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Other/Mixed Mechanical tension for hypertrophy

Other strength modalities (e.g., Clubs), mixed strength modalities (e.g., combined kettlebell and barbell), other goals (flexibility)
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bluejeff

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Rather than hijacking the thread from which I quote Watchnerd below, I figured I'd just start a thread about this.

We often hear that the three main drivers behind hypertrophy are metabolic stress, muscle damage, and mechanical tension. However, more recent research has been narrowing in on mechanical tension being the main driver. Linked to this is the idea of "training to failure." As I understand the literature I have read, the closer one is to "failure" per set, the more tension the muscle fibers actually experience. The researcher below explains much of this. Much of it requires a basic understanding of how muscle fibers fire and contract.

Links to books, FAQ, and blog

Article list

For those of you who maybe just want to know how to implement these ideas into training, refer to the last section of the FAQ: "how can we optimize strength training programs?" and "how can we implement periodization and ongoing variety?"


As to the topic of mechanical tension and hypertrophy:
We don't 100% understand, mechanistically, what causes hypertrophy. If it's tension, where does metabolite induced fatigue fit in? Is 'the burn' just another way to create mechanical tension via the size principle exhausting all the little fibers first? Or is there something else going on in terms of adaptation?

I certainly don't have all the answers, but this from the same researcher I linked to above. I haven't even had time to comb through all of this, though the more I read, the more the same ideas and conclusions are seen.

This one is specifically about why mechanical tension may be the main driver behind hypertrophy. Interestingly, he cites how denervated muscle fibers have been shown to hypertrophy when exposed to stretch. The entire article goes into how the ideas behind hypertrophy have been tested, and why mechanical tension seems to be the most likely cause. For those who don't want to read the entire article in its technicality, the large black and white text box at the very top of the article summarizes it, and there are big, colorful text fields that summarize each section/point.

This one is specifically about the "metabolic stress" theory, and the holes in it:
 
Yeah, there are basically two camps that I've seen:

"It's all tension" -- any other mechanism that induces hypertrophy (e.g. metabolic) is just another way to create mechanical tension, because muscle fibers are dumb mechanical sensors.

"It's also epigenetic" -- The ability of muscle fibers to change types, exhibit mitochondrial changes, and exhibit muscle memory effects seem to indicate that there are biological adaptive processes more complex than just tension on fibers.
 
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I can't recommend his books enough. I also took his 6 month mentorship and learned a ton. I need to go back over the content again because it is dense (for me).

Yeah, it's a lot to digest and you need at least a basic understanding of anatomy, physiology, biomechanics, and a little dose of biochemistry to get the most out of it.
 
Without reading all of the content and not trying to be argumentative, his assertion that metabolic stress does not contribute to hypertrophy fails to address BFR training and its consistent and notable results at low loads/not to failure.

I also am not wrapping my head around how training to failure esp with a moderate load increases tension on the muscle when:
- it is no longer exerting at a high % of its capacity and wasn’t to begin with
- is not being exposed to a heavy external load at length
- many of the units are plain exhausted and under reduced tension.

Admittedly with point 3 there will be remaining units that are possibly experiencing greater tension than the load would indicate, but then presumably progress will be quite slow as only a relatively small % will benefit.

Lastly, if tension were the main driver or indeed, the ONLY driver then isometrics would flat out dominate for strength and hypertrophy. Yet it only seems to induce notable hypertrophy when combined with glucose depletion either using longer holds or via some other mechanism, in my case HIIT. The time-dependent relationship hints at something(s) in addition to tension. A reactive response to fuel consumption by-products, signalling from the draw down itself, signalling from the conversion of lactate back to glycogen (Cori cycle by itself triggers anabolism) are all likely contributors.
 
Without reading all of the content and not trying to be argumentative, his assertion that metabolic stress does not contribute to hypertrophy fails to address BFR training and its consistent and notable results at low loads/not to failure.

