069 Evaluating a new hypertrophy model

Well, welcome back. Thank you for joining us for another episode. Chris, good evening. How are you doing today? I'm doing very well. Thank you, Jake. I just showed you. I don't always show you the plan we're going to talk about ahead of time, or sometimes I keep it a little bit of mystery until you when it's from something like that, but I did show you this one. And you didn't seem too excited by this plan. You question whether I, in fact, really wanted to share this plan. So here we go. Let's jump into it. It's a two day, I think there's interesting things to note about this plan. So we are going to talk about it. It's two days per week. I don't recall if we've even talked about a two day per week plan. So I think that in and of itself is really interesting. And a lot of people do have this assumption that they need to be in the gym more than twice a week. And I think if you do a good plan, if you got a plan well, you don't need to be in the gym more than twice a week. Obviously, there's benefits to doing whatever, and you can split your session up more and whatever. But if you've only got two days a week, you can get amazing results. So let's talk a little bit about if this plan is doing two days a week well, if it's not doing it well. So this is Verne Weber. So kind of bodybuilder also Olympic lift, strong man type character. He was part of the York mob back in the 60s. And this routine came from 1961. So, you know, this is at the point where Annabelle Xer has sort of started to become popular. You know, a few early adopters have been on Annabelle Xer at this point, maybe for a year or two. And so it's hard to say, you know, what he'd been enhanced at this point was he's still natural. I don't know. But we're just going to have a look at the plan. Now, worth acknowledging that again, he had been coming from a bit of a strength background, some, you know, oldy lifts. And he was moving into becoming more competitive in the bodybuilding world and in the coming years, he would start to win shows. So this is really like in there, that sort of intermission, intermediary period before he sort of became quite competitive in a bodybuilding world. So two days a week. Now, it's an AB, but it's kind of like him and blended AB. So the workout is fairly similar with a few differences. So workout one, we start with an incline press. And that's something, he are almost everything. He's done for three sets of five. Okay. I'll tell you otherwise if it's, if it's different, but three sets of five. So starting with the incline, he then goes through preacher curl. He then does a pull down. I'm not sure what, what grip he did for that. And then he did a single set of good mornings. And this was done for a single set of 20. Then he goes back to three sets of five for the seated overhead press. I think I was done with the barbell. He then did three sets of five for push down for a seated cable row and then finished with three sets of five on a squad. Now, after he done his resistance training, he then this was not his idea. This came from his trainer, I believe at the time, but they would use a heavy sand bag. He would bare hug said sand bag and walk around the gym bare hugging this hundred or two hundred pound sand bag. So I guess kind of like a farmer's carry, but he's, he's bare hugging the thing. I guess he saw that as conditioning work as something of the like. So that was his first workout. Now, the second workout of the week was almost identical. What differed here is he did a flat bench instead of his incline bench. He did standing barbell curl instead of preacher curl. The pull down was the same. He then got rid of the good morning and he did leg press for three sets of five. The overhead press was the same, push down was the same, seated cable row was the same and then he used a trap by deadlift instead of a squad. He once again concluded with his heavy sand bag. So almost identical sessions, but two or three exercises did differ. Okay, you weren't, you weren't too taken with it. Tell me what are your thoughts. So yeah, I mean, I think that as a, as a twice-a-week routine, it's not actually as horrible as I thought it was when I first looked at it. I think the issue was that my eye kind of picked up the differences in exercises, whereas the reality is that as you pointed out when you analyzed it, before we jumped on the podcast, most of it is the same. So even though it kind of looks like an A, B twice a week, which would be horrible, is actually an A with a couple of small changes. And if you take it in the context that they didn't really do hamstrings training in the silver ear anyway. So the good morning is just kind of a waste of time. It's the token kind of gesture. Yeah, it actually kind of works. You end up with too much quad work really, too much. I mean, we've got a kind of a, okay, fine. One day is just squat, but the other day we've got a leg press and a trap bar deadlift, which I think is just silly. I mean, you can get away probably with, with six sets, I guess, once a week and then three sets the other day. But, you know, I would generally kind of top it to five sets if you're going to do something like that. But, you know, not horrendous. And as regards the rest of the exercises, I mean, it's a pretty standard kind of set to exercises for the silver ear. I guess the pull down is a nice, nice to have in there, not really noticing anything else unusual. I don't think there's any calf work in here. Yeah, no cars in the no hands that you touched on basically. But, yeah, I mean, fairly straightforward to exercises. Yeah, just the weirdness with the good morning for one set, once a week, which is just bananas. It is odd. I didn't wonder what that was about. Do you think to make a case for this good morning? So, on the other day, he has a deadlift and he has a leg, oh well, trap by the lift and he has a leg press. And then on the good morning day, he's got the good morning and the squat. Do you think that there's a little bit of something he's not getting in the squat that he's getting the trap by the lift, whether that's directives, whether it's a little bit of hamstring work and he's maybe having a good morning in there carrying over some of what he might be getting in that trap by the lift, albeit not that efficiently. But I do wonder if maybe he's getting something tiny out of it. I mean, the thing about trap by deadlift is that they're kind of designed to try and minimize external momentum lengths. So, they're kind of trying to put you, you know, really in the center of the, of the kind of the equipment. So, you don't have this offset of the barbell, therefore, an external moment arm to the hip and an external moment arm to the knee. That's why you can generally lift a heavier load with a trap by deadlift. And people who don't understand the moment arm get really, really excited about that. They're like, oh, wow, you know, I can move more weight. I'm like, yeah, but the talk is the same but the hip and the talk is the same. So, you kind of, so I doubt it's particularly interesting in that respect. I don't think it's, um, I mean, if it was a different deadlift variation, I'd be inclined to agree with you. You know, if it was a stiff leg and he'd got a stiff leg on one day and a good morning on the other day, I'm like, okay, well, I can see what he's trying to do there. But I mean, maybe that is what he's trying to do. Maybe he was falling. I'm sure you say something to do the trap by deadlift where they kind of do keep the legs fairly locked out until the bottom. Maybe he just happened to be one of those people who is performing the trap by in that particular way. It's like people do like rdls and stuff with the trap bar, you know, maybe, maybe that's what he was saying. Who knows? But yeah, I mean, as I said, the first time I looked at it, my eye was drawn to the differences, but I've been gone through again. Look, it's actually not a horrible routine at all. I mean, again, you know, you could do this. You could make some tiny changes. You could, again, you could just take out the good morning and the leg press and replace them with stiff leg deadlifts. And there'll be an awesome other program that you could run twice a week. Yeah, if he would just had repeated that good morning or stiff leg and then on the other day, even if he wanted to stick with the same set. Even if you're any good to single set. Yeah, you could, you could just do single sets. Yeah. Now with that good morning, I don't know if you want to go into this, but that single set, would that be enough for sarcomyogenesis or not? Yeah, I mean, it's very possible. It's very possible. I mean, that's, it's a really interesting kind of question. Because it does look like the amount of volume necessary to get sarcomyogenesis in a meaningful way than is net sarcomyogenesis across the whole week. Does look like it's quite a lot lower than what you would get with a hypertrophy model. So, you know, I genuinely, I don't think the data exists to really pull together a proper sarcomyogenesis model, whether it's for static stretching or for eccentric training or for strength training with long muscle lengths. I don't think it's, I don't think there is enough data out there to do that exercise at the moment, but we are moving in that direction. And it does look like the numbers will probably be different. It does look like you can go away with less in terms of the amount of volume and possibly therefore the frequency. Interesting. Okay. Okay. Well, I think this is a pretty interesting two-day week plan. And yes, I do think that AA would have been better. And that's how I produce in my two day a week plans. But for someone who wants trained twice a week, I think this would be a good format for one to use. Three sets of five, I really like that. If you're happy, this would be a fairly long plan, to be honest, if you're doing this, especially if you're doing this like in a home gym and you've got to set up the bars and everything else, like this is probably going to take you close to an hour or 45 or doing my guess. - I think it draws attention to, the fact we have to ask the question of why somebody wants to do twice a week. Because if somebody wants to do twice a week, because three times is too much, then this is not a good program. - Yeah, too much, like too much volume, you mean? - It's too much, 'cause I think it's on. - Okay, it's just too much to do three times a week. - Well, I'll tell you when this would be a good plan. When I used to live in the other side of the country ish and the closest gym there was not absolutely horrendous, was 45 minutes away from me. This is when that