Gaining volume with Kyrpa

@timeit

(1) this is where we have debated a bit previously in this thread. The question is what the best baseline measurement is. But frankly, with this newer research, it doesn’t really matter because we are no longer questioning the existence of an elastic limit. So whether you start at flaccid length or closer to BPFSL, shouldn’t really matter other than time under heat. If you plot a load-strain curve starting at the flaccid length, you would just see a much longer toe before getting to the heel of the curve. What we are really discussing here is strain beyond the heel. What I do is gently warm the penis with radiant or conductive heat (IR and rice pack) just to get things going. The minor stimulation from getting the device situated ensures that I’m at maximum flaccid by the time I’m ready to go. The most convenient starting point is just a bit less than BPFSL, which if the penis is slightly warm can be accomplished with about 1Kg load. I’ve got two ways to apply load in my extender. The precision adjust is an ultra fine thread micrometer on a translation stage that strains about 0.5mm per revolution. But the travel on that is only about 27mm so I only use that once I’ve gotten to a good starting point. Prior to that there is a more course turnbuckle which I turn slowly under ambient heat until I reach 1Kg load. This takes about 5 minutes to reach the starting point, just be careful to realize at this stage we are not trying to stretch anything yet. I haven’t seen any evidence yet that we need to be too careful about the rate at which we approach the normal physiological limit, except that we might assume that flirting with the limit at too great strain rate is undesirable. We just wanna sneak up on it slowly so as not to trigger an inadvertent modulus increase. In any case, the baseline from which we measure strain is a bit ambiguous.

(2) ideally the strain would not require body movement at all. There is no reasonable way to shift your body 1mm/minute. So with the sand clock type setup, you’d just hold still and allow the sand to gently increase the load. The drawback to this is that it implements a creep protocol rather than stress relaxation. IMO, SR has modest benefits in terms of cyclic strain, but I think creep can also achieve good results if rate is controlled. Also, one big difference with the pully setup is that it doesn’t anchor off the pubic bone, so the ligs are experiencing a fair amount of strain as well depending on the angle of pull. This would probably be viewed favorably here because of an increase in total penis length, but I’m not after lig gains which just confuse the issue. I’m after the science of whether the actual shaft can lengthen.

(3) look at post #943 on this thread. I’ve since added a turnbuckle and electric motor with foot switch. The benefit to this device is that it anchors off the pubic bone so I can get incredibly accurate strain readings at any time during the treatment. There is no need for tugging on the penis after the treatment is done to figure out what the new BPFSL is. Also my device rectifies things like turkey neck and hair growing up the shaft due to excessive lig stretch. Because my extender stretches the shaft skin simultaneously.

To be clear, my methods might be somewhat frustrating here because some of the desired measurements won’t be provided that would otherwise align this research with previous on this thread. For example, I won’t be using the same conditioning process prior to the strain session. So the total % strain will not be comparable. I won’t be tugging on the penis before the session to try to get a BPFSL reading. I won’t ever be pulling hard on the penis outside of the treatment protocol because I suspect that any strain produced at a high strain rate and especially without 41C heat results in a counterproductive biological response. Some guys on here are jamming the ruler into the bone so hard it’s about to bruise the tissue, and then pulling so hard their face is turning blue. IOW, their measurement technique is actually a micro strain treatment. I won’t be subjecting the penis to any strain outside of normal erection unless it is part of the precisely controlled protocol.

As I’ve said before, my interest here is not getting a bigger penis. I want to figure out the science of what is happening and demonstrate that there is an optimal and reliable way for this to work for everyone without all the confusing and frustrating plateaus and ambiguous decon requirements. I’ll relate it to bodybuilding science. For years the bro science insisted that reps to failure were best. Numerous recent studies have shown that while reps to failure produce the greatest hypertrophy response from a chemical standpoint, it is actually counterproductive in the aggregate over a period of several weeks or months. It turns out, getting to within 1-3 reps of failure with each set produces the greatest hypertrophy. This seems to be because going to failure destroys too much tissue which consumes too much material resource to rebuild alongside the desired hypertrophy. Also, the resulting fatigue results in disproportionately long rest cycles and/or lower quality future workouts. Also, many used to preach explosive lifting techniques for fast twitch hypertrophy. More recent research has really dialed in the optimal lifting tempo, which as it turns out, is not just “as fast as you can throw the weight up”. This is analogous to PE. It’s not just about punishing the penis until the tissues give up and have to rebuild themselves. That might produce the greatest gains in a handful of sessions, but the body will certainly protect itself at the expense of future progress.

All of my focus is on stationary hands free heating. In the RF realm, Cutera Tursculpt is capable at a cost of around $20k and $50/treatment. In the US realm, the Therasound with the Autosound applicator is capable, which is four transducers lined up in a single head pulsing sequentially at 1 second each. This costs a bit over $2k.

