The Science of Hypertrophy with Paul Carter

Hello and welcome to the podcast that's dedicated and improving your understanding of human movement and movement system podcasts. I'm your host Matt Castoro, Dr. Physical Therapy and Certified Strength and Conditioning Specialist and in this episode we're going to have a discussion with Paul Carter, all about the science and physiology of hypertrophy. Paul is really an expert in hypertrophy training. He's worked really closely with Chris Beardley who is also an expert in physiology of muscle hypertrophy. I'm really excited to have him share all of the newer research on muscle hypertrophy and the mechanisms and help myself as well as you guys listening, understand those mechanisms a little bit better so we can make better training decisions for our clients and athletes. This is a really great discussion. Paul does such a good job of articulating the complex physiology and also making it actionable. So I'm really excited for this episode. 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I guess today Paul Carter, the hypertrophy expert, he's here to tell me all about why some of my thoughts on hypertrophy and the research that I've known about hypertrophy in the past have been more or less updated and are not so correct anymore. And I really appreciate this the way this podcast came about is basically through Instagram some of the stuff that I was posting about mechanisms of muscle hypertrophy that I had learned probably over the past 10 years or so since I'm getting my exercise science degree almost 10 years ago now has been updated and there have been kind of new findings and Paul is staying on the front of this and really an expert in this so I was going to shoot shoot it out here ask some questions I put on my Instagram story that Paul was coming on and you guys asked tons of great questions for him so basically that's how it's going to work Paul is going to kind of share a little bit about his background to start out and then we'll just kind of go through Q&A style so Paul welcome on. Thanks for having me on, but and I appreciate the fact that when this topic came up and I ended up commenting you were like super professional receptive and I want to commentate you on that because that is so rare in our field that somebody can say hey this stuff is like not really accurate anymore. There's got a lot of new information so my says oh man I'd love to know like share with me so dude you are the consummate professional and the guy that a lot of people I think they relate themselves after because you're totally open to like hey I just want to do you know get the best information I can know as much as I can and that kind of stuff so I just want to give you all the accolades for that. Thank you I really appreciate that yeah and I mean the goal is just like if you're wrong just like get better you know like share the best information so yeah let's let's do that. All right where where do you want to do the Q&A or do you want to kind of cover the kind of the broad level hypertrophy mechanisms kind of we were talking about a little bit in those I mean I'm cool with whatever you shoot. So here let's set the foundation so for anyone listening so there's probably some of you guys who are staying on the front of the research here and right there with Paul but maybe some of you guys listening are more like me where you've heard some different things over the past 10 years maybe you read some old books and you're more behind a little bit so where my thought process is on hypertrophy is I learned this kind of triad of muscle hypertrophy mechanical tension metabolic stress muscle damage all work together to stimulate muscles to grow and the kind of old mechanisms or thought processes around it is that you do a workout and you create micro trauma to your muscles and that is repaired and then you have bigger muscles but I think there's a little bit more nuance and more updated science that we can get into so Paul you want to lead off to anyone who kind of has maybe that understanding and into some more modern thoughts on it. So that let's you we can start with that one so that was kind of considered the muscle damage one and that one still goes around all over the place and I think is probably still the most consistently repeated and I think the reason there's a few reason why that it's repeated number one I think it's kind of easy to get your head around that idea that whole hey when you train there's this micro trauma these little tears have happened at the muscle fiber and then those repaired and the response is really good. So that's not really accurate that so that goes back to the hypothesis behind that goes back to around 1991 and it kind of took off from there and there's been a multitude of different transitions throughout the idea behind muscle damage causing hypertrophy so the couple like we'll kind of high level over this the one is the mechanical damage or the fact that there's tears or whatever and that generally is kind of related to the popping sarcomer hypothesis and I don't know if you're aware kind of where the popping sarcomer hypothesis the idea is that the sarcomers are stretched out beyond their operating length and then they kind of pop or tear and then the response to that is to repair and then you would either have to add sarcomers or mild fear goes one way or the other in order to create hypertrophy. Okay so that's kind of the one the popping sarcomer theory is the one theory that that was postulated behind that then so the other one was the idea and I think covered this too you kind of touched on this is in muscle damage there's the kind of the satellite cell response and then the satellite cell response so it switched over it and initially started off as kind of the mechanical damage you stretch the fibers out but the sarcomers can stretch out there's a popping of the sarcomers there's the the tear. The tearing of that stuff at that at that layer and then that one kind of went on and I never really panned out the whole popping sarcomer theory and then the other one was the idea that the satellite cell response would create a greater amount of malnuclei and then the malnuclear domain and then the idea was that it increased that hypertrophy and then it increased that much of the situation. So now that you have a larger amount of the domain, grow larger and so forth and so on. So over time either one of those had panned out and I think even the people that kind of proposed the muscle damage theory they've even started kind of backing away from that as you know we've had a few decades worth of data now or because I know even like Rick Contreras had posted and us like a tweet the other days like hey we used to all believe that muscle was torn down and go back up bigger we kind of know better than that now. So I think there has been a shift with the with that one so we can kind of cover both of those a little bit so the one we we do see the idea was that mechanical damage is so is what they call sometimes is that this working a muscle at a longer muscle length calls that popping sarcomer calls micro tears or whatever. So then that calls for muscle damage and then that was repair so there's two things actually really going on there we actually do see that even short muscle and contractions can cause muscle damage the degree is less significant but we actually understand the other mechanisms behind this now so you can try to muscle at a short length and still get muscle damage is just less significant. The reason why that is less significant is because we actually understand that what causes muscle damage is the overload of intracellular calcium so you have these calcium ions that get dumped off into the cytoplasm and this causes an activation of a protease called calpens so that is a frozen protein degradation at those at those levels with the basically that entire so. The actual sarcomers themselves the extra salio matrix that's what causes all this damage that you see one of the tell tell signs that should really be the first indicator to people that the training itself they'll training along muscle week is not causing this damage is we don't see the damage occur immediately post work out we see the damage occur hours and hours and hours later after these proteases have had time to do the protein degradation. So when you actually go through the literature and you look you'll see oh you're like this happens anywhere from six to eight hours later and sometimes doesn't peak for a few days so if the damage was actually occurring from the training itself we would actually see that damage happening like immediately post work out or like in a very short period but we don't see that we see it happening either hours or potentially peaking even days later. So that's the one reason why we do okay that that's not really happening the mechanical damage the tearing that's not really what's happening muscle damage the reason why it occurs at greater length longer muscle links is because when you train a muscle along with the link those the stretch ion channels get flooded calcium ions so those those ion channels get opened up and there's an even greater influx of that intercellular calcium. So whenever you have that happens always a greater degree of muscle damage so the reason why it happens less that shorter links is because you don't have that as much and because the tabletic emulation can interfere with that too so there's a multitude of physiological processes that happen that we know okay this this whole tearing popping of sarcomers tearing a five percent building up. back up bigger is not really what it's had. Now, kind of the, I'm not going to say the nail in the coffin, but the really what gave us even more insight was the work by Lepe Demas out of like with Stu Phillips and those guys. And they looked at muscle damage that was occurring and then myofibral protein synthesis. So with myofibral protein synthesis, we're actually looking to protein synthesis that actually repairs the damaged myofibrals protein synthesis that actually adds new contractile proteins. So what they saw was, and you'll probably this will probably be your aha moment here too, is over the first week or two. Myofibral protein synthesis was high, but it was all related to muscle damage. And once the repeated bout effect started kicking in and those protective mechanisms were in place, and you had a little bit of that fiber type shifting and stuff like that will go from a more like a lytic type fiber and shifts a little bit more to a protective more oxidative fiber. Once that started happening, you saw the muscle damage attenuated and then that myofibral protein synthesis could go towards adding those new myofibrals and contractile proteins. And we actually saw that the muscle damage kept the hypertrophy from occurring, but once the protective mechanisms were in place, then that cellular response could be allocated to increasing echology. Okay, I think for a lot of people this is going to be like drinking from a fire hose. I'm going to kind of run, walk back on a few of the ideas that you just shared and try to clear. I wanted to get all of that out of the way first. Okay, so so essentially I'm going to dump that down. So somebody like you said that just hard that goes what an hell. He just said, I'm going to