would be a good plan. - Yes. - Yeah, so when you've kind of got a limitation on how many times you want to make that journey per week, then yeah, that would be a good plan. But yeah, when somebody's just like me and I can't hand all three times a week, then I wouldn't be recommending to do three sets of all of these exercises twice a week. It could probably be single sets, you know? - Okay, I think that's it for this plan. Again, I do think this is quite nice. If you're training twice a week and there's a particular situation where it works for you, like you live 45 minutes away from the gym, have a look at this plan, 'cause I think you might enjoy it. Now it didn't pass me by, then you used to word model a moment ago when you were talking about circumvent genesis. And that's a very topically used to that word because that is in part what we're going to be talking about today. Now I'm going to pass over to you to introduce this. This is much more down the philosophy of science side of things than my knowledge of philosophical interests. So I'm going to be leaning heavily on you today. - Okay, so essentially a long time ago, I said that if anybody built a hypertrophy model, then I would review it on the podcast. And so as a result, when Mano Hanselman's introduced his model, I reviewed that and now Andrew Horst has produced a model and so we're going to review that. So you know, this is just me kind of making a commitment to looking at alternatives to the stimulating rep model. So I think it's useful before we kind of talk about this particular model, I think it's useful to start by asking the question of what these models are all trying to do. I think the best way of doing that is to go back to the original kind of metabolic stress model in the early 1990s and then talk a little bit about how that was then integrated into a hypertrophy research, kind of literature largely through the efforts of Brad Schirmfeld, but you know, kind of it dates back before that point. And then maybe then mention again, Mano's model and what that kind of tried to do as well. And I think that would be useful context to try and understand what it is that we're actually talking about here because a lot of the time, I think when this topic gets discussed, people make assumptions about what is being discussed and what is not being discussed and those assumptions I don't think are necessarily valid. Okay, let's go back to the beginning. So essentially the metabolic stress explanation, if you want to use a better word for the moment, let's call it an explanation. The metabolic stress explanation hypothesis was coined to explain why you could have two otherwise identical strength training programs, one of which had intracet rest period and the other one didn't. So essentially you were going closer to failure on one kind of training program than you were on the other training program. But to all intents and purposes, they had the exact same amount of volume load and in fact, four-time integral. So really kind of from a mechanical point of view, an external kind of work done if you like. If you want to use that, it's not strictly true. It was four-time integral, so it wasn't any work, so it was isometric, but anyway. Essentially, you're kind of looking at an external mechanical variable and you're saying that's equal. So how am I getting different muscle growth? And essentially, explanation was that when you didn't have these intracet rest periods, then you would get metabolites accumulating in the muscle, which we understand from the fatigue literature is pretty normal. And those metabolites were signaling for hypertrued to occur in some way, shape or form. And that's the essence of the metabolic stress hypothesis. So what you can see there is that a group of researchers are trying to explain a strength training observation that you can have the same external kind of mechanical variables going on outputs, but you can have a different hypertvee kind of result. And it must be because of something kind of unique that's happening as a result of being close to failure in the kind of group that's accumulating metabolites that's not got intracet rest periods compared to the group that has got intracet rest periods and is not accumulating metabolites. So it's an explanation. So you can then kind of see where that goes next, because when the literature started to test different rep ranges and they were going, OK, if I do three sets of 25 to failure and three sets of 10 to failure, I get the same hypertvee if I do the same number of workouts per week for eight, 10 weeks. How is that happening? And again, you've got a difference in kind of the external kind of mechanical variables. So in the case of the light loads versus moderate loads, obviously, you've got a heavier actual load on each repetition. You've actually got lower volume load. You've actually got less work done. Generally speaking, those kind of variables tend to be maybe sort of one and a half to two times greater in the light load group. So you've got these differences in the actual external mechanical variables compared to what you're dealing with as the output, which is the muscle growth theory observing. So muscle growth is the same, but you're looking at a different mechanical kind of quantity, whatever that variable may be, you're measuring that could be work done, could be volume load, whatever it is, doesn't matter. Force time integral. They're all kind of trying to get the same idea. So the metabolic stress hypothesis or explanation was then picked up and used for that. And we're like, OK, well, what's happening is you're getting more mechanical tension in the-- and this is interesting because they identify kind of tension as like in instantaneous terms in each repetition, ignoring the fact that you're getting more volume load in the light load group. So that's worth kind of being aware of, but nevertheless. So they're saying more mechanical tension in the kind of moderate load group. And then you're getting more metabolic stress in the light load group. And that combination together allows you to create the same hypertrophy. Now this is really interesting because when you go back to the original usage or the place where the metabolic stress hypothesis was coined, it was coined in order to explain why more hypertrophy was happening in one condition than another. It wasn't trying to explain why two things were the same. It was trying to explain why one was more than the other. Now, when you then move on and say, well, we're now going to use it to explain why two things are the same. You've actually got a slightly different problem. Because when you're trying to show that one thing is more than the other, you just have to show that one thing is more than the other. You have to show that they're actually matching each other in any perfect way. When you've got two different training programs and they're producing identical hypertrophy, and you're saying that they're doing it through different mechanisms, you actually have quite a big problem. Because what you've got to do is you've got to explain how they are somehow magically always ending up in the exactly the same place. Even though you could change the rep range is all over the place. You can go anywhere from five to 30 repetitions and you're still going to the same hypertrophy. And it's like, well, how is it possible you somehow always manage to get this perfect combination of metabolite stimulus and mechanical tension stimulus. And it always seems to add up to the same number. That really strains our ability to believe that if you follow me. So that's where this whole meta-well-extressed journey kind of went. It started out, as I say, trying to explain the difference between failure and not failure. I think that moved on to trying to explain how different rep ranges produce the same. My hypertrophy is slightly different perspective, ultimately using the same explanation. So they're using a physiological observation like the accumulation of metabolites as a physiological observation. They're interpreting that. They're saying that it has a stimulating effect on muscle growth and that's been the sticking point for the entire hypothesis because it doesn't. But you know, they're kind of making a physiological observation and then they're using it to explain a strength training phenomenon, which is that in one case and the original case, failure versus not failure produce different results, even though mechanical kind of variables are being measured that they're basically the same. Force-time integrals are identical. And then later on, you know, different rep ranges are producing the same hypertrophy when you do the same number of specific failure, the same number times per week. So yeah, basically using this physiological observation to explain a strength training observation. And ultimately, that is what we're all talking about here. Whether it's, you know, the original meta-well-extressed model, whether it's the original one before that, also damage model, whether it's Menos model and Menos basically proposed a equivalent of a kind of a force time into a type idea, you know, essentially kind of going back pre-metabolic stress observations. And you know, what we've got now, a stimulating rest model, which I kind of described in a moment, and then Andrew's suggestion, which we're going to talk about later. So is all of that making sense so far? Yeah, so essentially you need to have these observations to begin with, right? Like, you don't just come out of your life, we're going to come up with this model. It's like, no, no, these, these are a series of observations. We need to have a series of observations that we need to try to explain. And then we come up with this model, hopefully a physiological explanation for why we're seeing these things happen. And it seems to me like they expanded out, right? So you're saying we had muscle damage initially. And then there was like, hey, here's some new observations. They don't fit within this muscle damage model, if you will. And so now we're going to push out one set further and create this metabolic stress plus muscle damage model. And then that goes a step further later on. Like is that essentially what's happening? We're just expanding these models. So, I mean, broadly, I think it, I mean, obviously human behavior is messy. I mean, you don't like physiology is messy. You don't always get, you know, kind of perfectly, one of described scenarios repeating themselves, but broadly speaking, the metabolic stress observation was trying to provide an explanation for why some strength training programs were behaving in a slightly unexpected way. I mean, essentially