Is Load Progression Necessary For Hypertrophy?

So I'm going to invent an experiment in order to illustrate the HST idea of relative tissue conditioning and using load as a means of increasing stimulation.

Imagine we have 5 different groups who are 1) all trained people, with randomization etc. properly performed and 2) have taken a couple week break before our training experiment and 3) we know their RM's for 60-75% 1 RM.

Group 1 = 60% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 2 = 65% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 3 = 70% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 4 = 75% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 5 = 60% 1 RM, 3 sets to failure performed twice in week 1. 65% 1 Rm, 3 sets to failure performed twice in week 2. 70% 1 RM, 3 sets to failure performed twice in week 3. 75% 1 RM, 3 sets to failure performed twice in week 4. More reps performed on the 2nd session of each week if possible.

If I had to guess, I don't know that Group 1-4 would have any different results at the end of 4 weeks. I suspect they wouldn't. But the HST hunch/guess is that group 5 would outperform the other groups, because of the effect of relative tissue conditioning. Repeated bout effect might be the wrong word, it could be anabolic resistance, but if part of what we're adapting to is the load itself in our training sessions, then group 5 is the only one that would be trending towards staying ahead of the adaptive curve.

So another way of asking what I've asked in this thread is, what do you think the results would be? I'm honestly not sure, but if I had to guess if any of these groups were to win, my money would probably be on group 5.
 
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Imo it's because you keep looking at load out of context. I don't think I've seen anyone put forward the idea that load out of context is better. The only suggestion I've made so far is that greater load might be better in the same context (same volume/duration), e.g. bumping up our weights to 62% of 1 RM from 60% 1 RM for 3 sets of 12 after we've already done that 60% 1 RM for 3 sets of 12 the session prior.

I think we have a different idea of 'context' then....
To me, activation (participation of the fibers) is the context equalizer. If you do less reps with the lesser load, all the fibers aren't even feeling that total load.

And the reason the 30% fail group would have higher hypertrophy is simply because the duration of load applied is so much higher, enough to override any advantages that load might have since load is just part of the equation. Much longer spent cooking. I feel like even people suggesting load is part of the hypertrophy stimulus would concede this point, that you can make up for higher load with much longer durations. The old TTI logic.

And that's the whole point IMO, it's not load, it's not time, it's time x load that is the factor. Load is nothing without time and time is nothing without load, but load is just a part of the recipe.



I see what you're saying, because we're comparing load in two different contexts. Good point. But how about this...why not work/duration match the 30% fail group with another 90% group? That to me gets at the idea better of the role of load. Didn't that old Campos study basically do that?

Well, work is pretty much equalized if you take say 5RM to failure and 20RM to failure, it's 'actual internal' work equalization. The most important thing with the TTI studies was knowing that ATP usage is EXACTLY matched with total crossbridges which is EXACTLY matched with actual fiber force.

this would be the way to see this...
Take a single fiber, so we don't have recruitment messing things up...
Have it display max fresh tension from the start, for a time then have another fiber pre fatigue ramping up to max fatigued tension. Then compare hypertrophy.
the issue I think your seeing is a fiber WILL have max tension reguardless of external load if fully activated when fresh. the only way it will have less tension when fully activated, is if it's pre-fatigued which takes time with less activation, thus more reps with lighter vs less reps with heavier. See the conundrum? remember it's per fiber, not whole muscle, so that's where time is bothering you.






I see what you're saying. But my confusion is the "more load probably won't help increase the stimulation over time" part. If we increase the load with set volume equal, we are increasing the work. If we're trying to treat load as an isolated variable, isn't that a necessary consequence?

Yes, that's why you cannot have equal actual time and compare loads, the real main idea is run every fiber to max so they display their max tension, and compare. That takes going to or close to failure with either load.

I guess your reply, then, would be that the load part wouldn't necessarily be the driver, it'd be work. It's confusing I guess - if we're calling "tension-time spent at/near max recruitment and rate coding" the fundamental stimulus, which I think we are, that gives us a sort of equation where we have a particular context and then a tension-time formula, which is tantamount to work. But I think it'd still be accurate to call the tension part of tension-time part of the fundamental stimulus, no?

