I’m joined today by Samuel Buckner, PhD, a professor and researcher at the University of South Florida. In this episode, you will learn the fundamental elements of hypertrophy for strength and muscle growth, broken down to a cellular level.
Dr. Buckner is also conducting a no load / low load study on how the Neubie can induce hypertrophy. Tune in, learn, and share!
[Garrett salpeter] 0:53
I’m joined today by Dr. Sam Buckner, who is a PhD professor at the University of South Florida and the director of the USF muscle Laboratory. Dr. Buckner got his bachelor’s degree from Temple University master’s from Florida Atlantic, and then he did his PhD at the University of Mississippi. He’s been teaching at USF for the last three or four years running his laboratory there as an assistant professor in exercise science, and he his research, you’ll, you’ll come to find out why we’re so excited everyone the show, because his research is focused on skeletal muscle adaptation, on how to use low load training to build strength and muscle and also on the relationship between muscle strength and muscle size.
[Garrett salpeter] 1:42
He’s gotten over 60 papers published so he’s really, you know, a prolific and excellent scientist. And an interesting note, I when I met him in person, I was very impressed by his handstand push up skills. And at one point, he actually held the Guinness World Record for the most consecutive 90 degree pushups as well. Do you still hold the record Dr. Buckner?
[Samuel Buckner] 2:02
I no longer do I lost it when I was working on my PhD.
[Garrett salpeter] 2:06
Ah, yes, yes. The sacrifices we make along the way, right. Yeah. Well, thank you so much for being here. I’m really excited to, to talk with you, and, and be able to dive into some of your research and also talk about some of the research we’re doing together on the newbie. Yeah, I would be here. So this this, there’s a lot a lot of different things I want to cover before we get into some of our studies and different things. Could you for the benefit of our listeners, could you give just maybe a couple minute overview on muscle hypertrophy, what it actually means to grow muscle and what the most important contributing factors are in muscle hypertrophy.
[Samuel Buckner] 2:51
Certainly. So, I’ve done a lot of work studying muscle hypertrophy, and it’s one of the areas that interests me most, and a lot of people will enter the gym, the goal will be muscle growth, they want to hypertrophy their muscles. And what that means when, as a scientist or a researcher, what I’m looking for when I say hypertrophy is typically an increase in the contractile component of skeletal muscle.
[Samuel Buckner] 3:19
However, you don’t always know that’s what’s increasing, we have other components within the muscle as well. But basically, if we think about the organization of muscle, we have our entire muscle belly, which is, you know, what we see when we look at ourselves, we see a muscle, that muscle is made out of fascicles. And a fascicle is basically bundles of muscle fibers. Right? So we’ve heard a muscle fiber before. So a muscle fiber is a skeletal muscle cell. And that skeletal muscle cell that fiber is made out of something called myofibrils is basically levels of organization. And that myofibril is made up of something called a sarcomere.
[Samuel Buckner] 4:00
And a sarcomere is basically scaffolding proteins and then contractile proteins. And those contractile proteins are called actin and myosin, right? So actin and myosin basically interact with one another, and basically pull each other closer together, which causes shortening. So it happens at this most intricate level. Now, what we believe happens when we hypertrophy is we add additional sarcomeres to muscle fibers. So remember, sarcomeres make up myofibrils, a bunch of sarcomeres.
[Samuel Buckner] 4:35
And those myofibrils make up the fibers themselves and a bunch of fibers make up muscle. So we’re adding these proteins to our muscle, in series and in parallel, depending on what study you read. And over time, we accumulate enough to be able to pick these up with different imaging techniques. Right, and the technique we use in my lab, I use B mode ultrasound. Actually, I’m ultrasound behind me today. And we’re able to look at the muscle bone interface, and the muscle fat interface up at the top of the image. Actually, this is a picture of my bike. I don’t know why I keep it on my wall next to me. But we can see in this picture, and this is an old ultrasound, but we can see the bone here, the bottom of the image, at the top, we can see the muscle fat interface. So we’ll measure that distance over time, I don’t know how well that’s coming off on the
[Garrett salpeter] 5:33
Screen. If you’re listening, just listening to an audio here, he’s showing us an ultrasound picture. And we can see some bones and muscles and fat. And he’s looking at a measurement, basically a vertical measure to some of these dimensions to measure the muscle size.
[Samuel Buckner] 5:49
Yeah, yeah. So we’ll measure muscle thickness at multiple points across the muscle belly. Because we do know that when we train, muscle growth is not homogenous, so it’s not the same, from the top to bottom of the muscle, it may grow differently across the muscle belly. And when we’re training to induce muscle hypertrophy or growth, there’s several ways we can go about it.
