While I’m waiting until I get the energy to get aggro again, and I will, I wanted to write about a topic I’ve been meaning to address for a while, a detailed look at the idea of muscular tension. What it is, why it’s important, how we can or cannot measure it and what confusion comes out of the concept in a practical sense.
I’ve sure as hell typed up most of this in my Facebook group enough times to make this easier for me: I can type it up once and just link to it in the future. Honestly, that’s why I write most of what I write. Write it once, link to it forever after. Eventually, maybe put it in a book. This series will certainly be long enough.
As well, this article is going to act as a background piece for some stuff I intend to write about going forwards regarding training, muscle growth and what the actual PRIMARY driver on growth is (hint: it’s still not volume). But since I’ll likely have several articles using this information, it’s faster and keeps the articles shorter to write it up once and link to it. Even if this thing got rapidly out of control.
So with that short introduction, I want to look at the concept of muscular tension. What it is/represents, why it’s important to the training process and, perhaps more, err, importantly, how so many people completely misinterpret the concept in a real world training way.
To address the latter, I’ll have to make a couple of digressions but, hey, let’s remember who I am and how I (over) write. And it will take multiple parts.
How Muscles Work
Ok, so picture one of your major muscles, pecs, biceps, quads whatever. The muscle has several components. At either end is the tendon which attaches the muscle to the bone. Tendons are just dense connective tissues although their density changes from the bone end to the muscle end getting less dense as you move away from the bone and towards the muscle. When the tendon meets the muscle, this is called the musculotendinous junction.
Fun-fact: when people ‘tear’ a muscle, it is almost unheard of to tear the tendon from the bone because that connection is insanely strong. Rather, the relatively weaker musculotendinous junction is typically where the injury occurs: the muscle tears away from the tendon (rolling up like a window shade when a full tear occurs).
So between the tendons is the muscle itself which is also made up of multiple components. This includes the myofibrils themselves, the actual contractile components of the muscle which generate force. There is also the sarcoplasmic component which is mostly everything else: fluid, enzymes, glycogen, everything that’s not the myofibrils for all practical purposes (as I wrote about a few weeks ago, despite years of debate, it’s now looking like the idea of sarcoplasmic hypertrophy is an actual phenomenon).
There are also various connective tissues, titin, desmin and a host of others that connect the myofibrils in all sorts of complex ways. Some run along the muscle fibers, some connect the muscle fibers to one another in a grid, some connect it to the other parts of the cell. It’s just this interconnected lattice of stuff. Here’s a basic graphic showing how all of this works/fits together, linked from this page.
So it’s time to generate force. The brain sends some signals, which move down the motor nerve until they reach the neuromuscular junction. Then a bunch of stuff happens causing muscles to contract, generating force to (hopefully) accomplish whatever is being attempted. I’ll discuss some of the details of this in a bit. As I’ve discussed previously, there are a fairly large number of factors that can influence on the actual force produced.
The big one of relevance here is the physiological cross sectional area of the muscle or muscle fibers. So imagine you took a cucumber and cut it down the middle top to bottom so you’re looking at the round end. That diameter allows you to calculate the cross sectional area. If you cut a muscle in the same fashion, that distance across would be the same thing essentially. I said ESSENTIALLY.
And the amount of force a muscle can generate is related to this measure times what is called specific tension. Specific tension is the amount of force per unit cross sectional area that can be generated.
The Initiator of Muscle Growth
For decades it was stated that “We don’t really know what makes muscle grow” and this assertion was used to defend the absolutely goofiest bullshit training approaches that you can imagine. If you can’t say what generates growth, then any training system you can dream up is fair game so long as it “works” or at least seems to.
It didn’t help that so many things seemed to work. Well, especially once steroids got into the game and literally anything did work because steroids build muscle without training to begin with. Any stupid shit you do in the gym works so long as your dose is high enough (the main volume component of training is volume of gear used). Hence any stupid shit got defended for training because we supposedly didn’t know what triggered the process of muscle growth.
This isn’t to say that a variety of theories weren’t thrown out over the years.
The most common and still believed to this day was probably the idea that training breaks down muscle which is then built back up to higher levels. This was based on the almost wholly incorrect idea of supercompensation but that’s another topic for another day. It also doesn’t work that way in the least.
It was also related to the idea that muscle damage per se was a stimulus for growth (why so many people continue to chase DOMS/soreness) although that’s mostly thought to be incorrect. Many types of training stimulate growth with no damage and if anything, muscle damage may be detrimental to growth.
This tied in somewhat with an energetic theory of growth, the idea that training reduce skeletal muscle energetic status (i.e. ATP/CP) which somehow triggered growth. In my first book The Ketogenic Diet, I wrote about a then highly regarded theory that training would cause a depletion of ATP in the muscle causing it to reach ‘rigor’ and lock-up with the subsequent lowering causing the damage that turned on growth.