I also am not wrapping my head around how training to failure esp with a moderate load increases tension on the muscle when:
- it is no longer exerting at a high % of its capacity and wasn’t to begin with
- is not being exposed to a heavy external load at length
- many of the units are plain exhausted and under reduced tension.

Admittedly with point 3 there will be remaining units that are possibly experiencing greater tension than the load would indicate, but then presumably progress will be quite slow as only a relatively small % will benefit.

The "pro tension" camp would say its mostly #3.

It relates to the size principle -- the theory is that high reps / low weight will exhaust all the small fibers until there is nothing but big fast twitch fibers left, which experience high tension because the little guys can't help anymore.

This camp discounts the idea that metabolic stress is a separate hypertrophic pathway distinct from tension -- they say metabolic stress just leads to tension, which then leads to hypertrophy.
 
I think of it this way:
When motor units drop out, they are no longer contracting. Yet, unless the muscle has reached absolute failure, the motor units that have not dropped out will still have to move the load. They now experience greater tension as they resist the weight being moved. The motors units that have dropped out still experience at least some degree of the tension, as they are still part of the muscle (fascicle).

Beardsley does take the time in this article to explain the apparent misconception that external load dictates the mechanical tension experienced by the muscle fibers.

This article in particular cleared up much of my confusion about the role of mechanical tension and how it actually works.



One thing he discusses is the force velocity relationship regarding muscles and their force output. It seemed counterintuitive when I first read about this, but it made more sense the more I read into it. It basically states that a muscle produces more force at lower speeds. Faster speeds elect more motor unit recruitment, but less overall force. An easy way for me to wrap my head around it is to think of how light of a load you need to express maximum power. I can throw a 15lb dumbbell straight up, but I have to grind my 24kg up.

Warning: muscle science words ahead….

“Muscle fibers exert high forces when they shorten slowly, but low forces when they shorten quickly. This is because slow shortening speeds allow lots of actin-myosin crossbridges to form at the same time, and actin-myosin crossbridges are what allows each muscle fiber to produce force. In contrast, fast shortening speeds cause the actin-myosin crossbridges inside muscle fibers to detach at a faster rate, and this leads to fewer simultaneous crossbridges being formed at any one time.”

It’s all in the link I posted in this post, but this means that there are greater forces on the fibers at lower speeds. We all know that you can make a training session with a 15lb dumbbell brutal by lifting it slower.

I also am not wrapping my head around how training to failure esp with a moderate load increases tension on the muscle when:
- it is no longer exerting at a high % of its capacity and wasn’t to begin with
- is not being exposed to a heavy external load at length
- many of the units are plain exhausted and under reduced tension

From the same article:

When we lift a light load deliberately slowly, muscle force is even lower, because we are causing the mass to accelerate less. Therefore, the stretching force or mechanical tension experienced by the whole muscle-tendon unit is even lower. However, since the level of motor unit recruitment is greatly reduced during a submaximal effort, the number of active muscle fibers is greatly reduced, and each individual muscle fiber exerts a high force due to its favorable location on the force-velocity relationship.

As you can see, the mechanical tension experienced by whole muscles is very different from the mechanical tension experienced by each muscle fiber. Muscle force (and therefore mechanical tension) decreases from the fast lift with a light load to the deliberately slow lift with a light load, but individual muscle fiber force (and therefore mechanical tension) increases substantially from the fast lift to the deliberately slow lift.”
 
The "pro tension" camp would say its mostly #3.

It relates to the size principle -- the theory is that high reps / low weight will exhaust all the small fibers until there is nothing but big fast twitch fibers left, which experience high tension because the little guys can't help anymore.

This camp discounts the idea that metabolic stress is a separate hypertrophic pathway distinct from tension -- they say metabolic stress just leads to tension, which then leads to hypertrophy.


That whole argument fails to explain why hitting it with much, much higher tension prior to fatigue fails to induce a better response unless done for longer. Why does GTG not induce hypertrophy better than single session training? How is the time dependent factor explained in a way that accounts for the above?
 