make it really simple. So we're training for muscle damage occurs because of the fact that anytime you have those new type novel simulases or you have an influx of calcium ions that cause muscle damage, the body wants to do the first thing that it wants to do is put in protective mechanisms against future bouts of that. And that's we talked about, you know, I mean, you know the repeated bout effect, right? Yeah. So the repeated bout effect, those highly glycolytic fibers, the largest ones we have those type 2x fibers if you have any, because you're not everybody has a lot of type 2x fibers, but if you have those, they're damaged quite easily. So the particular mechanisms for just for the body to kind of do some fiber type shifting in the repeat about effect. So it gives it a more glycolytic type makeup and more glycolytic fibers tend to have more mitochondria. And the mitochondria is what removes those extracellular calcium ions. So when you have that, then we actually are able to have the protective mechanisms. So what people used to think happened when you trained was there was muscle damage. And then the response to that was I'm going to create larger fibers as a response to that. What actually happens first is there's protective mechanisms first. So once the body is able to kind of withstand that a little bit better, then it says, okay, I can allocate those physiological resources to adding more muscle. I think I get it now. That was a second. Was that a little better? Yeah, that no, that does help a lot. So let me kind of walk back a couple steps here. So first of all, we know that now that short muscle length training can also cause muscle growth. Right. And this is an indication that we don't need mechanical damage damage to cause muscle growth. Because if that was the case, then you could just do a bunch of even low load stretching and like eccentric and you would get a bunch of growth. But that's not the real mechanism, right? Like it's more dependent on calcium ions. So that is that actually that topic leads us down completely different path. Because then we have about length attention relationships and the muscle and how tension is general but essentially you are right. It's when we can train depending on the muscle muscle, looking for a muscle that is shorter muscle length and get equivalent hypertrophy outcomes, depending on the architectural makeup of those fibers. So we've seen that. Well, plenty, I know everything right now is and I don't know how much you've seen. Like everything grows better longer muscle length. I'm like, that's actually not the data. So we have plenty of data on short muscle lengths and we have plenty of data on long muscle lengths and some muscles do grow better at longer muscle lengths and novice. But generally not advanced. We actually have quite a bit of data on train guys and there's not. You don't get that extra stretch mediated hypertrophy because all of those particular adaptations have happened too. But yes, you're absolutely correct. If it used to be thought, well, you the whole reason why you got sore or you grew better or you're training at these longer muscle links and that the mechanism behind that was like this damage and these tears and the response to those tears was added muscle. That's not really what's occurred. Okay. So here let's let's talk about this from the perspective of the muscle fiber type transition because I think that's that's going to be relatable to some people. Now, I know this works kind of on a bigger spectrum than just type one type two. It's a little bit deeper than that is like our type one and then our more intermediate type two A fiber. Yeah, the so it's kind of like it's hybrid fibers. So it's like there's a lot of people just think type one or type two and there's really kind of low. When you look at the heavy and light miles and change, there's almost always like some fiber type. Like hybrid fiber types that you have something that's like it's like a you have fast like a lid type two fibers and then you have like moderate type two fibers and then you have slow type two and then course type one or also so there's like that hybrid fiber. So we have the fiber type shifting. They're really highly oxidative fiber types those type two X like we were talking about can shift into a more hybrid type fiber. So that it's a little more protective. So it gets a little bit more like a little comparatively. And then when you D train and this was a thought too right I don't know if you remember that what was that it's called nucleus overload training. Do you remember that that the idea that you would D train and then we started training you know you grow back new larger than you keep all the mile nuclear domain stuff. And we know like that doesn't happen now either. So the thought process was kind of related to muscle damage during that time right was that one of the things that would happen if you D train is that those you would get a fiber type shifting back to a little bit more of that like a lid type because you don't need to be about affect mechanisms in place. But so the body kind of does that stuff but we don't see a we're not going to you're not going to train and see a shift for more more glycolytic fiber. So I know somebody's listening like well how would I get a shift back to the larger you're not the bodies would always shift even in it would be the magnitude of the shift you would always have a fiber type shift going towards more oxidate so that's kind of the main principle behind the feedback effect is that we just getting a little bit more oxidative fiber types because the mitochondrial density is greater. Yeah okay so here let me let me try to explain this and see if if I make any errors here and you'll recognize me if I do okay so we have our type one fibers that are more more likely to be a bit of an endurance based we don't tend to see a giant shift from type two to type one but rather we have these type one fibers that kind of stay in place and they can experience some high perch feet but more so we're talking about our type two's now and on them type two's we know that it's it's a bigger spectrum but we can broadly classify them as kind of our type 2x which are very like a lidic and fatigue very fast. It's not that athletic grid doesn't have that great endurance or like capacity for the repeated doubt effect or type 2a though is more of that hybrid fiber or that like that oxidative but still more fast switch fiber. Now what we see generally is that shift from the type 2x towards the type 2a with training and with this that type 2x fiber that we're shifting away from that had decreased capacity it wasn't a great fiber to be able to handle a lot of training or to be able to shift training resources towards growth but once we do a certain amount of training we could shift away from type 2x towards type 2a that fiber has more mitochondria it's better at removing calcium ions I think you said yeah and that fiber is more resistant or I guess fatigue resistant. Yes yes and having that fiber type then allows us to with hard training direct that training effect towards growth more so is that based on. Do you know that you absolutely yeah you crush it do that was fantastic got it got so we do this fiber type shifting from anything that's more glycolytic into the more oxidative right and so those type 2 fiber so type 2a's will still have like great capacity for hypertrophy right so growth but they're they're not as easily damaged as like a type 2x but anything that we see that's going to be damaged at that type 2 level we'll have a little bit more of a shift over into kind of a more oxidative type fiber like. We talked about the hybrid fibers so the type 1 fibers they definitely are more in dear space but the type 1 fiber can get a lot they can they still have a good capacity for hypertrophy and a lot of people think of a type 1 fiber they give what they get mixed up there are the fibers controlled by the difference in the high threshold more units in the low threshold more so it's the fibers control by the low threshold more units really good for a lot of people. really we grow from those just from daily active right so it's the high threshold more to use all of those fibers have the all greater capacity. So a lot of people get those mixed up but a type 1 fiber if you grow actually quite large not as large just like of course type 2s that can increase more force they can grow larger and that kind of stuff but they can still grow by far so you still can get because we've even seen that with like controlled e-centrics like slow e-centrics that you get a more of a type 1 fiber type apart. Okay and this is kind of unintuitive to some people I think because they think like you want to be the most fast switch and have like the biggest fibers because is it is it true that the 2x is actually have like the motor units of the 2x is probably have the most fibers but those the characteristics of them change fairly early with training. So like I yeah and the other the other part I think that people don't get about that of course you would love to have all of your fear of your goal in life is to be as massive and muscular as possible you would love to have the greatest abundant type 2x fibers that you have but the issue is is that most people just don't have a lot of them and I want to say there was some testing for like Olympic like really high-level Olympic sprinters and stuff that had a higher degree so it really comes down to mom and pop that stuff right like if even as something as simple as regional hypertrophy a lot of people have larger areas of particular muscle and it just comes back to the bundles in that area do they have a lot of type 2x fibers that have a greater degree of those type of any type 2 fibers comparatively to type 1 so most of that stuff you can't like like not even most of that stuff all of that stuff you can't control it's just whatever you're born with in terms of fiber type distribution whatever mom and dad gave you that's what you're gonna have so that's why people like this guy did this these crappy exercises or whatever and through a like well yeah because it was mom and dad like that's like you know you can't you can't train to overcome those specific limitations yeah yeah but it sounds like there's still like a lot of potential for growth no matter what like wherever your fiber type distribution is like you can maximize what you have I think at the end of the day and you know Chris and I went over this in in our podcast is that you can't worry or think about that kind of stuff because you legitimately have no control over it so the best thing you can do is figure out what kind of training that you respond to best in accordance with whatever your goals are right so like if you're a goalist like I want to give this massive possible you can't control any of your fiber type distribution and that kind of stuff so you just have to figure out what kind of training is going to give you the greatest amount of stimulus create the least amount of fatigue and then approach it from that direction okay gotcha I want to walk back to one thing you said earlier just in case anyone else was kind of interested in this and that was about the the timeframe for protein degradation and how that has to do with overloading intracellular calcium so I think