Dan Duchaine’s Bodycontract training system (something that probably 3 people reading this will remember) was based around this: a set of 8-12 to failure to deplete ATP and then 3 heavier eccentric reps to cause targeted muscle damage after the muscle fibers had hit rigor (he called it ‘targeted intensity’). I doubt this model in fashion anymore given that muscle damage doesn’t seem to be a big player in growth overall. I certainly haven’t seen it discussed in a lot of years and I wouldn’t argue nor defend it 20 years later. Mind you, it has elements of the actual picture but isn’t entirely correct.
There were ideas related to ischemia/hypoxia (basically low blood flow/Oxygen) which were dismissed for years but may have some merit when you consider some of the blood flow restriction work (BFR). I’ll be writing up another longwinded article on this but short version: hypoxia would appear to be an indirect contributor to growth in that it helps the body to recruit more muscle fibers.
Others felt that flooding the muscle with blood was the key: the pump theory of growth, essentially. This might actually have some validity if you’re on steroids to keep the drugs within the muscle longer so that they bind to the receptors longer. Maybe. But big picture the pump doesn’t seem to mean very much. Humorously, others felt that keeping blood moving through the body was the key, hence the PHA training system (that maybe 2 people reading this remember).
There’s also been some theorizing about cell swelling for over a decade now but I haven’t seen anything particularly convincing in that regards (most of the research seemed to be in liver cells under non-physiological conditions such as saline infusion and such). I’m not saying it doesn’t play some role. I’m saying I’m not convinced it’s that big of a deal in the big picture under normal conditions. I could be wrong. If this were a thing in muscle, pump training might play a role in that it could conceivably cause cell swelling.
A super goofy study came out recently using ‘sarcoplasmic specific’ training protocols that generated immense increases in muscle thickness immediately after training due to fluid shifts. But you wanna look good in the club for a few hours, this is your jam. Go get your pump on and then go get your drink on and you might get lucky. Perhaps Arnold was right.
Currently there is interest in the metabolite theory of growth although, as I’ll write about eventually, it’s unlikely to have much merit (I’ll address it briefly in Part 2 or 3 of this series) in terms of metabolites directly stimulating growth. Like hypoxia, accumulating metabolites probably just help to recruit the highest threshold muscle fibers at the end of a set (this will make sense when I explain the process below). Don’t get hung up on this right now, I have a tediously long article coming later.
Then there was the hormonal response theory, that the testosterone or growth hormone response to training, was important. And, pretty much it’s not with any effect being extremely minimal since those small spikes in hormones just don’t amount to much. At best it plays a very minor role; at worst it is 100% irrelevant. Sure, injecting supraphysiological levels of drugs matters. Spiking testosterone or growth hormone for 15 minutes not so much. The growth response to training is almost purely local.
The one I’ll mention last, because it was probably the closest to right, was proposed by Vladimir Zatsiorky. He pointed out that during any given set, a certain number of muscle fibers would be recruited to generate force. But that recruitment per se wasn’t sufficient. Rather, those fibers had to be fatigued as well (this was based on the idea that fatigue of a fiber per se triggered growth which isn’t quite right). Basically you had to recruit the fiber (unrecruited fibers aren’t trained) but you also had to subject it to sufficient work to cause it to adapt.
So with all of those theories floating around, it seems easy to understand why people would argue that “We don’t know what causes muscle growth.”
As it turned out, the idea that “We don’t know what causes muscle growth” was wrong to begin with. As early as 1975, researchers had the picture about 90% worked out and it had been established that the primary initiating factor for growth in adult skeletal muscle was the exposure of muscle fibers to high levels of tension with the researchers concluding:
It is suggested that increased tension development (either passive or active) is the critical event in initiating compensatory growth.
Yet people maintained that “We don’t even know what causes growth” for decades afterwards. Well, I’m sure they didn’t know. But physiologists sure as hell did. Or had enough of a model, that would then be shown to be more or less correct.
Now tension can be generated in different ways and you will read about active vs. passive tension. I’m not getting into this in any detail but passive tension are things like those goofy ass studies where they tie a weight to a quail’s wing for 30 days. The chronic weighted stretch exposes the muscles to passive tension overload and causes rapid growth along with an increase in muscle fiber number (hyperplasia) This doesn’t work in humans, by the way. Active tension is what we are interested in, when a muscle is forced to actively generate force.
One nifty way they create increased active tension in animals is through what is called the synergist ablation model. This is a nice way of saying that they cut one of the muscles (the synergist) that supports a joint. This causes the remaining muscle to be overloaded to an insane degree overnight.
And growth is absurdly fast and potent. It’s like 50% in a matter of days in animals or something (don’t swear me to that number). So in a human it would be like cutting the soleus so that the gastrocnemius has to take over. Suddenly the gastroc exposed to an enormous overload since it has to take over for the cut muscle. It might be the the only way for some people to get calves. I am joking by the way. I think.