Yes tension is for sure part of the fundamental, we cannot activate a fiber without it creating tension.
  1. But does that fiber have to create full tension when fresh vs creating it later when fatigued?
  2. Why does a 1RM not produce the best hypertrophy when the fiber is creating literal max tension? Why does fatigue first, (reps of a set) then creating momentary fatigued max tension, but less absolute tension cause more hypertrophy? (force loss from use up to a lower absolute tetanic tension from fatigue)

Think about this....
Even with the tension time 'formula', less time with a lot more tension is still inferior to a fatigue with a final way less max tension (for a fiber). When those people hit failure at rep 30, the fibers in tetany were creating and feeling WAAAAAAAAAAAAY less tension than the ones were feeling with 90% load. What's that say about actual fiber tension and hypertrophy?
 
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So I'm going to invent an experiment in order to illustrate the HST idea of relative tissue conditioning and using load as a means of increasing stimulation.

Imagine we have 5 different groups who are 1) all trained people, with randomization etc. properly performed and 2) have taken a couple week break before our training experiment and 3) we know their RM's for 60-75% 1 RM.

Group 1 = 60% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 2 = 65% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 3 = 70% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 4 = 75% 1 RM, 3 sets to failure performed twice per week for a total of 4 weeks. Load remains static all 4 weeks, more reps performed if possible.
Group 5 = 60% 1 RM, 3 sets to failure performed twice in week 1. 65% 1 Rm, 3 sets to failure performed twice in week 2. 70% 1 RM, 3 sets to failure performed twice in week 3. 75% 1 RM, 3 sets to failure performed twice in week 4. More reps performed on the 2nd session of each week if possible.

If I had to guess, I don't know that Group 1-4 would have any different results at the end of 4 weeks. I suspect they wouldn't. But the HST hunch/guess is that group 5 would outperform the other groups, because of the effect of relative tissue conditioning. Repeated bout effect might be the wrong word, it could be anabolic resistance, but if part of what we're adapting to is the load itself in our training sessions, then group 5 is the only one that would be trending towards staying ahead of the adaptive curve.

So another way of asking what I've asked in this thread is, what do you think the results would be? I'm honestly not sure, but if I had to guess if any of these groups were to win, my money would probably be on group 5.

My absolute honest guess? All groups would have almost identical results. By all going to failure, time and load were equalized. If any group were going to grow more? I'd honestly say group 1 would be the best results. They are leaning more toward the 30RM fail scenario, and they'd have the best chance of 'also' getting sarcoplasmic hypertrophy.

If one want's to 'beat tissue condition'?
Here is what I would say would be the superior group...
Group 6 = 70% 1RM, add weight just to stay in that range, but.. week 1= 1 set to failure, week 2= 1 set to failure plus one myo set week 3= 1 set to failure plus 2 myo sets, etc.
 
I think we have a different idea of 'context' then....
To me, activation (participation of the fibers) is the context equalizer. If you do less reps with the lesser load, all the fibers aren't even feeling that total load.

I guess I don't see any other way to isolate external load, however, and let all else remain constant. It's like we agree but are almost having a semantical debate at this point imo.

And that's the whole point IMO, it's not load, it's not time, it's time x load that is the factor. Load is nothing without time and time is nothing without load, but load is just a part of the recipe.

Kinda what I mean though, didn't I concede this in literally the first post of this thread? Lol.

Well, work is pretty much equalized if you take say 5RM to failure and 20RM to failure, it's 'actual internal' work equalization. The most important thing with the TTI studies was knowing that ATP usage is EXACTLY matched with total crossbridges which is EXACTLY matched with actual fiber force.

This is an important differentiation, I suppose. I haven't been talking about literal internal work. I've been talking about the actual weight x reps definition of work, which is generally how I see it used in the literature, I thought?

the issue I think your seeing is a fiber WILL have max tension reguardless of external load if fully activated when fresh. the only way it will have less tension when fully activated, is if it's pre-fatigued which takes time with less activation, thus more reps with lighter vs less reps with heavier. See the conundrum? remember it's per fiber, not whole muscle, so that's where time is bothering you.

I see it, and this goes back to the idea of per-fiber tension that I thought was central to the idea of tissue conditioning. You're saying that lower loads = lower per-fiber tension by virtue of the fact that lower loads require first going through time with less activation before reaching peak activation.

Yes, that's why you cannot have equal actual time and compare loads, the real main idea is run every fiber to max so they display their max tension, and compare. That takes going to or close to failure with either load.

My thought experiment should satisfy this then, but we don't agree on what the outcome would be. Are you aware of any research even vaguely like this?

But does that fiber have to create full tension when fresh vs creating it later when fatigued?

Obviously not, which is part of your argument, otherwise lower loads would never equal, much less beat, higher loads.

Why does a 1RM not produce hypertrophy when the fiber is creating literal max tension? Why does fatigue first, (reps of a set) then creating momentary fatigued max, but less absolute tension cause more hypertrophy?

