Gaining volume with Kyrpa

Also interested in thoughts around strained vs unstrained healing. Evidence supports the idea that during the repair process collagen will orient itself longitudinally in the direction of the strain, if it exists. Otherwise the matrix takes on more of a random mesh structure.

At first blush, longitudinal orientation sounds advantageous, but upon deeper reflection I can’t help but feel that it is actually counterproductive. Oriented fibers are typically much less elastic in the longitudinal direction.

“Fundamentally, I understand and can mostly support the concept of sustained low-load cell proliferation driven growth. This is essentially the process involved in earlobe and lip stretching. The problem with that comes with the introduction of collagen dense tissues. Basically, when structures like the TA are involved, the process starts to resemble something more on the timelines of leg lengthening; brutally slow.”

I agree that the mechanism of action for collagen dense tissues is different. As far as distraction I’m not aware of anything that doesn’t require an osteotomy of some sort and therefore the healing occurs at the wound site for which mechanisms of actions are well studied and known.

But this is a good example of looking for known mechanisms and then speculating on what is going on here. I remember when I first came here and the stuff I read varied from “micro trauma” or “controlled trauma” to stretching leading to cell proliferation.

The reason I included the above reference is that when it comes to contracture as an example there is specific signaling and if you simply introduce the signaling to a tissue without stimulus the contracture occurs. So with that how can WE possibly know what we are doing.

Is it just signaling that we’re causing? What does that lead to? Cell proliferation, or just cell lengthening, enlargement?

I have no idea. And with that I can have no idea regarding the idea of healing in the elongated state. And I don’t mean to be harsh but I have not seen any evidence here to support that there is a benefit. My suspicion on this is that when low loads are used depending on the load that it takes a long time to get to the plastic range and perhaps the percent of fibers that are taken into the plastic range is smaller, but none the less occurs. I suspect in other cases the load is so low that the number of fibers entering into the plastic range is so low that nothing is actually happening. Something that you pointed out above. That’s what I actually think is happening under the auspices of healing in an elongated state. But truly I don’t know.

The big thing for me is to not have limiting beliefs regarding this to stay open.

Partly for the same reasoning about being less elastic I have decided to not follow the “healing on elongate state” principles. So on signing off from IPR protocol ,
where the prolonged use of ADS – equipment is one of the major aspects of the P phase.

Other reason is I think to have covered this aspect enough in my concept already.
If you look at the documentation I have posted, you can find out that after the BPFSL gains start to diminish I stop the cyclic manual stretching completely.
Carrying on few weeks with stretching exercises targeting to repeatedly approximating the elastic limit with lower loads, but not trying to produce more elongation.
I am certainly not the only one achieving permanent results without the prolonged ADS use.

Third reason is that I question the whole IPR concept as it is introduced for PE.
Anecdotal evidence suggest that with the approach I have adopted there should not be any major inflammation.
This is as long as backing off when the BPFSL gains start to diminish and kept away from the yield region altogether.
There should be certain reactions on collagen matrix, but we are way far of the IPR protocols promoted from the scar tissue healing,that the concept fit poorly in to this environment precisely IMO.

That been said there is no proof of anything. This is why I prefer not to make any theories and also very hesitant to even discuss about the theories presented.
Everything is just a theoretical chat until the day first studies on the bunch of cadavers, or volunteers giving biopsy specimens with a history of PE arrive to the scene.
As you mentioned that the procedures following your seven step example are debatable, this is my initial take on this particular debate.

I will the first to give thoughts on the types of growth of these types soon after the previously mentioned studies are available.
There have been debates on these string after string, and I am afraid if we have anything to add.

As long as we keep concentrating on applications which have proven to produce penile growth, I am in and committed.
And when it comes to improving these applications and forming concepts based on these refined tools, I am even more happy to join in conversation.
When it comes to debating how the growth occurs, for me personally it would be pointless case of better guessing without medical examinations available.

