Gaining volume with Kyrpa

Great, thanks for the info. Yes I’m thinking of trying without the inner diaphragm as my glans fills the chamber pretty much. Actually I have the green hose connection that came with the PMP so I could try that first, just not sure I can suck out enough vacuum by mouth - will experiment. Otherwise I will see if I can adapt using LeLuv and heat shrink tube, I should still have some of that from before.

Cheers

I am pretty sure you can get better vscuum with suction than with the pmp pump.

Yes for sure compared to the green bulb, I was more thinking of trying out that green tube connection that is the alternative to the bulb, where you suck out the air by mouth. Didn’t use it before but might try….

Kyrpa if you have time could you have a look at my post here =

Any advice would be much appreciated.

pudd1ng - Knowing whether you are limited by Dorsal Thickening/Septum

Kyrpa, your level of record keeping will definitely be an asset in sorting out the best protocol for PE I think.

With the amount of observations and measurements you have collected, do you have a view on the following?

1. Is penis growth due to PE driven by enlarging the fascia and inner structures of the penis, the proliferation of smooth muscle cells, changes to the rate of blood flow into the organ, something else, or a combination of the above?

1a. If fascia and inner structure (connective tissue) lengthening is driving the growth I think you would see the growth of the penis occur faster for length than girth, assuming the outer length fascia is longer than the circumference of the inner girth fascia. But my experience and I think most PE’ers experience has been the opposite. I have considered the possibility that people doing PE could be using too much force trying to lengthen the penis, causing length gains to be reduced while girth gains are unhindered.

1b. I have tested things which cause the proliferation of smooth muscle cells and the budding of new capillaries, and yet have seen no increase in penis growth I can attribute to it. I have reason to believe this route has worked for some, but I have no experimental evidence of it, possibly due to some missing factor or concomitant angiogenesis agents. I’ve mostly abandoned investigating this, but can restart if there is more evidence indicating SMC proliferation is the driver of PE.

1c. Changes to blood flow into the penis, namely an increase of it, doesn’t seem to have increased the rate of gains either based on my own tests, but I haven’t tested implanting a stent for obvious reasons and I have not tested increasing the blood flow to the level of high flow priapism.

2. Have you graphed total penis volume against the rate of gains? Have you graphed the length against the rate of length gains? Have you graphed the girth circumference against the rate of girth gains? Which of these graphs shows the strongest relationship between the two variables? Do you think that showing volume growth rate correlating with penis volume (or length to length growth rate, girth to girth growth rate) would be a good indicator of what is driving PE?

2a. I am on my second PE journey, I stopped for about a decade and experienced shrinkage. What stood out to me recently when using an online calculator for penis volume is that while my penis changed significantly in length and girth dimensions, the volume was nearly identical before PE and after a decade of shrinkage. That makes me think there is something that determines the volume of the penis independent of the fascia and that elongating the fascia may not have anything to do with increasing the volume of the penis. There were more relationships I noticed that indicate to me that PE is driven by something that determines the total volume instead of the length of the fascia that I wrote about here: Sigmoid - Can girth be converted to length by pumping with a thinner tube?

1.Mechanotransduction. The cellular structure reacts and responds to mechanical stress by growth response.

This is something which has been studied a lot in recent years, and in fact recently Buckfever posted a study where they did not mention a word of stretching ligaments or elongating collagen fibers when they evaluated the review on extender studies. They talk about growth.

Growth response induced by mechanical stress on extracellular matrix and the cells themselves, inducing collagen proliferation. More collagen type I is produced and the ECM itself adapting for the stresses caused. Several enzymes indicating anabolic environment and growth factors secreted by the ECM and SMC´s.
The sign the the collagen type I is up means no inflammation response is present. There is no injury, no markers of inflammation, there is no scar tissue forming. Straight on the proliferation phase.