So out of curiosity, ~80% of 1 RM is right near the range where you're at max recruitment immediately, right? But that's also like an 8 RM. I suppose rate coding would still go up throughout a set of 80% 1 RM, but would the fibers ever be pre-fatigued per se since activation is actually max off the bat?

I ask because I'd guess 80% 1 RM should be enough reps to satisfy that "hard workings set at moderate reps" rule.

Even with the tension time 'formula', less time with a lot more tension is still inferior to a fatigue with a final way less max tension (for a fiber). When those people hit failure at rep 30, the fibers in tetany were creating and feeling WAAAAAAAAAAAAY less tension than the ones were feeling with 90% load. What's that say about actual fiber tension and hypertrophy?

Using the rubber band example, this is why I always thought of it almost as a damage type thing. A single rep for a limited duration will see you stretch the rubber band really hard once and then return it back. I always envisioned a lot more reps as straining the rubber band more, more cycles of contraction/lengthening that would be more conducive to mechanical strain.
 
I see it, and this goes back to the idea of per-fiber tension that I thought was central to the idea of tissue conditioning. You're saying that lower loads = lower per-fiber tension by virtue of the fact that lower loads require first going through time with less activation before reaching peak activation.

YES!!!
remember, stimulation is per fiber.
So a fiber has to be activated to 'be used', 'to create tension'.
This means, you have to do 30 with 30 RM just so those later fibers even 'get to' create their max tension (even though it's lower from pre fatigue) yet that causes hypertrophy.
See what I mean? The 'go to failure' is the equalizer. Not literal 'time'. It's 'time for the fiber in question' not 'time for the whole muscle'.

that's what 'good reps' are... like last 5 reps with 8RM are good reps, last 5 reps of 30 reps with 30RM are 'good reps', so it's equal.

So out of curiosity, ~80% of 1 RM is right near the range where you're at max recruitment immediately, right?
For most muscles yes, small muscles about 50%, mid sized muscles like biceps 65-80%, thighs 95-100%

But that's also like an 8 RM. I suppose rate coding would still go up throughout a set of 80% 1 RM, but would the fibers ever be pre-fatigued per se since activation is actually max off the bat?

OK recruitment is max right off, not activation (activation is recruitment and rate coding total). So for sure, 1st rep with 8, the largest MU is BARELY helping, rep 2 it's helping more, rep 3 more.. rep 8 it's finally in tetany and 'feeling' 'creating' it's max , albeit pre fatigued, tension.

Like....
sOzCHz.jpg


and then think of this.... all the people who aren't training to absolute killer failure, are NEVER causing the last MU's to create max tension, even in a fatigued state, yet so many get huge anyway... The MU does get used, and if volume is there, it gets fatigued, but never highest tension... yet they get big....


Using the rubber band example, this is why I always thought of it almost as a damage type thing. A single rep for a limited duration will see you stretch the rubber band really hard once and then return it back. I always envisioned a lot more reps as straining the rubber band more, more cycles of contraction/lengthening that would be more conducive to mechanical strain.

OK I see how you look at it.. although in reality I don't think the fibers get 'stretch issues' from contracting, but maybe when strain is high, something 'turns on' or a 'port is opened' or something?
 
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Btw Ron, what happened between when you posted this and now to change your opinion?

http://thinkmuscle.com/community/threads/ah-ha-think-i-caught-on-to-something.43466/

I'm reading through old threads and your first post here is eerily remniscent of what I was getting at in this thread, including you proposing a similar thought experiment, about load's potential role of keeping the stimulus going. We apparently arrived at the same conclusion in light of the same new data, but between then and now you appear to have changed your mind. Just curious what new evidence made you think in that direction?
 
One more quick post to try to tie this all together since we've tangented all over.

The original article of discussion in this thread is whether load progression was necessary for hypertrophy. The research used to justify this position by Brian Minor and others is the emerging research showing RM's at widely varying loads produce similar hypertrophic outcomes. E.g. 15 RM seems to equal 12 Rm seems to equal 8 RM if the sets are all taken to failure. The idea, then, is that programming load increases aren't necessary to induce (or optimize) growth, they're just a natural consequence of getting stronger over time from having grown previously.

Contrasting this position, load progression is built into the HST model, so clearly Bryan et. al believe that load progression IS necessary, at least to optimize hypertrophy.