[Samuel Buckner] 6:17
And in the literature to date, I think most researchers agree that intensities are loads around 30% as low as 20 to 30% of one RM. And as high as 7080 85. Some studies make muscle growth Hadwin 90% of one RM, this wide range of training loads, seems to induce growth. And why do these training loads induce growth, the speculating mechanisms behind growth currently, mechanical contributions and metabolic contributions. And what that means when you pick up a dumbbell, that dumbbell is a mechanical signal, right, your muscles activate and sense that load. And that load tells your muscles to grow. Right through turning on the fibers, the fibers have to be turned on, they have to be activated to lift the weight.
[Samuel Buckner] 7:16
So that’s a mechanical component. We also believe we have a metabolic component. And what that means is when you contract your muscle, right, the production of ATP, which is the energy currency of our cells, when we contract muscle, we produce metabolic byproducts that we the one most people are familiar with is lactate production. Hydrogen ions. Basically, when we create energy, we get byproducts. And those accumulate within muscle cells, and cause muscle cells to fatigue. And when muscle cells fatigue, we hack that have to activate more, right to continue to exercise. So the simplest example if I left a heavyweight, and let’s pretend I have five motor units, and a motor unit would be one organization of muscle, it’s an alpha motor neuron in the fibers that innervates. So you got to activate a certain amount of fibers to lift a certain weight. Right.
[Samuel Buckner] 8:23
So a heavyweight takes a lot of fibers, a lightweight doesn’t take a lot of fibers, when you lift that heavyweight, the mechanical component makes you activate all those fibers. If you lift a lightweight, the mechanical component makes you only lift let’s say one quarter of those fibers are activated, right. However, if you do enough reps, the fibers you’re turning on are going to become fatigued to metabolites. Right, and you’re gonna have to train additional fibers. So the endpoints the same, we activate all of the fibers associated with that movement and fatigue them sufficiently. And I think most people would suggest, and there is some disagreement here.
[Samuel Buckner] 9:09
But ultimately, if growth is what you’re trying to achieve, you need fatigue. Right, so fatigue the fibers and if you lift heavy weight, you can fatigue the fibers and eight to 12 reps. If you lift the lightweight, you might need 20 to 30 reps, but you reach that same endpoint, which is eventually turning on all of the fibers involved in that movement, activating them right and stimulating a signal. We have signaling proteins within our fibers that get turned on when the fibers are activated. And they tell that fiber to grow right to stimulate something called muscle protein synthesis to synthesize new fibers or new proteins associated with our myofibers and our myofiber again, made of sarcomeres which are made out of action and myosin, and various other proteins. If you want me to add one more layer to that yet, I can just bring in the sarcoplasm. But I might be going too deep for our first intro question.
[Garrett salpeter] 10:12
Let’s, let’s do one more layer. Let’s do one more layer.
[Samuel Buckner] 10:15
Okay. So this is just kind of the emerging new controversy. And this actually, it can tie right into muscle size and strength as well if we want to go there. But the newest discussions around muscle growth are in this idea of differentiating between something called myofibrillar growth, and sarcoplasmic growth. And a lot of individuals chasing growth. Think that, okay, we might be stimulating depending on how we train, we might be stimulating something called sarcoplasmic growth, or we might be stimulating something called myofibrillar. Now, myofibrillar growth is the growth that most people believe contributes to strength, because myofibrillar would be proteins associated with a myofiber.
[Samuel Buckner] 11:04
And if we remember myofibers, make muscle fibers, right, which contribute force, so the contractile apparatus of muscle, the sarcoplasm, is basically everything surrounding those muscle fibers, right, the organelles that support they store calcium, right? It’s basically the area surrounding the fiber. And there’s been one study that came out that showed that sarcoplasmic hypertrophy was disproportional to myofibrillar hypertrophy, when you did really high volume training, right? And that made people go Hmm, that’s why bodybuilders are sometimes disproportionally strong for how big their muscles are.
[Samuel Buckner] 11:55
Because the sarcoplasmic component in theory, would be less contractile. And more, I guess, just supportive for the muscle itself. But the data we have on that currently is not really strong. We have one study with they took a subset of their data and analyze that subset to come to those conclusions. But I tend to think, and I think most experts tend to think that when you stimulate growth, you have an increase in both the myofibrillar, the contractile component and the sarcoplasmic component, which is basically everything else in that cell.