With these devices I just strap the applicator on a turn up the power.

Ingenious work, Tutt.

The slow stretch makes perfect sense.

If someone who is more versed in engineering helped me to create the sand clock technique, I would be intrigued.

Or even better, I would gladly buy a device like Tutt’s with the micro motor but I am afraid it is a few years too early haha.

My current very basic method works well, but the seed in my mind has been planted.

Mainly I was fascinated by the strain attribution. Until now we’ve been approaching this with the simplistic view of tissue level strain. It was very valuable to have someone use techniques in xray microscopy to determine what effects are experienced at the molecular level. This is the first study to have the technology required to validate and explain what I was seeing with my micro-adjust extender. This is a giant step forward because none of us was going to have the resources to make this discovery. It is difficult for me to overstate how critically important strain rate is. 41C heat + 0.5%/min strain is probably >85% of the puzzle. Everything else is just incremental steps to figure out the most optimal rest periods.

IMO, without keeping the strain rate below at least 1%/min, the plateau is inevitable. It doesn’t matter what concoction of rest and decon we come up with. It’s possible that at 0.5%/min with proper heat, there doesn’t have to be a plateau.

Tutt my friend, this is a very bold statement. Hypothesis which leaves lot of outside.
There is more in the limitations of growth than this alone.

By all these heat and strain rate talking do you mean state where “regular” methods where 100 % stretch/load is put in straight from the start, ie. Hanging, do not produce gains anymore?

Something like that happened to me and many others. After gaining first inch quite fast with high force methods and random heat usage, it was impossible to gain any more length. I hope decon break really does decon some of tissue toughening. Just coming off 3 year brake.

I will repeat this. I stated this years ago at MOS, while I was actively researching and looking for answers to my dead end. My gains had stopped many years before. There was no way to grow length. Tried everything including chemicals that only produced girth but no length. All I knew after self examination and retrospection of my own history, is that I had reached a dead end due to the septum.

And this is what I stated years ago: We all have seen by now those chinese guys who lift heavy objects attached to their penises. We have seen them hanging massive stones, pulling cars, even pulling and airplane with their dicks. If our approach of hanging using every day heavier and heavier loads, and equalizing the achievement of a heavier load to some sort of progress that will bring gains in return, IS WRONG. Because if that was the case, all these chinese guys would have dicks of 1 meter long. True, we have not seen them naked, but I can guarantee you that if that was the case, it would be a very known fact. They would, or at the very least one of them, proudly display the side effects of his ancient ritual. Not the case. So far, not a single one has come up forward with a massive record guiness dick. Why? Because the dick doesnt work that way.

And it was under that principle that I walked away from all those “techniques” the vets were promoting, some even selling “coaching” to grow anything guaranteed. Until I came across with this new novel science led by Kyrpa and others. And the rest is history.

Hypothesis, sure. But it is supported by the literature. When fast strain rates are used, a ligament begins a physiological response starting modestly at 2-4 weeks and then accelerating rapidly at 5-8 weeks. Basically, it is well demonstrated now that your ligament will not respond to a single excessive strain to protect itself. In fact it takes a couple weeks of repeated stress to initiate the beginnings of a response. At the tissue level, this response manifests as a rapid modulus increase (as much as 50-60%). So there is an observed stiffening at the tissue level. This corresponds well with each of your cycles as well and leads to a decon period at a relatively predictable point in time. The question was, what is causing the modulus increase? Could’ve been many factors; fibril orientation, primary bond formation, neocollagenesis creating more fibrils and/or thicker tissue, etc. One study in particular found that once the ligament is allowed to rest, the modulus begins to drop and actually returns about 85% of the way toward baseline within 4-6 weeks.

I was encouraged by that until I compared the MRI and echointensity. There was a drop in MRI resonance a month after detraining and returning to baseline within 3 months, corresponding directly to the modulus decrease. This strongly suggests that the short term stiffness we are experiencing is coming primarily from fibril orientation limits. Unfortunately, echointensity remained elevated beyond 3 months. This is bad news for PE. It means fibril orientation returns to normal fairly rapidly during decon (3 months should be sufficient to get noticeable results within a new cycle) but increased tissue density and fibrosis remain well beyond 3 months. An extrapolation of the decay rate would suggest a return to baseline after more than 6 months. To quantify, at 6-8 weeks of repeated stress, there is a 25% increase in MRI signal intensity which returns 85% to baseline in 2-3 months. There is only a 9% increase in echointensity at 6-8 weeks, but it decays very slowly over several months (likely with the half life of collagen apoptosis). This is because the MRI is responding to simple fibril orientation while echointensity is responding to new collagen and more dense tissue that will only decrease with programmed cell death.

