Is Load Progression Necessary For Hypertrophy?

[NWlifter]

You read my mind was thinking of condensing too!

OK yes... and... recruitment and rate coding increase at the same time. So just in case anyone reading this is thinking we increase recruitment, THEN rate coding goes up, no it's all at the same time.
It's like one signal coming in, as the signal increases, the first recruited increase firing rate, kinda like increasing the voltage on a motor, it spins faster, then it 'spills over' to the next MU, it starts out lowest firing, the signal goes up, it fires faster, that spills over, then next one comes online, etc.

So... if like your saying you start a set with say an 8RM and for the muscle, ALL fibers are recruited right off the bat. The first are at max rate coding during the first rep, larger MU's are progressively less up to the largest that is at minimal firing rate. Each rep, firing increases for all, but the first ones are at max so they don't fire faster, finally at the last rep, even the last MU is firing as fast as possible.

Ok lighter load, none ever drop out, but they do lose force as they continue to be fired over time. The higher the rate coding, the faster they lose force. Then effort increases which is supraspinal output, the 'voltage' so to speak, causes larger MU's to fire faster to make up the force lost by other MU's./fibers.

Yes, and for 'whole muscle', the last reps, what people call good reps, are 'better' , at that point, all fibers are working hard enough and many have lost so much force from the previous part of the set, that fibers are getting stressed and stimulated.

Right recruitment actually has zero to do with fiber stimulation, except it has to be recruited to 'be used and stimulated', but MU 1 doesn't need MU 35 to be recruited for 'it' to be stimulated. recruitment is just how many are working. But rate coding, firing rate, that leads to higher fatigue.
Yes that's the thing, you can't get the last fibers at high rate coding unless all are recruited, so that's all recruitment has to do with stimulation. It's like you have a group of 100 people, if you have 3 of them working, when they get tired, you add 2 more to help, then they get tired, add 3 more ect. So adding the later guys doesn't change anything for the first ones working, but it does for the guys you did recruit. Did I word that at all in a sensible way ? LOL

Ok actually YES what you said there... that is a good point!
If tension was the key then rep 2 with a 4RM would have the same tension as rep 12 with a 12 RM. and thus the same hypertrophy.. but it doesn't....
That's why I'm saying , the tension thing just doesn't fit...
BUT...
If you run a fiber until rate coding is high/max, regardless of actual generated tension, then keep running it, it starts to lose force, and THAT IMO is THE stimulus. It explains why 5 -30RM has the same hypertrophy, why running them hard until fatigue, .... is the common denominator... and it's logical, the only reason a cell needs to adapt, is if it is stressed and it's current capabilities are inadequate and it threatens cell survival.

 

[NWlifter]

Here does this help? I made it so maybe it's too lame lol
numbers horizontal across bottom are 10 motor units
numbers vertically are the rate coding level
first one you can see MU 10 isn't even recruited but MU 1 is recruited and at max rate coding
mu 2 is recruited and at level 9 rate coding, etc.
as the reps go on, MU 1 stays at max rate coding while others increase.you can see every rep is a 'good rep' for MU1 the grey one, most reps are 'good reps' for MU2, and only the last few reps are 'good reps' for MU10

 

[mikeynov]

Those graphs are actually great, and I think I mostly understand your argument now. Fair points that recruitment and rate coding increases occur concomitantly, and "dropping out" was probably misleading as you said, as they're just fatigued but still contributing some force still.

I have two main thoughts though in response:

1) If you're suggesting that the fundamental stimulus is a loss of force of muscle fibers as they fatigue, this would seem to imply that "metabolic stress" should play an important role in hypertrophy, no? As per Menno's talk, there appears to be some reasons to doubt this that he lays out. I can outline these in the thread if it helps illustrate the issue.

2) Similar and as part of #1, if what you were saying were true, I would think training literally to failure would be superior to training a couple/few reps shy of failure, as rate coding would ultimately be higher with more total motor units having a reduction in force output the nearer to failure you are. This does not appear to be the case, however, hence the argument that it's both the magnitude and duration of tension moreso. I.e. if the fibers experience a certain level of tension for long enough, they grow, and what's happening with metabolic fatigue just so happens to occur alongside of that. Sort of the reverse of your argument.

