# Hypertrophy And Effective Reps - Incomplete Model?

Awesome discussion! There is some great insight in this thread.

I just want to add the idea for those not sure how to frame this discussion in their minds, that biological tissue is "fuzzy" in the way they used to say "fuzzy logic".

From Wiki, "Fuzzy logic is a form of many-valued logic in which the truth values of variables may be any real number between 0 and 1 both inclusive. It is employed to handle the concept of partial truth, where the truth value may range between completely true and completely false."

"By contrast, in Boolean logic, the truth values of variables may only be the integer values 0 or 1."

The reason I bring this up is that there is a temptation by thinking lifters to define the ideal set using boolean logic, instead of fussy logic. It is tempting to try to prescribe the ideal number of reps, or weight, or time under load, etc. When in reality, as a biological system with both mechanical and chemical components, there will never be a fixed quantity of any of the variables involved that will always be true or "ideal". It is fuzzy, there is a range of possible quantities that will work for stimulating a system that has a range of possible "states".

It is for this reason that we have the HST principle which states, "The effectiveness of any load-stress depends on the condition of the tissue at the time the load-stress is applied." And the condition or "state" of the system is dependent on what load-stress it has been most recently and chronically exposed to.

Additionally, it is difficult to say what RPE is ideal without considering the fact that we have a moving target with mechano-sensing cellular protein structures such as costameres, intregrins, and adhesion GPCRs fluctuating in sensitivity all while the chemical milieu within the cell is ever changing.

Now I'm not saying discussions like this are futile, on the contrary, they are great and certainly do a lot to help lifters understand what they are shooting for when executing a set. All I'm saying is that, like an electron, we can't ever say for sure where it is at any given time, at best all we can say with some certainty is where (a range) it should be.

Ok, back to the discussion!

Great thoughts Bryan!
Man that is so true, it's funny how we assume things like 5 RPE is 'such and such'. ... in reality, like your saying, it's fuzzy.. one mans 5RPE might be very different than anothers, and that same person's RPE might be different on Wednesday over Tuesday... or this or that...

One aspect I never considered until just now, was a forest for the trees thing.. with load. I would focus on the tree (load) and not think about the forest. What I mean is, is even if load itself doesn't vary per fiber tension, load at a rep range, would vary 'volume load' (ie work, tension-time, etc.). I know you didn't say that in your post, but somehow your post made me realize that....

This thread wasn't really meant to be prescriptive in terms of do X sets of Y weight for Z RPE, but rather trying to figure out the big players on the practical end (sets and reps stuff) for hypertrophy. E.g. the little picture I made was just an illustration of the concept of RPE vs. stimulation and cumulative fatigue/stress, rather than saying "do exactly this." We actually discussed some caveats to even that picture - novice vs. trained, compound vs. isolation lifts, undoubtedly other inter-individual differences. For the subject of this thread, I was highlighting the idea of effective reps being popularized currently in some circles, and arguing that it's probably something more like "effective sets."

Either way, I think the concept of something like effective sets/reps appears strong, which is that to maximize the hypertrophic effect of a set, we 1) want to reach a point of full recruitment (either by being heavy enough or close enough to failure) and 2) have the set last long enough to accrue enough tension-time and/or metabolic magic. As per the fuzzy logic above, it's hard to say exactly what RPE that represents for #1, and even the number of reps for #2, so we can't guarantee what those numbers would be on a case per case basis. Though we can certainly look to research for reasonable starting points (in this case, >= ~5 reps and probably RPE ~5-6+). Like most things, people still need to trial and error stuff, and one of the ideas that's often missing in discussions of research is that it's kind of average case scenario, when there are always outliers, so even if the best fit prescription works at the population level, it's always possible that you as an individual could be an outlier that needs your dose skewed way lower or higher.

But yah, these sorts of threads are basically exercises in trying to understand the implications of the latest research on hypertrophy, and I like to have them with Ron et. al to catch myself up on this stuff from time to time.

edit: moved rest of discussion to next post.