[Samuel Buckner] 12:36
They seem to increase typically in proportion as we train, but one of the reasons that was a tempting hypothesis, and I think it still is, is because we’re constantly trying to explain why in research, I think in in practice, we see instances where people grow, but don’t necessarily get stronger. And it becomes this discussion of, is there something called functional hypertrophy and nonfunctional hypertrophy? Meaning is sometimes growth contributing to our strength into our function, and sometimes, is it not? And that’s a loaded question, of course. And I suppose it depends on what view of muscle growth that we’re going to subscribe to. And there’s a lot of debate amongst experts currently.
[Garrett salpeter] 13:34
So at one end, it’s the seems like if when you train to that fatigued state, you get both sarcoplasmic and myofibrillar hypertrophy. What if you’re an Olympic lifter, or a power lifter, and you’re training singles and doubles, you’re only doing you know, one or two or three reps at a time taking plenty of rest?
[Garrett salpeter] 13:58
Yeah, is, is that and you’re and you’re having to, you’re trying to limit muscle growth, so you can stay in your weight class. So are those types of athletes? Is there evidence that shows that they’re getting more myofibrillar hypertrophy and less sarcoplasmic? And it’s more of that, like you said, quote, unquote, functional? Or is that just kind of a theory that hasn’t been proven?
[Samuel Buckner] 14:18
It’s a theory that hasn’t been proven, and it’s only been done in one study, and it was hypertrophy style training. They’re using just really, really high volume. But I think it was artifact I think that study had like remarkable damage, and inflammation, and I think it was interpreted as, like disproportional sarcoplasmic hypertrophy. My hunch is that hypertrophy is going to happen where we increase the amount of myofibrillar protein and we also increase the amount of sarcoplasmic protein to support those structures.
[Samuel Buckner] 14:57
Because the sarcoplasmic component of our muscle It supports the myofibrillar. Right? We have the sarcoplasmic reticulum, which stores calcium, that calcium would be captured in the sarcoplasmic component, but it releases calcium. So it can bind to the myofibrillar component. So muscle can contract.
[Samuel Buckner] 15:17
So I think it just makes sense that they would work together and increase in a similar fashion, it’s going to be interesting to see what the research eventually reveals. But I think the in the example you gave, they were training with a high level of specificity, right, the movements that they need to perform in their sport. And I think, you know, that’s probably the best way to train to not prioritize growth, when they need to focus on their weight class, but prioritize that skill acquisition and getting as efficient as they can in that movement, and taking advantage of various neural adaptations that are likely going to take place to enhance their strength. Okay,
[Garrett salpeter] 16:05
That makes a lot of sense. Thank you for that. And then the other end of the extreme, if we’re talking about people who are, you know, like you said, who are going into the gym because they want to build muscle, and they are interested in hypertrophy, that’s their goal as their priority.
[Garrett salpeter] 16:20
So we heard from you that in training, you have to reach that endpoint, whether using 30% or 80%, of what your one rep max, you got to reach that endpoint of fatigue and build up those metabolites and trigger proteins that does this. And then the soy proteins, and then muscle growth happens during that protein synthesis phase, right, during the recovery period. And what are the biggest drivers of that we need to have proteins and raw materials? You know, is it insulin or other hormones or growth factors? What are the biggest things that that move the needle on muscle protein synthesis? What are the kind of the biggest requirements that we need to have kind of metabolically and otherwise?
[Samuel Buckner] 17:02
Um, I mean, yeah, we, we need protein availability. And this is, I’m not in the area of protein, I’m a reader or an occasional reader and the protein research, where we know that you obviously the diet needs to be there, if we’re going to support growth of our muscles. I do think a lot of that literature, and this is probably a topic for a different day. I think the protein literature exaggerates the amount of protein we need and nothing literature as a whole, but a lot of emerging recommendations are like pushing this more and more and more protein.
[Samuel Buckner] 17:46
And I don’t think anything is going to discontinue to have a dose response, you know, for its ability to induce growth. And as far as hormones, I’ll try not to overstep my area of expertise. But I will speak on the hormone hypothesis, which was really, I suppose relevant in, in the early days of resistance training, we recommended always lifting heavy for growth, because lifting heavy stimulates a much greater hormonal change than lifting lightweight, right. So if you lift really light weights, you don’t have this large increase in testosterone from pre to post exercise this acute change to cesarean and growth hormone.