This thread was an attempt to tease out what's causing what. My posts on per-fiber tension were trying to understand, mechanistically, how at the level of an individual fiber, load progression might be increasing the stimulus, and how this might affect our training decisions. The thought experiment I introduced of the 5 groups (I probably should have stretched out the timeframe to 6+ weeks, but same idea) was meant to try to illustrate this. Ron, you also introduced a near identical thought experiment in the thread above. The idea in these thought experiments is that it's not about widely varying loads inducing equal growth out of context, but rather something RBE-ish limiting our growth with a given load such that increasing the load winds up an increase in stimulus to keep us growing over time.

So the "point" I've been trying to get at is still related to the original article. I.e. is load progression necessary to induce growth, or at least optimize it? The HST model clearly indicates it is, and I still have tendencies leaning towards it probably mattering as long as something RBE-ish exists. This has gotten pretty confused with all the back and forth, but this is the gist of this thread and what I'm trying to figure out. As per my previous post, I think Ron got to the exact same place I am currently back in that old thread, so I'm still trying to understand what changed his mind. :)
 
I think it was just thinking more about it, looking at the studies more...
Just so much that more load less time wouldn't increase things I don't think. I think 'work' (load and time) have to be increased. I don't think , well, haven't seen a study or anything that shows just load is the factor that sets tissue condition. When I think about it, if a person can move from 2 sets with 180 to 5 sets with 150 and grow, then that shows it's 'work', not load.

then I was looking around and found people saying on here they had the most growth with the 10's not the 5's...

I started thinking, load can for sure be used and probably is the best 'way', but it needs to be used to bring up the equation... 5x3 is no better than 3x5... (that's times not sets, like 3 times 5)
So not like this...
Load =5 time= 10
increase to load= 10 time= 5

But would have to be
Load= 5 time= 10
increase to load =10 time =10

Now it would increase things. Or would could use
Load= 5 time= 10
Move to load =5 time= 15
but volume is harder to manage and way larger steps than what we can do with load.
 
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One more quick post to try to tie this all together since we've tangented all over.

The original article of discussion in this thread is whether load progression was necessary for hypertrophy. The research used to justify this position by Brian Minor and others is the emerging research showing RM's at widely varying loads produce similar hypertrophic outcomes. E.g. 15 RM seems to equal 12 Rm seems to equal 8 RM if the sets are all taken to failure. The idea, then, is that programming load increases aren't necessary to induce (or optimize growth), they're just a natural consequence of getting stronger over time from having grown previously.

Contrasting this position, load progression is built into the HST model, so clearly Bryan et. al believe that load progression IS necessary, at least to optimize hypertrophy.

This thread was an attempt to tease out what's causing what. My posts on per-fiber tension were trying to understand, mechanistically, how at the level of an individual fiber, load progression might be increasing the stimulus, and how this might affect our training decisions. The thought experiment I introduced of the 5 groups (I probably should have stretched out the timeframe to 6+ weeks, but same idea) was meant to try to illustrate this. Ron, you also introduced a near identical thought experiment in the thread above. The idea in these thoughts experiments is that it's not about widely varying loads inducing equal growth out of context, but rather something RBE-ish limiting our growth with a given load such that increasing the load winds up an increase in stimulus to keep us growing over time.

So the "point" I've been trying to get at is still related to the original article. I.e. is load progression necessary to induce growth, or at least optimize it? The HST model clearly indicates it is, and I still have tendencies leaning towards it probably mattering as long as something RBE-ish exists. This has gotten pretty confused with all the back and forth, but this is the gist of this thread and what I'm trying to figure out. As per my previous post, I think Ron got to the exact same place I am currently back in that old thread, so I'm still trying to understand what changed his mind. :)

OK good thoughts... I totally see what your saying, man how can I not babble too much and make what I'm thinking , just be easy to see .. how I see it... ummm lol

OK...
First, lets separate load increases from LOAD increases. As , compensatory load increases (keeping up with strength so your still at the same RM) vs moving up in RM levels (like HST).

Obviously, compensatory load increases do work for sure, it's how 99% of people train. Hang out in the 8-10 range, add weight when you can. It works, for sure. But HST was about gaining faster than that... the idea is, the anabolic resistance makes the gains small with that standard format, beating the 'wall' causes 'beginner gains' the whole time. (now me, I think beginner gains are mostly due to untapped satellite cells and under used nuclei, all those are ready to hurry up and increase PS like mad, then it maxes out) But... anyway, so the idea is, tissue is conditioned to load, vanilla HST is 1x15, then 1x10, then 1x5's . I myself, don't think 1x5 is a step up from 1x10. 2x5 would be, of course so would 2x10. We KNOW going from 1 to 2 sets with the same RM range will increase hypertrophy. So I don't think load 'itself' is the 'surpasser of anabolic resistance' I think 'work' or 'fatigue' or... something like that is.