I don’t really understand the science of hypertrophy but I see and have experienced the incredible diversity in training approaches that build muscle in practice. It would be nice if there was a single theory that explained them all, everything from Schwarzenegger-style “blast the muscle“ programs, Mentzer’s HIT, Wendler’s 5 (or more) reps in reserve, Schoenfeld’s high or low (whatever) reps to failure, recent research on people building muscle with 50% of reps in reserve (eg 10 reps at the 20 rep max) etc etc. On top of that is the role of diet and whether at least in some individuals that’s more important than their training approach. I’m left wondering whether there is a way not to build muscle
 
I think of it this way:
When motor units drop out, they are no longer contracting. Yet, unless the muscle has reached absolute failure, the motor units that have not dropped out will still have to move the load. They now experience greater tension as they resist the weight being moved. The motors units that have dropped out still experience at least some degree of the tension, as they are still part of the muscle (fascicle).

Beardsley does take the time in this article to explain the apparent misconception that external load dictates the mechanical tension experienced by the muscle fibers.

This article in particular cleared up much of my confusion about the role of mechanical tension and how it actually works.



One thing he discusses is the force velocity relationship regarding muscles and their force output. It seemed counterintuitive when I first read about this, but it made more sense the more I read into it. It basically states that a muscle produces more force at lower speeds. Faster speeds elect more motor unit recruitment, but less overall force. An easy way for me to wrap my head around it is to think of how light of a load you need to express maximum power. I can throw a 15lb dumbbell straight up, but I have to grind my 24kg up.

Warning: muscle science words ahead….



It’s all in the link I posted in this post, but this means that there are greater forces on the fibers at lower speeds. We all know that you can make a training session with a 15lb dumbbell brutal by lifting it slower.



From the same article:


Force velocity has a lot of moving parts, when you move a load rapidly the initial spike is much greater than with a slower acceleration. Force only drops off as inertia is overcome and or movement speed reaches muscle contraction speed.

Also, super slow training generally is inferior to training methods that use faster contraction speeds.

Color me extremely sceptical that training to failure creates higher tension at low load than the muscle experiences at heavier loading. 70% of repmax and heavier recruits all fiber types from the get-go, why the need for a level of fatigue?

And again, what of BFR that requires very little tension, no need for failure? If that doesn’t conclusively point to a metabolic trigger I don’t what further evidence would satisfy.
 
Color me extremely sceptical that training to failure creates higher tension at low load than the muscle experiences at heavier loading. 70% of repmax and heavier recruits all fiber types from the get-go, why the need for a level of fatigue?
I don’t think he’s saying that it creates a higher tension than a heavier load, just that it explains how you can see hypertrophy across any loading, because it is a way to experience relative high tension in the motor units that are active.

What I’m getting from reading through the material is that mechanical tension is present whenever hypertrophy is present.

And again, what of BFR that requires very little tension, no need for failure? If that doesn’t conclusively point to a metabolic trigger I don’t what further evidence would satisfy.
I’m still reading through this stuff and trying to process it myself.

Found this, though:

The gist of it is that BFR increases metabolite concentration, which increases muscle fatigue. The need to continue a set as fatigue sets in leads to a greater voluntary effort, which increases higher threshold motor unit recruitment. He also points out that when BFR is applied to resting muscles, and metabolites are allowed to accumulate, no hypertrophy occurs. If metabolites alone were responsible, they’d see hypertrophy. So perhaps, according to this model, metabolites play a role, but it’s not just their presence that induces hypertrophy.


I thought this was interesting, regarding lactate:

When lactate is produced during glycolysis, it is immediately shuttled out of lactate-producing cells and into lactate-consuming cells. Lactate-consuming cells include other muscle fibers of the same muscle, other muscle fibers of other muscles in the body, and organs, including the brain, liver, and kidneys. In being shuttled to such organs through the bloodstream (especially the brain), lactate does have signaling effects, thereby acting like a hormone.