[Samuel Buckner] 18:40
But you do see that when you lift 70%, or one or M for four sets to failure, and for a long time, we thought that that acute shift in hormones was causative for growth and adaptation. And I think now most people would agree that that short transit increase, you know, it’s elevated, I don’t know how well it’s back down to baseline hours after exercise. That doesn’t seem to be playing a large role for the muscle growth adaptation. It’s more so the activation of the just protein cascades, right. So whether it’s the, I don’t think metabolites or direct stimulators for growth. Metabolites are indirect stimulators for growth because they just allow us to activate more muscle, right? If if you turn on a motor unit, because you only need one to lift that weight, well, if the weight so like the only one more unit, that’s a motor unit you’d probably typically use for aerobic exercise. Does that make sense?
[Samuel Buckner] 19:55
Because aerobic muscle is designed to more so far very light, non-intense activities. But if you are able to bring yourself to the point of failure, you fatigue those ones out. And you turn on motor units that are associated with lifting heavy, even though you’re not lifting heavy. And those motor units once they’re activated, right, there’s there’s some activation of a protein signaling molecule, it’s called motor. And lot of people are familiar with the the mTOR complex, we stimulate this protein and this protein activates protein synthesis within the fiber. And this seems to be what’s important. So through some type of metabolic signal or mechanical signal, right, we’re able to activate a protein cascade through various signaling proteins.
[Samuel Buckner] 20:54
It’s called the signal transduction hypothesis. Right? So we activate a protein and this protein has downstream proteins that it turns on. And the end result is we’re stimulating protein synthesis. And when we have enough protein synthesis occurring, we add contractile components to our muscle. And over time, eventually, we’ve added enough that we have maybe a noticeable visual difference, we can see it right. But after you train, you’ve stimulated that response. And muscle protein synthesis will be elevated for several hours, right. But you train and you come back the next day, no one’s going to say, I grew a lot from that session I did yesterday, right? What they’ll say is, I feel like I really stimulated my muscle, right? You told it to grow. And whatever its capacity to grow over a 24 hour period, that’s what’s occurred. But it’s going to take several of those sessions to accrue enough of that growth for it to be meaningful.
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[Garrett salpeter] 22:38
That makes sense. That’s I really appreciate that overview. And that makes a lot of sense. Overall here, I’m really interested in getting into some of this difference between strength and growth. But let’s talk let’s talk first while we’re on the topic of hypertrophy. And, you know, we realize now that this goal, the goal is to reach this endpoint of inducing some fatigue building up these metabolites. We know that that’s your business, we know that, and that some anabolic hormones are helpful in the process.
[Garrett salpeter] 23:15
Fair summary of what you said so far. Yeah, thanks. And so in your research, you’ve been looking at ways to induce hypertrophy, to reach that endpoint of inducing some fatigue, with little to no external resistance. So that’s a two part question. So can you talk a little bit about the work you’ve done? And then let’s talk a little bit about some of the research that you’re doing now with the newbie along those same lines using the newbie to get that type of muscle recruitment with a hypothesis that it may be able to induce growth? So we’ll start first with a little bit of your research background and how you’ve been able to evaluate that hypothesis of can you reduce muscle hypertrophy with little to no external load?
[Samuel Buckner] 24:02
Yeah, yeah. So um, I guess it’s still my research career in 2015. Somewhere around there, and I’ve done quite a bit of work using blood flow restriction, so restricting your blood flow during exercise, while utilizing low loads, so lightweight, with restricted blood flow, and what does this do to skeletal muscle? So we did several studies over the past four or five years, looking at low level alternatives, and essentially what we find when we use blood flow restriction, is that the combination of lifting when you lift, lightweight, and a lot of people have probably experienced this, one of the complaints that you might see is, well, you just have to do so many repetitions, right? So a lot of times the frustration of lifting light weight is the fact that
[Samuel Buckner] 25:00
You might be in the gym for a very long time, if you’re doing something effective, right? So we said that the contributors for growth, we need some level of fatigue. And we’ll clarify when I say fatigue, my recommendation is typically to failure or near failure. So you don’t have to go to absolute failure. I always tell people, that’s an insurance policy, but it’s not absolutely necessary. But anyway, we, we know that doing low loads can be very time consuming. So blood flow restriction is a technique where you add a cough to the top of the arms or legs, and you restrict the blood flow into the muscle, right. And at the same time, you limit venous return, so bloods going into your arm, right, but blood is having a really hard time leaving your arm. Right, so you’re lifting that same really light dumbbell. But now you’re not clearing metabolites, right, they’re stuck.
