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Exploring the Science of the EtP Model

Originally Posted by Para-Goomba
Wad, I haven’t followed this debate much, but do you have evidence of your point #2 (directly above) other than your own experience? I’m unsure whether other guys retained their increased F:E ratio after stopping active PE workouts, the way that you did for a long time.

Unfortunately, no.

While I’ve tried to establish the lessening F:E ratio of gains, I have only my experience of the downside. Really, the only one responding to this - who’s also made gains, then ceased PE for at least 3 years - is lil12big1. And I’m not sure if he saw a relatively larger shrinkage of his flaccid.

One of the tricky problems is getting an accurate/consistent measurement of the damn flaccid size.

…Just a few more installments…. :)

Originally Posted by iamaru
I get confused contemplating LOT theory so this is all a tad confusing for lill old me.

EtP theory basically states in a nutshell, that gains come from deforming the tunica (thick fascia layer, multiple layers covering the penis). Essentially once you deform (go from elastic to plastic) those cells are permanently deformed. However, your body regenerates new cells that must be worked, but it doesn’t replace cells all at once, it replaces cells here and there. Therefore, if you were to stop PEing all together, eventually (years) your dick size will go back to pre-PE with nothing to show for it (like what happened to Wad). However, it also states that once you achieve your goals, a simple maintainence routine is all that is needed to keep your gains, because when you do your simple workout, all you need to deform is the small number of newly regenerated cells (the rest are permanently deformed).

GvM theory is basically the bodybuilding theory, it essentially states that PE is like bodybuilding, and when you stop PEing (like if you would if you stopped lifting), you lose a significant amount of your gains quickly, and the rest fade away slowly. It also states that you need to keep up high intensity PEing if you want to maintain your size (just like a pro-bodybuilder has to do in the gym).

Because Wad’s gains took a long time to go away, EtP theory fit his situation and many other people’s scenarios. Keep in mind, both are theories, both have people who believe in and support both. Wad made a great case for EtP, and this is honestly what I believe is going on. EtP seems to be the simpliest explanation for why PE works. The good news with EtP is that as long as you keep up a maintence routine, in theory you should not lose much of what you have gained, if anything at all.

Does this help?


My goal is to be the best me, mind, body and soul, PE is part of achieving the best me.

HardbodyPEer, that’s a pretty damn good summation.

Originally Posted by wadzilla
Unfortunately, no.

While I’ve tried to establish the lessening F:E ratio of gains, I have only my experience of the downside. Really, the only one responding to this - who’s also made gains, then ceased PE for at least 3 years - is lil12big1. And I’m not sure if he saw a relatively larger shrinkage of his flaccid.

One of the tricky problems is getting an accurate/consistent measurement of the damn flaccid size.

…Just a few more installments…. :)

Yeah flaccid measurements can be tricky, some people probably lay their dick on a ruler and measure, others probably put the ruler on top as the dick hangs, and then we have the problem of the penis being warm or cold. When I’m cold or nervous, my dick shrinks up to a nub, its unbelievable and depressing. Other times, it hangs pretty decent.


My goal is to be the best me, mind, body and soul, PE is part of achieving the best me.

Originally Posted by wadzilla
HardbodyPEer, that’s a pretty damn good summation.

Thanks, you deserve credit there, you explained it very well in your EtP Deformation theory.


My goal is to be the best me, mind, body and soul, PE is part of achieving the best me.

Flaccid & Erect Gains do Not appear to be simultaneous

1) Anecdotally, there appears to be quite a high number of PE’ers who’ve reported that their very first gains were in flaccid size. Only later did they realize erect gains.

2) Even amongst experienced PE’ers, many have reported that the “newbie pattern” has continued for them – even after already making appreciable gains.

Every paysite states that this is to be expected – and the explanation they all give is “increased blood flow.” As I dealt with this earlier, I won’t belabor the point – only reminding you that “increased blood flow” = tunica loading (i.e., “erection”). You might have more “chubbers” after you’ve began PE, but you won’t get that extreme “turtling” – even when your tunica seems completely unloaded, (i.e., very soft & very flaccid).

* Note: This following is pretty much free speculation….

Could EtP Tissue Deformation be a 2-stage Process?

Before any “super-expansion” (i.e., erect increase) is manifested, does the tissue deformation process work on the low end first – vis-à-vis flaccid increases?

From the following excerpt (regarding the stretching of connective tissues)…

“When stretched, the connective tissues appear to be viscoelastic in nature. When a force is applied against the tissue and then removed, the tissue behaves as if it has both plastic and elastic properties. The elastic response is shown by recovery of the tissue to its original shortened position, while the plastic response is characterized by permanent elongation. Optimal plastic deformation of the tissue results with applications of long periods of low force stretch. The tissue slowly remodels because a biochemical, triggered by constant force, results in a loosening and shifting of the fibers’ connecting point within the tissue.”

Contracture.pdf

While this particular extract refers to connective tissue (which is not expansive like the penis), perhaps the earliest stages of this “remodeling” (for penile tissues?) might be when the tissues don’t quite retract to their original flaccid shrinkage.