prior to that point, the idea was it's mechanical tension at the muscle level. And so they were expecting that to train in programs with identical four-time integrals would produce identical hypertrophy. They didn't find that because one was close to better than the other because the one had interest at rest and the other didn't. And so they ended up with a, kind of a sort of unexpected result, which then required an explanation. And they provided metabolic stress as the explanation. That is essentially what all of this is all about. We're trying to say, here are some strength training program observations, here are some physiological observations that might explain why that is happening. And so what's stimulating rep theory tries to do is to say, when looking at the metabolic stress explanation, there are two really big problems with it. The first is that it really doesn't make sense that you can have, you can compare any two rep ranges to failure that you like, and somehow always mechanical tension analytical. It's always going to add up to the same number. There was always going to be one going down, one going up, and they're always going to end up perfectly the same number at the end. That is just to me, just, it's just not possible. You can't have that degree of, you know, perfect correspondence with two variables moving against each other all the time. There's always going to be one kind of point that maximizes both of those two things and kind of, you know, you wouldn't expect them to always add up to the same number. And secondly, you know, ultimately metabolites don't stimulate hypertrophy. So the physiological observation itself was kind of really on week, kind of sort of standing. It was never really like a strong place to start from because there isn't any data showing that double rights can directly stimulate muscle growth in any way, shape or form. And every single kind of spin off area that's ever been done to try and, you know, sort of prove that point has failed miserably. And I've done a, you know, complete categorical analysis of every single one on the FAQ because, you know, ultimately it's in my interest to make it clear that that model doesn't work because it's really the only competitor to the stimulating mass model. Now, a model can be quite small in what it's trying to answer, right? So theoretically, you could have models within a model. You present an example of that early wrong when you said to me, you know, kind of soccer meridensis. I mean, ultimately, soccer meridensis is a one word model answer to the question of why do strengthening programs with four ranges of motion or ostrich positions are often caused more hypertrophy than strengthening programs with smaller ranges of motion, more partial ranges of motion, especially in contact positions in certain muscle groups, in certain populations. And the answer to that question is one word, it's soccer meridensis. And so you can have an explanation that kind of does the job very, very easily. And that's a great example of that. And I could, like, that essentially fits within the simulating of this model. So, I mean, ultimately stimulating rates model is about hypertrophy, not really about soccer meridensis. I mean, the soccer meridensis literally fits dovetails beautifully with the stimulator model. It just adds on the side of it. It just says, you know, you've got this stimulator as more going on. I mean, ultimately to be fair, it's alongside the metabolic stress model. I mean, it literally just says, anytime you've got a straight position, you've potentially got an additional source of a totally different type of tension that's creating a totally different adaption, which adds muscle volume. I mean, like muscle volume is, if muscle volume is your output that you're interested in, then, you know, all of the hypertrophy models give you maybe 80% of the answer. The soccer meridensis is going to give you another 20%. So really, it's just kind of adding an additional kind of piece of information that is being partitioned off. Now, yeah, I mean, if you don't bring soccer meridensis in as the example, then you are going to be running around trying to find something else. And actually, that's one of the reasons why we have a three-part model with metabolic stress muscle damage and mechanical tensions, because muscle damage was being used as a way to explain why esendrics and long muscle length exercises cause more muscle growth because they cause muscle damage. But if you bring soccer meridensis in, then that model drops away. And you actually just go back to the mechanical tension and metabolic stress model instead. I mean, ultimately, this is all about using physiological observations, muscle damage, metabolic stress, muttonic equipment, force veloc iterations, whatever they may be, to explain how strength training programs are in the literature of producing the results that they produce. Yeah. Yeah. Okay. So some models fit nicely together and others conjured each other. So some simply, yeah, okay, great. And this matters because A, it helps you actually know how to program and know what variables one should focus on and things like that. But also, it's important when it comes to actually where the research goes. Or an example of that. An example of that. If you follow the metabolic stress model, then you would be incentivized to try and find ways to increase the amount of metabolite accumulation in the muscle's wild strength training. So you would be incentivized to chase kind of lighter loads, drop sets, ways of enhancing this metabolite accumulation, muscle swelling that goes with that and the kind of burning sensations that you feel that are accompanying that as well. So it actually does change the way you think about the way you're constructing a strength training program. Absolutely. Yeah. Yeah. And we'll also influence the types of studies that are done and we'll influence. I mean, it, it feels to me, and this is maybe a super over simplification, but it feels to me a little bit like what glasses you're putting on when you look at a study. And it's like, well, this is how we think all this works. It's, like, for me, there's a lot of studies that look at it. It's like, men, this is, well, not again, so great example of that. Again, a great example of that would be going back pre-metable exercise hypothesis. The standard kind of assumption was that if you maintain mechanical variables equal, like four-time integral equal or volume load equal or whatever it may be equal, whatever mechanical variable you want to point at, you should end up with the same muscle growth. And you can still see people chasing that today. You can still see people chasing it today saying, "Well, volume load has to be the same." And so, well, there's never been a study that shows that if you were great volume load in that same muscle growth, you know, pretty much every study that's ever been done points in the opposite direction. And so this study's been that we're not just trying to. Yeah, but it's not a real model, like because it hasn't been validated. Because it's never actually been kind of proposed as, and, and kind of challenged. So, like, the metabolic stress model has been put through the ringer. I mean, it has. I mean, it's been absolutely put through the ringer. So, why, why when you look at studies? Why do I pick up a study sometimes? And it says, we, you know, kept participants in, you know, reps and reserves to a great volume load. Why does it not say we equated stimulating reps? That's a, that's a, that's a sociological question, which I'm not answering. But basically, what you will find is, as you say, that they often will talk about equating volume load, which is nonsense. I mean, it's really silly, and it absolutely should never happen because there's never been any, any data showing that they're actually equating. In fact, as I say, the very first metabolic stress study that was ever done started to the whole kind of hypothesis that's taken us 30, 35 years to get through, that very first study actually disproved the idea that you could hold external mechanical variables the same, and ended up with the same muscle growth. It actually disproved that, you know, so, you know, chasing that and saying, always standardizing in this way is, is lazy and is ignorant, and it really should not be done, you know. So, and as I say, I mean, just look at the light load versus moderate load literature, you'll find that pretty much every light load group is doing one and a half to two times as much volume load as the heavy or moderate load group. Examples are just all over the place. Tripover, for example, is just walking through the literature of why volume load cannot be used as a standardization tool. It can't be. But I don't want to spend today ranting about how it's silly to use volume load as a standardization tool, because ultimately the researchers are doing it. It's just going to get upset, and you know, people are going to get indignant and say, well, what am I supposed to do? I'm not supposed to do your job, but you know, that's a big question. Okay, so similarly in your roughs bottle, so what did that was an anomaly that occurred in the literature that wasn't explained by these other models, and that's what led you to developing this model. Tell me about it. So basically, the stimulating rough model appeared in my mind when I made two observations. One was an observation that I've already drawn attention to today, which is the fact that it's really difficult to make myself believe that you can somehow combine a mathematical extra stimulus and mechanical tension stimulus and end up in the same exact amount of hypertrophy irrespective of rep range. That, for me, is just, that's not the kind of thing that happens in nature. You know, it doesn't. You're going to end up with a local maximum somewhere. Simultaneously, I was looking at the problem with the pre-metabolic stress kind of assumptions, which is that, you know, this kind of the idea that whole muscle force was the driver for muscle growth. And I was reading the review paper by Stuart Phillips, and I should have pulled the paper up to remember the exact title. But basically, it's something like muscle muscle hypertrophy is a virus-specific phenomenon or something like that. And it was like this kind of realization hit me, and it was the explanation of why both the pre-metabolic stress idea of equating mechanical variables was, you know, kind of. Sorry, the pre-metabolic stress idea of muscle force being the driver of hypertrophy, and therefore equating mechanical variables was a way of kind of guaranteeing the end of the same muscle growth. And then