But let’s move to something a bit more physiological as an example of active tension. For example, lifting a weight where muscle fibers must generate force to perform the movement. This requires them to generate/exposes them to high tension which, as above, is the initiating factor in muscle growth. Like I said, we knew this in 1975. Or at least had an inkling that this was the case. And it turns out to absolutely be the case (literally any review paper you read on mechanisms of hypertrophy regardless of the author or their bias will list tension as the primary factor in initiating growth).
What we didn’t know up until fairly recently (by which I mean like 15 years ago or so) were the actual biomchemical pathways that were involved in turning on protein synthesis. And we now know that the primary mediating factor for muscle growth is something called mTOR (the mammalian target of rapamyacin).
Training activates mTOR and so do amino acids, especially leucine which is where the whole BCAA thing comes from (they are still garbage, for the record). Yes, there are other pathways and factors involved such as AKT and ribosomal activity and many others but mTOR is kind of the key or final pathway. If you block mTOR (with rapamyacin), protein synthesis from training is blocked no matter what else you do. You can think of mTOR as sort of the final pathway for all of this stuff.
What was missing for a while was how the first achieved the second. That is, how was a purely mechanical signal (muscle tension/mechanical work) being translated into a chemical/biological signal? Because at some level, this didn’t make much sense. How can a mechanical process activate a biological one?
What did make sense was that some biological change in the muscle, ATP or lactate or hormones or whatever was causing it that it was related because it makes sense for one biological change to trigger another. This was clearly a case of a mechanical effect causing a biochemical pathway to activate.
What was going on?
Bioengineers to the Rescue
As I originally heard the story, the muscle physiologists couldn’t get anywhere with this and got some bioengineers to come take a fresh look at the problem. This was kind of before all of that other connective tissue stuff like desmin and titin I mentioned above were known about mind you. The idea that muscle fibers were connected to other parts of cell wasn’t a thing at the time . You just had muscle fibers kind of running down the length of the muscle with tendons on the end and when they contracted, movement occurred around the joint they were attached to. And somehow that could turn on this biological growth process.
And supposedly the bioengineers were like “Ok, so if you had some sort of tissue that connected the actual muscle fibers (running lengthwise down the fiber) to other structures in the cell, that could explain how a mechanical signal turns into a biological signal. The fiber contraction would pull on those other tissues which alters cell structure and could translate into a biological signal.” This would provide a mechanism for mechanical tension to turn on a biochemical cascade.
And I’m sure the muscle physiologists were like “Lol, ok” and then looked for these supposed structures and were like “WTF, they were right” or something. And then probably took credit for the idea when it was all said and done.
Now I may have dreamt all of the above up (it wouldn’t be the first time) but, even if I did, it turns out that this is exactly what is going on. Essentially, there are mechanosensors within skeletal muscle that, when activated, transform a purely mechanical signal (muscle fibers generating/being exposed to high tension loads) into a biological one, the activation of mTOR.
Note: I don’t know exactly when the above model became a thing but it was somewhere between 1993 when I graduated from UCLA and the early 2000’s when I took an advanced exercise physiology class at UT Austin.
So what are the mechanosensors? So far as I can tell, they are currently calling these things Focal Adhesion Kinase which, when they do their magic, activates mTOR (this appears to be mediated through the generation of phosphatidic acid which is why those supplements were popular a while back). Going forwards I’ll just abbreviate this process as FAK/PA/mTOR.
Boom, a mechanical signal is converted into a biological one. Tension overload
activates mTOR and growth is stimulated. Problem solved.
Note: Other systems have this too. Bone is an interesting one where high force impact loading activates mechanosensors called osteocytes within the bone that turn on the process of increasing bone mineral density as an adaptive response. Even more interesting, after some number of high force stimuli, the osteocytes become refractory to further stimulation. That is, there is a per workout or per day maximum to the stimulus. Hmm, that sounds familiar. Even the cell swelling theory is thought to work through physical stretching of the cell where the mechanical stretch turns on biological processes even if I remain unconvinced that it’s a major pathway in skeletal muscle growth. But, fundamentally it’s mechanosensors all the way down.
And, once again, that is the primary initiating event in turning on hypertrophy: high tension forces generate a biochemical cascade that turns on protein synthesis. Yes, there are other players in this process but this is the key one. Importantly, it looks like there need to be a sufficient number of high-tension contractions for this to occur. It’s not just a function of exposing a muscle to a singular brief high tension load. You have to do it a number of times for the mTOR cascade to get activated.
But at this point nobody knows how many contractions are required on either a per set or per workout level (though it’s funny that everything seems to be coming back to Wernbom’s recommendations from 12 years ago and it won’t surprise me in the least if he was right all along). A single maximum daily contraction doesn’t turn on growth and a group that did 5 maximum single reps twice/week showed no growth so there’s clearly more to it than just high tension. Some volume of high-tension contractions is required (and nobody including me has ever said differently, that volume doesn’t matter. I’ve said that it wasn’t PRIMARY because it isn’t). Put more succinctly.
High muscular tension is REQUIRED but not SUFFICIENT to stimulate growth.
