Is Load Progression Necessary For Hypertrophy?

Discussion in 'Hypertrophy-Specific Training (HST)' started by mikeynov, Jun 29, 2019.

  1. NWlifter

    NWlifter Active Member

    Very interesting....
    Apparently, in real life, most motor units 'come online' with close to full tetanic tension, they pulse in and out. So the logical (seemingly) idea that rate coding slowly increases fiber tension 'in real life' is not quite right. Theoretically, it would, but seems that's not what happens. Fibers are never on during exercise, for such a short time that they only 'twitch' (low tension) without summation. (range of tetany)

    Further, we can't also forget that the only time a fiber can actually create and thus 'feel' maximum tension is at full tetany near the stretch position for optimal actin-myosin over lap. (most actual cross bridges attaching) So even a 1RM with an exercise where max effort is in the mid range to contraction area, still wouldn't cause maximum 'tension in a fiber'. Chasing max tension seems futile...

    What does this mean?
    That in real life, a 5RM probably isn't increasing the actual tension that fibers are feeling/producing over a say 10RM. They just create max tension more often. That was how I first learned this, and posted about it. Then found more info. and changed my outlook. Now I see this and it seems the first rendition was more correct. MU's only vary their actual tension at very low or very high maximal contractions. Most 'come on line' at, or close enough to, full tetanic tension. It's more about how often they 'produce' that tension that varies whole muscle tension.
    Last edited: Aug 23, 2019
  2. NWlifter

    NWlifter Active Member

    The picture I'm getting from all this, is that during a 'set' , since it's not super light, and barring if the person is literally pushing with 'do or die' all out crap their pants effort, most motor units pulse on and off with a higher level of rate coding, and therefore high tension, in a narrow range of tetany. The actual firing intervals between MU's is staggered and frequency of actual firing varies so the contraction is smooth, At any millisecond in time, various MU's might be actually creating tension. Recruitment means they are involved but does not mean they are just flat out solid on for the whole period of time when needed.

    I'd say it's almost like you have a tug of war with hundreds of people pulling, when a person pulls, it's a sharp hard tug but not all are in sync with those tugs, so more like...
    number 1 tug, tug........ tug................tug.. tug............tug............. tug
    number 2....tug.... tug,... tug............tug..........tug....tug......tug.........
    number 3.......tug.............tug..........tug...tug.......tug.....tug........tug
    number 4..tug...tug.........tug....tug...tug.......tug.........tug.....tug.....
    number 5 ...tug.....tug.........tug....tug.........tug........tug.....tug........tug
    number 6tug....tug......tug......tug.........tug........tug..tug..........tug
  3. NWlifter

    NWlifter Active Member

    Mr. Mike, where'd ya go , any thoughts on this or your other thread? I saw you tag me in the other one, curious on your take on both of these, cheers dude!
  4. mikeynov

    mikeynov Super Moderator Staff Member

    Sorry Ron!

    I actually did read these posts, and looked at that old study you posted. I'm not sure what to make of it per se, other than it's kind of more evidence that per-fiber tension doesn't meaningfully change in the context of it actually being recruited in the first place, as you said.

    I still think you're probably right that something about the activation/frequency of it generating that tension is probably corresponding to some sort of microstrain-y type event that is kicking off the cascade of growth past some fatigue threshold. Which would explain and correspond to the idea of "effective sets" I've been proposing.

    As an aside, I have a spreadsheet I've been working on to start making use of some of these ideas. Basically the ability to plug in a bunch of exercises at known/current weights (I'm defaulting to an upper/lower split), reps and RPE's, and then create your own RPE prescriptions in anything from 1-12 week cycles. The RPE table is customizable, and I have a bunch of different options you can easily plug in, or just plug in your own values (better) so the RPE's correspond to meaningful percentages.

    I can upload this if you or anyone else are interested.
  5. NWlifter

    NWlifter Active Member

    OK cool, yes, that's how I learned all this many years ago, then reading about theory on fibers I guess mixed it up. 'How' a twitch works isn't how it actually 'happens' in real life. I guess it's kinda like a car engine, we could read about force from a single piston firing and assume a car engine can put out as low as 1HP, but it real life, it doesn't happen that way.
    But to me that doesn't negate the basic HST model, it just alters it from only focusing on whole muscle tension for an increase, to focusing on 'tension and time' together to increase the stimulation.