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As a separate issue Bryan, since this thread seemed to get your attention, I was hoping you could shed light on this HST principle a bit more. As Ron and I have discussed, I'm not sure what your thoughts are on this HST principle in light of more recent research, namely that pertaining to similar hypertrophic outcomes at widely varying loads (~30-35 to ~5 RM) when taken to/near failure.

"The effectiveness of any load-stress depends on the condition of the tissue at the time the load-stress is applied."

The best place to start for this discussion would probably be this article by Brian Minor:

In the article above, Brian (as opposed to Bryan!) makes the case that increasing load, in and of itself, does not appear to achieve "progressive overload." Rather, increases in load are more like evidence that progressive overload has already occurred. Or stated differently, we add weight over time not because the act of adding weight keeps us ahead of something like RBE, but rather because we need to increase the weight to keep the relative effort (RIR/RPE) the same after having already achieved progressive overload by doing enough hard sets.

I think what I'm trying to suss out here is the difference between something like RBE, which is inextricably tied to our HST model in terms of tissue conditioning, and something like "anabolic resistance," which appears a similar concept but without quite the same implications. From what I've seen, RBE appears to relate more to muscle damage rather than hypertrophy, per se. Anabolic resistance is similar in that the idea is that, obviously, we can't keep using the same magnitude of stimulus over time to keep growing, but anabolic resistance doesn't appear to invoke RBE to explain itself. It appears to be more like "the closer you are to your potential, the greater the magnitude of stimulus needed to keep growing," with the stimulus relating more obviously to volume rather than load.

Any insight you could offer would be much appreciated.

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One thing I gotta pop in here, is if we leave the actual 'method' blank but just look at the HST principle, progression is like this, compared to standard

Regular progression
Tissue condition 2
workout level 3
Big stimulus
Tissue condition increases to 5
Compensation progression workout level 3 (raise things to match adaptations)
Medium stimulus
Tissue condition increases to 8
Compensation progression workout level 3 (raise things to match adaptations)
Small stimulus

HST progression
Tissue condition 2
workout level 3
Big stimulus
tissue condition increases to level 5
Over progression workout level 5
Big stimulus
tissue condition increases to level 8
Over progression workout level 8
Big stimulus

The base idea of HST is to keep having workouts higher above current condition. It seems like that should work, I think it might take a 'volume-load' increase not just a load increase.

Stronger dudes might get away finishing their 6-12 rep sets with 1-2 RIR. Less strong guys might need to take all their moderate to high rep sets closer to failure.

To expand slightly on what Ron is posting above, the confound here is relative effort, or "how far away from failure we are" in a given set when considering the role of load. The number of reps in reserve we have on any set.

For example, in a standard HST type setup, I might do 2-3 sets of 10 multiple times per week for 2-3 weeks, going from something like ~60% 1 RM to ~70% 1 RM. Realizing inter-individual differences will make the following estimations imperfect, 60 1 RM is probably close to a 20 RM for a lot of people, and 70 is more like 12, and near-ish the limit for what we'd be able to do for multiple sets of 10.

So at the start of that cycle at 60% 1 RM, each set has roughly ~8-10 reps in reserve (again, average case scenario, YMMV). However, as we rapidly increment the weight, we have fewer and fewer reps in reserve, going from ~8-10 at the start of this minicycle to maybe ~1-2 per set at the end. So relative effort changed throughout the course of the cycle, and our sets are literally getting harder.

So if sets of 10 at 60% 1 RM were enough to grow post strategic deconditioning, then ramping up the weight while still doing 10s is one way to raise the stimulus, but not because the weight increased per se, but rather because the relative effort increased.

Now imagine the same sort of cycle, going from ~60 to 70% 1 RM, but we took every set to/near failure, i.e. had the same relative effort. If we started our HST cycle with ~18+ reps or whatever at 60% 1 RM, and wound up using ~10-12 reps per set at ~70% 1 RM a few weeks later, did raising the weight, in and of itself, actually increase the stimulus for growth?

This is what I'm trying to get at - what is the role of load, in and of itself, in driving hypertrophy. In and of itself would mean that we'd need to compare the same relative efforts to avoid having that as a confound in our comparisons.