the post-metabolic stress idea of kind of combining these two stimuli and end up in the same place, which is very, very difficult to do. I realized that if you simply assume that hypertrophy is fiber-specific, and you then interpret that through the lens of basic physiological observations, which are motina accruement and force force to relationship, suddenly you end up with the explanation that the only the last couple of reps in each set, regardless of what load you start with, are stimulating and provide pretty much the same stimulus, regardless of the rep range. And that was it. I mean, that was the simplest possible variation. And since then, I've kind of developed it to include how fatigue works, you know, which makes it a lot more powerful and a lot more usable in practice, we can talk about that later on. But ultimately, it was just this objection I felt to both existing models. On the one hand, you know, the idea that muscle force was triggering hypertrophy, which, as I say, the paper by Stu Phillips made very clear to me is just not what's happening. And simultaneously, if I were to work stress model was just really straining our ability to believe that two things could always magically add up to the same number. Do you still mean I could always magically add up to the same number? So yeah, essentially, just kind of realized that the force velocity relationship at the fiber level is what's determining the mechanical tension. So essentially, if you were to do all of your repetitions in the maximum effort, you would be way too quick for the first repetitions of a set to do your temperate max, for example, first repetitions would be too fast to produce meaningful tension at the fiber level. So you wouldn't get any growth. Only has the velocity start slowed down, has been tabulated, you get some mechanical tension being meaningful at the fiber level. Acroement, essentially, if you're doing that set with maximum effort on every single repetitions, maximum and every single repetition. So it doesn't really matter. That's staying equal. Conversely, if you do the other way around, you just allow the kind of rep speed to be whatever the rep speed is, then what you end up with is gradually recruitment increasing. So either you end up with low recruitment or low or low retention at the beginning of the set and those reps don't count. So that's kind of how you end up with this sort of stimulating rep zone at the end of the set when you've got the simultaneous high recruitment and high mechanical tension at the fiber level due to the slow movement velocity. OK, so this stimulating rep model is essentially force velocity and it's answering why we saw similar hypertrophy outcomes with lighter loads, higher loads. Essentially, it's in the language that, you know, kind of not the language, but the perspective that I know that you take from a philosophical point of view. What it's doing is it's objecting to two specific things in two other models, one in each model. It's subjecting, in the first case, it's objecting to the fact that the tension that stimulates hypertrophy is not muscle specific, it's muscle fiber specific. That's the first observation. The second thing that is objecting, and so therefore external mechanical variables are irrelevant, really. And then secondly, what it's doing is it's objecting to the fact that a metabolic stress model, my only has a problem because metabolic stress isn't a thing, metabolic accumulation doesn't stimulate anything, really. The second thing, the idea that you can have two stimuli always adding up to the same number is just really difficult to believe. It doesn't really fit, you know, kind of what happens in nature. So, yeah, basically, there's an objection to those observations going back to the sort of drawing board, going, well, what do I know? Well, I know from the force velocity relationship that you've got, you know, velocity determining fiber tension, and fiber tension, you're going to increase as you go through the set. Tablet lights don't really interfere too much with mechanical tension. And then on the other hand, you've got recruitment, and that determines how many fibers. So, ultimately, what it's saying is, if you've got a high number of fibers activated, and you've got a high level of mechanical tension at the same time, then you're going to end up with a meaningful amount of muscle growth. And anything that happens before that point is not really going to do anything, either because the velocity is too fast, because you're doing maximal effort on every single rep, or because you're not going to high enough level of recruitment. Now, if you kind of run down that road, you can figure out why you need a high level of recruitment in order to get to a meaningful amount of hypertrophy. It's because the fibers at the lower end of the motunit pool are already fully grown, and that's another physiological observation, which is the size principle of strata muscle. So, essentially, the stimulator as model is cool, because it doesn't invent anything. So, metabolic stress is an invented, I call it a marketing term. I mean, it was invented. There's never anything that started anyone saying, "Oh, look, metabolites stimulate hypertrophy." There's never any kind of empirical data suggesting I was literally just like an observation coin to explain our strength training result. But an immense size principle very well described, forced velocity determining five attention, very well described, size principle described, the muscle very well described, that literally just observations exist in physiological litter, nobody had ever bothered to use. And this is one of the reasons why I get very, very rude about hypertrophy searches, and people get very indignant when I do this. But it's because they don't read the physiology, and they don't import the physiology into what they're actually trying to study. And I'm like, "Well, if you did that, I wouldn't be rude about it, would I?" So, your model identified, "Hey, here's some things here that don't make sense with the existing models we've got." And then it superseded the metabolic stress model, the muscle damage model. I mean, I guess, do we have that triple tier, like metabolic stress, muscle damage, mechanical tension? Is that like the model, I guess? So it managed, I think it managed about sort of seven to ten years. So, that's pretty good. I mean, ultimately, I think it got, from a sociological point of view, I think it lost a lot of its influence when Philippe de Mass did his studies on showing how muscle damage didn't really appear to be positively associated with muscle growth. But I would say, from a physiological point of view, it was when it became clear that psychameradenesis was causing the additional growth in situations where you've got esendricks or strage positions and things like that, because it really sucks all the power out to the model, because you don't need muscle damage to explain anything once you've removed those variables. If you explain them in a different way, then you don't need the muscle damage model anyway. I mean, there was other stuff happening as well. I mean, muscle damage was getting kind of losing a certain amount of its influence in terms of muscle growth for other reasons. But I would say the the the the the master studies were probably the important thing from a sociological perspective, from a research literature and community perspective. But for me, more important physiologically was probably the psychameradenesis angle, because that just pulled all of the rationale for talking about it in the first place, to be honest. I know when I was coming up through the the worlds I was coming up in in in the fitness world and bodybuilding space, that model was still being taught and muscle damage, metabolic stress, mechanical tension. And I probably wasn't until I actually came into contact with you whenever that was, that I realized I was an alternative to that model. You know, up until that point I didn't realize with any other explanations. So it's clear to me having had you explain that what your model was speaking to and what anomalies had occurred for that to be, I guess, to evolve. Now, at this point, so we've got this other model we're going to talk about in a moment, is that when people are coming up with models now and you talked about Menno's model, are they seeking to address questions and anomalies that aren't being explained by the stimulating reps model? - I mean, that's a really good point. I don't think so. I don't see that, I think the motivation is different. I don't think the motivation is that the stimulating reps model is failing to explain things. I mean, ultimately it explains the rep range problem very, very well, which is the primary problem that had been struggled with previously. It explains the proximity to failure problem very, very well, which again was something that previous models had been struggling with. So, but there isn't anything extra that is not kind of. Okay, obviously it doesn't predict everything, it doesn't predict volume dose responses. I mean, that's kind of where you need a separate kind of tool, which is what we think that stimulus model is doing. So, if you kind of start with the basics of what the stimulating reps model is built out of, which is motina cumin being high at the same time as mechanical tension being high, then you can overlay fatigue, and you can say, well, if fatigue happens that impairs recruitment from a CNS point of view, or if fatigue happens that impairs tension from say a calcium unrelated point of view, then you can start to say, well, okay, well, now we have an understanding of why volume dose responses happen, because you can start to see as you get through a strength training workout, you start to reduce recruitment because of the supospinal and spinal sinus fatigue, and you can start to reduce the kind of tension, because the calcium unrelated point of view, so you can start to derive a volume dose response from these stimulating responses. It's not that the. So, on the one hand, you can say, well, the stimulating response model is just this kind of very simple recruitment plus tension thing, and I, okay. But if I want to map it to effort and velocity, then I have to use fatigue and understand that there are some fatigues that are negative and some fatigues that are slightly kind of permissive. So, but if you do that, then you've now got a model that is completely not necessarily predictive, but is completely continuous with dose response, kind of of a hypertrophy to training volume across a workout. So, it's not that the model, you know, doesn't fit with it, it does. If it fits with it