[Samuel Buckner] 26:03
And when metabolites get stuck, they induce fatigue, right? So you create this scenario, where your arm is not recovering, right? You’re doing bicep curls, for example. And there’s this burning sensation, it doesn’t feel good. Metabolites are bathing that muscle essentially. And maybe, with let’s just say, a 20 pound dumbbell, you used to be able to do 40 reps. Well, with BFR, because we took advantage of metabolites, right, metabolic induced fatigue, instead of doing 40 reps, we can now only do, let’s say 20, or 18 reps, we’ve reduced the volume of work, we have to do to reach the same endpoint. So in a lot of ways, the kind of what I think of my research is finding different ways to reach the same endpoint and this endpoint is, let’s activate the muscle. Let’s take the muscle. And let’s see if in response to this it grows. So we took that a step further, I suppose. In one of my colleagues, Brittany talents, it was her thesis, we wanted to remove the external load completely, right?
[Samuel Buckner] 27:20
So we know we can lift lightweight, what if we lift no weight? Can we still make a muscle grow? So we, we actually coined this no load training. And essentially what it was, is going through a range of motion for a bicep curl, and doing four sets of 20 repetitions, right. But what if you were to do no load training, you no longer have an external cue? To tell you. Okay, I need to contract this much to overcome this. So there’s no load to overcome. So excuse me. Instead, what we said was maximum contract your bicep. Right?
[Samuel Buckner] 27:59
So we just had people flex as hard as they could up and down. Right? And it turns out, that’s actually not easy to do. But what it does do, is it maximally activates the muscle. Right? And it still is relatively fatiguing. Right? And it’s all internally focused. Right? Meaning you’re focusing internally on the muscles tension, as opposed to focusing on a weight in your hand. Now, I don’t recommend this training strategy for anybody. I think it’s really hard because psychologically, I think it’s a bit more taxing. But it demonstrates something, I think it’s important it demonstrated, the growth is not at all load dependent. Right? It’s dependent on creating the signal and creating this activation. Right. And this could be a pretty smooth transition, if you think about new fit.
[Garrett salpeter] 28:59
But let me ask you before him as much as I love the smooth segue, let me just ask you a question there. So is that fair to say, to call that quote unquote, no load training, because if you’re really squeezing the bicep is overcoming mechanical tension, mechanical resistance of the triceps of the ear. There’s the antagonist musculature there. So there is some resistance. How do you how do you factor that into the conversation here? How do you how do you look at that resistance? Yeah. Musculature it’s,
[Samuel Buckner] 29:28
So technically, it’s no external load training. And, you know, there’s been research I would call this research pretty similar. They didn’t find a huge difference, but they had people lift dumbbells. I think it was dumbbells, I don’t remember exactly. But they would tell them to either focus on lifting the weight or focus on squeezing your muscles as hard as you can. And the group that focused internally is, as opposed to externally have larger growth over the study period. Which was eight or 12 weeks.
[Samuel Buckner] 30:02
So internal focus in this case was more effective than external focus. And what I would say is that if you’re focusing internally, you’re probably producing more force and you need to, to overcome that weight. Right. And I would say, with no load training, you’re still producing probably more force than you would need to, to overcome. I don’t even know what weight we could place in the hand, and it’d be the same level of contraction. Right? So mechanistically, what does that tell us? It’s, it’s the internal tension, right? Between the actin and myosin.
[Samuel Buckner] 30:45
That seems to be what’s important for creating the signal and it can happen independent of an external load. And why might that be important? I think people get in the mindset that you have to lift heavy if you want growth to occur. Right. And there’s areas where we do not know everything yet. I did a podcast recently. And we talked about muscle density. Because I know a lot of the bodybuilding community thinks that lifting heavy is important for muscle density. Right? I don’t have any data right now to really answer that question. Just some speculation. But we know that we can lift lightweight, we can let’s heavyweight we can lift, no weight, technically. And as long as we’re activating, right, internally, those fibers growth as possible.
[Samuel Buckner] 31:38
And typically, in these studies, we compare the growth that occurs to the gold standard, and the gold standard for as long as I’m familiar with the literature is 70%, on one or M, you know, three or four sets to failure, right, or eight or 12 repetitions per set. That’s kind of the traditional comparison group that we compare these things against. So the no load training was compared against traditional high load training. And a lot of these low load alternatives of BFR have been compared against traditional high load training. Does that make sense? Yeah, it
[Garrett salpeter] 32:15
Does. And that’s interesting. To me, I see it almost as three as three groups. One is traditional resistance. One is, you know, very low load, where you’re using BFR for the metabolites. And then one is, like, like you said, the internal focus is creating a similar mechanical tension as the higher load but doing it internally, rather than with that external weight as the stimulus. Is that kind of fair to break it up into those three?