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This is what I'm trying to get at - what is the role of load, in and of itself, in driving hypertrophy. In and of itself would mean that we'd need to compare the same relative efforts to avoid having that as a confound in our comparisons.
9-10 days of SD loses some adaptations, so the perceived effort of working with previous loads leads to recovering the lost grounds, nothing more. Otherwise we'd be cycling SD+unchanged loads forever and growing In reality it seems that working loads have to stay in the 85-90% range for each rep to be "effective" regardless of failure proximity, or going closer to failure with lighter loads. Meaning if a person's 85-90% loads no longer feel heavy, he either has to do more reps and/or use shorter rest to feel the effort, or increase the load to stay in the 85%+ range.

In reality it seems that working loads have to stay in the 85-90% range for each rep to be "effective" regardless of failure proximity, or going closer to failure with lighter loads.

Not quite sure what you mean here, to be honest. 85-90% of what? Research has shown comparable hypertrophy effects from something like ~30% 1 RM (something like a 30-35 rep max) to ~85% 1 RM (something like a 5 rep max) as long as both are to failure. So heavier to failure is no better than lighter to failure, as long as you're somewhere in that range.

If you mean something like 85-90% effort, i.e. high-ish RPE, I think I'd agree with the sentiment, though it's probably not quite that all out.

Otherwise we'd be cycling SD+unchanged loads forever and growing

I think this part gets to the heart of what Brian Minor is trying to address with respect to load. I'll link it one more time in case you haven't read it yet:

I agree that we can't just use the same loads forever and keep growing. But I don't think it's because adding weight to the bar cycle to cycle raises the hypertrophy stimulus per se. I think it's because the weights would quickly represent too low of effort (RIR/RPE) to trigger significant growth as our initial cycles got us bigger/stronger. So we don't increase the weight because increasing the weight = more growth stimulus, we increase the weight because we're attempting to maintain the same relative effort, and we're forced to do this as we get bigger/stronger from training properly.

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Yes, 85-90% of 1 RM. Contrary to higher rep sets 5RM loads don't even need to be done until failure to elicit growth response, every rep is effective.

I think the big issue between some of the research results (tension, 'effort', etc.) is the 'in-vivo' factor.
In the HST Faq, one study in particular from 2003 shows an absolute causation of tension to the level of p54 levels, and the JNK levels have been shown to lower myostatin levels and lead to hypertrophy. So how can there be a mis-match with studies comparing lighter loads to higher loads in real people actually doing an RT workout?
either or both of these must be true
A) there are other factors that also stimulate hypertrophy (if p54 is lower, something else that also does this must be higher) so the end stimulation product is very similar
and/or
B) the control of muscle fibers (ie. coming online in tetany anyway) in-vivo ends up with actual similar per fiber tension anyway.

I should go back and read all the older HST FAQ stuff again, it's been years I think.

In terms of figuring this out from the practical/research end, I still think a study with this kind of logic is needed as we previously discussed:

http://thinkmuscle.com/community/th...sary-for-hypertrophy.43525/page-4#post-262025

I just need to become some sort of Elon Musk like business magnate and, instead of funding car and rocket companies, spend billions on all manner of hypertrophy and other resistance training oriented research.

Yes agree. Theory is great, but sometimes creating a program based on individual molecular changes doesn't really match reality... real tests of load, anabolic resistance, the whole their would be really helpful.
I've seen studies where people's PS levels stayed pretty constant for a couple months with normal training, they didn't get lower and lower like HST says.

SD is in my opinion the essence of HST, as its core concepts - load, frequency, volume- are based on it, or more precisely, on how much of RBE it manages to "unroll".

As a separate issue Bryan, since this thread seemed to get your attention, I was hoping you could shed light on this HST principle a bit more. As Ron and I have discussed, I'm not sure what your thoughts are on this HST principle in light of more recent research, namely that pertaining to similar hypertrophic outcomes at widely varying loads (~30-35 to ~5 RM) when taken to/near failure.