Newbie gains can be categorized as a systemic elastic expansion which is reversible in quite large capacity.
There are guys who have spend 6 months on newbie program or extending, and they lose all the gains quickly once they stop.
No matter how much they have gained. Or should we dare to claim not gained.

Not before the TA or ligaments have been exposed under some degree of plastic deformation there are no permanent gains.

I prefer to concentrate majority of the heating on septum and dorsal thickening which are forming the t -shaped “back bone” and most dense, rigid and thickest collagen structure of the penis.
Lengthening these structures the whole penis is triggered to adapt as the TA lengthens within, and the smoothmuscle and the collagenous sinusoidal space volume of the CC is forced to follow behind.
This is observed to be supposedly happening here when these penises get bigger.

This also means permanent gains. Again how the growth occurs any of us still have no clue at all, even the theories are plenty.

Concentrating on TA stretching you still have plenty of stimulus on the structures of the base ligaments as well. Even being in the extender setup.
Weakening the supporting ligament system assumption might be just opposite in practice. As have plenty of hangers find out with their base girth enlargement.

Being it then from the Ischiocavernosus muscle thickening as the longitudinal TA layer in fact is a collagenous continuation of these striated skeletal muscles,
which are intruding also inside and between the penile chambers not just in tunica alone.

This is strictly anecdotal finding and not documented, but I suspect based on palpation that the thickness of the
dorsal thickening at the base of my unit has increased further during my gains with PE.

How can you be sure that with the few minutes under 0,5 kg you can repeatedly produce the same results day after day. There are too many aspects to take in to consideration. Temperature, nutrition , having or not having sex, recovery from previous exercise etc.
Toe region is not eliminated without equipment you have described earlier. I think that it would be only eliminated testing in laboratory environment with the precise tools to plot the complete curve out.
Therefor I prefer to refer to the total strain percentage. Pre exercise BPFSL and Post exercise BPFSL are both measured in similar fashion same day in same circumstances.

I have tested how much the penis elongates with different stretching methods, loads and timings per event. Then decided not to go above 4 % strain as we now know what starts to happen there after.
Exercises and heating cycles I have chosen happens to produce average of 2.5% strains which have repeatedly produced permanent gains. Not trying to produce any particular percentage or millimetrical lengthening , rather keeping this maximal strain percentage of 4% in mind then repeating these events with the program we have chosen for weeks.

When the strain percentages these exercise are producing starts to diminish we are not going to increase load , heat cycles or stretching time.
Instead we simply turn the focus on producing this new maximal length for some weeks. Maintaining this anabolic environment with exercises which are supposed to lead in increased production of growth factors and sustaining the collagen remodeling already started etc.

Well , here you have it in nutshell what I have been trying to produce here.

I agree with the studies showing better and especially faster achieved strain with the cyclic stretch. But I am not sure if we need to do more than one heat cycle per exercise because that seems to be productive enough.
If the total strain percentages have tendency to stay low , then it would be better idea than increasing other variables.

Proportionality limit is then the threshold limit which I have been reaching. My documenting shows that I can produce repeatedly new lengthening for several cycles before the gains start to diminish. Mankos´s experiences indicate same kind of trends.

“There are guys who have spend 6 months on newbie program or extending, and they lose all the gains quickly once they stop.
No matter how much they have gained. Or should we dare to claim not gained.”

Only thing that I would add here is that we have known since the 70s that histologically elastic fibers are not fully remodeled after a year. Whether those gains or even some of those gains were in the plastic region, it does not surprise me that those gains were lost. Moreover that in itself, given those gains were entirely lost, as intimated by Kyrpa does suggest that those “ligament” gains were elastic in nature. Collagen having largely turned over in 240 days, should have seen some gains retained. FWIW

Kyrpa, I think your approach is the most fundamentally correct that I have seen, which is what enticed me to participate here. Your points are very valid. Theoretically, you are probably correct in that the elongation value of the heated stretch occurs at a single point in the protocol. That is, I don’t think that heating with every cycle will result in a notable strain increase. You are likely to reach the same 2.5% stretch. In my protocol it would be the final strain that is heated. However, I was basing my requirement for heat at every cycle on numerous studies showing heated tendons experience significantly less microtrauma under load. Albeit, this doesn’t necessarily mean a US targeted 42C would be required. A generalized 39-40C via FIR or rice sock would accomplish the objective, and would certainly be more convenient.