[Samuel Buckner] 32:44
Yeah, I definitely think so. Because the no load would not comfortably fit in. And either, we could add a fourth, if you had BFR. To know about, I think no load becomes a lot easier, because now you can create metabolites within that muscle as well. And we actually did, we did a study, it was no load training with them without BFR.
[Samuel Buckner] 33:08
And the idea was, if you’re, a lot of people haven’t had access to a gym lately, putting a cuff on and fighting that cough, and doing some contractions, you probably have to focus less on maximum contracting, if you can accumulate some metabolites. So I mean, for the purposes of our discussion, I think three categories are fine, but then within those, you can maybe move the meter, well, let me add more metabolites to this type of training, right, Let me decrease metabolites here, let me increase or decrease external load component here, or let me increase or decrease the internal focus on any given type of training. So yeah, I think all of those are really beneficial, and things we can take advantage of.
[Garrett salpeter] 33:53
Okay, so we know the variables, these are all ways to get to our endpoint of inducing fatigue and metabolites within the muscle. And just to be clear, so everyone kind of understands the bigger picture when we’re talking about wanting to do low or no load training. A big part of that is because of rehabilitation, or wanting to reduce the risks of injury or reentry. Right, that’s those are some of the main driving factors here.
[Samuel Buckner] 34:19
Oh, absolutely. Yeah. The clinical implications are that’s where this has the most impact. It’s living here in Tampa, there’s a very fitness industry culture, and they’re more interested in bodybuilding powerlifting applications, but where it has the most bang for its buck is clinical populations are people recovering from injuries that they can’t bear a heavy external load. So it’s nice that we have effective alternatives to lifting heavy weight
[Garrett salpeter] 34:52
and for people who want to train but you know, even if, even if they’re not injured, or maybe they have some aches and pains, but they do Just want something that’s more sustainable, to be able to do some days with less strain on their joints, right and reduce the risks of injury.
[Samuel Buckner] 35:07
Yeah, it just avoid contraindications. Yeah. And I think another one we don’t even think of is, you know, there’s a blood pressure response to lifting heavy weight. And I think about this one less, but when I teach cardiovascular physiology every year, I’m reminded that during a double leg press, your blood pressure could get up to 400 millimeters of mercury at its peak, right? The highest blood pressures I’ve ever seen in literature, and I won’t pretend I’ve exhausted the like, search the literature, but lifting weights, creates a blood pressure spike.
[Samuel Buckner] 35:45
So it’s not like you have a 400 millimeters for 30 minutes. But for a brief moment, you spike your blood pressure up very high. Because you increase peripheral resistance, that resistance from your legs contracting, right, and push pushing blood upward. So there’s other reasons to why people would want to avoid heavy weight, outside of muscle, skeletal, there’s cardiovascular implications as well, where you could perhaps get the benefits of hypertrophy, right? Without the risks of heavy, heavy weight.
[Garrett salpeter] 36:19
That’s awesome that especially when I hear that one, it’s a fabulous point. And two, I can’t help but think that in an aging population, for people who you cannot lift as heavy, you know, for because of those cardiovascular reasons to be able to maintain muscle mass and get all the health and longevity benefits. I mean, there is, to my understanding, you know, pretty well established significant research that shows maintaining muscle mass as we age helps reduce all-cause mortality helps improve quality of life is a big goal that we should all have if we want to age gracefully, right?
[Garrett salpeter] 36:54
There. Yeah. So here’s the version.
[Garrett salpeter] 36:58
That’s a’s a great a great point. So now let’s, let’s take that segue into the newbie here. So you talked about blood flow restriction buildup, metabolites, helping us reach this endpoint to kind of accelerate the rate at which we’re reaching this endpoint of fatigue and metabolites? How do you think the newbie fits into this framework that we’ve described here? Around hypertrophy?
[Samuel Buckner] 37:26
Yeah, so this one’s interesting. And I’m excited to see what we find because it too is a bit unique. And it might most closely resemble some type of hybrid between the no loads, right? Because I think you almost mimic this intense internal focus, right. But without the psychological aspect of having to do that voluntarily. A maximal contraction is not always easy to produce. So I think there could be some value in removing that component, right, which might provide a means to get a fairly intense training session without the perceived exertion. I’m not saying it’s easy, but it’s probably a different kind of hard as opposed to normal training.