what you said was like after training if it was just purely mechanic or largely mechanic or or something we would be able to see that as soon as you were done with training these mechanical elements would would show and we would see the damage right away but instead what we're seeing is protein degradation that's six to eight hours or often even a few days after training is ended which is indicating that this has to do with overloaded intracellular calcium and it takes time for the sarcomeres and the extracellular matrix to respond to that degree of damage that was caused during the workout and that's happening hours after which is indicating this is more to do with the calcium less to do with the mechanical elements of overload 100 percent so the as I said the when you have a significant degree of calcium ions that get flooded into the the sarcoplasm right the side of both then that will activate those protein degradation in as far as we're talking about with the proteases called cowapids and what they do what's the word I think it's a posses I can ever say that when you're talking about a possesist or whatever that that protein it's basically cellular death right so that's what happens so when you have that happen when those get released that's when we see all of this significant amount of damage that occurs and that occurs more at longer length training than it does as shorter muscle training so because in the long-legged training you activate those stretch IOB channels and then the extra-cellular calcium just gets flooded in there when you're training at a shorter muscle link there's actually a greater degree of metabolite accumulation and then the metabolite accumulation actually kind of keeps that from the hurt so we do see there's still some damage that occurs even at shorter links but comparatively the magnitude is much smaller so that's also why we know it's like you're talking about is that we see plenty of muscle hypertrophy at different links isometric links short links long links it just all depends on some of the architectural properties of those particular fibers so some fibers are gonna grow because they get succumbia or genesis they get muscle added at a longer fastical link and some do it more laterally due to the nation and so it just depends on that linked to tension and relationship muscle but as far as the damage goes that's all gonna be relatively the same I see so here's the thing like that I'm thinking now is we are a lot of people wonder about like trying to maximize it I think this leads to a bunch of really weird hypotheses of like oh if stretching what would cause hypertrophy that would be the case if only like the mechanisms of stretching was the only thing that was important but we obviously know that we wouldn't get a lot of calcium released just from stretching because there's no neuromuscular there's little neuromuscular stimulus right or like signal can we stretch it is a little stretching is a little different so we can get hypertrophy from stretching but it's you have to stretching and then strength training range of motion and how all that works are actually quite different so in a so in a string training session when you're using specific join angle ranges motion you're more limited whereas in stretching you can actually stretch past further right than you get in in most string training exercises and so this can actually stretch the sarcomere the stiff segment of the sarcomere and Titan to cause passive tension in those muscles so you can get some longitudinal hypertrophy what we think of as stretching media hypertrophy with static stretching but it's quite different than what we think of as string training exercises because in a string training exercises Titan is basically cow has a calcium ion sensitivity so it does get activated in string training exercises so when you're doing the an eccentric or training at a longer motion right you still have a degree of passive tension that's going to occur depending on that muscle but when you do stretching you don't you don't clearly you're not loading those muscle fibers right so with with a load right so it's a passive stretch so there's a completely different kind of approach there when you think about it because all of those fibers get stretched out beyond what you would be using in a normal string training session so if they had the capacity to experience passive tension in a stretch and we saw that with the cast training training study they did I don't know if you were aware of that one when people in dorsiflexion for like an hour a day their calves grew a whole bunch yeah that was like pretty intense protocol right that was like pretty I remember thinking I was like I one of the persons gonna ask me that you can't grow calves like should they buy a cup some of those boots and put themselves in dorsiflexion for an hour a day see if their calves grow like at least seven out of ten pain level or something I think they said it was it was like and that's exactly what I'm getting at so yeah a lot of people think well oh so I just stretch and like that's gonna grow but I'm like actually you have to kind of get to your stretched tolerance and kind of hold it there because you're getting to a range of motion you normally don't get to yeah that's not the same with string training right like you don't really push to a stretched tolerance position to hold it for any specific period so those things are kind of different like discussion as far as like we can get some hypertrophy usually kind of like distally or it'll be it'll be something like we get like the stretch me hypertrophy we're stretching but you have to get to ranges of motion you don't normally get those fibers too okay gotcha what kind of chalk that up is like a different mechanism and discussion that we might want to hold off on it for a different day yeah I mean there's that this whole stretching thing has come up before because Chris and I work off like basically a physiological model that pretty much anytime you have a study come out you can pretty much look at it and be like well this is why that happens so the stretching component is good the completely different topic because it's really doesn't quite follow the same constructs as you would see in like a string training normal string training exercise like so it's kind of it's a little bit of a different discussion as far as how that creates hypertrophy we're using just like isometric stretching yeah and for anyone listening who's wondering Chris Chris Beardsley and and how would you describe Chris Chris is such a smart guy in probably informative yeah I think if I like I feel very fortunate happy Chris and I've actually been working together for quite a few years I was the first person to ever figure out his physiological model so I always have that kind of feather in my hat so we've been working together for a few years now I personally I think I think Chris is the best in the world at physiology. I don't think there's anybody else that even comes close. So I always feel very fortunate, like that he's kind of become what I consider, like my mentor these past few years as far as physiology. I don't think you could get a better person. So. - Yeah, and I'll put a link to obviously your Instagram. - Oh, great. - I've created this a lot to that here. - Yeah, and what's funny is, as I started working with Chris more and I started getting into all of these mechanisms, these are not new. Like one of the things that we, he and I laugh and talk about quite often is when I don't go through a lot of these mechanisms, I'm talking decade, we've known this, but they've been largely ignored by the, what I would consider like the evidence-based community as far as the hypertrophy topic still muscle growth goes. These are not like, some people will go, well, that's an old study. I'm like, yeah, but that's kind of a, that's it, that nausea because I'm like, just because a study is older, does it mean that it's not relevant or at least it's not a good study? You should know that from going through research, right? Some of the older studies in physiology we have are still some of the best studies that we have. And the main thing that we want to look at is how repeatable some of these outcomes are whenever they test some of these things out. Like is this a repeatable process that happens over and over again? And if it is, we can usually kind of stick that into the model physiologically to how these things happen. And most of these things like the calcium ion related stuff they create, muscle damage you create, you can test it with low frequency fatigue. So all this stuff we've seen over and over and over and over again, we're like, okay, that pretty much a sound mechanism can kind of stick into this model that we know occurs anytime this happens. So a lot of the research that I got into, when I would go through it, I'd be like, well, this is from like 1990 here. This is from like 1985, we've actually known, this is pretty funny. We've actually known how tight work since the 1950s and it hasn't changed. Like, the fun thing about anatomy and physiology, it doesn't really change that much. Now, some of our understanding of mechanisms does evolve. But some of the tight research goes all the way back to 50s. I will be understand about muscle growth and mechanical tension, there's research going back to the 70s for that. So a lot of this stuff isn't new, but it's kind of funny because it's like people been sitting around for 20 or 30 years and I wonder how muscle hypertrophy works. There's literally research from the 70s going, it's just mechanical tension. Yeah, actually, so this bridges the gap really well to like some of our listener Q and A. And someone asked, what is mechanical tension? OK, so mechanical tension, let's say if we can do this in like fifth grade terms, right? I had, I don't like the name names, and I don't do names because I don't actually, I'm not a throw people under the bus kind of guy for the most part, I'm really not. I don't make content where I like go, I don't know if you ever go over about my content. And I'm like, if you're an educator and you're making content about people rather than ideas and mechanisms and stuff, you're not really an educator. So I don't name names of people, but I had a guy with a PhD come at me like a minute ago and we were arguing about mechanical tension. He absolutely could not explain mechanical tension to me, but post about hypertrophy all the time. But he absolutely cannot explain mechanical tension. It was a big long conflated explanation. So I'll try to do my best to explain mechanical tension to people. So mechanical tension essentially exists on the force velocity relationship. And that means that the force capacity of a muscle is predicated by the contraction speed. If you are in a slow contraction speed, that means force is high. So the force velocity relationship, you know that one. I know you know that, right? So the force curve, as the contraction velocity slows, the force curve goes up. And then eccentric contractions is mostly flat on the other side. So what we have to look at are two things. What fibers are activated during those contractions, right? And then what is the contraction speed? So if your contraction speed is relatively fast, that you can have-- you can be recruiting high