Possibly the “completion” of each of these stages results in the plastic response being displayed (or “completed”) during optimal expansion (erection).

Or, maybe not?

But this type of flaccid/erect (relaxed/flexed) disparity between size does not occur in the known GvM model of hypertrophy. One’s relaxed arm measurement doesn’t increase first, followed by a lag before the flexed measurement increases [of course, I’m not talking about the temporary bloating of the muscle - “pump” - caused by a workout].


Last edited by wadzilla : 01-26-2009 at .

Some Scientific Views on Tissue Deformation

In an earlier Post #32 to marinera I said,

“Let's all be honest. What you take for “scientific evidence” is nothing but disjointed extracts taken pell mell from all over the place….

(1) They often involve non-human subjects

(2) When they do involve human subjects, they virtually never deal with the penis - but usually tendons or ligaments, or even skin graftings, etc.

(3) When they do deal with a human penis, its usually in the setting of some pathology: peyronie's disease, chordee, megalophallus, impotence, etc.

(4) Or they focus on ill men suffering impotence due to various ailments: diabetes, MS, hypertension, etc.”

Nonetheless, I’m not averse to looking at any interesting finds….

The following excerpts contain some useful information on heating & force…

From Deformation: Intensity, Method and Recovery - Shiver (July 20, 2004)

“Infrared heat increases the extensibility of collagen tissues. Tissues heated to 45C (112 °F) and then stretched exhibit a non-elastic residual elongation of about 0.5 to 0.9 percent that persists after the stretch is removed. This does not occur in these same tissues when stretched at normal tissue temperature. Thus 20 stretching sessions can produce a 10 – 18% increase in length in tissues heated and stretched.”

I don’t think it is important what the heat source is. In the quote that I pasted they were selling Ultrasound machines, which is why they mentioned that method. I think 112 °F is pretty hot, but not too hot to bear I would have thought.

From the research on collagen extensibility it would seem that a long-term stretch under low force would be best (score one for the hangers).

“When stretched, the connective tissues appear to be viscoelastic in nature. When a force is applied against the tissue and then removed, the tissue behaves as if it has both plastic and elastic properties. The elastic response is shown by recovery of the tissue to its original shortened position, while the plastic response is characterized by permanent elongation. Optimal plastic deformation of the tissue results with applications of long periods of low force stretch. The tissue slowly remodels because a biochemical, triggered by constant force, results in a loosening and shifting of the fibers’ connecting point within the tissue.” [from Contracture.pdf]

If you look at the research on Ultrasound treatment they also have some points on how much to heat structures for the best results:

“The thermal effects […] on human tissues are well documented, and are utilized to […] increase the extensibility of collagen allowing tissues to be stretched more effectively. […] Tissue temperature need to be raised 3-8° C to obtain the increases in tissue extensibility associated with heating.”

And about duration…

“Sapega et al. describe a program designed to lengthen functional connective tissue structures in an a traumatic fashion. They advocate a moderate but tolerable force to stretch contractures for 20-60 minutes, depending on tolerance. The joint is placed at end range. Several 30- second breaks can be used.”

Some hints about heat and penetration from various studies I found in the net:

“Far-infrared light can penetrate up to 1 to 1.5 inches where heating pads mostly heat at the skins surface.”
About heat packs: “Greatest degree of heating is at 0.5 cm depth from the surface and takes 6-8 minutes to reach maximum.”
“Muscle temperature at 1-2 cm depth increases at lesser degree and takes 15-30 minutes to reach maximum.”
“Stretching window is 3 minutes. After that the tissue temperature drops past tissue extensibility.”

Best heating source, btw, would be infrared, followed by moist heat. Thermotex sells and produces infrared pads, but they are very expensive and don’t have the right size for PE.

Actually one study had this to say regarding that issue:

“In order to deform, and then reform a ligament into a more desirable length and form, the applied “constant” load must reach over 40% of that particular ligament’s “ultimate load”. A ligament’s ultimate load is defined as “the final load reached by a structure before failure”.”

This is supposedly ideal force so that the fibers don’t revert to their original state but rather remain elongated. (No word on whether heat changes this threshold though.) Now, we don’t know the ultimate load of the tunica and/or ligaments but considering lig pops and other phenomena I’d say that manual stretching, if fairly intense, should at least approach that 40% cut-off.

But the take home message for the high intensity guys is taking adequate time off between sessions depending on the nature of the excercise, and depending on what part of the healing phase the tissues are in. I’ve listed some of the stress amounts listed below, while being high, are withing the realms of hangers and stretchers here.

You can get the full article here.

The stress is divided into four bands which are defined very roughly as follows:

A <80N (<18lbs)
B 80-180N (18-40lbs)
C 180-280N (40-63lbs)
D >280N (>63lbs)

From Connective tissue- FIRST “THREAD OF THE YEAR” - hobby (Aug. 14, 2002)

With any given stretching force, the resulting proportion of plastic to elastic response depends primarily upon two stretching force variables: time and intensity. Research on these variables has produced three significant findings: 10, 16-18

1) Short duration stretching of high intensity favors the elastic response, while prolonged duration stretching of low intensity favors the plastic response.

