Medical Verification

It’s got promise, that’s for sure. But why throw in the massive erection after the workout instead of before it? Wouldn’t we want to weaken the tunica first and then stretch it? Am I going about this wrong?

I understand the balloon analogy, but is it complete? A balloon cannot be grown so of course its size has a limit. But why can’t new tissue (be it elastic or inelastic) be made?

I have the same thoughts. This is one PE theory among many and hopefully it does not explain all PE gains, because that would mean that in the end genetics will limit you not dedication and hard work. :(

I have stated before that my first gain ever came before I knew anything about PE, I was dating the girl for 3 month. We we both had a lot of money so we no longer worked and were only 23 years old so no care in the world. We would have sex 4 to 8hrs everyday (not strait) after the 3 months I was .5 inches longer and .25 inches more girth. The girth stayed and I have added to it. The length has still not fully came back. It stayed for about 6 months after we split up. I did nothing but the extended sex and I also did what on this board is called amazing iso’s but I didn’t know of any PE board at the time, they just made since to me that they might work.

Look, the reason the medical community doesn’t believe in PE is because they assume that we think we’re claiming to achieve “bodybuilding effects,” and they know that the penis is NOT composed of striated skeletal muscle. You don’t hear doctors claim that you can’t add an inch or 2 to your biceps or chest, etc. But they dismiss this because they know that you can’t *bodybuild* your dick.

Obviously, if they conducted in-depth studies, they would see “enlargement.” And this enlargement, I believe, they would attribute to plastic deformation. It’s no more complicated than that.

We’re not really “building” dick, we’re stretching it, via externally- and internally-invoked forces. And our ultimate capacity to stretch is based upon, I would reason, our existing levels of elasticity.

There is one thing that I’m curious about. I remember hearing a doctor state that we’re a “new person” every 7 years, in that by that time we’ve replaced every cell in our body - hence, we’re “new.” So, I’m wondering if there’s long-term potential to jumpstart gains even after we think we’ve hit our max. But this could only be seen over extended years.

Doctor said that officially? Its really interesting, because I thought its only belief.
I read that renovation of body last one year, with exception of bones - they need 7 years. Anyway, idea is simple - “new” cells copy information from “old”. So, this theory confirms two things in PE: gains are permanent, few months of cementing is needed to keep them.

So, is anything growing (in the “building” sense)? I don’t understand why we need to take rest days if not.

Also, assuming one has no problem getting a 100% erection, does the tunica always determine the size of the erection or could there be some other limiting factor?

Sorry for the barrage of questions, but this is the first PE theory that actually sounds “right” and I want to make sure I understand it.

As I understand it, no, technically you just decrease the elasticity in the tunica so that it can reach it’s full potential. The size of the tunica is fixed but the elasticity holds it back from reaching it’s full potential.

Check this out (link):

It doesn’t seem like the tissues in the CC’s puts up a big fight once you expand the tunica.

I mean aside from the tunica. Other tissues in the penis may grow (in the “building” sense). Otherwise, Wad’s quote about doing decon to “help prepare the penis for another round of growth” doesn’t make sense. What needs to be prepared?

Let’s assume yes, other things need to grow or stretch or whatever, besides the tunica. This is why I brought up whether the tunica is really always the limiting factor. Sure, the corpora act like a sponge but that doesn’t mean they can expand indefinitely.

The glans, for instance, is made of a similar material but has no tunica. No tunica, yet it has fairly limited expansion. The glans is also notoriously difficult to grow (in whatever sense). Perhaps the ability of the glans to expand is an indicator of how much the other corpora can expand.

I’m just not sure the tunica is always the factor which determines size.

About the breaks, I can’t answer for him but when he used the word “growth” I don’t think he meant actually growing something, as in adding mass to the tunica, but simply stretching out the tunica. But I must agree, I am not really sure what exactly a break would do to help gains, in the context of this theory. I do believe the tunica it is the main limiting factor, or more precisely, the dorsal thickening (some might say septum).

Hey wadzilla, great thread! First, I must say that I do agree with you that the penis enlarges by plastic deformation of the connective tissues. I have been researching collagen for a few weeks not, and physical therapy research has shed light on these issues for me. Nevertheless, the penis is made up of 50% connective tissue, and 50% smooth muscles, which is completely different from skeletal muscle (as you know). This smooth muscles does not hypertrophy. I have to do more research, but I believe that it grows by creating micro-tears in it, which are then filled in with new tissue, and the result is longer smooth muscle tissue. This is not hypertrophy.

Now, back the connective tissue. Plastic deformation is also used in engineering mechanics to describe a material that has been permanently deformed. It is used in bio-mechanics (the mechanics of living tissues) to describe the same outcome, but what occurs in the molecules of each is different. In metal, micro-tears occur in the molecules, and that is it. Little micro gaps then exist which makes the total length of the metal longer. In connective tissue, the collagen fibers or fibrils experience micro-trauma, or micro tears. Cross linkages also break during plastic deformation. Now is where things get different. After the micro-trauma is induced, the healing cycle of Inflammation, Proliferation, and Remodelling begins. Some scar tissue is also created, but to the extent of scar tissue can be controlled to some extent (well, in physical therapy it is possible). After, the whole healing process is completed, the micro-tears no longer exist. They have been filled in by new collagen, type I, but mostly type III, along with some scar tissue. So, in essence you have created new tissue, but the total end result is PLASTIC DEFORMATION of the connective tissue AS A WHOLE. Plastic deformation of living tissue is therefore interchangeable with the words “permanent elongation”. Some people are thrown off by the fact that in non-living materials molecules are deformed, and that is it, end of story for the non-living materials.