Therefore, if lactate (or any other hormone for that matter) were to have a signaling effect on muscle fibers to increase in size, then it would increase muscle size indiscriminately around the body. In fact, the muscles that would increase in size most would be those that contain lactate-consuming cells, and not the lactate-producing cells themselves. This would contradict everything we see when taking measurements of muscle size after strength training, which is that increases in muscle fiber size are very localized to the muscles (and even the regions of muscles) that produce force during a workout.”
 
That whole argument fails to explain why hitting it with much, much higher tension prior to fatigue fails to induce a better response unless done for longer. Why does GTG not induce hypertrophy better than single session training? How is the time dependent factor explained in a way that accounts for the above?

I don't have a lot of faith in it, either.

Yes, there is no doubt at this point, based on tissue tests results of muscle fiber biopsies, that tension is a factor in hypertrophy.

But, as you point out, there are a lot of cases that seem inconsistent and there are other things going on.
 
He also points out that when BFR is applied to resting muscles, and metabolites are allowed to accumulate, no hypertrophy occurs. If metabolites alone were responsible, they’d see hypertrophy.

I’d say this statement applies to tension as well. Tension alone does not account for adaptive response. The assertions re BFR can sort of be applied to isometrics, a short exposure of the highest tension the body can generate triggers very little hypertrophy and the strength gains quickly top out limited by muscle mass - they’re explained easiest by changes in tendon stiffness and firing rate. Coincidentally it generates very little metabolic stress…

My personal theory based largely on isometrics and HIIT is that tension “opens the door” to metabolic triggers. Without high tension you need to generate substantially more metabolic signalling (BFR, typical “to failure” BB training) to get the same amplitude of effect. But both need to be present.

With higher levels of tension, the door is opened wider/ a smaller metabolic trigger is needed. I do not know what precisely this door is - I doubt it is muscle damage but honestly I don’t know. I do know that if I do a HIIT session of about 12 minutes it generates a large “pump” effect if done within 48 hours after isometrics. On its own, HIIT does not trigger this at all.

With standard isotonics these two factors are largely inseparable, is simply a question of ratio.
 
My personal theory based largely on isometrics and HIIT is that tension “opens the door” to metabolic triggers. Without high tension you need to generate substantially more metabolic signalling (BFR, typical “to failure” BB training) to get the same amplitude of effect. But both need to be present.

With higher levels of tension, the door is opened wider/ a smaller metabolic trigger is needed. I do not know what precisely this door is - I doubt it is muscle damage but honestly I don’t know. I do know that if I do a HIIT session of about 12 minutes it generates a large “pump” effect if done within 48 hours after isometrics. On its own, HIIT does not trigger this at all.

This largely maps to my subjective, absolutely not scientifically tested, bro-science experience.

But not without data.

I have anecdotal data, it's just n = 1.
 
Anecdotal evidence typically precedes scientific evidence. People figure out what tends to work, then someone figures out how to explain why it worked.

And the science is constantly being updated as more accurate info becomes available, case in point the thought that lactic acid causes muscle fatigue. Anecdotal evidence stands on its own as an observable fact.
 
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And the science is constantly being updated as more accurate info becomes available, case in point the thought that lactic acid causes muscle fatigue. Anecdotal evidence stands on its own as an observable fact.

And to that point:

It's only relatively recently at that there have been a lot of hypertrophy studies.

I'd be surprised if they figured everything out in the first 10-15 years.

Especially given how many of the studies are done on a particular set of demographics (young untrained novices).
 
When I started bench pressing, my pec muscles grew noticeably (which is to say they grew from near-nothing to something), so let us then consider the "form follows function" school of hypertrophy, whose thesis is: You'll grow what muscles you need to perform whatever movements you choose to perform. As I powerlifter, I sometimes perform assistance exercises in order to address weaknesses, but that is different than addressing small muscles just because they're small.

-S-
 
You'll grow what muscles you need to perform whatever movements you choose to perform.

Yes, there is little scientific dispute that (for the most part) your body adapts to applied stimulus. This has been well researched for well over 50 years.

What isn't as well understood is the mechanistic cause at the cellular level.
 
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