Is Load Progression Necessary For Hypertrophy?

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

  1. NWlifter

    NWlifter Active Member

    https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1954.sp005161

    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
    etc.
     
  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

    [​IMG]


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

    [​IMG]
     
    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.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5786199/

    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...

    https://www.nrcresearchpress.com/doi/full/10.1139/h2012-022

    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,

    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0020993
    ER stress induces anabolic resistance in muscle cells through a PKB/PRAS40-induced blockade of mTORC1.

    https://www.researchgate.net/public...ein_sub-fractional_synthetic_responses_in_men

    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.

    ftp://www.pcultrasound.com/Public/Articles/article_50.pdf
    The repeated bout effect can occur without mechanical and neuromuscular changes after a bout of eccentric exercise
     

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