The best place to start for this discussion would probably be this article by Brian Minor:

In the article above, Brian (as opposed to Bryan!) makes the case that increasing load, in and of itself, does not appear to achieve "progressive overload." Rather, increases in load are more like evidence that progressive overload has already occurred. Or stated differently, we add weight over time not because the act of adding weight keeps us ahead of something like RBE, but rather because we need to increase the weight to keep the relative effort (RIR/RPE) the same after having already achieved progressive overload by doing enough hard sets.

Any insight you could offer would be much appreciated.

Sorry to quote so much but it helps to have it there for reference.

First, I disagree with Brian’s perspective that we increase the load because we have adapted to the previous load. I also disagree with his world view that effort is the key to muscle growth.

Load progression: There are two ways to apply the principle of progressive load. The first and more traditional way (promoted by the ACSM) is you prescribe a weight that your client can lift 10 times. After some number of workouts your client will grow stronger and be able to lift the weight 15 times. At that time you increase the weight so that the client can only lift the new weight 10 times. Repeat.

For HST we use a different approach. We intentionally expose the muscle to ever increasing loads irregardless of the rate of strength increases. In this way we are able to maintain the level of stress at a given ration to the level of adaptation. Yes, we are trying to stay ahead of the rate of adaptation. If you do not, your growth rate will slow. There is an interesting paper you might like to read, Taber LA. Biomechanical growth laws for muscle tissue. J Theor Biol. 1998 Jul 27;193(2):201-13. In it the author shows,

“The total growth, therefore, depends on how fast the active modulus (effective stress) decreases relative to the growth rate (rate of adaptation). The slower the decrease in [effective stimulus relative to the rate of adaptation] the greater is the final muscle thickness, and vice versa. This example shows that neglecting changes in material properties sometimes can lead to erroneous conclusions.”​

I had to make a couple edits here because he’s actually using mathematical symbols which I can’t type correctly here. So yes, I am actively increasing the severity of load-stress at a rate that matches the rate of adaptation so that growth can continue more quickly than it otherwise would.

There is also anecdotal evidence from studies where one group progresses weight loads the traditional way and the other group uses “periodization” (i.e. lifting heavier weights and lowering the reps). In the end, the group that was exposed to the heavier loads sooner grew more. Now, before you go looking for counter examples, and you will find some, it is the principle that I believe in after seeing all of the data on both sides of the argument. You will grow faster if you don’t wait until you are stronger before exposing the tissue to heavier loads.

As a separate issue Bryan, since this thread seemed to get your attention, I was hoping you could shed light on this HST principle a bit more. As Ron and I have discussed, I'm not sure what your thoughts are on this HST principle in light of more recent research, namely that pertaining to similar hypertrophic outcomes at widely varying loads (~30-35 to ~5 RM) when taken to/near failure.

I think what I'm trying to suss out here is the difference between something like RBE, which is inextricably tied to our HST model in terms of tissue conditioning, and something like "anabolic resistance," which appears a similar concept but without quite the same implications. From what I've seen, RBE appears to relate more to muscle damage rather than hypertrophy, per se. Anabolic resistance is similar in that the idea is that, obviously, we can't keep using the same magnitude of stimulus over time to keep growing, but anabolic resistance doesn't appear to invoke RBE to explain itself. It appears to be more like "the closer you are to your potential, the greater the magnitude of stimulus needed to keep growing," with the stimulus relating more obviously to volume rather than load.

Any insight you could offer would be much appreciated.

As for the principle, “The effectiveness of any load is dependent on the condition of the tissue at the time the load is applied.”

You mention research showing that light loads can induce hypertrophy if the set is disruptive enough to the homeostasis of the muscle tissue. This does not lie outside of our principle. If you chose to lift light loads thinking that you will grow continuously because the study showed that light loads can make you grow, you will be disappointed. In time, those light loads, even taken to failure, will no longer have any effect. They will not make you grow. They will not make you grow anymore because the condition of the tissue is different than it was the first time you did it. And yes, we call this phenomenon the repeated bout effect.