threshold motor units. You can be recruiting fibers controlled on the low end of the motor unit. So we have to look at really kind of really toothed. So we're looking at the size principle of motor unit recruitment and conjunction with the force velocity relationship. So if we're talking about hypertrophy, then what we're thinking about is proximity to failure. As we get close to failure, and we have to actually create a high degree of effort, we will recruit those fibers controlled by that end of the high threshold motor unit core, write those largest fibers that are controlled at the very end of the largest motor unit. So as we get near the end of the set, close to failure, we're recruiting those largest fibers. Now because the contraction velocity is slow, as we're getting close to failure, right starts to slow down, there's more overlap between acting myosin. When there's a greater overlap cross-perching between acting myosin, they produce more force. And more force is essentially seen as more tension by those active fibers. So the common issue you want to look at there is a fiber-active-- because it has to be active first, I've heard people try to explain that a well, a fiber doesn't actually have to be active to grow. I'm like, well, that doesn't make any sense. Because I've heard that theory postulated before. I'm like, yeah, I'm just not going to buy any of that. But a fiber fits active. And you have a slow contraction velocity. We're talking the concentric side, of course, right now, but if it's active and there's a slow contraction speed, there's a high degree of force being produced. And that is essentially mechanical tension. So that just won't consider how to increase mechanical tension. Now to back up, I've had another guy go, he's like, well, you're always experiencing mechanical tension throughout the day. This is true. So the mechanical tension that your fibers experience that just cause you to grow from time when you're like a little baby and walking around and doing normal life stuff, those are all the fibers controlled by the low threshold modernness. There's just a whole lot of them. They're not large. They don't have a great capacity for growth. But you have those that experience mechanical tension all day long. If you move your arm up and down like this, those fibers still that are controlled by the low threshold motor units, they're still active and they experience tight-to-grid tension. But if you start weight training, that's the only time you get a chance to activate those largest of the fiber types, who discuss those, right? Those type two fibers. So the only chance that you really get it in terms of activating those and letting them experience mechanical tension, that slow contraction speed is when you're training. And then you're training either to failure or very close proximity to failure. Gotcha. So just to try to see if I can summarize that, especially towards the end of sets, whenever velocity is naturally slowing down, even if you're trying to move to the bar fast, but because of the T-- So right there, I don't want you to miss that point. That's a super important point. So when you-- something you said right there, when you're trying to move the bar fast, that means you're getting close to the end of a set, right? And you're applying a lot of effort. But the bar still moving slow. There's really two cool things that high degree of effort is what causes that higher degree of motor unit improvement. So that's when we get those-- So motor unit recruitment, you hear a lot about that. And it's completely effort determined. A low degree of effort is a-- you're basically you're not going to recruit the highest threshold of motor unit, right? And a high degree of effort recruits those fibers controlled by the high threshold motor unit pool. So when you get close to the end of the set, like you said, and you're really pushing hard, but everything's going slow, what happens is that you have those largest fibers they finally get activated. And then they have that cross bridging between the active myosin and they pull, it's like a stretching. So they're trying to resist that stretching, right? It's happening at the fiber level. And then that is what gets detected as tension by the mechanical reception. Gotcha. Yep. And actually, this is like a really practical takeaway for people training. Or people training people. Or people training athletes is like, that effort has to be there. So like, we shouldn't-- because I see this so many times is like, people think that because bodybuilders are doing slow reps, they should grab their 20 pound dumbbells or 30 pound dumbbells, even though they could do 50s. And they just do really slow reps. And I'm like, the effort's not there. The intense not there. Yeah. And that's really-- so that's the-- yes, exactly. So that's the time under tension thing that you hear about a lot. People use a slow concentric, like five seconds. And they're-- I'm like, OK, so let's back up. If you have low external forces, and it requires low effort, right? And you have-- so if you're moving at a dumbbell, if you set a 10 pound dumbbell really slow, there's a low degree of effort there. But if I take a 20 pound or a 30 pound dumbbell, and I move it as hard as I can, there's a high degree of effort there. And that means I'm putting the largest fibers or getting close to it. So I increase my mobility. So we have to have that combination of the effort. I mean, you're really nailing that, bro. And then that slow contraction speed. And I actually like to rephrase it in voluntary slow contraction speed, because we're trying to move it as hard as we can. But it's still just moving slow. And I think that's an easy way for people to get their head around. So mechanical tension is I'm trying as hard as I can to move this as hard as I can. And those muscles are now experiencing the kind of potential. That makes sense. That makes a lot of sense. I think we're good on that. What I want to get to is some other people's questions here, which is like, if-- here's one. If you don't have a chance to do it, you can do it. If metabolic stress doesn't account for hypertrophy, why does blood flow restriction training work so well? It actually works the same way. With blood flow restriction, you get this massive buildup of metabolites very quickly. What actually happens is that metabolic feedback is just a fatigue mechanism. There's aspirin feedback with the nervous system that this hurts and it's very painful and it's a fatigue mechanism. The actually in principle, the guy is one of the guys in all of blood flow restriction stuff, his name's Nick and he actually does pretty much all of the blood flow restriction research. The reason why blood flow restriction works is because the fatigue mechanisms call you to have to push harder, which creates a higher, you see where it immediately works to go with that. There's a very fast acute degree of metabolite accumulation occurs. This gets feedback, this creates the fatigue mechanism. This is the fatigue. Anytime we hit fatigue, everything you just said will start tying into this conversation. When we hit fatigue, we have to make a choice. We're going to continue and if we're going to continue, we have to push harder. The effort has to increase. When we increase our effort, we have more reunion improvement increase and then there's going to be the involuntary slowing of contraction speed. With blood flow restriction, they've actually, I'll send this one to you after we talk, but they tried to use blood flow restriction in another study where they had people, I want to say how they did it, they had them train a failure and then slapped on the blood restriction immediately after to see if the metabolite accumulation would cause an additive effect and it didn't. You have to be able to somehow separate off lactate and metabolite accumulation and that was the segue into that other one was the whole metabolic stress. You have to separate off. Is metabolic stress, if it creates an additive effect, then you have to be able to separate that off somehow from mechanical tension because you have to be able to remove mechanical tension from the equation to see if this also is stimulating the need for adaptations that have the physiological level. Does that make sense? I think so, yeah. We know mechanical tension causes, right? That gets picked up by the mechanical receptors and then mechanical transduction happens and then we have this mechanical signal gets converted into the biological process and then we get the addition of mylfibrals. We know that all occurs. In order to understand if, like we were talking about earlier, if muscle damage causes hypertrophy or if metabolic stress causes hypertrophy, we actually have to remove mechanical tension from the equation and say these alone create a hypertrophy adaptation without mechanical tension in the mix of that process. You can't have them both because I can just keep saying mechanical tensions there, mechanical tensions there, mechanical tensions there. You have to be able to remove it off an isolated and some kind of way. So we've actually had multiple studies. We had one study where they injected people with lactate. We're just seeing if that would create a hypertrophy and about a significant response in it. So we've actually tried multiple ways to kind of isolate off lactate and metabolite accumulation as a way that kick off the muscle growth process and it doesn't happen. The stuphillips and his group just did a lot. I think I said you that one right through DMs. I was like, there was just a literally just a lactate study done. It was the third one in a row. They have been trying to test in a myriad of ways to try to say how can we connect metabolic stress to muscle growth. It never works. So with blood flow restriction, what we actually see there is that there's just an increase and metabolite accumulation that occurs very quickly. And so the reason why you can think of it this way, it's like you can you get the same effect where you're training heavy loads because they've done research where they've done heavy loads versus blood flow restriction. And there's no, the hypertrophy outcomes were the same. I want to say in any time you talk about volume equity conditions, not volume load, but volume equity where you talk about sets to fail. So anytime they've ever equated that there's no difference. So what happens with the blood flow restriction stuff is there's just a very almost immediate fatigue. There's fatigue mechanisms and those fatigue mechanisms cause you to have to say, I'm going to continue doing this set, which creates the motor unit equipment we just talked about and the involuntary slow interactions. Yeah. Well, I think just practically just like relating this back, there's some really really good use cases for blood flow restriction training in rehab, especially like it's basically has, it's a certain early stage of post op ACL and they can't load through their knee in a closed chain way. The same way that they could if they were healthy. Well, now we can do an open chain exercise, add some blood flow restriction and. Dude, I think blood flow restriction. Dude, blood flow restriction, I think that we have, I think it has so much potential across the board because you can essentially get the same results that you