For me it has been clear that increasing the BPFSL is the catalyst for the growth despite the fact we cannot see the biochemical markers.
What I can see is that the highly productive efforts for elongating the structure has triggered the growth response seen as a volumetric growth. If we can increase the BPFSL the BPEL follows little bit behind.

2.BPEL therefor is purely volumetric growth to fill the already expanded structure. If the volumetric growth is from the SMC hypertrophy or hyperplasia we don´t know. Or if it´s just SMC elasticity with expanding sinusoids, we don´t know either. There are no one having biopsies of their units to prove anything.
I don´t see any difference on which way the penis grows, it grows volumetrically in the direction there is room to expand. How it is achieved Is a different thing. Molding the structure larger we trigger the growth response not the other way around.

I have kept volumetric graphs and I can see that the volumetric enlargement rate has been steady for a year now. The expansion during the first half year was huge and after that I have been keeping the same volume increase rate no matter if the gains have been on length or girth.

At the moment I need to say that gains are plateauing but it is another story and I come to it later on.
And I am going to spare a word or two on ECM homeostasis and adaptation when talking about plateau.

BPEL 22.0m ->22.4 +0.4cm
BPFSL 23.6 cm->23.9 +0.3 cm
MSEG* 15.2 +0.0 cm
*Documented mseg is average from base (16.4), midshaft (15.0) and behind the glans girth (14.2) for more accurate volume calculation

I have gained slightly past the previous best with BPEL and equaled the BPFSL best.
Second goal with volume is now achieved with +10 cubic inches gain in 18 months.

Looks like the plateau with BPFSL is near coming as the there is significant drop on the gain rate.
The slope is nowhere near the margins of previous Periods.
P1 to P3 I had the BPFSL gain rate going significantly ahead of the BPEL gain rate.
Now the rate is similar to BPEL the slopes going parallel on the graph.
I believe that I can´t get much further with the BPFSL as the plateau will be inevitable.

What is the reason for the top reached deserves another post on fundamentals of growth and basics of the decon break use. But basically it is diminishing returns signaling.

I have come to this point not using traditional progressive workload concept.
Working hours count, used loads, exercise duration or the amount of sets have not been increased nor cumulative.
This is the classic case of adaptation to present input. It is intentional as I like use this journey as a study.

The BPFSL and BPEL difference is 1,5 cm so I am still enthusiastic on getting erectile size gains as the workouts still producing gains and strain percentages being in the gains bracket.
Therefor I keep hammering until the usual 60 to 70 days as previous periods.

2 days on 2 days off

Phase 1 CONDITIONING STRETCH
Measuring t_0 BPFSL
Stress Relaxation stretch for 40 minutes with rice sock heating. Load 2.5 kg. Using elastic band and hook scale.
Stress relaxation is produced by putting the tension and then letting the vacuum cup rest in the edge of the sofa not pulling any further. Every 5 minute reloading the band.

Phase 2 HEATED STRETCH
Stretched OTL with the elastic band for 12,5 minutes each side. Load 3.8 kg. Heating with two 1.6w /cm^2 1MHz transducers. The shaft laying firmly
against the skin of my thigh the heat is felt very easily and by the dual approach the heat is distributed nicely all around the shaft after 5 to 8 minutes.
Stress Relaxation happening the band have to be re-loaded once per side.

Phase 3 MANUAL STRETCHING
Interval timer for 16 stretches 30 second work and 15 second rest.
Stretching all imaginable direction mirroring each side. Manual fulcrums and bundled stretches included in.
The load averaging 6kg ( test run for calibrating the feel)
Measuring t_3 BPFSL

Strain percentage have been evolving from 3.2 % to 3.6 %

Awesome work Kyrpa! Especially the scientific approach you take to your PE. Keep it up.

This experience seems really common among those who gain size, the so called newbie gains. Would you happen to have a hypothesis on the physiological reasons why this occurs? Could we draw an analogy to someone starting their bodybuilding career and gaining lots of mass during their first year?