Now, I know all of this is already self-evident to you. The RBE is the sum of the consequences of repeating a bout of resistance exercise. These include, less trauma following identical workouts (through a number of mechanisms), an increase in muscle size, and increase in muscle strength, a change in metabolic capacities, to accommodate future metabolic demand, and finally, an increased threshold for all of the above. “Anabolic resistance” is part of the RBE. That is the anabolic resistance associated with resistance training and not that seen with aging, illness or starvation. We can, if necessary, go over the mechanisms for these changes, but it is quite complicated sometimes getting into areas of biochemistry that is over my head.

It is true, we don’t see a linear dose-response by increasing the weight. I have been saying this since introducing HST, based on some research showing equivalent increases in fiber size regardless of weight loads. The seemingly equivalent results from widely varying weight loads demonstrate a “threshold” effect. As with other threshold-type models, once the threshold is crossed you see diminishing returns as you push things higher. The same is true for weight; heavier doesn’t necessarily mean more effective. The only time heavier equals better is when you haven’t reached the effective weight threshold for your specific situation.

What this means is that, the load or effective weight threshold that one must cross to achieve hypertrophy is not static; it changes as the condition of the tissue changes. As the muscle tissue adapts to the previous loading sessions it pushes the threshold higher. Repeated training sessions cause the effective weight threshold to go up and reduce the effectiveness of any previous load whether training with light or heavy loads.

Before I quit, always remember to interpret research using untrained lifters with the appropriate considerations. Once a lifter is highly conditioned, and close to his genetic maximum, there is not much that will allow him to get bigger short of serious over feeding.

Now I have a question..

you wrote
The seemingly equivalent results from widely varying weight loads demonstrate a “threshold” effect. As with other threshold-type models, once the threshold is crossed you see diminishing returns as you push things higher. The same is true for weight; heavier doesn’t necessarily mean more effective. The only time heavier equals better is when you haven’t reached the effective weight threshold for your specific situation.

How does work/volume factor in? somehow it does... like..
2x8 with 10RM can be exceeded by
2x8 with 9RM OR 3x8 with 10RM

Also, I've moved from heavy to much lighter training and started growing after being stalled, I went from 3x5 with 7-8RM to 3x8 30 seconds rest with about 2/3'rds of the previous loads, started growing and kept growing for a couple months using regular 'progress as I can' kinda thing. Somehow the 'density' so to speak of the lighter loads (120 lbs 3x8 30 seconds) surpassed 3x5 2 minutes rest with 180.

It seems like load is only better if 'load-volume-density' (?) is higher? Does that make sense?

I just wanted to say Bryan I really appreciate you taking the time to share your thoughts on the subject. I'll definitely need to take some time mentally digesting this

There is also anecdotal evidence from studies where one group progresses weight loads the traditional way and the other group uses “periodization” (i.e. lifting heavier weights and lowering the reps). In the end, the group that was exposed to the heavier loads sooner grew more.

This has always been one of the questions in my mind that I've never seen quite answered, and this is an interesting suggested solution. Meaning you see DUP style setups seem to do better sometimes in the research vs. linear style incrementation, and relatedly, there's other research showing improved effects by actually doing multiple variations of a lift in a week vs. just a single variation. I've long been curious what the novelty factor is in either of these situations that explains these sorts of results, but it's interesting to think about it from the perspective of relative tissue conditioning with respect to big swings in loading.

One more thought, it is important that when we are trying to figure out all the variables of training that we don't forget the actual biology and chemistry that actually happens in the process of adapting to a stimuli. In other words, before accepting a new principle, make sure you can explain why that principle would be true based on the physiology at play. What mechano-sensitive cellular structures are at play and why would they respond in one instance and not in another? What signaling pathways are at play and why would they be activated or not activated by a given change? The same holds true for growth factors, myokines, and even genes. For example, in order for a person to say that more volume (or more load, or more fatigue) will lead to more hypertrophy, they must also be able to justify that claim by explaining what is happening inside the cell when volume, or load, or fatigue is increased, otherwise they are just guessing.

We find that when we hold ourselves to this standard, things start to get very complicated, and there is a lot of uncertainty. Especially when the animal models of muscle hypertrophy are included which usually throw a lot of what people know about training a human out the window.

Anyway, just a thought.

good thoughts Bryan!

I think what bothers me sometimes, is when research ignores reality and tries to show that something 'doesn't work' that actually does.