Without a high tension stimulus, growth isn’t turned on (and note that I didn’t say high LOADS, I said high TENSION which I’ll explain later). But other factors play a secondary role to the presence of mechanical tension. Volume is one of them. You need some amount of contractions under high tension conditions to turn on growth. We just don’t know how many yet.
Which is basically what the Zatsiorsky model of growth I described above is getting at. He put it in terms of recruitment and fatigue which is wrong but his general picture was still right. Just making a fiber generate high tension isn’t sufficient to trigger growth. Some number of contractions is also required to activate the FAK/PA/mTOR cascade.
High tension is still the key which is why running and other low intensity activities don’t generate muscle gains. Ok, that’s not true, they do in total beginners where even that low intensity activity probably is a tension overload for a little while. Then again, so is Wiifit at that level. But beyond a certain point, those activities do not increase muscle mass. I’ll address the low-load/BFR stuff, which seems to contradict this (except that it really doesn’t), briefly later in the series and in excruciating detail eventually.
So we ask: how do we generate high tension in a muscle? Now I have to digress into some details.
Recruitment and Rate Coding
Fundamentally there are two ways that the body can get muscles to generate force. The first is through recruitment, actually making the muscle fibers themselves activate to generate force. The second is through rate coding, the rate at which signals are sent down the motor nerves to those fibers which impacts on how they fire. The combination of the two determines the force output of the muscle and the body has different “strategies” for using one or the other depending on the situation (and this gets insanely complex and I am so not going to try to get into it because it’s not big picture relevant).
I should that there are two primary types of muscle fibers, Type I (slow twitch, oxidative) and Type II (fast twitch, glycolytic). There are also a bunch of sub-fiber types like IIa, IIx, IIax and some hybrids but I’m going to ignore the details here since they aren’t really important. I’m just going to pretend that there are Type I and Type II to keep it simpler.
Type I are typically smaller, contract slightly less quickly, generate less force, are more aerobic and fatigue very slowly. They are good for endurance activities. Type II are typically larger, contract a bit more quickly, generate more force, are more glycolytic and fatigue more quickly. They are better for high-intensity activities. Type II fibers generally have more potential for growth as well.
During activities, muscle fibers are recruited in a fairly orderly way from smaller (Type I) to larger (Type II) depending on force requirements according to what is called Henemman’s Size Principle (not to be confused with Henneman’s Wife’s Size Absolutely Matters Principle). So Type I are recruited first, with Type II coming in later progressively. And there is a continuum of both types of fibers with a continuum of characteristics that will come in progressively as the intensity of activity goes up. It’s also way more complex than this, don’t worry about it.
At around 20% of maximum force, basically lower intensity aerobic work, only Type I fibers are needed. This is why it can be continued for extended periods: Type I fibers are highly aerobic and don’t generate many waste products. You can go until you get bored or dehydrated. I mean, ultra-endurance “runners”, who may be going 3.5-4 mph (a brisk walk) will cover hundreds of miles at that pace. It’s all Type I fibers at this level.
As force requirements go up, Type II fibers will be recruited to a greater and greater degree. So you move to faster running and start to recruit some Type II fibers. Now Type II can still be somewhat aerobic, especially at this level. So you still don’t fatigue particularly rapidly. Forever maybe become 6 hours on the bike or when glycogen runs out.
Now you’re running near your maximum sustainable speed, something you could do for an hour. Lots of Type II fiber recruitment. Not all of them, but more. There’s waste products being generated but they are not accumulating. It hurts but you can keep going. Then you go all out sprinting, HIIT type. Depending on the intensity you probably get damn close to full recruitment. Waste products build up rapidly and you fatigue in 45 or 90 seconds.
And that’s how fiber recruitment basically works, at low intensities the body only needs low-threshold Type I fibers with higher threshold fibers being recruited progressively with increasing intensity. At least up to the point where full recruitment occurs.
What is that point? In a weight training sense, maximum recruitment occurs at about 80-85% of MVIC (maximal voluntary isometric contraction which I will roughly take to be synonymous with 1 repetition max even if it’s not exactly the same). At that level, all muscle fibers are recruited. Beyond this point, the body generates more force with rate coding and other complex neural stuff as there are no further fibers to be activated.
A quick note: there is a long held-belief that the body can only recruit a small portion of available muscle fibers but this is fundamentally wrong. Using a technique called the Interpolated Twitch Technique (ITT), it’s been found the people can recruit 98-99% of their biceps fibers. In contrast, they can only recruit 88-90% of their quadriceps muscle fibers (low back is down at 75% if I recall correctly and I suspect this is to protect spinal disks). This leads me to speculate that the “empirically observed” and “semi-research suggested” idea that legs need more volume than upper body might be related to this. If even during a hard set you can’t get full activation of your quads/legs, you might need more total volume to get the same overall growth stimulus. We really need more structured and systematic work on this.