    To me, a basic idea to take advantage of this, would still be to use load, but to keep the reps the same. For example, the base routine....
    instead of
    2 weeks of 1x15 with 15's
    2 weeks of 1x10 with 10's
    2 weeks of 1x5 with 5's

    would be
    6 weeks of 12 reps, starting with a 20RM, with an ever increasing load and using something like rest pause/clusters. So once you can't get 12 reps in one set, you might do 9, rest a bit do 3 more.. later it's even heavier, you might do 7 +3+2. Eventually your doing 5+4+3+ etc. This way work increases instead of matching.
  6. NWlifter

    NWlifter Active Member

    I myself am positive there is something about 'time at tetany' that is a strong trigger.WAY back years ago, me and Dan started an e-book on this theory, then I didn't hear back from him for a bit and he was creating max stim at the same time and released that. I still have the first few jumbled pages of the book we started to write about this. Over the years, the more I read and dig, the more this seems to still fit everything.
    Last edited: Aug 24, 2019
  7. NWlifter

    NWlifter Active Member

    Here is my theory that takes into account tension, time, volume and frequency. I'm sure this is how fiber size operates.

    *Sleep for example is an atrophy input, it doesn't happen as strong as the input, but it's pulling down on protein synthesis, there is no PS upregulation signal during this time. If it continued, fiber size would slowly drop like the 'bed rest' studies.The natural level of PD would outweigh the very low PS level.

    *Regular daily activity has little bursts of tension, those are tripping a little increase in PS that offset the times when no signal for PS increase is present.Average PS matches average PD.

    *The workout puts up a huge 'intention for PS, it lingers long after the workout thus negating any 'down pulls' from dis-use later that day. PS outweighs PD for 12-72 hours


    So over time, all the pulls up and pulls down that vary actual PS levels in each fiber average out

    Last edited: Aug 24, 2019
  8. HST_Rihad

    HST_Rihad Active Member

    It's a bit funny to see people arguing about what the best way to cause hypertrophy is, when in reality all you have to do to make your muscles grow is overeat.

    That said, RT does favorably impact overall body composition, probably by improving a person's p-ratio.
  9. NWlifter

    NWlifter Active Member

    Some interesting studies I ran into recently...

    The contraction stimulus driving MPS
    From a systems perspective, the input into a skeletal motor unit–muscle fibre to lift a weight would come from the neural signals it received, and these signals would determine whether to fire or not fire and at what frequency. The surrounding nutrient milieu would then dictate (to a variable degree) the response of the fibre in terms of MPS (Biolo et al. 1997), which would ultimately sum to yield hypertrophy over time. When viewed from this perspective, there is an underlying commonality between many RT variables such that application of any variable in such a way to induce muscle activation ultimately serves to activate the same intramuscular signaling pathways necessary to stimulate MPS and potentially training-induced hypertrophy. Indeed, many will argue that the phenotype of ultimate importance with any program of RT is both strength and hypertrophy and we do not disagree with this. However, a common link between these variables is hypertrophy,
    ER stress induces anabolic resistance in muscle cells through a PKB/PRAS40-induced blockade of mTORC1.

    We aimed to determine if the time that muscle is under loaded tension during low intensity resistance exercise affects the synthesis of specific muscle protein fractions or phosphorylation of anabolic signalling proteins. Eight men (24 ± 1 years (sem), BMI = 26.5 ± 1.0 kg m(-2)) performed three sets of unilateral knee extension exercise at 30% of one-repetition maximum strength involving concentric and eccentric actions that were 6 s in duration to failure (SLOW) or a work-matched bout that consisted of concentric and eccentric actions that were 1 s in duration (CTL). Participants ingested 20 g of whey protein immediately after exercise and again at 24 h recovery. Needle biopsies (vastus lateralis) were obtained while fasted at rest and after 6, 24 and 30 h post-exercise in the fed-state following a primed, constant infusion of l-[ring-(13)C(6)]phenylalanine. Myofibrillar protein synthetic rate was higher in the SLOW condition versus CTL after 24-30 h recovery (P < 0.001) and correlated to p70S6K phosphorylation (r = 0.42, P = 0.02). Exercise-induced rates of mitochondrial and sarcoplasmic protein synthesis were elevated by 114% and 77%, respectively, above rest at 0-6 h post-exercise only in the SLOW condition (both P < 0.05). Mitochondrial protein synthesis rates were elevated above rest during 24-30 h recovery in the SLOW (175%) and CTL (126%) conditions (both P < 0.05). Lastly, muscle PGC-1α expression was increased at 6 h post-exercise compared to rest with no difference between conditions (main effect for time, P < 0.001). These data show that greater muscle time under tension increased the acute amplitude of mitochondrial and sarcoplasmic protein synthesis and also resulted in a robust, but delayed stimulation of myofibrillar protein synthesis 24-30 h after resistance exercise.
    The repeated bout effect can occur without mechanical and neuromuscular changes after a bout of eccentric exercise
  10. Clayton