Though it's my impression that part of their argument is that fiber tension is NOT scaling with external load. In this sense, lighter loads at similar relative intensities (proximity to failure) would ultimately see similar recruitment/rate coding, and thus the magnitude and duration of tension experienced by your fibers in both scenarios would actually be similar.

 

[NWlifter]

Those graphs are actually great, and I think I mostly understand your argument now. Fair points that recruitment and rate coding increases occur concomitantly, and "dropping out" was probably misleading as you said, as they're just fatigued but still contributing some force still.

OK cool

I have two main thoughts though in response:

1) If you're suggesting that the fundamental stimulus is a loss of force of muscle fibers as they fatigue, this would seem to imply that "metabolic stress" should play an important role in hypertrophy, no? As per Menno's talk, there appears to be some reasons to doubt this that he lays out. I can outline these in the thread if it helps illustrate the issue.

I think , just as with tension, it's more a side effect.... metabolic stress can be seen when fibers fatigue. I think some studies show it can have a factor in stimulation itself, but I bet it's more 'part of' the fatigue (fatigue as in force loss) effects. Possibly mechanical fatigue is more important? Literal physical effects of contraction on physical components.

2) Similar and as part of #1, if what you were saying were true, I would think training literally to failure would be superior to training a couple/few reps shy of failure, as rate coding would ultimately be higher with more total motor units having a reduction in force output the nearer to failure you are. This does not appear to be the case, however, hence the argument that it's both the magnitude and duration of tension moreso. I.e. if the fibers experience a certain level of tension for long enough, they grow, and what's happening with metabolic fatigue just so happens to occur alongside of that. Sort of the reverse of your argument.

OK yes..
I am willing to bet that....
1) if we compare 1 set to failure vs 1 set short of failure, the set to failure will have higher post workout MPS
2) For SURE going to failure taxes the last recruited MU's more. (max neural output is the only time the last MU has a chance even of hitting tetany).
3) Also that say 2 sets short of failure, make up for a bit less activation with more 'time' at that level. Just like 12 with 12RM makes up for less tension by having more time, over say 6 with 6RM.

But I still think, what ever systems in the cell are stressed enough, will be 'stimulated' to adapt. Just making a fiber display high tension with no ill effects, is it's job, if it can do and does and isn't stressed, all is good. No need to adapt, but if you make it work hard, and ask it to keep working hard and it's failing to maintain force (it's only job), it seems logical 'that' would be what signals for an adaptation. If energy is stressed, sarcoplasmic increases occur (see Cody Haun's latest paper), if physical is stressed, I bet that's when fibrils are stimulated.

I'd say force loss, is the visible indicator that the cell is 'stressed', it just can't keep going....

 

[Jester]

I still advocate progressing load but after personal success with myoreps, I'm sure there is something to what you're talking about. I've seen growth after having scaled load back significantly from what I was using for months/years prior.
I'm sure you're already aware of how a regular myoreps setup works, but i went from 5 to 10 RM loads to using 20 to 25 RM range loads. Myoreps also incorporates double progression where we progress the reps on myosets until you're getting the full 25×5,5,5,5,5 and then progressing the load. And that works great.
However, it is all built around a fairly standard HST style template so there is still that component going along with it.

Tldr; I experienced some rather profound gains with myoreps.

But do you need to continue to progressing them myoreps load over time?

TL; DR the rest

 

[mikeynov]

I've gone back and reread our exchange NWLifter, and I think I am understanding your argument even better. I'm attempting to differentiate it from what people like Menno Henselmans, Brian Minor and Eric Helms are suggesting, or maybe more accurately my interpretation of their thinking.