In any case, this recruitment threshold of about 80-85% 1RM (and some put it closer to 90%) has a couple of implications. The first is that beyond about a 5-8RM you don’t get any more fiber recruitment. Doing a 3RM or 1RM won’t recruit any more fibers than a 5-8RM. You’ll certainly see different neural patterns, rate coding and such. But from a fiber recruitment standpoint there is no real difference and going heavier beyond a certain point won’t lead to further recruitment. I’ll come back to the other implication later down.
Fun fact: The above only holds for large muscles like arms, quads, pecs, the ones we care about. In smaller muscles like the eyes and fingers, recruitment occurs up to about 50-60% of max with rate coding dominating after that. This provides much finer muscle control; if it didn’t work that way, your eyes would fly back and forth as you tried to read this and you’d have no control over your fingers for fine motor tasks. This is also why all those finger and thumb muscle strength or endurance studies have less than zero relevance to training (and why citing them to make any argument about real-world weight training is not only pointless but shows a lack of basic physiology knowledge by the person doing it). They simply don’t apply.
Ok, so that’s recruitment and rate coding and implies that getting full recruitment of a muscle means training at 80-85% or heavier. Except that that isn’t correct.
Two Ways to High Tension
So if you start at 80-85% of MVIC, maybe a 5-8 RM you get full recruitment from repetition 1 and throughout the entire set and I’ve written previously that if you had to pick a single repetition range for growth, this is it. I based the argument on optimizing both recruitment and total mechanical work. Because working in this range will cause full fiber recruitment from the first repetition and allow you to perform the most repetitions under that condition compared to either heavier or lighter sets. Knowing that we need fiber recruitment and some number of contractions this would arguably be the most efficient way of achieving that.
In any case, if you do a 5RM you’ll get 5 total reps at full recruitment. If you do 3 reps with 5RM you get 3 reps with full recruitment. Of course, you can probably do more sets of 3 at a 5RM than sets of 5 at a 5RM and might get more total per workout contractions. Those sets of 3 will be a higher quality technically or in terms of bar speed as well. So you can do 5 sets of 3 with 5RM for 15 effective reps versus perhaps 2 sets of 5RM for only 10 and with better technique and speed. This is how strength/power athletes typically train, using a heavy load but not taking it to failure so that more total high-quality sets can be done. The same principle can hold for hypertrophy but let’s move on.
But now lets ask the question what the process of fiber recruitment looks like if we start below 80-85% of max. So let’s say we’re lifting at 70% of max, maybe a 12-15RM on average. Now, by definition, the body doesn’t need to recruit all muscle fibers in this situation since force requirements can be met by less than 100% fiber recruitment. For some number of reps in the set, full recruitment will not be achieved since it’s not needed.
But as the set continues, some of the initially recruited fibers will start to fatigue. When that occurs, the body will recruit higher threshold fibers to maintain force output and continue the set. And more fatigue will occur. And more fibers will be recruited. And this will occur until, at some point in the set, full recruitment of all available fibers has occurred. And that full recruitment will be maintained until the set is terminated either because the lifter stops or muscular failure occurs (defined here as the repetition not being completed no matter how much force the lifter exerts).
So, hypothetically, say you start lifting at 75% of max, about a 10-12RM or so. For the first 5-6 reps you won’t reach full recruitment as the body can generate enough force without needing all muscle fibers to contribute. As fibers fatigue, the body will recruit more fibers and over perhaps the last 3-5 reps (or whatever number) you will get full recruitment. Which means that it’s only over those last 3-5 reps that the highest threshold/Type II fibers are being recruited, hence exposed to high tension, and doing mechanical work and hopefully activating the FAK/PA/mTOR cascade.
Which raises the question of when in the set do all fibers reach full recruitment. I am aware of two studies on the topic.
In one study, trained men performed a set to failure in the leg press at either 90% or 70% of 1RM with surface EMG (admittedly limited as a methodology) being used to determine activation. On average, the subjects got 8 reps at 90% and 18 reps at 70%. Without getting into the weeds on what they measured (it was a bunch of peak and average EMG), what the study ultimately found was that the peak EMG at 70% was the same when compared to the “matched repetitions” of the 90% set. Which is a weird way of saying that the peak EMG was the same for the final 8 reps of the 18 rep set as for the 8 reps of the 8 rep set. Either way you get 8 repetitions with full recruitment. You just have to do 10 non-full recruitment reps first with the lighter weight to get those same 8 full recruitment reps.
A similar study in untrained women using rubber tubing found the same thing. It looked at trap activation during a lateral raise at either a 3RM or 15RM set. And what it found was that full activation was reached from the first rep in the 3RM set as would be expected. But full recruitment was not reached until the last 3-5 reps in the 15RM set. So in the 3RM set, 3 total reps were done under full activation, in the 15RM, 3-5 reps at full activation were done. Both groups got essentially the same number of full recruitment reps. The 15RM subjects just had to do 10-12 reps without full activation to get there. And I do wish they’d stop using such extremes, comparing perhaps 85% to 75% or whatever to see how it differs.
What you see is that submaximal loads lifted close or to failure
can cause similar fiber recruitment patterns as heavy sets.