perfectly well, it's just that there isn't an easy way of turning the numbers into something that will give you an up, and that's as I say, what we can, it's the most model is posted. Okay, so at its most basic level, the stimulating reps model, it could have just been descriptive, right? Like, this is what's causing hypertrophy. - It needs numbers. - I mean, you didn't need numbers. I mean, numbers are to make it practical. - Yeah, I mean, that's basically what the numbers are for, and I know that, I think, you know, again, speaking sociologically, I think the issue is that, when somebody who has a practical kind of, sort of perspective on strength training comes and looks at the stimulating reps model, the only thing they see are the practical bits. They see the five reps, and they see, you know, kind of that's the answer to everything. Okay, so I can just do the last five reps, the only ones that matter. And then that leads them to ask questions about things like, you know, rest pause and drop sense and stuff like that, and you have to say, well, you know, if you want to use stimulating as model in a practical context, you do need to understand how fatigue works, you do need to understand that if you try and doing like drop sets, for example, then those reps aren't going to be that stimulating because of the fatigue mechanisms that you've got in place at the end of the set, you've just done. That's just fatigue physiology. - So the other thing is an interesting distinction there, 'cause you said, if you want to use it in this way, so technically speaking again, at as well as basic level, it doesn't seem to be- - It's an explanation of how muscle growth happens. - Well, the metabolic stress explanation is an explanation of how muscle growth happens. But now this lay is that you can apply the fatigue layer, you can apply whatever else. - Talk about sentences, yeah, exactly. - And now it starts becoming formative as to how strength training should be prescribed to actually result in this outcome. - Yeah, I mean, you can literally use it to govern all of the kind of different advanced techniques, which ended up basically being pretty pointless. You can use it to explain the rest period duration, you can use it to explain exercise order. I mean, ultimately, overlaying the fatigue literature on top of it and saying, well, if I'm always chasing tension at the fiber level and recruitment to the muscle level, then I just need to make sure that my fatigue inputs don't mess around with those two variables. And that's fine, that's gonna work. - So, you know, I think ultimately the stimulus model is very facilitated to be, I suppose, of using the fatigue literature in the context of strength training programming, whereas metabolic stress model is not, now there's a muscle damage model, because both of those are treating fatigue mechanisms, metabolism and muscle damage are both fatigue mechanisms. They're both treating them as hypertrophy stimuli. And as soon as you do that, your model breaks, in my opinion, that was a, I'm trying to be objective and descriptive in this podcast. That was me kind of expressing an opinion. Yeah, I think it means that your model breaks, because ultimately, I don't think fatigue mechanisms are stimuli for hypertrophy and as a result, that's why the stimulus model is constructed in the way that it is. It's constructed in a way that fatigue actually always, apart from in the case of double H being permissive of slow velocities, it pretty much always creates fatigue mechanisms as a negative. So I'm finding this really interesting, 'cause it seems to me now that when people make criticisms like, oh, it's not just the last five repetitions of a stimulating, or this is not how fatigue works, or whatever-- It does have fatigue works, I promise you that way. But like, do you say, well, you know, whatever, like to say-- I do have to define a sensitivity that doesn't mean this much, or whatever, you know, like ultimately, it feels to me like they're making criticisms of how these other things are being overlaid onto the stimulating of some model. And it seems to me-- - Yeah, a lot of people will, as I say, color, like you pointed out earlier, they each person will bring their own colored spectacles to the model and look at it in their own way. And I think, as I say, people who have a practical perspective, they have spent their, you know, kind of free time reading, strength training from a practical perspective and thinking and set some reps and programming terms and they've been steeped in that kind of coach-led literature. They will come to the stimulating of this model, and all they will see is five reps to fail. That's all they're going to see. Because-- But you have to-- Again, I made this point on mainstream stories. You have to understand where people are coming from. You have to understand that I came from reading a lot of basic physiology, muscle physiology, before I started putting the model together. And so all of my starting points are, well, what is a muscle fiber actually doing in this situation? What is-- you know, how is the central noses actually activating muscle fibers in response to what's happening? You know, what actually is muscular failure? How does it actually work? Again, I mean, like, you know, most of the time and the model won't be able to tell you that. But I think that's the important thing. Is everybody's going to have their own starting points perspectives and they will look for the thing that they are most interested in. And a lot of people are looking for a practical output. And so all they will do is see that five reps. And so they will come and, you know, kind of square up to me and go, well, it's not just the last five reps. And I'm like, honestly, we are so far apart in terms of what we're each interested in that this is a pointless conversation. Well, it feels to me though that that's not the model. People are arguing about the application of the model at that point, right? And I think there are some people who are arguing about the actual model. I don't think there's many, but there are things that are a few, but ultimately, I think most of the people who think that they're arguing about the model, are simply arguing about how to apply the model. Probably, yes. I mean, ultimately, sociologically again, I think it's an interesting observation that at this point, very few commentators. I nearly said researchers then, and that's not true, because there's a lot of them still locked in the volume load kind of space. I think very few commentators are going to come out and argue that hypertrophy is called by anything other than high recruitment and eye tension. I mean, there are people who are making those arguments. There's some, but there's not many. But most people are going to start from the point that hypertrophy is high recruitment and eye tension. And they won't generally want to go much further than that, because as soon as they do, they're going to find themselves agreeing with me. But generally speaking, those are the two points they're going to make. Yeah, I think I can basically, I think this is Luminary. like I'm going to be opening up social media coming out of this and I'm going to be seeing all these criticisms of your model and I'm going to be seeing it and realizing none of these criticisms of your model, they're all taking for granted your model and then probably disarging how to apply it. Probably. But that's because of the industry is a strength training, it's a practical, yeah, people are interested in strength training from a practical perspective, they're like, what am I supposed to do? How am I supposed to use this? And so those are the questions and those are the topics that interest them. It just so happens that those aren't the questions and topics that interest me. Because I want to know how to say that. I realized that after years of conversations with you, I'm fairly straightforward. I mean, I just want to know how things work. Okay, having established what a model is, what your model is, with this whole new perspective I'm wondering if this model we're about to talk about, where this falls in, is it just say an arguing about the application for your model, I don't know, but let's talk about it. Can you introduce us to Andrew's model? Yeah, I'll do my best. So essentially, I'm going to go off the basis of a couple of social media posts and I'm going to try and avoid inferring too much. I'm going to leave things hanging if I don't know how to resolve them, for example. But basically, what it presents is a slide that looks very, very similar to the practical presentation of the stimulating as model, which basically shows five reps before failure producing hyper to stimulus. What this does is it expands the number of squares out to 30 kind of rep max, essentially, and shows a graded coloration of low stimulus at 30, 29 reps in reserve as it were moving towards a higher and higher, more intense color as you get close and close to failure. So what it's arguing essentially is that there is some stimulus, sorry, what it's presenting visually is that there is some stimulus on all repetitions, it's just that the amount of stimulus increases gradually over the course of the set. So that is the basic kind of presentation of the model and I don't believe that it has a name as yet. So if Andrew wants to create a name for it, then we can start referring to it. Or if he has already, I apologize, I didn't know what it was. Okay. So essentially, all reps are stimulating and that's in contrast to your model, which is saying, "Hey, we need these conditions to be met for a simulated repetition." Yeah. Now, as I say, it only shows 30 repetitions and I'm assuming that is alluding to the general belief in the hypertrophy community that you can get the same amount of hypertrophy with anything between five and 30 reps to failure as long as you do the same number of sets and frequency and what have you. So but it's not explicitly stated why that is being done, not clear whether it's possible to continue this rep range up to 100 or whatever. There's no kind of explanation of what's going on there. So in terms of the stimulating res model, I have a very clear explanation of why that happens but I don't know whether Andrew is using the same one. So it's not really a big deal to be honest. Ultimately, what I think is there's basically there's one philosophical problem with the model that Andrew has presented and let's do that first. So the philosophical problem basically is that it's not answering a need, it's not addressing a gap, it's not actually saying, "Hey, here is a observation that is being made in the strength and