So for sure, eventually, compensatory is required, but that's not a load increase, that's 'load maintenance', you get stronger, now your 8RM is 120 instead of 15, so your not increasing the tension, your maintaining the tension. Think of a muscle,if it's size A and you use a load, there is some amount of 'tension per square inch', if the muscle is larger, you have to use more load to have that same 'tension per square inch'.
 
This post by Bryan is probably one of the better descriptions I've seen of his position in that same thread:

http://thinkmuscle.com/community/th...ught-on-to-something.43466/page-2#post-259226

I recall Bryan previously describing his reasoning, and I think his argument is that looking at a fiber out of context isn't actually possible. That even fibers which aren't recruited still have to receive tension from fibers that are by virtue of the fact that they're literally hooked together structurally. Or stated differently, we can't simplify this to the level of an individual muscle fiber because the tension experienced by one fiber will affect adjacent fibers etc.

In this sense, I think he's looking at it on a macro scale, that "whole muscle tension" and the tension component fibers experience will scale with external loading, and whole muscle tension is a factor in growth in terms of the muscle's current conditioning.

A contracting muscle experiences a sudden and dramatic shift in its internal chemical (and genetic) environment. It also experiences significant distortion/stretch of its cytoskeleton (i.e. the protein structures that give the cell its shape and provide rigidity for contractile proteins to anchor themselves.) This shifting and distortion is a dynamic process, meaning that both are temporary and constantly changing while the muscle is performing reps. Subsequent anabolic signaling within the cell is in response to these sudden and dramatic changes.

The muscle will respond differently to the same combination of weight and reps over time. This change in how the muscle responds is caused by the following factors; 1) the “resulting” condition (due to previous bout) of the muscle at the time load was applied, 2) how much time has passed since the previous time the muscle was trained, 3) the ability of the tissue to respond anabolically to the current bout (due to genetics, age, nutrition, hormones, rest, stress, etc), and 4) the extent of adaptation (both metabolic and structural) since the previous bout (i.e. RBE). These variables or “unknowns” can be described in other ways, but you get the point. These variables are like electrons, you can’t know exactly where they are at any given time, but you can have a good idea of where they should be.

I think these two quotes get to the heart of the HST argument. So to me the last piece of the puzzle is what you said here:

I don't think , well, haven't seen a study or anything that shows just load is the factor that sets tissue condition. When I think about it, if a person can move from 2 sets with 180 to 5 sets with 150 and grow, then that shows it's 'work', not load.

This is why I was hoping to get Bryan or someone's input on RBE vs. anabolic resistance and maybe more insight into what exactly we're adapting to. Part of the confusion in this is whether metabolic stress is a factor, in and of itself, and it's why I linked that Menno video that Totentanz liked in my original post. If metabolic stress is its own unique stimulus, and it seems like both Bryan and Borge think it is, then there's a certain logic to 150 causing new growth in the sense that you're wildly increasing metabolic stress. If metabolic stress is NOT an independent driver of growth like Menno argues, then maybe it really is just "work" we're adapting to. But I'm not sure what the practical implications of that are over the longer term.

This is all reminds me of what Dane Trudell of Doggcrapp training said in his original Cycles for Pennies article back in like, shit, 2000? If I only give you 135 lbs to growth with, can you really grow forever just by increasing reps and/or volume? Or at some point do we actually need more load to keep driving you towards your potential?
 
I would love to see a study though showing a slack fiber can be stimulated from another fiber pulling it, what I read is the fiber has to have high calcium (calcineurin is permissive) so must be activated, but maybe that's not true... and then I think... well high load would have all fibers working so there would be 'less of that', less load would have more of the scenario where a tetanic fiber would be tugging at a less activated fiber.

Right but read what I said above about compensatory load increases vs actual RM increases. maybe you posted the above before seeing my post just above that.

I'm pretty positive (not totally but pretty sure) RBE and anabolic resistance are two separate things... When RBE is low, we get damage and the high PS is about repair, that's now what we want. That's similar to Vince Basile's old posts about DOMS = Growth.
 
Right but read what I said above about compensatory load increases vs actual RM increases. maybe you posted the above before seeing my post just above that.