get from heavy load training with very light load training, but your fog might, you're not, you don't, if you having somebody do a rehab and, you know, we can't load that joint very heavy right now or, you know, multi-breasons or we get like older people and we're trying to save all sarcopenia. Like there's so many different things that we can do blood flow. I think we just, we've just hit the, the cusp of kind of all the applications for somebody who's healthy, if they want to do blood flow restriction training, I'm, that's fine, but it's not giving you anything you're not getting from normal strain train, right, with heavier motor loads. And with heavier loads, the other thing that you get, you wouldn't get some blood flow, is the kind of the bone density increases that you, like so we, I think it's 80 to 85% load as you have to be yet to kind of get that bone density increases. So with blood restriction, you wouldn't get that particular benefit, but as far as you to stave off muscle wasting and stuff like that for people who can't train or rehab, who are older people, whatever, people who really can't lift heavy loads for whatever reason, it's like a really, did you know the story behind how that came? No, I don't actually. So it was a guy, I think he was sitting on his, like, you know, like how you do like a kneeling, like you kneel down. So like if you're like, like if you're like praying, right, like you're like knelt down, like in your like, I think it was, it was over in Asia. I'd have to remember the story, but basically he noticed that he sat down for a long time like that and his calf would get super, super, super pumped. And he figured out kind of the, the, the hypoxia that was occurring there that maybe there was something to that. And he started testing blood flow restriction. And that's how it came about. Interesting. Yeah. That is interesting. Yeah, I mean, I was like right in school 10 years ago or so whenever the blood flow restriction research was really starting to take off. And I saw it, I saw it in the research setting where there was like specific cuffs and specific protocols that they were following and the hell is this in the gym where people were just like getting an influencer is like thing and just wrapping it around their arms and just going for it. And it's interesting. I haven't seen it be as popular in the gym lately, but I think in a lot of research settings and rehab settings, it's still I think for rehab stuff, dude, it's like a miracle kind of thing for that. Yeah. Yeah, it really is. And I think that's where it's going to you're going to find that it has probably its greatest potential. I do think there was a recent study that came out that showed that there was a gosh, I think there were shoulder to still some shoulder and peck growth that happened from it as well. Yeah. Yeah. Yeah. Yeah. Did you see that one? I think there was some stuff that came out that did show because for a while, it was just like legs and arms, right? Yeah. Like your blood flow restriction legs and arms. But actually, you see you're going to be able to get some peck growth, some delt growth, some other stuff from it. So I think we're just kind of on the cusp of looking at welfare restriction stuff. But from the physical therapy side, I think it's going to change that whole landscape. Oh, yeah. I mean, we've had people with knee injuries. We've had people who can bench. Like if you think about it, like we've had people with peck tears that are a D1 football player going to, we had a guy who's going to play it or he is playing it Michigan, but whenever he tours peck, it was like, okay, how are we going to load this guy within the first three, four, five, six weeks where if you can bench three, 65, I think, I'm like, how am I going to load him in rehab to build back up to that? Like the, the, the, and now you can take now it's changed your whole rehab protocol, right? Because you know, like, dude, you don't have to sit here wasting away and build back up over the course of like three months or six months or whatever. You're like, we can actually keep most of your muscle immediately with light loads by throwing this both a restriction on. So I, it's just like really miraculous in terms of like rehab and getting people back and stuff like that. Yeah, absolutely. Okay. So I want to get to some other questions that people had. Best time for hypertrophy. Professor said five to ten minutes, which threw me off. What? I don't know. What's that question? Is that a question? Maybe we'll skip that one. So there's always some silly questions like regarding like, oh, like what time of day should I train or like what? Like little stuff that I'm like, that probably doesn't know. I have, I have, I think I sometimes have this unfair reputation online for like being used. or grace of it, I answer stuff. And then when people actually talk to me, I think they get like my energy's different than it comes across. And I call those like weak people questions. And the reason why I call them weak people questions is because as I'm not trying to be a a holo, technically I still have to jump in it. But they're weak people questions because I think you're focused on the wrong things. Like at the end of the day, that's not gonna make any kind of massive difference. And what I mean by weak people questions is, I see this kind of paralysis by analysis that happens online where guys are so focused on all the minutiae. They're just missing kind of the big picture stuff. And that's why they're frustrating to stock. So one guy's like, should I have 20 grams of cyclic dextrin before, during after training? And if I train at 315, does do I need to drink it at 3 o'clock? Or do I need to actually drink it at 330? Which I'm like bro, that like all that for the most part is you're just missing kind of the big picture stuff. So I'm not sure what that, what he means by that question, but that feels like a weak people question. - That's fair enough. Here, there's two questions that are kind of similar here. Is it only the last five reps or so that are increasing the effect, or increasing the effect and contributing towards growth? Or are studies showing that you can grow with six reps in reserve? - Yeah, so the last five reps is kind of what is the effective reps theory, effective reps model or stimulating reps model. And that is exactly what we're just kind of covering before where we're talking about mudding improvement and the force philosophy relationship. Now the reason why that this exists, we're gonna get some more fire hose action going on here. The reason why that this exists is because throughout all of the EMG research, what we tend to see is that activation. And I know EMG is not perfect, but like we have what we have. So we see in terms of activation, full mudding improvement that we're gonna get tends to be maxed out at around 85, 88% somewhere in that range. So whatever you get starting from there, you get full mudding improvement from almost like rep one. So when you look at a 86, 88 kind of one rep max load, you're looking at about five reps, right? That's somewhere we're gonna be in your five reps. And then through the rest of the research that we see is that when they do train your failure, when they've looked at this, is that somewhere in the four or five reps, the last four or five reps is that it flattens out or your improvement, the action potential is kind of flattened out. So if you think about that from the mudding and your croutons step point, that's why I set that up earlier and I said you have to start with mudding improvement. You have to look, so am I getting the maximum amount of mudding improvement that I'm gonna get? And if I am, when does that occur? And so somewhere around the last five reps, so to set the failure, is when that maximum amount of mudding improvement is going to occur. So now we get a chance to mechanically load those largest fibers. So to experience your kind of attention. Now there's a caveat to all of that, of course. And this is something that I've actually brought up in you times, just because a set potentially contains about five effective or stimulating reps within that set, like the failure, there's a few things here. Doesn't mean you're always gonna get five. Maybe you only get two or maybe you only get three, because fatigue mechanisms exist. So fatigue mechanisms either occurring at the central nervous system or at the peripheral level. So at the peripheral level, that means that even the fibers that are active due to the calcium influx that we talked about earlier, the one of the other effects that it will cause is something called excitation contraction coupling failure and that happens kind of at the triad. You probably later say in this part too, go ahead and say that's thing you're stuff you're sparking out of. And it happens at the triadic junction between the bolts of sensor and the calcium ion store. So if they can't communicate, then you don't get the calcium ions that get in, 'cause you still have to have calcium ions in order to stimulate muscle contraction, right? Because it has to unlock that proponent, right? The trope of myocene chain and the proponent that occurs. So that way the myocene can attach to the act and bind inside. So when you have the other one of the other factors that can occur there as far as fatigue goes at the peripheral level, can occur due to that calcium ion. Influx, and it can cause excitation contraction coupling failure. So when that occurs, you're not gonna get, you're gonna have those largest fibers, even if they're activated, they're not gonna experience mechanical tension, right? So because they're not gonna actually be able to get those calcium ions in to cause the cross-perjion. - Yeah, I think you lost me just a little bit on that. Can you walk back one more time on what contraction, excitation contraction coupling failure means? - Okay, so whenever you have an actual potential, right? That sit down the spine, and it gets to the triadic junction, right? There's the communication that happens between that voltage into there, the triadic junction, and it happens to calcium ions stored. So the actual potential that is sit says, hey, you need to release some calcium ions, 'cause we gotta do some muscular contractions, right? So once we have too much intracellular calcium, one of the other side effects of that is something called excitation contraction coupling failure. So now that communication, both the centric and its broke, it can't communicate with the calcium ions stored. So muscular contraction by those largest fibers are not gonna happen. - Is that because the calcium is flooded and it's not getting back? Or what? - Because it actually causes the damage there at that level. So we can actually see that happen when there's an influx of a high degree of intracellular calcium overload can happen relatively quickly as far as excitation contraction coupling failure grows. Now, if you train too failure, and I'm talking about you hit that last rep and it's grinding, grinding, grinding, grinding, grinding. There's more calcium ion overload that happens on those particular reps that happens on, then if you're leaving one or two reps and reserve. - Okay. - So there is, it's already getting five stimulating reps. You, there can be times where you don't get five because of the fatiguing interference mechanism, right? - Oh, thanks, yeah. - Are you, now I just saw like, you had that little bit of, ah, get it now. So if you have, so remember right, we're getting back to all these five stimulating reps. But if a muscle cannot actually experience that contraction, right, those fibers can do to that excitation. So since the active potential down, can't communicate the voltage sensor, can't communicate with the calcium ion stool, then those particular fibers are not gonna experience began to potentially. Now, the other one is any type of fatigue that we experience at the central nervous system level, whether it's gonna be super spinal at the spinal level. What will happen there is that we don't actually fruit. We have a lot of central nervous system fatigue. We don't end up fruiting those largest fiber. Now, I'm gonna throw this one actually, I think this will complete this for you. - Okay. - Two, there was a meta analysis and meta regression that looked at training to failure. Did you keep up with these? It just happened lately. - Hey, me. - Okay. So this will blow your mind a little bit, but I think this will kind of collectively bring it together for you. They both had, people were going crazy 'cause the first one said, if you train three reps in reserve, you get the same stimulus as training to follow, which is just, that's not true. - Okay. - Okay. - Or needs clarification. But what I like to look at is, what are the consistent findings that we find across? Here's the things that we keep finding, right? 