The US just happens to be very effective in targeting the heat and giving more possibilities on stretching with a lighter loads.
There are guys which have used IR, and based on their logs I find that it is not efficient enough method for all of the users.

I hate to form any opinion based on beliefs but I am convinced that taking the temperature beyond +40C has tremendous effect on stretching efforts.
For this opinion I find lot of backing on published research with collagenous tissues.

IR reach the TA for sure, but there is enough anecdotal evidence that the TA is not the most restricting structure when it comes in severe difficulties to gain.

This is why I fundamentally believe that newbie gains are primarily just what someone would typically call a lig and muscle stretch. In the absence of strain, connective tissues tend toward a shortened state. For example, chronic bad posture doesn’t just create tight musculature, but actually results in shortened connective tissues. There is no reason to assume that the penis is any different. During the newbie period, muscles loosen, cells elongate, and some secondary bonds are broken. But little in the newbie stage has been taken past it’s natural state. It would be expected to revert to the contracted state once the chronic strain is removed. Just like a desk jockey who starts yoga. Going from poor mobility to above average is relatively easy and rapid. They aren’t asking the body to do anything unnatural. But if they stop for any extended period, the body begins to tighten.

Others may disagree with me, but I don’t think newbie gains have much to do with the elastic limit debate. Just shifting from the lower end to the upper end of normal tissue laxity.

Sorry, I absolutely agree that above 40C is a huge benefit and US is the only accessible method to get there. I was trying to say that in a cyclical train protocol, US would only be absolutely required on the last big stretch. Using heat on the preceding cycles I think is still marginally beneficial, but doesn’t need to reach 42C and could therefore be done via FIR if it’s easier.

Agreed.

And agree with the post earlier. If the gains are reversible, then there have simply been operated under the natural limits of the users penis structure.

Apologies also if I made it sound harsh on theoretical debates on these matters at hand being not so productive.
Of course there is some scientific backing even on my personal approach on this, as you have confirmed.
I haven´t yet to find it necessary to collect all the references under one umbrella ,as I have no intentions to sell or prove anything.

But when it comes to “cracking the code” as Buckfever mentioned, we simply have time or other resources enough.
There are lots of debates from decade ago where some of the participants actually were on it. Each and every one have gone silent since.

“But when it comes to “cracking the code” as Buckfever mentioned, we simply DON´T have time or other resources enough”

“However, I was basing my requirement for heat at every cycle on numerous studies showing heated tendons experience significantly less microtrauma under load.”

Are we assuming that the microtrauma is to be minimized? What if that is the very mechanism of action that we seek to induce?

Kyrpa have you ever run your protocol without heat?

I don’t disagree with most of that and I think it explains why I, being older, experienced outsized gains initially, because I was operating within the range of the “natural” state. As to whether any of those gains are durable, is where I’m less certain and I would conjecture that given a year or more of maintenance there would be cell turnover that would sustain. There is anecdotal evidence of that here.

The thing of this “natural state” is interesting to me. Because we know that developmentally there is a genetic component but also a signaling component, which occurs really early I think around 6 months. I wonder if each individual has a genetic potential size distribution. And I wonder if there is a genetic hard limit beyond the “natural state”. That’s one of the things that I find interesting about Kyrpa’s documentation, is whether at some point headwinds are encountered on a macro scale and diminishing marginal returns are realized.

Could you elaborate on what you mean by a ‘signaling component’? I’m kind of new at this more theoretical side of PE that you guys represent.

First I want to apologize in that I kind of have already derailed Kyrpa’s thread and I can’t find the exact research, but basically there is a developmental component to penis size, related to the anogenital distance, which is embryonically influenced by various “signaling” during development.