literature." And this new model I'm presenting is now explaining that for these reasons. So it's not sort of saying, what he is doing instead is saying that he objects to the physiology of the stimulating res model. So he's not looking for a problem in the literature that's not being addressed, he's actually just looking for a problem in the stimulating res model that he disagrees with essentially. So essentially what that leads us then to is one, I have to respond to why I think what he's saying is incorrect. Okay? So that's one thing. And the second thing, as I say, is a philosophical problem which is that it's not actually objecting to anything problematic in the literature. So there's no actual drive for the model to be built in the first place. Secondly, the model he presented goes back pre-stimulating res model, and it fails to explain the literature. Because if you now say that every single rep is stimulating, you're back in the metable extra place of saying, we've got these kind of stimuli that are all happening, and maybe they're all just tension, but somehow, somehow Palpatine returned, somehow you end up in exactly the same amount of muscle growth for rep ranges. Well, how? What's the explanation? And he hasn't got a physiological assumption to explain why that's happening. It's literally the exact reason why the metable extra stress hypothesis got used, as I say, popularized by Brad talking about different rep ranges. Exactly why the stimulating model was proposed to explain again why you get different hypertrophy in different rep ranges, Andrew's model doesn't do that. It actually goes back pre-metable extra, some pre-stimulating res model, and it lands in a place where you don't now have an explanation for how different rep ranges call to say my hypertrophy. Because it actually ends up with a circular argument because if you look in the comments when he's answering people's questions, he's saying, oh well, no, the strengthening literature says that all rep ranges produce the same hypertrophy when you do the same results to feel there. But that's circular. Using strengthening literature, explaining strengthening literature, what's the physiological observation? Why do all of your repetitions, that far away from failure, somehow always add up to the same amount of muscle growth, even though using different rep ranges? What's the reason? What's the physiological underpinning of that? And he hasn't got an explanation. Which is why I generally wouldn't regard this as a physiological explanation of anything. Okay. So is there an objection to the way that the stimulating model is using physiology? Yeah. So there will almost just be like an observation that, hey, I've observed all your repetitions of stimulating. I'm not physiologically explaining why I'm just saying all of your time. Let me pick up on that. Is that a true statement? Because when I look at the strengthening literature, I don't see evidence for 30 reps in reserve producing hypertrophy in anybody. So you've got a chart that shows some degree of hypertrophy stimulus out, 30 reps in reserve, 29 reps in reserve, whatever it may be. Well, okay. Can you show me a study or a bunch of studies? That support that. I can't, I can't think of any, I mean, you know, generally speaking, once you get passed about sort of six, seven reps in reserve, it becomes very, very difficult to find any, just showing any kind of hypertrophy and anything other than certain to all people, you know, and even those studies are imputed, they're not actually measured reps in reserve. So if there aren't any studies that show that, then clearly there's not that anomaly that's being so sort of. Well, that's what I'm saying, it's straight to it, where has this, where has this observation come from that has led him to create a critique, because it's not actually so model, it's just a critique of the stimulator has model really, because it doesn't actually use any physiological observation to explain any strength training observations, yeah? So like this is the whole point, that's why I spent the time at the beginning of this podcast explaining that, you know, when you look at metabolic stress as a concept, it's trying to look at the physiological observation, accumulation of metabolites to explain a strength training observation, why do different proxamistics failure produce different hypertrophy results despite the same mechanical kind of variable as being being measured? If you kind of, yeah, but Andrew's not got that, he's not got a physiological observation explaining anything. So how are you accumulating that training stimulus across different numbers of repetitions to failure and somehow arriving at the same total every time? It's the same problem the metabolic stress hypothesis has, except he hasn't got the metabolic stress to point to as an explanation for anything. So aside from the wanting physiological explanation, is it providing us any other directionally sort of pushing us in any other direction for you, spainly anything else or is it just ultimately saying? Well, that's what I'm saying. So it's actually the opposite because what you've got is you've got a scenario where it's making, it would predict things that aren't happening. So as I say, it would predict hypertrophy being stimulated at 15, 20 reps in reserve. You know, so that's not happening. So you know, how is the model kind of connected to reality if we haven't got studies showing that at that distance from failure, muscle growth can be stimulated because it's an assertion that he is making that isn't backed up in the literature. So let's say, let's say we did have studies that showed 30 reps of reserve with stimulating growth to some extent and maybe less than other sets or whatever. Let's just say that, you know, 30 whatever, that there was actually some stimulus and that was documented. So a model like this could exist without a physiological explanation if it was simply charting in this visual representation of what we're observing in these studies, right? But we're not we're not observing that in these studies. Well, so again, the presentation, the visual presentation doesn't give you a numerical output. So the stimulating model basically says, look, you've got five stimulating reps and I, you know, you can probably argue it's anywhere between four and seven. But I mean, the point is, it's giving you a quantitative estimate so that if you do a whole bunch of sets with two reps of reserve, you can kind of compare that with some sets to failure. You know, so it has, it makes in its own predictive output. You can go away and test that if you want to. Graded color on a graph doesn't do that for you. Yeah. So, you know, you can you can kind of present the argument, but you're not showing if you're not showing like specific percentages, then you're not actually and also, you know, how are you? When you if you do show those specific percentages, you are going to have to also show how they all add up to exactly the same number. So if you take three repetitions with a light blue rep, does that equal one dark blue? What I'm saying, yeah, that's why color grading doesn't work. So what you would have to do is you'd actually have to go in and figure out what all the percentages were for every single repetition. And again, as I'm pointing out, you'd have to make sure that they all added up to the same number and you'd have to provide a physiological explanation of why that was the case. Because if you do that, what you're going to find is if you've got a, let's say you've got a, a 30 rep max and you comparing it with a 15 rep max, like what you can't do. And I think the color chart implies this, but obviously, you know, that's not what's happening. But what you can't do is match the last 15 reps of your 30 rep max with your 15 rep max. Because you've got another 15 reps on the beginning of your 30 rep max. So what you've got to do is you've got to have an explanation of precisely why the last 15 reps of your 30 rep max is different from your last 15 reps of your 15 rep max and so on and so forth. And that's got to map across the entire chart. You would have an explanation of why that is the case. And no, referring to the strengthening literature and saying, Oh, yeah, but strengthening literature shows that all set to be the produce the same muscle growth regards as a reference. That's not an explanation. That's not a model. That's a circular argument. You've got to start from physiology. Well, you know, just be a list of observations, wouldn't it? It becomes a list of observations because it's, it's trying to clarify that's not because it's actually, it's actually making a claim for something that isn't happening, which is that muscle growth has been stimulated at 30 reps in reserve, which is not. Okay. Okay. Is there is is there any explanation in this model that you're aware of for why each rep is stimulating or is there any physiological explanation for any of it? Well, as I say, there is no attempt been made to link physiological observations with the strengthening literature. There are a couple of assumptions. I mean, so there are a few sections of description about how fatigue increases over a set, how external force changes, how perception of effort changes. Those are not connected with the model output. They're just descriptive and bolted on the start of the explanation. There's no connection. Interestingly, it's one of the things that I object to most when I did my personal training qualification a billion years ago, was that we basically were taught a whole bunch of physiology and crep cycle and other stuff. And I was like, and then we were taught strengthening programming. I'm like, how does this bit relate to that, Ben? I'm like, don't ask questions that we can't answer. I'm like, well, okay, I'm going to swim my life bridging the gut then. You've created a monster. So, but yeah, so there's some explanations of that, but then they don't connect with the what the model is actually doing. There are also some statements made which I disagree with very strongly, but again, they don't really change the model and I'll read them out, but, you know, I mean, they're not really important. The assumption is that all muscle fibers and the muscle experience, some tension on every rep irrespective of whether they're activated or not. There's literally no data to suggest that is true. It's literally just a contrarian observation against my point, which is that single fiber tension is generated by the muscle itself, muscle fiber itself, by acting the most in crossbridge overlap, which is what appears as he studies say. So, I don't know, other than to point out that it seems to be a