[Samuel Buckner] 38:34
And it’s very easy. For example, when I say do four sets of 20, and contract as hard as you can. So one effort is probably here, set to a tier three to tier, right. And you encourage them, maybe they maintain it, it’s hard to maintain activation, because it’s psychologically taxing. So I think in those ways, this has the potential to be a similar stimulus is this maximal contraction, but without that extra strain of it being voluntary. The metabolite profile? I’m interested, and I’m curious, and this is where, you know, we’re looking at the fatigue response to this protocol. Right. So bringing individuals through a training session, and we’re going to see how their fatigue right there. And one of the best ways to measure fatigue is an acute drop in performance. Right?
[Samuel Buckner] 39:39
So if you can produce a certain amount of force, and then you can’t produce that same amount, we would assume that you can’t produce that because you are fatigued. So indirectly, that data might tell us a little bit about the metabolic response. To a training session with a device. But regardless of whether it’s fatiguing, you’re not it’s very interesting. If it is fatiguing, it’s interesting that we achieve this fatigue with this device. And if it’s not fatiguing, then we have a low effort, low fatigue methodology that may induce growth. So I guess what I’m saying is, I’m interested in what we find. And scientifically, we could find one or the other. And it’s nothing more than interesting at this point. Until we get the long term data with the actual growth. I,
[Samuel Buckner] 40:43
I think there’s a lot of potential here. And, you know, if we do consider the mechanisms that we propose, which are activation and turning on of these fibers, right, when you use this device, you get this very clear activation that everyone who’s using it, so this maximum activation, at times it feels greater than maximal and that people feel very fatigued. Right? It’s a different sensation, then voluntary exercise, I think, in fatigue that we feel. So I’m curious as to what that looks like, over time. We’ve, we’ve also, you know, we’re tracking some different psychological things regarding effort, discomfort, these sorts of things. And then we’re also looking at muscle soreness, and the days following exercise. Right? And when we discussed hypertrophy, I didn’t. I did put muscle damage as a mechanism, which some researchers do.
[Samuel Buckner] 41:55
I think muscle damage can be present in hypertrophic protocols. But it’s not necessary. Right? So it’s just an interesting observation to see, is there or isn’t there a damaging response. And the presence or not presence of damage doesn’t guarantee things one way or another. It’s simply interesting physiologically, because if there is damage, then this would look more similar to a high intensity high load training program. If there’s no damage, it’s going to look more similar to a low load training program, if that makes sense. As far as the stress on the fibers themselves,
[Garrett salpeter] 42:38
So it’s just for just for clarification, there is the when you have soreness, does that mean there’s been damage? Are those two absolutely equivalent? Or are they related but not always one to one corresponding?
[Samuel Buckner] 42:51
Yeah, they’re, they’re related, but not always. So just because you’re sore does not mean you have damage. And just because you have damaged doesn’t mean you have soreness, the best indicator of damage, like the best indirect marker. And this is, I think, probably one of the most reliable ways is just a depression and your torque production. So we measure isometric strength. It’s how you pool at one angle. And if you come back the next day, and you can only pull 80% of what you pulled the previous day, then there’s, that’s a pretty good indication that there’s some level of damage, and that you’re limiting your force producing capabilities.
[Samuel Buckner] 43:33
So when we do a damage profile, we do multiple different proxies. So we look at swelling in the muscle, we look at torque decrement. And we look at soreness all together to try to give us this this picture of what’s happening in the muscle. So we’ll have all that data to kind of bring together and consider together and determining, okay, what is the 24 or 48 hour response to this type of training. But everything we need for growth is here. And I think I think we’re I guess before I jump ahead, I think we’re beginning to understand inflammation and damage a bit more. And that damage was classically considered some of the they call it Z line streaming.
[Samuel Buckner] 44:29
So the Z lines are the structural components of the sarcomere. And after damaging these Z lines, which would have proteins running perpendicular, right? They would be like misshapen they’d be like, you know out of not in line, right? That was called Z line streaming. That was classic muscle damage. But we know that there’s this delay, right? We can have this delay in the response, which I think has to do more inflammation Shin following exercise than actual structural damage during exercise. So it’s possible that inflammation is playing a role in soreness as we remodel the muscle. And in those sorts of things.