Something I'm noticing more as I'm re-going over Brian Minor's article as well as the links he provides to Eric Helms' article and video, is that they seem to be at least a little talking around what, specifically, is the thing we're adapting to at the level of individual muscle fibers. Eric Helms indicates that it's mechanical strain via mechanical tension for sufficient duration, and that's long been my understanding. Brian Minor is talking about how fibers need to be recruited in order to meaningfully receive the tension in question to ultimately experience sufficient strain through "impulse" (force x time), I think. He then refers to "impulse threshold," i.e. some amount of sufficient force/tension for a given duration (time) to experience progressive tension overload.

But in all of this it's not exactly describing what's happening at the level of the individual muscle fiber, what progressive tension overload truly means on a per-fiber basis. As you said, generating tension is what muscle fibers do, so what exactly do they need to adapt to? What you're suggesting, I think, is that if you zoom in to the level of an individual muscle fiber, the thing doing the "stress" to the fiber is the rate coding, i.e. its firing frequency and then then the mechanical/metabolic changes that happens to the fiber in that context. If it hits its maximum rate of firing for long enough, it will eventually tire out and force output drops, which you see as a candidate for the key factor causing the sufficient stress/train to require adaptation and growth.

In my own mind, I think I've long envisioned it as something like, in the context of us having recruited all our muscle fibers while lifting something heavy enough and/or close enough to failure, our muscle fibers are generating force for a certain amount of time per set, and if the product of this tension-time across enough sets is sufficient, we induce the required mechanical strain overload and get an adaptive response. But that's obviously more of a gross, whole muscle way of thinking, as opposed to questioning what, specifically, is happening at the actual fiber level. Or why just being activated for X amount of time at high tension is actually straining anything in the first place.

I guess I thought of it almost from a damage type perspective, with muscle fibers being sort of like a series of interconnected rubber bands, and as they all stretch and contract repeatedly over and over in these sufficiently challenging sets, eventually you get "strain" on the bands that, in a living system, would demand an adaptive response to repair and then compensate in a way to be more resilient to the strain they experienced.

So, to restate your position again, I think what you'd suggest is that the progressive overload event at the individual fiber level is basically that fiber experiencing maximum firing frequency for long enough such that you challenge its ability to generate force, and its force levels actually wind up dropping. More specifically, if we accumulate enough time under those sorts of conditions, presumably through enough high effort sets close to failure, we sufficiently strain the muscle fiber enough to get it to grow.

 

[Totentanz]

Just want to say... That video was great. If anyone hasn't watched it, I'd highly recommend it.

 

[NWlifter]

I've gone back and reread our exchange NWLifter, and I think I am understanding your argument even better. I'm attempting to differentiate it from what people like Menno Henselmans, Brian Minor and Eric Helms are suggesting, or maybe more accurately my interpretation of their thinking.

Something I'm noticing more as I'm re-going over Brian Minor's article as well as the links he provides to Eric Helms' article and video, is that they seem to be at least a little talking around what, specifically, is the thing we're adapting to at the level of individual muscle fibers. Eric Helms indicates that it's mechanical strain via mechanical tension for sufficient duration, and that's long been my understanding. Brian Minor is talking about how fibers need to be recruited in order to meaningfully receive the tension in question to ultimately experience sufficient strain through "impulse" (force x time), I think. He then refers to "impulse threshold," i.e. some amount of sufficient force/tension for a given duration (time) to experience progressive tension overload.

But in all of this it's not exactly describing what's happening at the level of the individual muscle fiber, what progressive tension overload truly means on a per-fiber basis. As you said, generating tension is what muscle fibers do, so what exactly do they need to adapt to? What you're suggesting, I think, is that if you zoom in to the level of an individual muscle fiber, the thing doing the "stress" to the fiber is the rate coding, i.e. its firing frequency and then then the mechanical/metabolic changes that happens to the fiber in that context. If it hits its maximum rate of firing for long enough, it will eventually tire out and force output drops, which you see as a candidate for the key factor causing the sufficient stress/train to require adaptation and growth.

