allow them to have more control and more turnover and regulation of the fibers, which we think, and we're guessing a little bit, we think that allows them to enhance their recovery so that they can train multiple times a day and more often than the rest of us.
Well, I guess at this point, the question then becomes, you know, let's say me and you are doing the exact same workout and you're recovering much faster. Is this something that we were born with? Is it genetics or is this something that can be trained a little bit? And is there a way to, I guess, increase the number of my nuclei?
Yeah. So the amount of nuclear number can increase because, you know, satellite cells can be differentiated and proliferate into an amount of nuclear. But so the real question is actually is the satellite cell number limited. And I would have to defer to Kevin or some other experts in that area because we don't exactly know a certain portion of that number is genetically determined, but whether or not you can augment that number through training as such it's a little bit left to be determined and it's most likely thought to be not confounding or confusing the factor a little bit more is the fact that it looks like now we have potential to increase nucleation without necessarily having to have more satellites. And so we don't know what's going on there. And so that could totally change what we're looking at. And we'll get in the future.
Having said that you mean back to your original question that could be one of the examples of why you recover better than I do. It could be other factors too. A lot of the molecular factors that are outside of genetics and those other factors are very, very transient. Well, I just published a paper literally yesterday that got accepted where we looked at a particular set of proteins that are called the map kinase or map care. So that's a family of proteins. So here's what they do. And this is not exactly how they work, but I'm going to translate a little bit. So it's easier to understand for non-scientific folks. So these are basically proteins that are inside of yourself and then what we call signaling proteins. So let's say you stretch the muscle fiber. The muscle cell gets stretched. It gets damaged which activates this protein because it's on the cell wall.
It talks to another protein, it talks to another protein, but stocks, another one kind of goes down the chain and eventually one of them, one of those proteins talk to the nucleus and tells the nucleus we've been damaged. This is what we think you should do about it. Express the genes that you have that code for the protein, say muscle to repair the muscle damage. Well, we found in endurance training and we've actually found this before in a spectrum of people from those that are sedentary. Those that are recreationally active, those that do like circuit training were what we would call a scientifically. So some combination of low-level weights plus conditioning, plus a lot of movement, you know, somewhat of a CrossFit workout all the way up to very high-level powerlifters and all the way through very high-level weightlifters. Now we just published our paper again yesterday on the other of the spectrum, which is the endurance side of the spectrum.
So good runners, moderate runners, all we have to very good runners and found a couple of things. So these proteins are activated through a process called phosphorylation, right, but we can just think of it as are they turned on or are they turned off. So what we see happen in both of those studies is differential responses based on your training load, which is a way of saying, you can either turn up or turn down the amount of that protein that's activated translation. That means it's more sensitive or less sensitive. So you and I may have exact same amount of these signaling proteins, but you are more hypersensitive. More of yours is turned on or turned off. So when we get the same exact stimulus, because your sensitivity is different, you get a different message communicated to the nucleus. The other thing that was very interesting, we found is the total amount of that protein.
So not just whether or not it's turned on or off, but how much of it's actually present is extremely responsive in terms of the training. So you may increase or decrease up-regulate or down-regulate the amount of that protein that's around and available, which also plays into your sensitivity. So you have multiple routes. For example, if you increase the amount of the protein and you have all of the turned on, you are extremely sensitive, and I could do the opposite, which is downregulate or get rid of a bunch of the proteins and have the ones that are available turned off. Now it's going to take a lot more activation for them to really get stimulated. And so what we saw happen through the continuum of training is that actually, it's a combination. So those of us that really turned down the amount of protein tend to turn on the ones we have more often and vice versa.
So that's stuff we're teasing out, but that would be another explanation independent of the nuclei as to why some people respond more or less than others because they have either more or less of these signaling proteins of which there are hundreds of thousands. We just looked at three of them or, you know, they're more sensitive. So a lot of potential explanations. Now, none of those are going to ever represent the entire equation because physiology is very complex and you have multiple systems that are integrated simultaneously. But at least from our perspective, from the muscles perspective, we're getting closer to some answers we think.
I want to dig a little bit into it, and I approached you about this afterward. And it was hypertrophy-based training. And I was at, at the, at the time I was thinking, okay, how does this kind of apply to maybe a master's athlete? And I, I would love for you to dig into, and I think in our space, I feel like we're, we're past the point where we're scoffing at, you know, bodybuilding style training. We realized that it has some value. Yeah, it, could you dig into maybe how that correlates to some of these satellite cells and even the concept of hyperplasia that you touched on?