So let’s say you were doing a 3 on - 4 off protocol until gains taper off (according to this expected at about 5-7 weeks depending on intensity) and then you decon for 3 months and start a new cycle. This will work for a few cycles because the 3 month decon is time enough to allow the fibrils to mostly reorient and modulus to drop near baseline. However, with each cycle the echointensity would build cumulatively by 6-7%, suggesting the your body is adding more fibrils to the mix. Interestingly, MRI shows that the tissue doesn’t get thicker for a long time, first it just gets much more dense. So after a year of this, your tissue is now measuring 20-25% more dense and you start noticing a dramatic slowing of gains with each new cycle and a requirement for higher loads.

That response will happen even within the normal physiological ROM if resistance is applied. But in our case we go beyond normal ROM and that is where the newer research comes in. If the strain rate is fast, the strain mechanism is an effective decoupling of fibrils as they slide past each other. This is shown to be associated with higher levels of fibril damage and tissue fibrosis. The body is recognizing this as a strain and responds by densifying the tissue over repeat occurrences. But if the rate is incredibly slow, the fibrils do not decouple and remain virtually undamaged so no fibrosis response. Instead the molecules elongate, gaps widen, and fibrils stretch.

I’m asserting that the slow rate not only allows for greater strain at lower loads, which is pretty much established fact at this point as it is supported by every piece of literature I’m familiar with , but also mitigates the accumulation of residual tissue density over time, thus avoiding the necessity for frequent prolonged decon periods.

IMO, “regular methods” here are highly counterproductive. They will easily produce quick apparent gains mostly from basic ligament stretching. This isn’t really gains as your penis didn’t get bigger. It is simply increased range of motion, just like stretching your hamstrings to touch your toes. Sure, with enough work there will be some elongation of the TA in the shaft as well, but ultimately the body will protect the integrity of the structure by creating a thicker and more dense collagen structure, making it exponentially harder to keep gaining. For most people, if you want to ensure you won’t be able to gain more than an inch or so, follow the typical hanging routines and other such outdated techniques.

I’m not aware of any literature that suggests a permanent thickening of a non-structural ligament. 3 years should be plenty to reach baseline again.

Sorry for the short answer, I will get to it properly later.

The tissue density remaining high.
It is what comes from residual cellular stress.

And it is a direct cause of the ECM growth itself. It is the primal reason hypothesized to be the natural limitation of tissue growth.
Being the growth from natural causes or self induced.
There is very little to do for lowering it than time. Totally leaving the PE for months or years after significant gains.

Elongating the structure at ECM level will cause accumulation of residual stress. It will most likely stop further growth being the methods as gentle as you describe or not.

People wiser than us don’t really understand it properly. Neither do we.

Therefor the statement of non existent plateaus does not sink well with me. IMO They are inevitable in any case.

Great to hear veteran like you that has put tremendous effort in and still could not gain, can actually gain again with decon and different methods. Gives hope to me. I was never hanging very heavy, 6-7 kg range, but I used to do manual stretches with quite high force. Actually almost as hard as I could pull. My theory was that I would make deformation with high force and then used ADS +12h a day to heal in extended state. Zero gains in 6 months. Then I stopped.

I thought I said mitigates plateaus, not eliminates plateaus. The question that has to be answered is which direction is the literature pointing? Towards heavy loads or modest loads? I think we agree the latter. Towards fast strain or slow strain? I’m suggesting that all the relevant literature supports slower strain.

Then it is just a question of what slow means. A reasonable starting point is where the literature shows only marginal benefit from any further decrease in rate. That is somewhere around 0.5-1.0%/min. I believe this is the second most important factor, next to 41C heat.

Third most important is probably max load. I don’t have a strong indication of where this is yet, but I suspect based on mine and everyone else’s trials here, it is somewhere around 2.0-3.0kg.

I think we actually have the same belief here Kyrpa, which is why you settled on stress relaxation. It is the mechanism whereby one might strain too quickly at first, but then allow the undesirable stress to relax. What I’m suggesting is that it’s much more optimal to strain at a slow enough rate in the first place, rather than a sequence of… too fast, pause, too fast, pause…

Yes. We agree completely on every aspect concerning the tissue stressing methods.

Stress relaxation allows greater initial stress used, as you say it starts to subside in huge portion soon after loaded.

I also have 100% consensus with you about the timeline tissue starting to get stronger as response to the repeated exercise bouts.

What I have thought and more so after you talking about this strain rate relations, is that the permanent elongation needs fibril sliding level change.

After all it is a crucial thing on natural growth bursts on teenagers.
It has been demonstrated happening due decorin biglycan bond release and re-organisation.

Same thing happening with the therapeutic heat to some extend.
In fact there is a study indicating total decorin denaturation at 45C, allowing fibril sliding at great extend. Once the temperature drops the re-organization starts and it quickly is normalized at resting temperature.
This will been seen as instant permanent elongation.