I do not believe that Kyrpa’s gains earlier in the year were classic newbie gains. My strong belief is that what is typically referred to here as newbie gains are in fact just a loosening of the pelvic floor structure (ligs) with perhaps a marginal amount of uncrimping of the ECM within the penile shaft.

Kyrpa’s gains seem to be primarily comprised of viscous reorganization of the ECM into a semi permanently uncrimped structure, followed by a certain degree of neocollagenesis as much as is possible in a 60-90 day window.

He appears now to be reaching the point where the gain rate will just continue to diminish until he commits to an extended decon rest period. We’ve discussed offline, and I believe the required rest period to be 200-220 days. This being the point where at least 80% of collagen will have turned over, albeit it would still take many more months for the new collagen to organize into type1. But there has been some intriguing discussion around how to speed that up.

If I should examine my personal newbie gains I would say that the first 3 months were purely considered as such, 1 cm gain on BPEL and 0,7 cm on MSEG resulting 12% volumetric expansion.
And if should have stopped there I would have lost all of it. Purely elastic reversible gains.
Anything after has come from or are merged inside the process Tutt described without detailing it further.

With an extensive experience from the bodybuilding world I can see lots of analogues from different level results. Gains coming basically from the same basis of addressing the tissue ECM with mechanical stress, we have the loose relationship. But the muscular tissue being very different to ligamentous structure having tendinous mechanical features we try to expand full analogy can´t be drawn.

The similarity is seen best with high gainers the majority have their biggest gains in first 2-4 years and they settle down to more mortal category in both PE and BB. Genetically favored extreme elite continue to gain at higher rate for decade or so. If we look at the professional level bodybuilding there seems to be trend that the world top 20 or so have gained enormous amount of basic muscle mass in their early years and spend the rest of their careers on maturing the muscle, getting more grainy and detailed look on their physiques.

What comes to a common gym-rats and average gaining PE practitioners the analogues are unreliable
because of uncontrolled variables both group have plenty of.

I agree with Tutt on the fundamentals of the gains achieved.
I will be needing the extended Decon soon. How long is under the debate as the basic cause of the long term plateau have not ever been really sorted out.

We have discussed it lately and there is not full consensus yet as there is unknowns in the process.
The time of 200-220 days is real with the remodeling process when the classical injury recuperation process is considered.
That is the time needed for the ECM reorganize and remodel the collagenous structure at 80 % maturity level. The rest 20 % to mature takes years as the progress follows logarithmic scale.

But as I mentioned few posts ago, there have been no injury and so on the collagen type III expression induced by inflammation response has been really minimal.
Using ultrasound thermal and non-thermal effects the elongation has been produced with a smallest possible structural damage. The proliferation has been produced with the Collagen type I with a high percentage from the start.
Therefor I hypothesize that with the method in use we are getting a headway on the process already.
How far we are is if not impossible but at least difficult to say. The collagenous structure with this amount of ultrasound therapy and the basic nature of the elongation happened, is remodeled already at high degree.

There is more to hypothesise on the plateau process than the remodeling and maturation of the collagenous structure.
The extracellular matrix (ECM) adaptation process itself could be the main source of the diminishing gains and in some or most of the high gainers stopping to gain completely.

I have been studying a lot on mechanotransduction, the ECM adaptation and recovery lately.
And what seems to be getting more clear the more I dive into is that the scheduled decons right from the start of the PE career are needed.
And the decons have to be longer than one month between the growth campaigns. The bigger the gain rate the longer the decons.

I will continue later but for now, there is couple of links which I would like to suggest everyone interested to read with a thought and investigate further.

The basic knowledge where to start with
Mechanotransduction and extracellular matrix homeostasis - PMC

From this on I would pinpoint the residual stress on the cellular level which is proportional to strain (and cumulative to elongation), and the rate it will decrease is logarithmic, meaning never to completely recover back to starting level once we start to gain size quickly.
https://www.res earchgate.net/p … _cell_migration

What do you think about the collagen to elastin ratio of the penis?