'Cause there's always some anomalies for various reasons that this happened and this one that happened with that one. But what are these consistent findings? So the consistent finding across both of those was that when you're training with heavier loads, you didn't need to go to failure to get the maximum hypertrophy outcomes. Now, something we just covered was, when you're training with heavier loads, you get maximum energy in fruit, and that's from the first rep, right? So you're getting that high degree of mechanical tension, really from the first rep with heavier loads, 'cause you have maximum amount of improvement, you have a slow velocity contraction speed. With lighter loads, they both, the Mata Analysis and Regression found the same thing. That with lighter loads, it was more important to get two failure. To volitional failure task value, not a reason why that is, is if you have all those reps leading up to the last five reps, all of those reps are creating fatigue. We just talked about with the bloodthaler restriction effect, right? So all of those are creating fatigue. They're not actually creating a high degree of mechanical tension for the fibers, but they are creating fatigue. When we get to the level where that fatigue accumulates high enough, and it's giving that affincy back to the central nervous system, and says, "Do you want to keep doing this? "Because it's really hard." And you have to get that high degree of effort, that's when we start recruiting those higher threshold more reviews. So when you're using lighter loads, it's more important to actually get the failure to achieve the same hypertrophy stimulus because we had to get there in order to create those highest threshold more reviews, right? So the difference was we didn't have the fatigue. If you take like a five rep max, right? If you knock out four reps with it, there's no fatigue. You just just hard from rep one, right? Like you're like, "Okay, this is heavy, it's hard." So that's maximum margin there. I didn't have fatigue, you mechanism is in place. And then I either hit failure, or I was very close to it by the yet. So if I did four reps, I got four good stimulating reps in, right? But if I'm going to light load, I'm going to have to do 13, 14, 15 reps. You know by the time you get to 11 reps, 12 reps, it's burning, it's hard, it's painful. You have to decide if you're going to continue. So you had to actually push two failure to get that same. same amount of my group as you got in the heavier loading with less reps. Okay. No, okay. I want to see if I could take this to like apply it. And this will be probably somewhat theoretical, but like, how do we apply this to some of the training decisions that people typically make? And yeah, that's always the practical application is what I am always the most interested in because I always ask my like, when I read that, I was like, well, how does that help that person or me or my training groups? Yeah. That kind of stuff. How do we use this to create better programming for people to achieve their goals? So if we understand that the fatigue mechanisms are exacerbated with higher repetitions, lighter loads, like shorter rest between sets, stuff like that, then what we want to do is if we want to maximize motor you through that and want to get the greatest amount of mechanical tension, that means that every set we do in the gym, right, is going to have a little bit more fatigue than the previous set did. So that means the hypertrophy stimulus is just a little bit less too. Right. So for the most productive set you're going to do in the whole gym, the higher, like the whole time you walk in is the very first set you do post-apheller. And then every set you do after that carries a bit of fatigue. So that first set carries some fatigue with it, but it has the least amount of fatigue and the most amount of stimulus. And then after that, every set you do has a little bit more fatigue than the previous set. So the stimulus comes down just a little bit. So when I, when we say that there's five reps, right, five stimulating reps in the set, there's a caveat there, because fatigue does exist. So how this gives us an idea, one of the lights that turned on for me in the last few years was I was like, so the most important thing that people don't think about when it comes to the practical application of this is that I have the training in a way that actually minimizes the amount of fatigue that occurs within the training session and after. Because remember, we talked about muscle damage can occur for like the, the, the, basically the outcomes for muscle damage can occur for days after. Now here's the other thing that occurs with that. There's an inflammatory response that occurs with muscle damage, right? That particular inflammatory response also causes a reduction in central nervous system. So like basically central, it creates neuro central nervous system fatigue due to the inflammation in the bloodstream. And that also reduces motor unit treatment as well. So the calcium ion related fatigue and the muscle damage that it causes actually creates a subsequent fatigue effect throughout those following training sessions to do to the inflammatory response that happened from muscle damage. So if we can mitigate as much muscle damage as possible, if we can mitigate central nervous system fatigue as much as possible within the training session itself, then what we can do is we can have the grace amount of progressive overload. We have the fastest amount of recovery, right? And then we have the grace amount of motor group and then we have the most amount of stimulating reps and sets that we're going to have within the training section itself. So that also reduces the amount of sets that we have to do, which also improves our recovery, so forth and so on. Everything comes back to mitigating how much fatigue we experience within the training session and then the subsequent days after. Yeah, this is where it gets I think really interesting for people because there's going to be people who are listening like myself who want to perform at running or sports or triathlon, but still want to make the most of like training session. There's going to be other people who are optimizing just towards being as big and massive as possible. And I think the people who are just trying to be as big and massive as possible, they're like whenever you said, I think a little bit earlier about like pushing towards like more and more fatiguing reps and say losing velocity, there's some people who are like, okay, that's fine. Like I'm going to do that. There's other people who are like, but I've been told by my strength coach, I'm typically trained that as soon as I start to lose velocity, and I said I cut it off because they're trying to maximize like the neuromuscular response. Yes. Those are like two really different discussions because getting to, so the strength discussion is really separate from the hypertrophy discussion really is because I think the approach to maximizing strength is quite different from the approach to this maximizing like hypertrophy outcomes. So the maximizing strength approach really comes back to the skill of what you're doing. Like that's a huge thing, right? You're talking about getting developed and those neural adaptations. So the rate coding that goes on, like how fast you're releasing those action potential, how fast all that's occurring, and then basically reducing the amounts of co-contractions that are occurring, the reducing the amount of antagonists, muscle groups that are involved because all of that stuff limits the amount of basically strength expression that we're going to have in that exercise. So when you actually train, there's kind of a weird thing. So when you train two failure like that, right? So there can be a part where there's actually almost like a loss in motorbure recruitment, too. So if you're training a strength training exercise, that's why that being explosive and sub-maximal lifting, I think is a better way for a lot of guys to approach actual strength training. And I actually posted about this in my Instagram last night, my Q&A was that what took my deadlift from like around 635 to 725 was sub-maximal training with explosive, training the deadlift explosively. And I actually learned that from Andy Bolton. And then actually as I learned more and more and more about these mechanisms, I was like, that was such a really smart thing. And when I put it into the practical application of my powerlifting training, all my lifts really jumped. And it was because I wasn't accumulating all this fatigue and grinding. And I was actually training the lifts of maximally. And then I would only have within a mesocycle, I don't have a few weeks because you still have to get into those heavier loads to create those coordination patterns and stuff like that, right? Because you can't just train light, be explosive all the time and then moves like maximal weights. That's not possible. When we see that consistently, I think both that's one of the things where the research and then anecdotal stuff really lines up is if you're trying to get stronger, you at some point you do have to look heavy. Like you can't get around that, right? If you're trying to create, but you can't lift dude doubles and triples all the time without number one increasing the amount of injury potential than the other thing is that if you're doing like a double and triple, like a squat and a bench and devilish and all that kind of stuff and those are all like all max doubles and triples and stuff like that and you're doing high volumes, a lot of guys would do. The you will incur a lot of towards the fatigue that way, which causes the central nervous system fatigue and all that kind of stuff, right? Because