I’d note and I’ll come back to this in a later part of the series that this is how low-load/BFR training essentially works. By taking a low-load set to failure (and this doesn’t happen if you stop short of failure which is a big pointer in to what’s going on), you reach or achieve full muscular activation near the end of the set. In a conceptual sense, you sort of have to by definition since failure is 100% regardless of how you get there. A 5RM is 100% effort at the end but so is a 30RM so long as both are to true failure. So the fiber recruitment patterns would be expected to be at least similar. And they basically are.
The same occurs with BFR with the metabolites/hypoxia helping with fiber recruitment. Simply, they increase high threshold fiber recriutment even with the submaximal loads. At the end of each set the highest threshold fibers are recruited and exposed to a tension stimulus for a sufficient number of contractions. Yadda yadda, FAK/PA/mTOR cascade. Mind you, you have to do 25-30 painful, pointless reps first to get to full recruitment and tension but that’s what’s happening. But it sure looks edgy on Instagram and isn’t that what training is all about?
Put more simply, whether you do a set of 3-8 with 80-90% 1RM, a set of 15RM with 70% 1RM or a set of 30 with 25% 1RM (or BFR it), you end up getting some number of repetitions under full recruitment and high tension. In the first case it’s from the first repetition and you get 3-8 reps under full recruitment. In the second full recruitment occurs around reps 10-12 and you get 3-5 reps under full recruitment, in the third case, you waste your life doing 25 worthless reps to get to the 5 or so good ones or however many it is.
But it’s all ultimately a path to high tension overload of the high threshold muscle fibers (yes, there is some speculation that low load/BFR may target Type I and this is assuredly a durational/fatigue issue that I’m not getting into here).
As I wrote on Facebook the other day: All roads lead to high tension.
It’s just a matter of how you get there.
While I’m on the topic I might as well address a relatively new concept which is that of “effective reps”. The idea here is that it’s only those repetitions of a set done under full (or near full) activation that “matter” in terms of the growth stimulus. The total sets don’t matter. The total reps don’t matter. It’s the effective reps that matter. I don’t know that I’d argue this in the strictest sense although it’s certainly true if you’re talking about the highest threshold muscle fibers. Clearly fibers are being recruited or trained without full activation. Just not all of them.
If you did a 5RM set, that’s 5 effective reps since they were all done under conditions of full recruitment. So if you do a set of 12 near failure and get full activation for reps 10 through 12, that’s 3 effective reps. If you do a set of 35 reps with 30% of your 1RM, you just fucked around for ~30 reps to get to the 3-5 or so effective reps. The end result is effectively the same. Get it? Effectively? Effective reps? Effectively? Nevermind.
Now we still don’t know how many effective reps are necessary to optimally activate the FAK/PA/mTOR pathway. Once we do, and if we also find out that it saturates at a certain point on a per workout or per week level we’ll be able to end this fucking volume debate once and for all.
So if we determine that 20 or 40 effective reps per workout or whatever (or so many contractions per week) is optimal and/or the limit to the growth stimulus, we have the basic answer of how to optimize training for growth. I still suspect Wernbom’s earlier data will turn out to be roughly correct.
Because we know that there are different ways to get the same number of effective reps. So consider someone doing multiple straight sets of 8 say 4X8 on a 2′ rest. Let’s say they start 2 reps in reserve/reps to failure, so it’s a 10RM load. Realistically, the first set might get a couple of effective reps under full fiber recruitment. With each successive set, assuming the rest interval isn’t too long to allow full recovery, as fatigue accumulates and the set gets closer to failure the number of full recruitment reps per set will increase. Becuase what will happen is that set 1 is at 2RIR and set 2 is at 1-2 RIR and set 3 is at 1RIR and set 4 is 0 RIR.
So on set 1 maybe it’s 1-2 effective reps, on set 2 it’s 2-3, on set 3 it’s 4 and on set 4 it’s also 4. What’s that, 11-13 total effective reps across the 4 sets. Do it for a second exercise and maybe you double that to about 20-26 effective reps or whatever it works out to. So that’s one way to do it: some number of straight sets with an incomplete recovery that results in an accumulating number of effective reps per set over the workout as full recruitment starts earlier in each set.
Or consider the various rest-pause approaches such as Myo-Reps or Doggcrapp (or simply rest-pause). Here you start with a heavy set, often called an activation set. The idea is to either start heavy enough (i.e. with an 8RM which is about 80% of max) or get close enough to failure with a submax weight to get full fiber activation in that first set. So you get to rep 8 with maybe 2-3 full activation reps and stop the main set set (Myo-reps used to use speed cutoffs, DC went to failure). Now rest 15 seconds, long enough to recover a bit but not completely.
Now you get 2-3 more reps which are probably also still under full activation so they count as effective reps (and they do that without requiring another 5 reps of a straight set). Rest 15″ and you get 1-2 more. Rest 15″ and you get 1 more. So maybe it’s 8-9 effective reps across that singular rest-pause set. If you do two of those sets you get 16-18 total effective reps which is about the same as the straight sets although it only took you two rest-pause sets versus 8 straight sets to do it.