In my own mind, I think I've long envisioned it as something like, in the context of us having recruited all our muscle fibers while lifting something heavy enough and/or close enough to failure, our muscle fibers are generating force for a certain amount of time per set, and if the product of this tension-time across enough sets is sufficient, we induce the required mechanical strain overload and get an adaptive response. But that's obviously more of a gross, whole muscle way of thinking, as opposed to questioning what, specifically, is happening at the actual fiber level. Or why just being activated for X amount of time at high tension is actually straining anything in the first place.

I guess I thought of it almost from a damage type perspective, with muscle fibers being sort of like a series of interconnected rubber bands, and as they all stretch and contract repeatedly over and over in these sufficiently challenging sets, eventually you get "strain" on the bands that, in a living system, would demand an adaptive response to repair and then compensate in a way to be more resilient to the strain they experienced.

So, to restate your position again, I think what you'd suggest is that the progressive overload event at the individual fiber level is basically that fiber experiencing maximum firing frequency for long enough such that you challenge its ability to generate force, and its force levels actually wind up dropping. More specifically, if we accumulate enough time under those sorts of conditions, presumably through enough high effort sets close to failure, we sufficiently strain the muscle fiber enough to get it to grow.

good thoughts and summation, that sounds how it sure seems to me.
to me, that also explains why volume and 'density' increase the stimulation, and how lighter loads also work as well.
It just seems so undeniably logical that the only reason a fiber would need to adapt, is if 'what it has isn't enough', since it 'can' lift a load, the actual tension it created must be 'enough', it did lift the load, so the only thing left is a loss of the ability to 'maintain force' as the candidate for stimulation.

I wonder too about damage... I know there is great evidence that 'damage isn't required' and even 'may hamper hypertrophy', but I wonder if that's not actually gross damage, maybe undetectable micro trauma (to use an old phrase) actually is a factor, maybe just even just in the sarcomeres... rather than whole fiber damage that they have seen. Remember that study that was posted on here oh so long ago, that DOMS is the remodeling process, not damage? Not saying we need DOMS, but maybe that process, whether it 'hurts or not' is the process.

It also fits with the high rate coding, a fiber doesn't truly reveal a lack of maintenance until rate coding is high and force still drops. Might not even need max rate coding, but just time at a high enough level to have these mysterious actual effects occur that kick off the signaling for a need for adaptations.

I remember the old 'energetic theory of muscle growth' from way back, it said that during high rate of contractions, energy is directed toward contractions, that blunts protein synthesis , mTOR, etc. Afterwards, it 'rebounds' to a much higher level. Might not be a causal effect, but maybe an interesting peek into it.

( I guess what bugs me, is it's always said, 'mechanical stimuli'... that's so freaken vague.
How do you drive a nail into wood? Mechanical stimuli. Ok so if I file it will it go in? that's mechanical, ..no that won't work.... how do you cut wood? Mechanical stimuli... and... oh it has to lead to removal of the wood substrate . There we go.. so muscle.. mechanical stimuli and tension that leads to.... what? ..I say leads to force loss of the fiber. When they talk mechano transduction, it makes it sound like just making a fiber do its job, even within it's capabilities, and create tension, that does the trick That' can't be right, otherwise, a single full out rep would do that in spades).

 

[NWlifter]

I just heard this today, with Brian Minor, it was a good listen.

One thing that bugs me with most of this...
The phrase 'Apply tension' to a muscle..
Muscles create tension, I think using 'apply' is very misleading, makes people think if they put 200 on the bar, they are applying 200 to all the fibers since the whole muscle 'sees' 200 so to speak.

 

[Jester]

I just heard this today, with Brian Minor, it was a good listen.

One thing that bugs me with most of this...
The phrase 'Apply tension' to a muscle..
Muscles create tension, I think using 'apply' is very misleading, makes people think if they put 200 on the bar, they are applying 200 to all the fibers since the whole muscle 'sees' 200 so to speak.

Conceptual sacrifice?

 

[NWlifter]

Conceptual sacrifice?

I don't know what that means lol

 

[Jester]

I don't know what that means lol

Sacrificed accuracy of a detail to better convey concept.