it's like if you're pulling a max double or max triple, there's like an enormous amount of that calcium, an intercellular calcium influx that we're talking about there and that continues on. So if you're training sub-maximal, really explosively, what you're doing is you're training that pattern, but you're also getting maximal mooring and recruitment every set. When we talk about efforts, high, mooring and recruitment, I always try to get people to understand that really simple concept because they will get the mooring and recruitment stuff mixed up in mechanical tension. I'm like they're they're combined, but they're not the same. So you hit on it early. If as your effort high, now just tell people this, let me make it simple for you. If your efforts high, mooring and recruitment, if your contraction velocity is high, your forces slow. So if your contraction velocity slow, your force is high and then get those mixed up. So if you have asked you to jump up the test of ceiling, your effort's hot. So you get in a high degree of mooring, but you know there's a training athlete, so what the athlete's right, is if you're trying to do an explosive move, if you're Olympic lifting, or if you're jumping, or you're sprinting, or you know any of those kind of explosive movements, the effort is very hot. So mooring your group is hot. So if you're training a deadlift or a squat, and you're training explosively, then you're getting a maximum amount of movement that you can, but you're also not beating yourself up, trying to move heavy loads all the time, but you're still training the pattern. So what I found was kind of finding it, who's the Russian powerlifting strength guy? Is it, is it, is it, is it not Smolov? It's a, thinking about Berkoshinsky? No, with Smolov? Smolov was the squat thing. Who's a ducky? I can't remember what you're thinking about, but anyway, the, the Russian high volume powerlifting stuff they do, the average when I was into powerlifting, and I was looking into the stuff like I'm going to show the average loading for their meso cycles between 68 and 72 percent of one arm. That was really good. All their work, but they did it with maximum loss. So the mooring your improve is hot. So that was a lot of what I ended up moving to as far as strength development, and then when I to a meet, I would push the percentages up the last few weeks. So I'd do like 72, 75, 80, 82, 88. So I only have a few weeks where I'd get in those top 80s and 90s, but I've been training the pattern so much like it was an easy transition into the heavy waste, but I just do it. Yeah, okay, so I'm just curious how did you implement that with deadlift? Like how were you in the 70, like 70-ish percent range? So that would put you in? Whenever I would, one of the things I did at the time was I moved my deadlift on my squat then. So I would squat and I would do five to eight sets of three to five reps, and it would be at the time it was four or five to four or 25 first fastest possible. So and I would try to get those in at like a specific period of time, but 20 minutes, I have to go in five sets of five, and they all had to move at the same speed. So if I got to my fifth set and the last, you know, three or four reps of that fifth set, they were slow, I would not move up and low. So I'd done based it off velocity based training, right? So I would look and say if I'm using 405, and I think my squat at the time was anywhere between 640 and 660, so I would move 405 so you can do the math on that or figure out what is that I don't even it's pretty low 68.5 68. Yeah it's like 68% or something like that right so I would try to do that as fast as possible and then I could knock out 5 sets of 5 with that load I would move up then so the goal was to stay sub maximal and then to get to where that was just so easy like I could move up in those sub maximal loads and then when I would push up I remember I hit my best I hit it a high bar cost bottle 605 for a triple easy after months and months of not squatting more than like 405 or 425 and so that was I was like wow and then I like I quit power some it wasn't too long after that so kind of just as I felt like I figured things out I actually I retired I don't know if you can retire from support that you suck at but I quit so I quit but and my day that's what really took my day with off because I was just be I'm not I don't have leverages to be a great day with like my lockout was right around my crotch right and a lot of times when I see those guys with big dead list their lockouts like right at me cap up and I'm like well of course you pull big what's your bench bro so like they'd always have like some 350 bench with 800 pull I'm like okay but I had I had a dead lift my lockout was like right like literally right below my like my prox level so I wasn't you got to pull that far it makes a massive difference so I figured out like I said it was mainly like a lot of what Andy Bolton was talking about a lot of P wild and Andy was such a great puller and he was built for pulling but he also figured this out and he was a smart guy and he talked about the fact I want to say when he pulled a thousand he never pulled more than was like 600 and his training or like like it only had like a week or two where he pulled up to like 700 and he pulled a thousand like there's no way to go so I was like well I mean I'll try it and then I was pulling I want to say it was anywhere from 455 to 500 but as fast as possible like and it was mostly like triple so I would do all my squats and if you do your squat and go to dead list you don't need a lot of warm up so that eliminated a lot of that stuff so I would literally go like 3 15 405 and I'd be ready and I would pull two or three sets of like doubles or triples on dead lists for as fast as possible and once again I would look at bar speed so if the velocity of that came down to me much I knew I was going to get it but you have to be honest with yourself you have to be really brutally honest you have to put your ego people like to say they put their ego at the door but if I pull I do I was capable of pulling I think at the time the internet were wild for this I've been around for a while and I had trained with Ed Cohen and I pulled a really fast 635 fast I mean like and I had never pulled more 635 I had been my max for a while like one of those mental sticking points and we went to I was training with that we were in in quad gym it was me and Ed Cohen and Pete Rubish and the Lilly Bridge family and that's for anybody involved with powerlifting we'll know those guys and we went to 635 and I pulled it like there's no way the bar I went to 660 and the 635 moves so fast I knew I should have been good for 700 and there's a funny story about this so I went to pull 660 and it came it came off the floor like lightning speed and then just stopped at my knees and I didn't make it and I was just destroyed I that was when I lived my pounds on the bar and next day I was still upset and I was like you know I feel really shitty because I didn't I missed that 660 and Ed looked at me he goes and you should and he's like you should feel really shitty he goes because you can pull that easily he goes but you told yourself that it was heavy so it was and that was a really big learning experience for me as far as the mental part and he's like he's like you he gets every time you walked up to the bar when we went from 315 405 500 500 600 600 600 he goes you just pull the bar off the floor like there was nothing you know as soon as we got past 635 you just you were walking around trying to get psyched up and I was in my own head but what I was getting back to with the ego checking there is when I was trying to make this method work it's um it's you want to go in and just keep putting weight on the bar to test yourself to see where you're at but you can't do that you have to trust the process and once I learned how to trust the process I remember I went in and I pulled 635 for a triple like when I started going back heavy and I mean like a faster was like whoa and then it went like 635 655 675 7705 7.5 like all fell like a year like really fast but during those times I stopped deadlift and heavy I would only have a few weeks here and there where I would actually I did what Amy talked about I would just have a few weeks but I would pull really fast for 2 or 3 sets after my squats and that is what really helped my deadlift the most yeah I think I think there's some interesting research developing in this about measuring like dynamic strength index and like how much of your force expression or how much of your force potential can you express in certain limited timeframes with like the lossy based training but it's probably beyond the scope of what we can get into for this thought yeah I've checked out so much from like the whole string this is what I really feel like I kind of come to the conclusion of last year I feel like that you can kind of just like you were talking about a little bit like the first year like here's the thing I studied 10 years ago and that I feel like I know about this and then one of the reasons I don't talk about nutrition anymore is because I just don't research that I don't have an interest in that area and I don't research anymore so I don't stay on top of it but I also think that most educators need to kind of focus on like an area and because I really do feel like most of these areas get incredibly deep and complex depending on how deep the rabbit hole you get into them and if you haven't if you're not really specialized in that area then like you know it's kind of like we were talking about you're like you know this is stuff that I was reading 10 years ago and I still talk about and have it had a chance to update my information and I mean like I said you're definitely a you know a guy that's like hey here's new information let me go learn this because you know I'm behind him the stuff yeah I think when you have like for example I'm really good friends with Alan Erigo I think it's just like one of the best in the field right with him training and stuff but Alan doesn't talk about like high perch for your string training right because he knows it's not it's right but if any you want to know anything about nutrition at all no matter what it is you can go to Alan he's got because that's his focus so with the Trink's string training stuff I have people ask me this all the time and they're like looking who does like the string training stuff that you do for a part training I'm like I don't I don't know like I know Chris does he does both sides of it but we never talked about the string training stuff I just once I once I quit powerlifting I just had no interest in it and I feel like I figured it out by the end like I was like okay so this is actually the best way to train for like powerlifting and nobody then I was like okay I'm really ready to do that because at that time especially that was when I was taking drugs and I'm always but I was always open about my drug use too which is really kind of weird thing too now because people think they still so well like if I was on steroids like you too I would and I'm like I've been off right years and I was always open I've fussed my blood work stuff like that but one of the things I made a promise myself is I'm not gonna be that guy that chases