Yes, one does have to stretch beyond the elastic range and into the plastic range to cause plastic deformation of connective tissue.

It will not snap back to normal after plastic deformation, but cross linkages in connective tissue can heal improperly. Also, an excessive amount of scar tissue shortens connective tissue.

I believe that some elastic characteristics will remain, but the actual deformation takes place in the non-elastic parts of the tissue. In the end, a higher percent of your penis will be non-elastic due to where the actual deformations occurred, you enlarged in areas that were non-elastic to begin with. This overall would make the penis less elastic because of a shift in the ratio of elastic areas to stiffer areas. Elasticity occurs by straightening of the “crimps” in collagen bundles. They may very well lose some of their ability to spring back into a “crimped” position after extreme changes have taken place. Some elasticity occurs from the connective tissue retaining fluid. Under stress this fluid is slowly expelled into the surrounding tissues, which results in creep. It is highly likely that the connective tissue will always behave this way.

If it is true that the Indian Sadhus lengthen their penises up to 18”, to the point which they no longer become erect, then this is evidence that PE can be taken too far.

Well, after 3 weeks of applying a tensile force to connective tissue, the collagen fibrils begin to line up the in most effective manner in order to resist further sub-failure damage (micro-trauma which results in plastic deformation). The body always adapts in order to protect itself. Micro tears are an early sacrifice that the body gives in order the save all of the tissue as a whole from tearing. Then after repeated exposure to tensile forces, it attempts to even prevent the micro-tears from occurring.

The second thing that makes the tissue tougher is the scar tissue that has been created. It is less elastic but has a lower failure point. So, it is said to be tougher, but not stronger. After the Remodelling phase has completely ended, which may take up 6 - 12 months, the scar tissue may be minimal. I’m not sure about this. Research says that new collagen is placed in the area, but I’m not sure that things return to a before injury state. So, I’m not sure if we can “re microtear” that same spot, or if we have to move on to new target areas. By spots and areas, I’m referring to distances micrometers apart……not very long distances. Think on the cellular and molecular level. I believe that this is why fulcrum stretches/hanging is effective. By using the fulcrum technique, one is able to target a new area and focus the force in that area to create micro-tears. This should be a last resort, or used in an effort to gain that last inch or so, in my opinion. You are then using your reserves.

If the scar tissue returns to near pre-PE conditions, you may very well be able to induce micro-tears in that same spot. I do not know if this will be possible or not, but I will try to keep an eye for any information pertaining to this.

I totally agree. By doing PE, we are not causing muscular hypertrophy. We are causing micro-trauma to cells. The fluid of the torn cell then spills out into the extracellular matrix and signals to the body that the healing process needs to begin. This is certainly what occurs in connective tissue. I need to research smooth muscle, arteries, veins, and skin to make a decision on those parts of the penis. If I had to put money on it, it’s all micro-tears. The difference will be the amount of force it takes to cause the tears in each one. Some will tear at lower forces, and some will heal slower or faster.

You know, I believed that PE occurred by cell mitosis for the longest time. This is true to a slight extent, but before new replacement cells are called in, some original cells must stretch beyond their limit and tear. Then the body produces the same size cells according to your DNA. Here’s the catch———- the area that previously required one cell may now require two of the same size cells in order to span the distance. Ah, but that Darn scar tissue……it is in there somewheres, no doubt affecting elasticity.

From the information that I’ve come across, the plastic range begins at about 3%. That is in human connective tissues. I’ve written a thread with information about a rat MCL reaching its yield point at 5.14%, but that same article showed in electron microscopes that cellular damage began at about a 2.5% strain.

Yes, I do have links for this information that I am speaking about. All of this was in my own words, so I’m not posting any right now. Also, it’s late and I have to get to work tomorrow. Last, I’m still putting information together for a thorough explanation in the future.

Great thread, Wadzilla!

Agree. I had the same thougth before reading this thread, and now it is reinforced; doing clamping we force the tunica.

Now, repeating 2-3 times this work (clamping) we are pushing the tunica to the extreme of it’s elasticity, near the point of deformation; at this moment the tunica should be at it’s weakest point, so stretching will put deformation in vertical direction, and not only in horizontal one.

Hope what I’m pointing is clear.

Isn’t this thread to some extent supporting the chemical PE approach whereby one has a chemically induced, maximum stress, erection for 3-hrs. at a pop?

If so why would we not all get some caverject and figure out how much we need to stay erect for 3-hrs. and be done with it?

I’m not sure I buy certain related the hypotheses in this thread as the chemical PE threads have died and to the best of my knowledge there is absolutely NO supporting member evidence that the approach works. In fact, it seems that surgery may have a better outcome track record than chemical PE if gone about in the right way.

Thoughts?

The only thing I would add to this, is that elasticity is the proper word, here. Flexibility describes an entirely different physical property. Flexibility is the ability to be bent and return to original shape without deformation. Elasticity is being stretched out of shape and being able to return without deformation. Thus, that which is elastic is not necessarily flexible and visa versa. Then you have ductability, maleability…

The trouble with chemical PE is that you need to induce an erection exceeding your natural one. To just pop a boner for hours won’t do it- or I wouldn’t even be here. And it’s just not safe to induce that kind of erection- a priapism. So, no this does not really support chemical PE, unless it becomes possible to predict and control the priapism so that plastic deformation occurs and not injury.