 

[NWlifter]

Sacrificed accuracy of a detail to better convey concept.

Oh ok, thanks! Never heard that phrase before

 

[NWlifter]

Hey Mike, you disapeared.

 

[mikeynov]

Hey Mike, you disapeared.

Didn't disappear, I'll come back with more thoughts as I develop them. Was also waiting to see if others popped in and contributed since I've already said a lot

 

[NWlifter]

OK cool , me too, I over babbled on this lol. Hopefully it'll continue in the future, fun discussion!

 

[mikeynov]

So to pose a question to re-focus discussion here, let's look again at the subject of the original post. Does increasing load, in and of itself, increase the hypertrophic stimulus, all else constant? The all else constant would be frequency, volume, and relative intensity (nearness to failure).

To me this boils down to whether per-fiber tension increases as load increases. If it doesn't, then fibers aren't "overloaded" just by raising the external weight. However, if more external weight results in higher per-fiber tension, then there's a case for programmed increases in weight to stay ahead of the adaptive curve along the original lines of reasoning as per HST.

I.e. if the hypertrophic stimulus is fundamentally a mechanical/strain one, i.e. sufficient tension-time at high levels of activation and rate coding, then the tension part of tension-time increases as load on the bar increases. But if it doesn't, and fibers experience the same amount of tension at widely varying loads dictated mainly by the relative intensity, then the fundamental strategy of rapid load increases doesn't seem to actually accomplish anything in terms of continuing to grow, and the original HST setup makes markedly less sense

I'm not sure if we ultimately resolved this or not, so I'm curious what people think. Does increasing the weight increase the per-fiber tension? Either way, does my reasoning above make sense to others?

 

[_Simon_]

Okay, am still reading through the responses haha but it's been riveting so far guys! Yeah I love this stuff too, and even though I don't get right down to really fine details at the cellular level I still find it fascinating.

Here Brian Minor lays out a case that load progression per se is not actually necessary to induce hypertrophy, i.e. progressive loading of the weight itself isn't the stimulus per se, but rather a natural consequence of having produced hypertrophy.

This is actually a really fascinating way of understanding it... and even though it sounds similar to progressive load makes you grow, it actually to me has different consequences of practical application. It now finally takes into account the all important condition of the tissue at the time. Which yeah HST is entirely based on!

If it was purely progressing weights = hypertrophy, the exact same progressions would/should probably produce the exact same percentage hypertrophy amongst different people (assuming diets are all controlled), but this doesn't happen due to the relative state of the conditioning at the time.

So the condition of the tissue is something of importance, and the relative growth level of the tissue not to mention the tension levels/conditioning it is used to experiencing would be a necessary piece of knowledge in knowing 'where to go from here' load-wise.

So hypertrophy is the 'go-ahead' to increasing load would we say? But in way that constantly stays ahead of the curve and ahead of current adaptions. Which is interesting... as that could then mean you should simply stay at one load/volume UNTIL hypertrophy occurs before you add load.

But to me that would be a very slow way of going about things, and conditioning would set in very quickly and halt things. Not to mention constantly having to measure your growth before you increase load haha.

So HST aims to keep ahead of the adaptive process, to keep a constant input so that there is no time or chance for stagnation.

And strategic deconditioning is just that, a way of resetting the current adaptions or the 'condition if the tissue' at ct he present moment. So HST principles are very respectful and aware of present conditions (something many other protocols compleeeeeetely disregard), but is aware of what occurs with the tissue and how quickly it becomes resistant to further growth, so it's then future focused in a way that keeps the resistant adaptations from setting in.

Okay dunno why I wrote all that haha, maybe just to clear it up for myself!

But I guess in light of this, it may not be a matter of:

increasing load to ---> produce growth

OR a matter of hypertrophy occurring ---> then permission to increase load

, but perhaps a mish-mash of it all at the same time in an attempt to stay ahead of the adaptive curve, whilst still with the understanding of all this driving that.