    Clayton Member

    Not trying to troll, but if I'm following Beardsley and Brian Minor (, doing a reverse HST would work if I'm making sure to increase the workload?

    I just started a new HST cycle, but if I'm still lifting consistently in 6 to 8 weeks, I think I may immediately do a "reverse HST" without taking a week or two off. Basically, after the 5s, I reverse course with the weights I previously did, but making sure to do more reps (mainly via clusters and Myo-Reps). Since, I'll have the recent weights/reps, it should be easy to track to make sure I'm getting more "effective reps." At the very least, weekly workload should be increasing and it should be good for my joints. I'm guessing the weight/rep range progressions will be 3 instead of the normal 6. So, kind of a 3 week deload back into the higher rep fun. Then, ideally, back into HST/standard periodization.

    I think it's safe to assume it won't be as effective as SD, then starting a new cycle, but I'm cutting weight, so it's mainly for the consistency with lifting. So, while progressing mechanical load is tried and true, I'll mix it up for fun...unless someone has already done this??
  11. NWlifter

    NWlifter Active Member

    Me myself, I know that can work based on my own training experiments.
    I've went from heavy to light but increased 'work' and grew. I've went from lighter to heavier with less work and lost size. I myself am positive that load itself isn't the key but more load, time with the load density, fatigue, etc
    Clayton likes this.
  12. Jester

    Jester Well-Known Member

    I would also bear in mind that very few of these studies have a sample size worth talking about (if we’re being honest with ourselves), and most of them aren’t repeated, ever.

    Short version is that doing what works for you is not simply dismissible as ‘broscience’.
    _dark_master_v2 likes this.
  13. Bryan Haycock

    Bryan Haycock Administrator Staff Member

    Forgive me for not having followed this thread carefully. I did what most people do when they skip to the end of a book just to see what happened. That being said, I wanted to remind folks about in-vitro experiments on loading muscle fibers. You can take a single muscle fiber, attach each end to a moving anchor. Then simply stretch the fiber repeatedly and if amino acids are available, it will growth. So load itself, does in fact cause muscle to hypertrophy. Each fiber has the capacity to growth within itself, independently of the organisms as a whole as long as amino acids are available.

    I know that this discussion is more about real world experience, but I just wanted to through that out for consideration so that load itself would not get thrown out so to speak. :)

    Also, about reversing the example HST structure, please remember that HST is not a workout. I know, I know, we say HST to simplify the discussion and I do it myself. My point is that if a person is curious if a training method/strategy will work or not, they should consider the principles involved, not the organization of the workouts. As a refresher, here are the principles.

    1. The body will adapt in a manner specific to the demands placed upon it.

    2. The hypertrophic potential of any load is dependent on the condition of the tissue at the time the load is applied.

    3. Once the anabolic load-stress stimulus threshold is reached any additional “work” fails to produce significantly greater anabolic effects.

    4. The loading stimulus must be applied with sufficient frequency to create a new and consistent environment.

    5. A given load-stress (or workout) applied in a consistent manner will produce diminishing returns over time.

    6. In order for any load-stress to continue to be effective over time the degree or intensity of the load-stress must be progressively increased.

    7. The resistance to further hypertrophy brought on by consistent loading of the tissue can be partially reversed by temporarily removing the loading stimulus.

    * Load-stress = both mechanical and metabolic load.

    As you can see, most training routines can/will produce gains as long as either (or both) mechanical or metabolic load increases over time. Doing HST backwards just relies on metabolic stress increasing as load stress decreases. Should still work for a while. And it might be a nice break from doing things the usual way.
    Jester, _Simon_ and Jawhari like this.
  14. NWlifter

    NWlifter Active Member

    Cool Bryan, great to see a post from you!