[Garrett salpeter] 45:19
It’s cool to know that there’s, there’s still a lot that we don’t know, there’s still a lot to learn. Yeah. And even even just on some of these real, you know, relatively simple, not common day, everyday topics. So, so right now, we’re just talking generally about some of the research approach and some of the questions we’re asking you, we’re about to you have completed data collection, the first study, and we’re going to save that for another time, once it’s been analyzed and published and everything.
[Garrett salpeter] 45:49
But the first study that your lab is doing with the newbie is looking at some of those toward production, soreness, psychological profiles, measures of fatigue, muscle swelling, using the ultrasound. So some of those things that you’ve talked about, can you just talk about the plan for the second study?
[Samuel Buckner] 46:06
Yeah, the second side of the plane, and we should be geared up to start this really, really soon. Is this do a train study, right? So over an eight week period, see how much growth we can induce no resistance train population, because we had some discussions, and I think this is a great population to really put the device to the test of its ability to induce growth. And if the acute data and you know, we’ll have a better idea once we look at the acute data, but the acute basically informs the long term and helps us understand what we see, you know, in the long term growth study, so we’re basically going to have people come in, they’re going to do knee extensions. And we’re going to compare head to head.
[Samuel Buckner] 47:04
Like I said, we’re doing a lot of these studies, we compare the new fad stimulus to a traditional heavy training program, right, and we see how do these compare across time. And I think the 70% Compare considered the gold standard. That’s not to say that sometimes things can exceed this gold standard. It’s typically a close race. But I think it’s going to be a pretty fun study, we have so much interest here, because everyone wants to use this device. And that makes my job as a researcher, quite easy. But yeah, we’re going to bring him in, do baseline muscle thickness, multiple muscle sites in the lower body. Within subject design, so one leg is going to do new fit training, the other is going to do the high load, heavy training, and we’re going to see what we can achieve.
[Samuel Buckner] 48:11
And yeah, I, I think one thing that people it’s easy to be critical of research, and we tried to pick the design, we thought would best answer our question. And this within subject design gives us a lot of control. Because if you think about it, when you’re training, sometimes we worry about protein intake, right, which we talked about earlier, well, with within subject, the right leg and left leg had the same protein over eight weeks. Right? The difference was, what was their training for their knee extension exercise for that eight week period.
[Samuel Buckner] 48:51
And you can look at, you could pick any, any indicator that could create a difference between, you know, your groups, within subject designs help with that quite a bit. So you have the same person’s genetics, the same, you know, some people respond to training and others don’t. So, you have a responder for the right and left leg, except now the right and left leg are getting two different stimuli. What does that growth look like over time? So we’ll do muscle imaging. And if growth occurs, we’re going to see it. And yeah, that’s the goal. We want to see. What is the muscle growth response to this type of training? And how does it compare to traditional high load training?
[Garrett salpeter] 49:36
That’s awesome. I’m so excited to be able to work with you and to see these studies evolve and see the data and and hear your analysis of it. And can we have your back on to discuss the studies when the when the data is out there and they’re ready to be published?
[Samuel Buckner] 49:53
Oh, definitely. Yeah. I’m happy to come back on and talk and yeah, I know a lot of people you In this device and with it, I’ve had great success. So I know people are interested to see the data. And I’m excited that, you know, we’re conducting these studies. And yeah, I can’t wait to share to share what we find.
[Garrett salpeter] 50:17
Awesome. Well, really, it’s a true honor for us to be able to work with such a wonderful and curious and knowledgeable scientist, and your team there. And we’re really grateful to, to have you come on the show. So thank you for sharing some of that knowledge and your perspective and experience. If people want to look up any more about you or your research, what’s the best place to find news website social media?
[Samuel Buckner] 50:42
Um, I am not super active, but I am on social media. It’s the same your Buckner on Instagram, I suppose. I have a Google Scholar page. So, just Samuel Buckner is my Google Scholar profile. And that’s where people can find my research if they want to read my specific research. Other than that, if someone has like a question related to what I do, I could take that question on Instagram. Or you can email me and my, just my school email, S l. buckner@usf.edu. And, you know, if it’s a research related question, to something I’ve published are some of this type of information. I’m happy to answer it when I get the time. So
[Garrett salpeter] 51:38
Very, very gracious of you. Thank you, Dr. Buckner. Really appreciate you coming on the show. And we’re excited to continue to work with you and have you on again in the future.
[Samuel Buckner] 51:48
Of course, yeah. Thank you for having me on.
[Garrett salpeter] 51:50
All right. Thank you very much. Thank you so much for listening to the undercurrent podcast. If you enjoyed this episode, please consider leaving a review and be sure to subscribe to stay up to date as we release future episodes.