contrarian, to stimulate your model assumption, I don't really know how to integrate that observation with the model that is built. And that assumption that each fiber is experiencing tension, is that based on his colligrating or is that based on when he says strict? It's just an assumption. It does not seem to connect to the way that the model works. So, is that the statement where he says, regardless of the fiber being passive or active? Yeah, it is mechanically loaded. Yeah, I tried to avoid using the word passive in my explanation because passive tension implies passive tension, which is not really, I don't think that's what he's referring to when he uses that word. And he's just saying not activated. Yeah, but yeah, my view, if a fiber is not activated, it's not going to experience any actin mice and overlap, therefore, it's not going to produce any relevant active mechanical tensions to stimulate hypertrophy in the strict sense or fiber diameter increases. You could stretch here and it would produce cycle regences and thus totus a production. So, but again, I don't see how that connects with the model that he has built and the model that he has built, you know, it ultimately, as I say, it lacks evidence for the stimulus of hypertrophy, hypertrophy rep max sorry, hypertrophy reserve, you know, and it actually ends up predicting some very strange things. For example, if you are working on a basis that with such a far degree of, you know, such a long way away from muscular failure, you could still stimulate muscle growth on every fiber in the muscle, because that's again part of the explanation that he's given. That would imply that minimal levels of intensity would actually be sufficient to stop atrophy from happening. You could literally do, you know, very, very minimal amounts of exercise in terms of intensity. And it would keep pretty much, you know, kind of natural bodybuilding levels of hypertrophy, which is, to me, not really continuous with anybody's lived experience and certainly not really with the literature. So, me, that would be a strange prediction. That doesn't really jive very well. You would also predict that something like clusters with 12-wret maxes or 15-wret maxes would be absolutely amazing for muscle growth, because you could literally just stack up a whole bunch of these little kind of shading to get destroyed all day. And you could just do it all day. And that would be a really good test of stimulating rest model versus whatever this is, because stimulating rest model would say, "Well, you're wasting your time with those first repetition." Because, you know, the fibers are maxed out. Excuse me. And maybe actually that is the source of the misunderstanding that he's got, because he's looking at things and he's going, "Well, you know, some fibers are activated and maybe they're shortening slowly and therefore there's tension." So, you know, "Why can't we call that stimulating repetition?" And like, "Well, because they're not going to cause muscle growth to happen, you know, will they actually cause the existing fibers to receive mechanical tension stimulus?" Yes. I mean, this is one of those things where I've made this point a bunch times. I've kind of commented on the idea that some people really can't get past certain words. I mean, Scott Adams, the creative deal, what he used to talk about, word thinkers, as people who, like, they hear a word and they think that that word then means, like, it's definition in every single context. And it's like, sometimes we're using words as labels and you have to actually dive into the situation and be, you know, kind of rummage about a bit and be, "I get to a better understanding of what the concept is, what's that word?" Just describing shorthand for, yeah. And stimulating, you know, and again, it's like when, I think, Andrew actually criticised stimulating response model for not including reference to other adaptions that are being stimulated at the same time. Like, well, yeah, it's estimulating, most model is a hypertrophy model. It was not designed to do anything else. So, it does look like he's got a word thinking kind of problem going on here whereby his tendency is to see a word and assume that that word has to mean exactly the same thing in every single context. It's like, well, it's just a label. It's a name, you know. So, the concept is a hypertrophy model. So, you don't need to include adaptions that are also being stimulated in recruitment or pendant stiffness or what have you. Okay. That's not what the model is trying to do. Is that a criticism that's been made? Totally. Yeah. In one of the posts that he's made, criticizing the. stimulating at the model. So, okay, right. So it's like stimulating, it doesn't adapt it. So, 10% of the time you've got to get stuck on words. So, yeah. But, yeah, the stimulating at the model says that you can apply the kind of content and stimulus to some fibres that are fully grown. And, yeah, they will technically be stimulated, but they won't grow. So, we're not going to call those stimulating because we just have to add the growth potential to kill those. It's potential. I mean, ultimately, if you were to, you know, kind of have an accident and break a limb and then put in a cast and then the end of that two month period with the cast or whatever and take it off and then start, you know, rehabbing it, you would notice that the muscle was very, very small and they would gradually grow back just doing daily activity. Yeah. You know, you're million miles away from muscular failure with daily activities stimulating at that point. It is. But that's because those fibres haven't, have now gone, have now gone past their shrunk below their maximum size. But, you know, in the day to day life that we've got, you know, those fibres are maxed out. So, I think ultimately it's one of those situations where I suspect is just getting stuck on the words stimulating and thinking that it has to mean what he wants it to mean, rather than trying to address the concept that is sitting underneath the label. Which is why the stimulating guess what a word for dig that if you did have someone who had atrophied, who had been immobilized or a very old person who had been sedentary or whatever, that actually further away from failure wouldn't fit me stimulating. It's definitely continuous with that possibility. I mean, I mean, I'm not immune to kind of word thinking myself and that's ultimately why I chose to call it stimulating rather than effective reps and just kind of run with what Borgi was doing. Because, you know, a picture rep model is a practical model. It's not a physiological model, Borgi said that himself. But, you know, ultimately, I get to very similar practical output, especially if you ignore fatigue. If you include fatigue, then the model's changed. But that's, that's by-by. But yeah, I mean, essentially, effective is even more kind of provocative to the kind of the word thinking community, not community, the word that you tend to see. Because, you know, effective really does sound like, you know, it's encapsulating everything that could possibly be good. Whereas stimulating at least tries to kind of, you know, sort of siphon off a little bit to that, that value judgment. But, you know, it's like there isn't really a perfect, maybe there is a perfect label. But I couldn't think of one at the time. I'm stuck with what I've got now. Is there more to the model than this? It feels, I certainly not. I mean, ultimately, I think essentially it, it feels very much like a mistaken objection to the stimulating at model because of a misunderstanding that you can have repetitions early in a set that are stimulating hypertrophy, that don't actually cause hypertrophy, because of the size principle of strata muscle, because you max out those fibers. If you understand that the size principle of strata muscle exists, then, you know, stimulating at model makes sense. But essentially, all of these kind of collagry that is inserting are literally just, you know, kind of creating hypertrophy or supposedly creating hypertrophy in fibers that can't experience hypertrophy. And I think that's probably why he's got a strange assumption about every single fiber being somehow mechanically loaded even when it's not active, which I think is very real. I think it's probably what he's trying to get around is trying to get around the size principle of strata muscle problem. But again, he's kind of pushing himself into a corner because he's still got to now explain, well, why are you ending up with all these different rep ranges produced in the same hypertrophy? And no, you can't just refer to the strength and literature as your explanation for that. You have to have a reason why it's happening. Otherwise, it's not a physiological model. You mentioned Boggy's effective reps model a moment ago, and you said it was, what do you say, an application based on that? It's a practical, an application based model. Now, and then you made a comment that fatigue isn't really overlaid into it in the same way. One could technically overlay fatigue into it, and then you probably have to turn into stimulating as model because it's not just, because it's not a physiological model. It was designed as a practical model. It doesn't have an explanation baked into it. If you put an explanation into it, you'll put the stimulator as model into it. And then it'll be a stimulator as model wearing an effective reps model overcoat. It won't be the effective reps model anymore. The regular rep model is literally just the observation that based on the strength and literature, it kind of looks like the last reps of the set of the only ones that are actually stimulating. It doesn't say why. The stimulator as model says why. It says that basically, you've got accruement, you've got tension, and you've got fibers that are already maxed out. There you go. So I actually think that most of the, the opposition I see online to the stimulating reps model is actually opposition to the effective reps model then. Probably. It's probably just objecting to the number of stimulating or effective reps. I mean, most of the time people are just going to argue saying, well, I think you can get hyper to five reps, six reps from failure. I'm like, good for you. It doesn't really invalidate anything I'm doing at all. No. Okay. Interesting. Okay. So there's nothing else worth mentioning. Andrew's model there. I think if I say any more than I'm just going to be even ruder than I have been, and I probably will mischaracterize elements of it, which isn't really very fair. So we'll see what happens. But for me, until he comes up with a physiological explanation for why all rep