    Can I kinda mix in my thoughts with the facts you presented, maybe form a question/hypothesis?

    OK so for sure ''tension' on a fiber stimulates hypertrophy
    Increased tension increases the stimulation

    I've grown using lower loads but more 'work/density'
    So somehow, time with tension must be a factor? Ie even 8RM for 3 sets is more stimulation than 8RM for 1 set (or is it that 'more fibers' were stimulated with more volume, rather than more stimulation 'per fiber')?
    X tension for Y time = X-2 for Y+2 for example (I'm sure not linear like that but just the idea of that).Kinda why 1x6RM is very similar to 1x10RM. More load less time = less load more time
    Since invitro, fiber tension is 'created' by the activation levels, whole muscle tension doesn't for sure predict 'per fiber' tension.
    Jester likes this.
  15. Bryan Haycock

    Bryan Haycock Administrator Staff Member

    Thanks for sharing that NWlifter. In my in-vitro example, the fiber never contracts. It is completely passive and is just undergoing cycles of stretch by a microscopic mechanism. SO the tension is completely passive, or coming from outside the cell. As the cell membrane is distorted by the stretch, mechanotransduction takes place converting mechanical stimuli into chemical signals and the cell starts building proteins for growth.

    Just a few more thoughts after reading NWlifter's thoughts.

    It's important not to think of muscle fibers in isolation. They are connected both physically (in series and parallel) and chemically by the extracellular matrix and paracrine system respectively. The extracellular matrix is a lattice of protein fibers crisscrossing (like a web) the entirety of the muscle. Each sarcomere is attached to the extracellular matrix so that when one muscle fiber is distorted either actively (contraction) or passively (stretch or compression) that distortion disrupts all other surrounding muscle fibers. How far out the disruption travels depends on the degree of disruption. Because muscle cells are "mechanocytes", meaning they react chemically to physical disruption, when one cell is mechanically disrupted, all its buddies are also disrupted and react chemically.

    All fibers are also connected chemically by the paracrine system. You're most likely familiar with the endocrine system, this is when glands send chemical signals out and into the systemic circulation. The paracrine system is similar but the signals don't travel out into the systemic circulation, but rather out into the extracellular space where they act on adjacent cells. So, lets say one muscle fiber is very active during a set of contractions and this stimulates mechano-growth factor to be produced. This growth factor will travel out of the cell and into the cells surrounding it so that the growth stimulus is spread even to previously inactive fibers or those fibers which did not work as hard, as long as they are in the surrounding area of the active fiber.

    When more growth results from more "work" (density), it is usually because of metabolic stress. We know this because full activation of a muscle occurs before reaching failure during any given set. So, if the muscle is fully activated, then the mechanical load is also fully present. What's left then is metabolic stress which will continue to accumulate set after set, especially if rest is reduced (i.e. increased density of work).

    Granted, there is also a fatigue factor, where some fibers or motor units may become fatigued and thus it stops supporting as much load as it did before. This leads to the load shifting subtly to other motor units in the same muscle. Thus the focus of the mechanical load can increase over time as fewer motor units are able to fully participate in supporting the load. Kind of like when people start getting tired during tug-o-war. The strongest guys end up supporting more and more of the load as weaker pullers give up.
    NWlifter likes this.
  16. NWlifter

    NWlifter Active Member

    Cool, thanks a bunch Bryan, very interesting and informative post. That gives me some new areas to read up on, thanks!

    Here is a follow up question (s)

    1) Are all or most of the fibers in a common motor unit physically touching (I'd think maybe yes, since the nerve is common)?
    What I wonder is, would it be common place for a fiber running at say 30hz to be right next to one that is barely active? Or are the fibers in an MU all bundled together?

    2) I also wonder what 'time' with tension does besides add metabolic fatigue?
    Like if we removed metabolic fatigue, why would a longer 'stretch tension' time increase hypertrophy over a short duration but equal tension bout?

    3) And the above makes me wonder also .... ok if two fibers are next to each other, when one is active but the other isn't, the lateral 'connection' force would be higher than if they both were active and scrunching at the same time? (like the tug o'war example, if two people each had their own rope to pull on, and they were also attached to each other with a bungee cord, if one guy was pulling and the other wasn't, the bungee between them would stretch more than if they both were tugging back at the same time.
    Last edited: Apr 23, 2020

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