However, as per my thoughts above, I'm not sure how to reconcile this in light of the relative intensity producing similar hypertrophy observation. If heavier weights translate to more per-fiber tension across a set, then the tension overload would seem to be, by definition, higher with heavier weights. If that is the case, then the case for progressive overload being a primary driver of hypertrophy would be back on the table, and you'd be back to how I originally understood HST to be - you apply enough mechanical tension for long enough to induce growth, and then you raise the weight next time to stay ahead of the adaptive curve because, implicitly, that raises the magnitude of tension the fibers experience. Eventually, you run into strength limits and so you strategically decondition to lower the threshold of mechanical tension necessary to induce hypertrophy again. That's kind of the mindset I've had in the back of my mind for a long time, it's just that this newer hypertrophy research seems to kind of contradict that, hence my confusion.

......

To me the biggest unanswered aspect of what I read and hear about from people like Brian Minor, Menno Henselmans, Eric Helms etc. is trying to understand the relationship between tissue conditioning, i.e. the "anabolic resistance" concept, and achieving mechanical tension overload. As Bryan did years ago I feel like we still need to understand why you can't just keep growing forever with the same load, though in the case of Brian Minor, he's very literally arguing you could as long as recruitment stays maximal and you accrue enough tension-time there. I'm not entirely sure what to make of this, hence the thread

Yeah this is what puzzles me a little too...

I guess in light of the ways growth can be achieved (and the papers from Brad Schoenfeld on the 3 mechanisms of hypertrophy make sense to me), I don't necessarily think that the recent stuff contradicts HST, but I think it reinforces it.

HST to me does work through all 3 mechanisms, but primarily I think it focuses on mechanical tension first and foremost, which I think has been shown to be the biggest and most potent driver of hypertrophy over time. I think metabolic stress creates a similar stimulus and replicates what can be achieved from mechanical tension-based hypertrophy, plus all the other metabolic goodies and factors along with it. It still can work to create maximum activation, and some sort of progression is still probably required.

And perhaps what Brian Minor is saying is that as long you keep the maximum recruitment occurring, growth will be continuous.

BUT is it possible (I don't know here am just pondering) that say for example you use a certain heavy weight for 8 reps and produces maximum recruitment. That over time of constantly using that weight, you become better at lifting it (ie stronger), so the muscles don't experience as much tension in order to lift that weight (through adaptions)? Is that a thing?

So Brian is perhaps saying that you'd need to still increase the load to keep at max activation, as the tissue is now working better and is much stronger to move those old loads without needing the same tension/activation, and a higher loader is now needed to keep that?

So maybe he wasn't arguing that you can just use the exact same load all the time, but just need to keep at max activation (same tension levels etc), by increasing load when the old load doesn't cut it anymore? (Apologies I haven't yet watched the video haha but I will)

So old load no longer will have the same effect, which can be reset, but I don't know if it's possible to have it reset completely everytime you strategically decondition it, and I would think progressive load would eventually be needed..

 

[_Simon_]

.
I'm sure tissue condition is a factor. It decides if what you did today was 'good enough'. but I think that separate from acute stimulation.
What I mean is, is I think people are getting sidetracked with 'mechanical' attributes, in the area that hypertrophy is proportional to fiber tension.
I really really think the research is showing that...
100 for 30 seconds is equal to 80 for 50 seconds, just for an arbitrary example.
So why is it that way?

I think it goes back to my post above, about 'cellular stress'. Obviously any parameter, load, tension, time, etc. isn't 'THE' stimulation factor. And logically, if a cell 'can do' something without stress, it doesn't need to adapt. It 'did it', no worries, no stress, .. no reason to change. BUT, make a cell do something where that task stresses it, threatens it, THEN it needs to adapt.
So what stresses a cell and what indicates it's stressed?

Now tissue condition... if 10 with 10RM is the same as 6 with 6RM for hypertrophy, how do we increase stress above either of those?
10 with 6RM would, 12 with 10RM would, .. more time with same, or more load with same time.