Is this making sense?
The corollary to this is that sets that are too light AND nowhere close to fatigue, may not contain any effective repetitions, or certainly not many (or certainly not effective reps for the highest threshold muscle fibers). If you do a set of 6 with a 12RM, you’re not recruiting the highest threshold Type II fibers at all. Not unless you do repeat sets with a short rest interval so that there is cumulative fatigue across the sets.
So if you do 6 sets of 6 reps with your 12RM but only rest 15-30 seconds between sets, fatigue will accumulate and you’ll reach full recruitment eventually. Maybe by the fourth set you’re getting some effective reps or whatever and that increases with each subsequent sets. It “works” although you basically fucked around for the first 3 sets to even get close to a meaningful training stimulus. As I think about it, Gironda’s 8X8 probably worked by this mechanism. It was an honest workout.
In this vein, there is a recent super stupid study that looked at what they called the the 3/7 method. Using untrained subjects, it compared a single set of 3,4,5,6 and then 7 repetitions at 70% of max (12RM) with like 15″ rest between mini-sets to a group doing 8 sets of 6 with 12RM. And the 3/7 method worked better than the straight sets (inasmuch as more or less everything works on beginners). Because with that short rest, it probably got at least some effective reps near the end despite being pathetically submaximum. In contrast, 8 sets of 6 at 12RM is a series of warm-up sets and I bet they were lucky to get even a few full recruitment reps during that workout.
I made similar comments about the Haun et al. study Mike Israetel was involved with. It used repeat sets of 10 at 60% of max with the subjects reporting 4 reps in reserve. So it was 4 reps from failure and there was an 8-10′ rest interval due to the goofy nature of the workout setup. So there was no cumulative fatigue (RIR stayed at 4 across the workouts and study). If I’m being generous let’s say each of those warmup sets got maybe 1 effective rep per set. Maybe it’s 2.
Don’t believe me? Go back to that 15RM study I described above. Full recruitment didn’t occur until rep 9-12. 10 reps with a 14RM load and you maybe get full recruitment on rep 9. 8 if you’re lucky. 1-2 effective reps per set at best.
First let’s compare a workout with 1 effective rep per set to a real workout. At 10 sets/week that’s 10 effective reps per week. NOT per workout. PER WEEK. You can achieve the same thing with 2 all out sets of 5RM. Go to 20 sets per week and that’s 20 effective reps per week. 4 sets of 5RM per week.
At 32 sets/week maybe they got 32 effective reps. I can do that in 4 all out sets of 8 in a single workout. I could also do 2 sets of 8RM twice/week and go home. In those 4 sets I might accomplish the same number of effective reps as 32 piss-ass sets. I’ve done 32 effective reps in 32 reps vs. 32 effective reps in 320 reps. 1/10th the volume by reps and 1/8th by sets.
If I go nuts and double my workout to 4 sets of 8RM twice/week, I’ve gotten 64 effective reps in those 8 sets. I’ve done 64 reps in 8 sets versus 320 reps in 32 sets for TWICE the effective reps. And that’s without spending 2 hours in the gym fucking about.
Even if you give the benefit of the doubt and say the 10 reps at 4RIR gave 2 effective reps per set, 32 sets is 64 effective reps PER WEEK. If I train a muscle group for 4 sets of 8 to failure twice a week I achieve the same thing. 8 sets for 64 total/64 effective repetitions vs. 32 sets and 320 reps for the same 64 repetitions. And I get to do it without having to live in the gym fucking around warming up for 2 hours.
Basically the workout in Haun et al. was a lot of pissing around. And maybe that’s why it needed such ludicrous volumes to accomplish anything at all. The sets were so piss-ass low intensity, low fatigue that almost none of the reps were an actual stimulus to the muscle fibers. These are warm-up sets at the rate of 6-7 sets per muscle PER HOUR. You could do that all day long until you went nuts from boredom. Seriously.
The fact that the growth appears to have been predominantly sarcoplasmic speaks to that. Actual myofibrillar protein synthesis wouldn’t be turned on if there aren’t enough high-tension reps to activate the FAK/PA/mTOR pathway. But you get a lot of volume and stress sarcoplasmic components with that kind of ineffective training. And if that’s your goal, go to town. Or just learn to train for real.
Because contrast that to the Barbalho papers on women and men where all sets were truly taken to failure and where the low volumes did just as well if not better than the higher volumes. Because in every set that was done, a large number of the reps were done under full recruitment and were effective reps. When they were doing 4 sets of 4-6RM in that week that’s 16-24 effective reps per workout because every rep was done under full recruitment from rep 1 until the end of the set. And that was true of every week since they were true RM loads (I still do not believe the squat workouts were achievable, mind you). It would take 16-24 sets of piss-ass low intensity work getting 1 effective rep per set to accomplish the same stimulus or 8-12 if you got 2 effective reps. So 1/2-1/4th the volume if you actually train hard.