ranges produce the same hypertrophy, I'm not really going to take you any further. I'm not going to look to any further because that's the thing that's missing. At the moment, as you point out, it's descriptive of the strength training literature. It makes some assumptions in order to do that. But that's a bit that confuses me because it's not descriptive of the literature because we don't see it as you say. Yeah. No, no, sure. So there's bits of it that it mischaracterizes like claiming that you can kind of stimulate hypertrophy with 30 reps of reserve or 29 reps of reserve. I mean, that is a mischaracterization of the literature. That's not what you see. So yeah, I mean, it's not very clear in that regard. But for me, from what I'm interested in, what I object to, and what I'm looking for when I don't see, is a physiological explanation of how you end up with all rep ranges creating the same hypertrophy. When clearly, what you can see is that you must have different stimuli being provided. If you've got stimuli all the way up to 30 reps from reserve, then you've got the same problem that multiple extras has got, which is that how do you magically end up with the same amount of hypertrophy in every rep range? It's really difficult to predict that. It's to want to be what the data is showing. So you've thrown out the challenge there to, hey, someone does produce a model. Obviously, we will view this as a standing challenge. I mean, anybody produces a model or a review. It kind of comes back to this point that people occasionally will message me and say, why don't you debate people? I'm like, well, I've got a standing offer for anybody who's made a model that I'll take it seriously no matter who they are. So that's me saying that if somebody is prepared to put the head over the parapet and put the name to something, because I don't think people realize how difficult that is. I think a lot of influence is if they've built themselves a platform and they're making a decent income and they're happy with their life. If you said to them, we want you to kind of put your name to a model and say this is how you think hypertrophy works and popularize it, I think a lot of them would just say no, because the risk of them completely torpedoing their entire business will be quite high. Because if you put a model out there and people rip it to pieces, then your reputation disappears. So I'm prepared to take anybody seriously who's prepared to do that, because I respect that commitment, I respect that courage. I'm not really going to take somebody seriously who's just going to sit behind the parapet and love stones at me. That is kind of what people want me to do when they say, oh, debate this person or debate that person. I'm like, have they produced a model of hypertrophy and explained how it works? No, well, I'm not getting rid of that. Because I want to see them commit in the same way that I've committed before I kind of go into that conversation. Otherwise, it's just me sitting there defending my model while they sit there in a very comfy armchair, lobbing criticisms at me. That's not a particularly fair contest. I need them to have something to lose as well as me having something to lose. I think a lot of conversations end up becoming not based on what a model actually is or is actually seeking to do. It ends up being like, hey, here's an observation that isn't explained by the model and therefore your model's wrong. Yeah, but if I'm the only one who's presenting the model, then I'm the only one who's defending theirs, so you can't change the point. And if you actually, if you look at the way the fitness industry in this little corner that we inhabit, if you actually look. at the way that pensions you work. Essentially, it's a whole bunch of influences, micro influences, and even bigger ones, arguing why I'm wrong. Right? Yeah. That's it. And then everything else that they argue about is like opinion-based. It's like, well, I think this exercise is better. I think this is better. I like the way I'm doing it. And it's all kind of like opinion. So they're protected. They're sitting in a very comfy armchair, you know, kind of, you know, being very protected against any kind of criticism and just lobbying criticisms at me. And then they're like, people will come to me and go, why don't you debate that person? Well, what have they done to indicate any indication I should take seriously? Where's their courage? Where is their commitment? It's not existent. So someone who created a model, like what would be some advice for how to do so? Like, it seems to me like, what's lacking in this model we've looked at today is an attempt to explain. I mean, exactly the wrong person to ask, because honestly, I think that the right person is right. Yeah, but you're the person who's built a model. You're the only one sitting in this room right now who's built a model. So you're the exact person I should be asking, how would one go about trying to build a model? Well, I can only tell you what I did, which is start from a clear understanding of what is happening physiologically. And then connect that with the strength training observations. I mean, observations at the time explained by current explanations of what was happening. Sure. But it has to fit all of them. You know, you can't have a model that explains some of them not others. It has to be continuous with all of the strength training data. So every time you start, and I would say, if you want to guarantee that, I mean, okay, why do I think the metabolic stress model was a disaster? The metabolic stress model was a disaster because they didn't verify that metabolites had a stimulatory effect on muscle fiber size to begin with. That was the disaster. If you are confident that the physiological observation that you're looking at does the thing that you want it to do in the model, you're on to a good start. Ultimately, they went, metabolites are occurring in this case where hypertrophy is stimulated and not occurring in that case where hypertrophy is not stimulated. That's correlation. So they're going, okay, so we're seeing a correlation. We're going to make hypothesis that metabolites stimulate hypertrophy. They had no prior reason to believe that that was happening. It was literally just correlation. So if you start from the principle that you're like, okay, we're confident that muscle fibers are growing and that tension is making them grow. Okay, well, now you can go and look in the literature and say, ask the question, what affects tension on a fiber level? Well, you've got a couple of things. You've got length tension relationship. You could look at that. You've got force-for-lost relationship. You can look at that and you've got calcium on weight of D. You can look at that. So you can start to actually look at the physiological underpinnings of the thing that you think is making the difference. And then you can say, okay, well, how do I deliver that tension to all of these muscle fibers in the muscle? Well, that's the hand-on-size principle. That's recruitment and ultimately, if you want to go that far, it's near mechanical matching. So you're looking at the delivery vehicle for that tension on the fibers in the muscle that you've got. And then you can go, well, okay, is there any reason that fiber wouldn't grow, even though I've applied his stimulus to it? Well, that's the size principle of straight to muscle. I mean, you're literally just walking through pages of a physiology textbook here. I mean, this is, again, I get aggravated when I talk about this, because this should have been done 50 years ago. This is not hard, you know? So ultimately, it's literally just going, you know, what is physiologically creating the stimulus? And how is it possible to deliver that stimulus? And what's then the predictive output of those things, you know? And then you look at the strength training literature and go, okay, well, these are the observations I've got. Repranges all cause the same hypertrophy, same number of cysts to failure. You know, training to failure, for leaving enough reps and reserve, suddenly the hypertrophy stops happening. You start to put those observations together and you match them up with what the physiology is doing on the other side of the page. And it fits perfectly. It seems like it'd be very hard task to create an opposing model given that it actually does fit very well. I have the wrong person to ask because I think the model works perfectly. I know, I just don't see what need in your model is when it explains the physiology, well, when the physiology explains the model and the model explains the literature that we've got, I don't know why we're looking at the alternative models. What you're really watching is a whole bunch of people negotiate with their egos. I mean, that's really what you're watching. I mean, from the sociological point of view, I don't think anything else is happening. And a lot of people want to characterize this is like, oh, you know, the model is gaining popularity or your model is not doing very well right now and other people are arguing against it. And I'm like, it's noise. Look at the signal. Look at the signal of the last kind of five years. Five years ago stimulating reps just not a thing. Now stimulating reps is basically the dominant narrative. Yeah, I think it probably is a sociological thing. This whole everything that's happening. I mean, even the people I'm seeing who are interested in this potentially competing model, which doesn't seem to actually offer much competition at all. These are people who do know the literature and who are still seeing to be interested in in this model. And it's like, well, this feels, this feels like it is just a sociological, you know, phenomenal now. It's not actually about the lack of predictive lack of your current model. So, okay. I mean, I was I was pretty confident that the model had won like five years ago. I think we're literally just waiting for people to come to terms with that now. Yeah. Yeah. And there's resistance to that. Which I mean, that's generally how new models work, right? Like a model gets proposed, so do places old models and it tends to be like quite a lot of opposition from people who have obviously invested heavily in those old models. Exactly. Yeah. Okay. It was a bit of a different episode for us. Anything you want to finish, you want to leave everyone with or you've said all you've got to say? No, I think I've said everything. So, yeah, if people have questions, I'll do our best to answer them on Instagram this weekend. Cool. Wonderful. Thank you, everyone, for joining us for another episode. We'll be back next week with a new topic.