Kind of what I was getting at with the Dante Trudell reference. Brian Minor said the same thing, load goes up because of a combination of 1) keeping things practical (who the hell is going to keep increasing reps past 20 in something like squats where you'll constantly want to die) and 2) the fact that, as you get bigger, you'll get stronger. So you wind up having to increase some combination of reps and load to keep growing, but not because those are a requirement of growth per se, but rather because you need to lift more weight or do more reps just to achieve the overload again since you're now bigger/stronger. They're the result of the adaptation, not the driver.

However, Dante Trudell's quote gets to the heart of that same issue. Or what Brian Minor kind of sidesteps by talking about keeping things practical. Assuming we didn't care about practical, could we give you a 135 lb barbell for squats, and have you squat in perpetuity with that load, just adding reps or adding sets, and have you reach your legs' muscular potential? As impractical as that is, I think the answer to that is the answer to this whole thread :)
 
I'm pretty positive (not totally but pretty sure) RBE and anabolic resistance are two separate things... When RBE is low, we get damage and the high PS is about repair, that's now what we want. That's similar to Vince Basile's old posts about DOMS = Growth.

Also, holy shit at this reference. I remember Vince! He had routines designed around inducing DOMS, basically whatever continued to induce DOMS = continued to induce growth.

As an aside, I've wondered if the damage part of hypertrophy gets screwed up based on the timeframes of most research. Meaning satellite cell donation and an increase in nuclei are longer-term adaptations. Let's say damage is part of what drives the satellite cell part of this. If we're not hitting our max size based on the number of nuclei in our fibers, in the shorter term, damage wouldn't really look like it's doing anything, because we're not running into those limits yet.

But if we stretched the timeframe to longer, then we'd actually see damage mattering. As most lifting research is like up to ~12 weeks max, it occurs to me that the muscle damage part of the equation could be getting missed.
 
Kind of what I was getting at with the Dante Trudell reference. Brian Minor said the same thing, load goes up because of a combination of 1) keeping things practical (who the hell is going to keep increasing reps past 20 in something like squats where you'll constantly want to die) and 2) the fact that, as you get bigger, you'll get stronger. So you wind up having to increase some combination of reps and load to keep growing, but not because those are a requirement of growth per se, but rather because you need to lift more weight or do more reps just to achieve the overload again since you're now bigger/stronger. They're the result of the adaptation, not the driver.

right, and that kind of load increase, IMO, isn't a load increase, so only proves that long term growth can be had, without relatively heavier loads.

However, Dante Trudell's quote gets to the heart of that same issue. Or what Brian Minor kind of sidesteps by talking about keeping things practical. Assuming we didn't care about practical, could we give you a 135 lb barbell for squats, and have you squat in perpetuity with that load, just adding reps or adding sets, and have you reach your legs' muscular potential? As impractical as that is, I think the answer to that is the answer to this whole thread :)

I'd say no, and not because load is too light but because other factors are ruining it. Like 100 reps with 100RM has so much metabolic and energy issues, you just cannot ever fully activate the muscles, so 'other things' get in the way.
 
Also, holy shit at this reference. I remember Vince! He had routines designed around inducing DOMS, basically whatever continued to induce DOMS = continued to induce growth.

As an aside, I've wondered if the damage part of hypertrophy gets screwed up based on the timeframes of most research. Meaning satellite cell donation and an increase in nuclei are longer-term adaptations. Let's say damage is part of what drives the satellite cell part of this. If we're not hitting our max size based on the number of nuclei in our fibers, in the shorter term, damage wouldn't really look like it's doing anything, because we're not running into those limits yet.

But if we stretched the timeframe to longer, then we'd actually see damage mattering.
ha you remember him too!?? LOL his posts were fun though!!

well, what I've 'read' anyway, is when a satellite cell is activated with damage, it pulls up, donates for repair, but it doesn't donate the nuclei 'into the cell' as another protein factory, that it's different. Donating for addition of working nuclei is a different process. I read that in some study when I was googling satellite cell stuff like a maniac one time lol
 
Hey Ron, I thought you might be interested in this post on the exodus board, in turn copy/pasting something Austin Baraki of Barbell Medicine has written on the topics of anabolic sensitivity (getting to our anabolic resistance concept), volume as the main driver of hypertrophy and the role of muscle mass in strength. I could give this its own thread, but it seems pertinent here as well. Some interesting implications about training "hardgainers" and older trainees, too.

https://www.exodus-strength.com/forum/viewtopic.php?p=73291#p73291

OK folks, brace yourselves: in an attempt to hammer this home I’m going to lay this argument out as clearly as I can:

1) The evidence shows that strongest predictor of force production capacity is the amount of muscle mass someone carries -- and this becomes even more true once basic neurological adaptations (e.g., skill and neuromuscular recruitment) have taken place. In other words, in post-novice trainees, the amount of muscle you have seems to make the biggest difference in how strong you are.