And no I’m not saying you need to train to failure. I’m making a point about how different approaches to training can generate vastly different numbers of ‘full recruitment/effective reps’ per set, workout or per week. You can do way more sets but if they are ineffective in terms of not achieving full recruitment for sufficient tension overload, they may still work worse (or certainly no better) than a lower number of sets that are actually challenging. And that alone might explain all of the volume debate or the discrepancies in the studies (which really don’t exist as currently 6 of 8 studies show the same thing with one shit show and one outlier people refuse to discount).
Because studies that use lower volumes of actually intense work (you know, all the ones supporting low to moderate volumes which represent 6 out of 8) are getting plenty of effective reps with a low volume of training. And if there is a per workout saturation point, higher volumes shouldn’t work better. And, in contrast, those that are using piss-ass intensities are not. They only appear to ‘need’ such high volumes because the workouts are so ineffectually designed.
You know, like a workout where supposedly guys did 5 sets of 8-12RM on 90 seconds in the squat or bench which is utterly impossible (PROVE ME WRONG, FOLKS). Which would ONLY be remotely achievable if “failure” were defined as about 4-5 reps before actual failure. Which if I don’t miss my guess is exactly what happened in that particular study (I would love to see video of even one of the workouts).
Because the workout is simply impossible to do once much less 3X/week for 8 weeks if the sets are anywhere close to failure. They can’t have been close to failure becuse the workout would be impossible at the higher volumes. Mind you, it’s not as if the statistics supported the highest volumes anyhow but I digress.
Because in 5 truly hard sets with a sufficient rest interval, you can readily achieve the same number of effective reps as 15 piss-ass intensity sets with a stupid workout design. You may only ‘need’ high volumes if you simply don’t, can’t or won’t train with any degree of intensity. And that’s probably exactly what is the case.
All those bros in the gym doing 20 sets/muscle group who get “big”. Well it’s probably taking them those 20 sets to get an effective stimulus as someone doing 4-6 hard sets. Which is what I’ve said before: If you think you NEED 70 sets/week for a muscle, you don’t know how to fucking train with any sort of intensity or focus. Visit me in Austin and I’ll prove it to you.
Summing Up Muscle Tension: Part 1
Ok, so this already got away from me and it’ll probably go 4 parts to address this all. The basic gist of Part 1 is this. High muscular tension is, without debate, the primary initiating factor in muscle growth and we’ve known this since the 70’s. And every review paper regardless of author or their personal bias or online bullshit states this.
This occurs through mechanosensors, probably Focal Adhesion Kinase which translate a mechanical stimulus (high tension in muscle fibers) into a biochemical cascade involving mTOR. Tension alone is required but insufficient. Some number of high tension contractions is required to turn on this cascade but we don’t know how many in either a per set, per workout or per week fashion.
What this means is that the process of turning on growth means 1) recruiting the high-threshold/Type II muscle fibers and 2) exposing them to sufficient amounts of mechanical work to turn on this cascade.
Towards that I examined how fibers are recruited in response to force requirements. The take-home is that you can get full recruitment with heavy loads of 80-85% of max or so or by taking lighter loads near or to failure. With lighter loads, as fatigue sets in, the body will progressive recruit higher threshold fibers, eventually reaching full recruitment at some point late in the set. Both ultimately end up causing recruitment of muscle fibers, exposing them to a high tension load. A heavy set of 5 and a set of 30 taken to failure probably both get about 5 full recruitment reps. The 30 reps to failure just made you do 25 pointless reps to get there.
This led into a discussion of the idea of effective reps, those reps in a given set or workout that are done under full recruitment/high tension conditions which, as noted can be achieved in different ways. Straight sets at a low RIR/RTF is one way, rest-pause is another. There are also stupidly ineffective ways of training that have so few effective reps per set that this might explain why some research or theorists suggest that the body needs an insane volume to generate growth.
When the intensity of your sets is utterly piss-ass low, you probably do need 5X the volume as if you actually knew how to train with some degree of focus or intensity. But you’d be better off learning how to train with some degree of focus and intensity than just doing more bullshit sets.
But regardless of how you get there, the key to turning on growth is doing a sufficient number of high-tension contractions. High-tension alone isn’t sufficient but without it, nothing happens. All of the insufficient tension work in the world simply doesn’t generate growth.
But this raises a question which is this: How do we measure tension in the muscle?
And the answer is that we can’t in the gym, not in any meaningful way. Not yet anyhow.
But we have something we can use as a proxy for tension. Something that we can measure and track to give us some indication of what tension the muscle might be experiencing. If you’ve read much of my work, you know what it is. If not, you’ll find out next week.
Where in addition to explaining what that proxy is (hint: it’s weight on the bar), I’ll move into a detailed discussion of the misunderstandings that come out of using that proxy. Of which there are many. Yeah, this is gonna be one of my stupid long article series for sure. But I need to get this written down once and for all. See you next week.