Ah very well said . Yeah no particular load, rep-range or parameter is 'the' golden ticket. It comes down to the conditioning of the tissue at the time, which then shows this whole thing is more of a bigger continuum and range.

And the perceived stress is what spurs on further adaptions. Over time the tissue gets used to certain loads, hence the need for progression of some sort. Progression meaning an increase in stress rather than what we could convince ourselves as progression!

 

[_Simon_]

Indeed. I appreciate wanting to shut up and lift, and I've for sure derailed my training many times as Jak indicated by experimenting too much, but the physiology side of this is fun in its own right.






I understand what you're saying, but the qualifier here is that you could theoretically accrue a shitload of tension-time with light weights, but unless it's near failure, then we can't equate the hypertrophy with heavier sets in which recruitment is maximal off the bat.

So being at/near maximal fiber recruitment seems to be a pre-requisite for this sort of comparison, which would, to me, mean that the primary driver of hypertrophy would be tension-time at maximum recruitment. Sort of like Borge's "effective reps" concept - or stated differently, widely varying loads taken near or to failure appear to have similar effective total reps, and thus similar hypertrophy outcomes.





I agree, but what I'm trying to get to is basically the heart of Brian Minor's article, whether it's accurate. And we need to be able to explain why widely varying loads seem to produce similar hypertrophy outcomes only in the context of being near failure. Does that make sense?





As per the above, though, if adding weight increases the amount of tension a fiber experiences, and it's still exposed to the same duration of tension-time, then a heavier weight DOES meet the criteria for "progressive tension overload" in and of itself. So I agree with what you're saying, but I'm trying to differentiate the argument Brian Minor is putting forth with what we all seem to believe, that adding weight to the bar is a way of staying ahead of the mechanical tension curve.



It would be both if we're correct, no? You have to lift heavy enough for enough total effective reps today to grow. And the next time you lift, you have to lift heavy enough again for enough total effective reps to grow. If adding weight increases the tension aspect of tension-time, then it is directly allowing us to stay ahead of the adaptive curve.



At the risk of beating a dead horse, though, the necessary context appears to be that we can only equate these sorts of comparisons if we're implicitly near/at maximum fiber recruitment. So it might not be as simple as lighter tension for longer duration equals larger tension for shorter duration. We'd have to also be at similar relative intensity for the weights we're using.



I think the answer is definitely mechanical tension induced disruption, right? As per Menno's talk in my first post (did you see this before?), mechanical tension appears to be THE primary factor in growth, and both muscle damage and metabolic stress can both be thought of as relating to growth only insofar as they relate to mechanical tension.



And this gets back to the original idea here - would adding reps forever literally work as well as adding load? If part of "anabolic resistance," i.e. the repeated bout effect as we used to call it, is us adapting to the magnitude of tension, then adding more weight will, at some point, ultimately be necessary. So this is getting to the nature of what, exactly, we're adapting to, as you alluded to with your cellular stress post.

Ahhhh I think I see what you're saying here....

But that's the thing I'm not 100% convinced we need to achieve maximum activation (or is that recruitment...) for it be an effective workout, but simply an exposure to a higher level of stress than before. Hence why in HST we spend time in submax ranges due to it still being above the current conditioning of the tissue.

Actually, I'm confused too hehe.

I guess if we look at the different mechanisms for growth to occur, we've got:

1) mechanical tension which disrupts the fibers in some way to produce growth/adaption. As long as the load is above the condition of the tissue, EVEN if we don't reach near failure, growth will ensue.

2) With metabolic stress, it's only in reaching quite fatigued states that its deemed as effective in producing growth.

3) muscle damage... not even gonna bother with at this stage haha.


The whole effective rep thing does throw something into the mix that is hard to correlate with this...

Is this primarily what you're putting out there and figuring out @mikeynov?

Am also trying to make sense of it... but I guess if we think of it as different models or pathways to growth then maybe there doesn't need to be a reconciliation between them, but just understanding different ways for growth to be achieved. Like how we can use a car or a bike to get to the same destination. Different mechanics, feet usage, timing, effort, but same destination... ?

? Haha