Elastin is not easily produced past a certain age. The penis seems to lose the elastic properties necessary for a firm erection when the penis collagen to elastin ratio increases.

Have you ever tested mechanotransduction without elongation by stretching or pumping? Or is stretching the fascia absolutely necessary to ensure the penis is remodeled larger?

I’ve started testing dynamic pumping, which should offer more mechanistic stimulation to the penis than static pumping, but so far I haven’t seen any indication it’s more effective than static pumping, rather it seems like it will be counter productive. Though, it’s too soon to have a firm opinion on it I think. It might also be a matter of finding the right parameters that avoid an injury response to make dynamic pumping more effective.

Whether elongating the fascia or growing via SMC proliferation, the rate of growth should not be static over time. Though remodeling of the pudendal artery to grow larger might be.

I’m just not satisfied without experimental proof of the mechanism underlying PE. It seems like we’re missing something fundamental to explain the patterns of growth. Having growth rate be predictable by volume, but not individual dimensions, rules out the role of the fascia completely in my mind. If SMC and angiogenesis were the drivers, surely my tests would have produced more growth, though maybe pumping was driving the maximum amount of capillary growth already so the substances I used couldn’t contribute anything more to the process.

If we knew the mechanism definitely through experimentation, we could refine it and create or re-purpose drugs that do it more effectively. Growing a few cm3 of new tissue a year for such a big capillary bed can’t possibly be as fast as the process can go. And if we knew definitely that SMC and capillary budding were the drivers, tissue or ECM transplants aren’t out of the question.

I have to say what you are asking is challenging. To be honest I am not an expert in every field, though it seems to be the case with the authors with medical degree as well. They seem to guess on this matter as much as we do despite the fact they have all the knowledge available we lack.

Well, like you said there is not much we can do about the elastin concentration on tissues and when we grow the collagen - elastin ratio will be affected with more collagen on the tissues. If it has any significance on gains, I don´t want to speculate. In tunica the elastin in general has been considered as a recoil for erected tunica when deflating the penis. The elastin compound crimps the collagenous tunica fibers into undulating shrunken shape while flaccid.

Another importance is the attachment of tunica layers which is elastin-based connection and of course the glans having elastin content greater than other parts.
What comes into elongation and strain during exercises we don´t need to worry about the elastin, as it is the collagenous bonding carrying the load.
The effects on erection seems to be more related on elastin content inside cavernous tissues. There the elastin may be crucial regulator with the smooth muscle content, and the active operator with the smooth muscle relaxation capabilities.

When I started to use the US heat I was first worried about the elastin because of the nonrenewable nature , but once I found out that the elastin can stand much higher temperatures than collagen I relaxed. Also the elastin has high cross-linking rate having 15 to 20 cross-linking per unit versus collagen which has 1-2.

The whole concept of PE has been driven by the attempts on forging the structure larger.
It is obvious if we look in to almost every possible PE format. We are mechanically stretching the structure with every exercise proven to produce gains to up to this date. The growth response we get from the ECM is highly proportional on strain we cause on the tissues, and via the strain the stress on the cellular level.
Being it the collagenous tissue or the smooth-muscle cells, we can find tons of studies showing both having highly promoted expression of almost every possible anabolic markers and growth factors during and after the mechanical stress addressed on them. There is not much left for believing, it is all about what we already know.
I can see that you are trying to grow the cavernous mass and volume and via the expansion somehow force the tunica bigger. I have to say that I highly doubt that going to happen in the large scale. Anything like we can see already happened with high-gainers with more traditional methods.
But don´t abandon the methods if you find anything giving even some positive feedback.
You can use it with better rate after you have stretched and grown the tunica for which ever direction.

I have had my unit growing at the rate of 4 to 5 cubic inches a year , before that 5 to 6 in six months. I am expecting it to decelerate in half during next six months.

Thanks Mr.Rocket ,

keep on stretching.