2) The neurological adaptations necessary to lift relatively heavy weights are best developed by handling relatively heavy weights (in other words, you MUST handle heavy weights to improve and demonstrate top-end force production using the muscle mass you already have). No one is arguing that at all, and the evidence is clear here.

3) Increases in muscle mass result from the process of muscular hypertrophy. The evidence unequivocally demonstrates the role of training volume as the primary driver of muscular hypertrophy, with data showing an incremental benefit to each additional set performed per week. Additionally (and very interestingly), there is also evidence showing that anabolic signaling progressively increases as you increase intensity from 20% 1RM to around 60%-70% … but above that, you don’t seem to get any higher anabolic signaling by using heavier weights. This helps to explain why you can get the SAME hypertrophic outcomes using weights ranging from 30% 1RM to 90% 1RM. (And has all been measured *myofibrillar* hypertrophy. The idea that using different intensities give you different proportions of sarcoplasmic vs. myofibrillar hypertrophy is bullshit.)

4) So, once we have someone who has developed the basic skills to perform the lifts, and has developed some of the necessary neurological adaptations in terms of neuromuscular recruitment (for our purposes, say, once they’ve finished the novice program), we need to get them MORE JACKED. This means that training volume per unit time MUST increase, *for everyone* (… which, of course, requires a reduction in average intensity). Note that doing the opposite — reducing training volume, increasing training intensity, and eating more — is an *incredibly* stupid way to train for gaining muscle mass (unless you’re artificially sensitized to training by being on tons of drugs, in which case you can do anything, like one heavy set per week, and make progress).

5) We have evidence showing that older trainees generate a lower anabolic response to training compared to younger trainees at low training volumes. However, we also have data showing that increasing this training volume for older trainees increases (and nearly normalizes) their anabolic response. This is the exact same phenomenon we see with protein intake. Similarly, there is evidence that anabolic signaling decreases the more “trained” you become (you effectively become desensitized to anabolic stimuli, i.e. more training resistant), and therefore need MORE TRAINING the more advanced you get. Duh.

6) It is true that an untrained older person is more likely to have a poorer recovery capacity than a younger person … though untrained people in general have poor recovery capacities. Fortunately, training with more volume and more frequency 1) improves your recovery capacity (evidenced by, among *many* other things, the rate of MPS after training), and 2) stimulates the Repeated Bout Effect, which protects you from the effects of muscle damage and DOMS … meaning you don’t get as sore — unless, of course, you’ve been told that as soon as you turn 35 years old you become crippled, unable to recover from anything because your testosterone is in the low-normal range. (In fact, we have evidence that fear-avoidance and catastrophizing behavior worsen the perceived severity of DOMS after training … and I’ll be talking more about this soon).

7) SO, the bottom line: Waiting as long as humanly possible before increasing someone’s training volume and frequency (or, *decreasing* it) means you are also 1) Waiting as long as humanly possible to develop the necessary work capacity to 2) TOLERATE the amount of training necessary, in order to 3) Stimulate enough anabolism and therefore gain enough muscle, in order to 4) Keep increasing long-term strength potential. On top of this, constantly TELLING people they can’t recover from doing an extra set and REMINDING them of how sore and achy they’ll get, further compromises this entire process from a psychological standpoint.

If you aren’t already familiar with this stuff, with physiology in general, and with the current literature, there is a WHOLE LOT to digest here. But that’s the argument we’ve been laying out in these podcasts.

This followup post with supporting evidence might also be worth pouring over :)

https://www.exodus-strength.com/forum/viewtopic.php?p=73294#p73294
 
that sounds really accurate from everything I've read myself on all this.
He's saying, and I've seen that too, that people kinda slowly get resistant to the stimulus, more volume surpasses it, but it's more an 'over time' kinda thing. Which makes sense, it's how we adapt, the resistance to the signal 'are' the adaptations.
 
that sounds really accurate from everything I've read myself on all this.
He's saying, and I've seen that too, that people kinda slowly get resistant to the stimulus, more volume surpasses it, but it's more an 'over time' kinda thing. Which makes sense, it's how we adapt, the resistance to the signal 'are' the adaptations.

Indeed, they seem to have a pretty good grasp of the research.