these like lifts and then is willing to take more drugs and all that kind of stuff so I once I hit a point it was when I was when I turned 40 you said I when I turned 40 I'm just gonna get out of this and I'm gonna get off drugs and that's what I did so I didn't hit all my goals I feel like in time I could have hit them but it would cost who knows and I wasn't willing to do that so in the drug culture and powerlifting is pretty big like pretty big some of the stuff that I take in powerlifting I'm like it's more in powerlifting than bodybuilding guys in powerlifting you take way more drugs and guys in bodybuilding people don't know that so that they'll leave one of those really lead level those guys are taking way more than anybody else that's crazy yeah and I was just never willing to do that so that's why so with the strength stuff there's probably all sorts of stuff that we can get now that I just say to talk about but I think the physiological stuff with muscle physiology and hypertrophy it there's so much stuff consistently evolving now that we're learning about like I said we've still been having to work on hey just you know can lactate stimulate muscle growth at this point now we know again metabolic stress really does it it's not really doing anything so at this point we know it's two things from all the research that we have mechanical tension and you can take antibiotics and just say that home and grow nice so yeah there's you know that's that study right the well they took the supergromo doses of of testosterone they give them 600 milligrams of test a week and they had four groups and one of the groups just literally sat at home for the 10 weeks and and actually grew more muscle than the natural guys that have to see this responsible to share off of the cats I don't know yeah I've talked that's true yeah I'm 100% not telling you guys to go to go take anything but as far as muscle growth yeah I can't explain all the mech the only thing I can explain to that is that um antibiotics make you anabolic for 24/7 so your body responds to that by basically increasing my favorite protein synthesis all the time yeah so and then the other way we know is for mechanical tension and mechanical tension kicks that off and like we talked about the the mechanisms that occur after that but when you think about it you know everything that we've just talked about you know like a new water hose series like there's actually so much in just this one area to know I don't ever feel like there's definitely time for our I feel like I don't know anything. It's the, you know, the Dunning Fugure thing. It's like I feel like everyone's well, I'm on the other end because I'm like, I don't really know anything because there's so much stuff. Do you have, do you not ever have those moments where you're like, you start, you dive into a topic and you might be six months into it. You're like, there's still so much stuff that I don't know. I was a computer engineer for 15 years. And the first few years I was a computer engineer, I really thought I knew stuff right. Yeah. By the time that I retired, I was like, there's so much to know, you just can't know it all. And so at that point, we would have guys coming out of college and I would be doing stuff like in meetings or like when we were talking about architectural design and they would be like, dude, who are you? And I'm like, what do you mean? They're like, just like you know so much. And I feel like even then, like when I retired from doing like computer engineer work, that I was like, there's so much to know that you just can't know it all. You know, and then there was new consistent, new technology coming out. You have to stay on top of it. And I really feel like that most times now with most of the physiology stuff, because I'm like, I got off into a rapid whole inter-facicular terminations like a couple of months ago and stretch me to hypertrophy. And I was like, okay, so this can only happen in specific mammal types with specific use of form fibers and specific in plates with type of motor neurons and not in other mammals for that. And then I said that and I thought, why not even know that? - Yeah. I mean, just to on that point guys, like for anyone listening, don't get overwhelmed by how many areas there are with experts, like that's like where this whole thing started. It was like, you know, I'm, I guess like personally, my fourth biggest priority in training is hypertrophy. And my athletes, their third or fourth biggest priority beyond behind skill, behind speed, behind a lot of other things, endurance and capacity. And then comes hypertrophy. You're not gonna be an expert on it. Just like if someone's an expert, just go talk to them and you'll learn stuff in an hour that would have taken you six months to figure out on your own. So, you know what I mean? - But dude, I've seen tones of your content. You're a smart guy. You put out good content. People would not be dismissed by like following you or getting information from you. You're a smart guy. And the other thing is you're not just a smart, intelligent and insightful guy. You're completely open to like learning and having good discussions. And that's so, it really is so rare. Because I think people, they attach themselves emotionally to some of these constructs, right? And then it doesn't become about the science or the physiology or any of that kind of stuff. It becomes about, I can't be wrong. Because then if I'm wrong, people will think, oh, you don't know what you're talking about. I'm like, dude, we're all gonna get stuff wrong. We're all gonna get stuff wrong. And I think what is important is kind of like, how people attach themselves to exercises or like ideologies or stuff like that. Like some people like, well, if you, if you, you got a squat, you grow big legs, you got, you're like, I'm like, why don't you have to squat? Like what if you're not, what if you have 12 foot long femurts and you don't squat well? Like you want them to squat. What if there's, is it possible another exercise will fit your anthropometry better than a squat? So like when people completely attach themselves, it's an emotional attachment. And then whenever that happens, you can't really logically have a conversation with those people. So if I point you out like these four mechanisms of how this occurs, and I can show you, like here's all the data that you're peedable up. To me, I'm like, if somebody comes to me and like here's like what happens with that, I'm like, oh, well, that actually just changes what I thought, no different than what you did. But I do think that such a rare thing. But you're, you're really right. And I, rather than people feel overwhelmed, the most important thing is for them to feel less overwhelmed, 'cause you're still gonna feel overwhelmed at times, but to feel less overwhelmed, is try not to learn. Not, don't try to be an expert in nutrition, strength, hypertrophy, athletic training, whatever. Because then what will happen is you're gonna have these massive gaps, the whole mat was a jack of all trades master of none, and you'll end up with these massive gaps in one way or the other. Which is why I'd like a while back. I just like, I don't, I used to actually study more nutritional stuff and now I just don't care. I feel like nutrition. From what I need to know about it's pretty easy. My protein intake, my calorie intake, fit my carbs and fats in, what I need to know. I don't really need to know anything else. And I can work that with either myself or my clients or my advantage. But if you want to become really, really, really good at a craft, you kind of have to focus on that one craft, right? If you look at athletes, well, generally speaking, if a guy plays football in the NFL, he's not playing a multitude, he's not playing linebacker and center and defensive back. He's just playing one position. And then he has to get really good at that one position. So I think that kind of the same thing applies in these examples is that if you want to get really good at whether you're going to be an athletic trainer, for athletes, whether you're going to train people for strength, I think it's just important to kind of focus on like, this is going to be Charles Pollacklum was one of my mentors too. And I worked with Charles for a long time. And Charles always told me that. He's like just chase knowledge. Get as much knowledge on that one topic as you can ever get. And that's going to be your most basically rewarding for fully thinking that you can do. It's just a failure knowledge base with that one thing. And the more over the years that it went by, the more that really paid off. Because I was like, well, I don't really want to know about all this other craft. I just really want to know like this thing. So yeah, definitely over the last few years, I just consistently focused on how does everything with muscle growth work? Yeah. Well, hey, we appreciate you sharing your knowledge on it. And coming in as the expert on that one area and being open to just saying like, here's all the stuff that I know and sharing it with people. So really appreciate that. Thanks for coming on. We're people find you if they want to learn more about this, if they are interested in maybe need to hear this a few more times to really get a district. I mean, my Instagram for one, the main one right now is Lift Run Bank 1. I've been saying for a really good change. The whole reason why that came up is because years and years and years ago, when I started my blog, I just wanted something that people would remember. And at the time I was doing MMA stuff, and at the time I was doing a lot of athletic stuff. So it was like lift run, it was like all about the whole bank. It was literally just what was called a variable in computer programming terms. And it even knows what a variable is. It's a word in programming that can mean a long string of commands. So the bank wasn't actually meant what most people say they think it means. The bank part was actually just lift run. And then what is your variable? Like what's your passion? Are you an athlete or your power lift, your bodybuilder? What is it that you do besides just like lifting weights and some conditioning and stuff like that? So it was actually a little deeper than what people thought it was, but it was catchy. But I actually just want to transition over to something like just coach Carter or something like that now. It's just like playing. So generally people can find me a lift run, being one. And Chris and I will have an educational portal that's going to actually come up soon where we have spent-- I don't know the last year and a half being gathered these video modules that covers all this stuff at a really high physiological level. It's going to be meant for high level trainers and coaches and people who are like they want to really descend to that kind of next level thing. And then they can also find me and all my programs at Train and Road. So that's kind of my two staples where I'm at right now. All right. Thanks. We'll put a link in the description to everything. Thanks for your time. Absolutely. I appreciate it. But you're awesome. All right. Well, if I have more questions down the road whenever all of this changes in a few years, we'll have you back on. Absolutely. But I look forward to it. All right. Take care.