Yeah. So a couple of things, the older we get it doesn't appear to really inhibit our ability to grow muscle mass except maybe really closer to terminal age. So 80, 90 plus maybe you lose that, but mechanisms appear to be the same. Now, as you get older, though, you become less sensitive from every layer, from the hormone layer to the cell level, to the molecular level, to the genetic level all the way down. So what that means is you probably need more of a stimulus to grow at that age. Like for example, we know very clearly it looks like older folks need more protein than younger folks. They become what we call protein insensitive. So we have to take that into consideration nutritionally as we start to train these individuals now making it no matter how complicated is the fact that they probably need more of a stimulus than younger folks, but they also can't handle as much work.
And so that's, that's your real conundrum is how do you balance not getting them so sore and trash that they can't work out for three weeks knowing that they need more of a stimulus. The mechanisms, the satellite cells do appear to be finite. So that is a as well, but again, Kevin's paper that he just published this week, last week, maybe suggested that the older individuals have an ability to overcome that given enough statements, but his stimulus was, was this thing called synergistic ablation. And it's not possible in humans. So we have to take that with a bit of a grain of salt, but we just don't know. And then alluding to your, to your hyperplasia comment.
The way that you grow muscle.
You know, you basically have two options, either all those muscle fibers that you have to get larger, therefore the whole muscle gets larger. So by larger, I mean, diameter, right? They get thicker, right? Hyperplasia should guess though the opposite, which is, well, maybe you just add muscle fibers. So hypertrophy, which is your muscle getting bigger could be either each individual fiber getting thicker could be you're adding more muscle fibers.
Or it could be a combination. And in
Kevin's model showed very good evidence that it's very, very likely that hyperplasia happened in his synergistic ablation model. And we've seen that a lot before animals. So I think it's pretty silly to think that it's not happening or it's not possible. The real question that we don't have an answer for is what does it actually take for it to happen in humans? I am of the belief that it happens a lot.
In humans, you can ask
For the scientific data, but it's one of those things, technologically will almost never be able to show it because we would have to take out a muscle fiber measure it, put it back in your muscle, assume that nothing changed train. You take that exact same fiber back out and then look at it again. And then that's just physically feasibly impossible right now. I mean, we're probably talking decades if ever, but we have so much in the mechanism understood. We know what happens in virtually every other mammal or at least as possible. So it's pretty difficult for me to believe the fact that it's not Kering. The real question becomes what's the actual mechanism. And I was literally having a long talk with Brad Schoenfeld. Who's the muscle hypertrophy guy. If you don't know his work, he's done more work in the area of muscle hypertrophy than any human on the planet, human muscle wiper tree. And, you know, the mechanisms that we could come up with are, it's either going to have to take one of two things, either tremendous
Insult. So picture
A ton of East-centric work in a really short timeframe or exposure over a very, very long period. So probably decades or more now, the second model, the decades, or more again, because of, you know, logistics timeline. I can't do a study that takes 30 years. I hope I'm not still doing science and 30 years. Well, I probably will, but those are just not possible, right? And the other one is also really, really difficult to pull off in humans because of the obvious reasons. It's hard to do so much damage to a person and make that ethical. So we're kind of left at this position where I don't know really how much farther we can go in that in terms of getting strong evidence in humans, but as the evidence continues to mountain animals, and we start to understand more about the mechanisms. I think we have to at least acknowledge that hyperplasia is not totally impossible. In fact, it's probable, but how much it actually contributes to normal human hypertrophies, it's probably minimal, but it's probably possible. And that's really, as far as I just want to see the conversation go tos, we gotta stop talking about it as if it's physically impossible and it never happens and says, yeah, it's probably minimal, but it's probably going on.
Okay. And then now you are the guy who is like the anti biohacking. Right. But then I remember during the talk you mentioned like there is this one hack, this one hack two, I believe it was more satellite cells.
Well, sure. Yeah. I mean, there, there's certainly a hypertrophy hack and, and it's not to add increased satellite cells that we really know of, although I'm standing to be proven wrong on that one. That's fine. But what we do think happens and this has been shown in a number of papers now that those that use exoticness testosterone have a dramatic increase in mom nuclear account. And it looks like that mouse nuclei are preserved even after the testosterone for years probably. And the, you know, the IOC and you saw it on Masada caught wind of this a couple of years ago. And a lot of people started making the argument though that, okay, so then what happens if I just do one cycle or if I've been caught one time for exotic testosterone? Well, you're suspended for six months. That's great, but you're gonna have this benefit at least for five years, maybe. So is that really fair? And so that's when you saw them actually really up there depending on the sport you're in, but they really up their probation or their punishment period from being caught with PDs. So that's an easy way around it, but you know, that's nothing new at all. We've known for a very long time. Anxiety, testosterone is very effective for muscle growth. We just have a bit more mechanistic understanding of it.