The frequency piece is interesting. Here's Menno's argument on that:

https://mennohenselmans.com/maximum-productive-training-volume-per-session/

I think the commonality here is that most of these people (Schoenfeld, Krieger, Helms, Israetel, Henselmans etc.) are suggesting volume, rather than frequency, is the main driver. However, there does appear to be a sort of per-session limit in terms of useful volume, possibly as low as ~5-10 sets per muscle group according to that Barbalho research.

So if you were going to do, say, ~10 sets per muscle group, a number already higher than what a lot of people do in the minimalist crowds, you could feasibly achieve this from anything from ~3 sets of 3 thrice weekly in a more standard HST setup to one day a week of ~9-10 sets with classic bro training. There might be a slight difference, but you're probably at least still getting most of the bang for your buck at 1x per week frequency. However, if you wanted to venture into exploring even higher volume, or if your training age and relative advancement were so high that you actually needed more volume to overcome your anabolic resistance, then that's where frequency starts to be particularly advantageous as you can spread around these higher volumes into more weekly sessions without running into that volume-per-day cap.

The thing to me is though, like Borge, I'm not totally sold on the idea of these crazy high, 10+ sets per week volume recommendations. And if we're not venturing into that high of volume, I think you can make a pretty strong argument for a classic split being a viable alternative, as per our previous conversations. That said, hedging on the side of, say, ~twice per week would probably be a good starting place for a lot of people and upper/lower type splits are probably a pretty good way to manage overall fatigue without going too nuts on frequency. I've written previous example of upper/lower type splits on this board before as it was my own sort of compromise of design I had concluded based on the research years ago, where it seems like at least most of the advantage of higher frequency is captured by even going twice weekly per muscle group when volume equated.
 
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ok yes, I've also listened to a ton of Menno's podcasts too.

BUT.... .... tissue condition , anabolic resistance.. is EXACTLY why I think lower frequencies, in practice, DO match higher frequency.

Here, read this.
If taking a 2 week SD, .........letting a muscle 'rest' for 2 weeks can allow a less than 15RM with less than max effort, the ability to stimulate, after the prior training 2 weeks before required high effort with a 5RM,, AND, we know as people get resistant, PS spikes are lower and shorter, then taking a week between workouts HAS TO at least allow a slightly higher stimulus the ability to 'still stimulate'. Read that again...
May 1st 3x5 RM with 200, 2 week SD, 3x15 with 20RM now is significant
Then for sure...
May 1st 3x5 RM with 200, 1 week between, then May 8th 3x5 with 205 has to also be significant and way more even than the above.

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Yes agree for sure. It really really goes down to the 'small stimulus more often' vs 'larger stimulus less often'. We see it in real life, it makes sense, it fits the science.....
Also agree, crazy high volumes are never needed for most, I guess if they train so gentle that each set is such a small 'inroad' (so to speak!), maybe a lot of them are needed to 'chip away', (also so to speak). Too many guys have gotten huge with low to medium volume, and even 1x a week per muscle, to say 'it can't work' or even is 'very inferior'.
 
Yep, I've actually made that argument myself here I think...15+ years ago? Jesus I'm old :( Basically that I could see a rationale for bro training with each week off between direct work on a muscle group as a sort of mini-SD, resensitizing us to a growth stimulus, and then the higher volume almost definitely assuring that we're continuing to grow, even if it might be slower on paper than higher frequency at first. And on that last point, that if you spread your volume too thin on a per-day basis as your training age advances with higher frequency training, that you might accidentally run into an issue where the acute, "right now" stimulus is actually not high enough to get an adaptation.

To illustrate this logic with an example, as a beginner, even 1 sets per muscle group per session is probably enough to grow, maybe even as good as 3 sets. So if we test 3 sets once weekly to 1 set three times weekly, we are basically comparing 3 growth sessions per week to 1, so the three times per week looks way better. But let's say, over time, as we become more adapted and anabolically resistant, we now need 2 sets in a given session to actually still grow. On those same protocols, we now have one option where we grow once a week on that 3 set session, and another protocol where we grow 0 times per week as no individual session is actually enough. So now the logic flips and only our once per week group still grows, but we'd miss this unless we followed our trainees for long enough.

In this sense, a more classic bro training split is an insurance card that, even if you're not truly optimizing the hypertrophic stimulus by nailing that per session volume/acute stimulus balance and breaking it up into more weekly sessions to squeeze out every last drop of growth, you're at least definitely still making long-term progress vs. screwing up that balance and doing too little per session. Which, again, might be exactly why people kind of gravitated to that in the first place through sheer trial and error.
 
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