2) There is a direct correlation between the duration of a stretch and the resulting proportion of plastic, permanent elongation.

3) There is a direct correlation between the intensity of a stretch and the degree of either trauma or weakening of the stretched tissues.

To summarize, the longest period of low force stretch produces the greatest amount of permanent elongation, with the least amount of trauma and structural weakening of the connective tissues. 10, 11, 16-18

********************************************

Interesting information – with the understanding that none of it results from any studies on human penile tissue.

Some “Hard Science” Regarding an Instance of (pathological) Penis Enlargement

As per my Post #32 to marinera I said,

“Let's all be honest. What you take for “scientific evidence” is nothing but disjointed extracts taken pell mell from all over the place….
……………
(3) When they do deal with a human penis, its usually in the setting of some pathology: peyronie's disease, chordee, megalophallus, impotence, etc.

……………

Unfortunately, the closest thing we have to hard science – regarding any instance of post-pubescent, non-surgical penile enlargement – would fall in that 3RD category: megalophallus.

I found, amongst my “disjointed extracts” on an old CD, a document file – megalophallus.pdf. After so much searching the internet in vain for a URL, I managed to locate a forum post: Megalophallus: 7.5” flaccid girth! (photo) by Para-Goomba * [You can see a photo at that link of a man suffering from megalophallus with – as the thread says – [more than] 7.5” of flaccid girth.

Apparently, the document had come from PubMed site; however, Para-Goomba wrote: “I can’t post the full-text article without violating copyrights (since the online journal is not publicly accessible).”

Therefore, I’ll do the same; further, I’ll refrain from uploading the PDF (I can’t even remember how the hell I got this!). But I’d like to highlight a few points from the PDF…

(1) Priapism is a common complication of sickle cell anemia; however, megalophallus is not generally recognized as a sequela of priapism.

(2) The patient featured in the paper is a 38-year-old African-American man with sickle cell anemia.

(3) This patient reported multiple short episodes of priapism in the past and an intense, prolonged, isolated episode 9 years previously, followed by a permanent increase in penile circumference and painless partial erection in two thirds of the penis. Nevertheless, a painless full erection was possible - but he presented an enlarged penis measuring 19.5 cm (7.67”) of girth at its widest circumference. No new episodes of priapism have occurred since the intense episode in 1991.

(4) The glans penis was normal.

(5) An ultrasound scan revealed good blood flow within the cavernosal arteries and branches, with areas of high velocity. Yet, fibrosis of the corpora cavernosa, as previously hypothesized should result in low flow by Doppler imaging. The reverse was true with this patient.

(6) An alternative mechanism (not fibrosis of the corpora cavernosa) was proposed for his sequela….

(7) The increase in penile circumference follows a sudden and permanent loss of elasticity of the tunica albuginea, brought about by a particularly intense priapism and a very engorged organ.

(8)The plausibility of this mechanism for megalophallus is supported by the lack of increase in the circumference of the glans in our patient and the one previously described.

We should all bear in mind the following: (1) this man suffered from sickle cell anemia, (2) he also suffered from priapism – which is a common complication of sickle cell anemia, (3) his severe & prolonged bouts of priapism led to megalophallus – which is not generally recognized as a sequela of priapism, (4) his megalophallus did not present fibrosis of the corpora cavernosa, (5) his megalophallus is believed to have resulted from a sudden and permanent loss of elasticity of the tunica albuginea.

Unfortunately a group of 8 simple measurements would’ve made this study, from my perspective, vastly more meaningful: beginning (pre-priapism) EL, EG & FL, FG; followed by current EL, EG & FL, FG measurements.

* Note: As a number of forum members expressed a lot of interest in exploring priapism (with the intention of inducing megalophallus?), several realities should be noted from the above extract…

(1) While priapism is common to sickle cell patients, priapism does not commonly result in megalophallus.

(2) This particular patient’s megalophallus – which allowed for painless erections and normal sexual functioning – is not the only “version” of the disorder. He did not present “fibrosis of the corpora cavernosa,” which would’ve changed things.

(3) By trying artificially to “duplicate” the nature of priapism (ingesting a lot of Viagra, wearing tight clamps for prolonged periods, etc.), you’re not even unlikely to induce megalophallus – you’re more likely to induce “deoxygenated hemoglobin in the corpora cavernosa ,” nerve damage, necrosis or perhaps fibrosis of the corpora cavernosa … i.e., “destroy your unit.”

I appreciate the time and effort Wad is putting into trying to figure this out. I am not at all interested in the arguing and shit-slinging that happened in the other thread. I am here to offer my experience to the mix, in hopes that it helps to ultimately draw some solid conclusions.

Regarding elasticity; I never really payed much attention to my BP flaccid stretch during my first round of PE years ago (2002/2003). Checked it a couple times (early into PE) back then, it was at about 1/2 inch longer than my real BPEL.

Now, having got back into full-time PE and started getting gains again, I have been keeping a closer eye on it. This, especially after reading the TGC theory thread from March 2008. My BP flaccid stretch is exactly 1/2” more than my true BPEL at this point. I will be keeping a closer eye on it now, as the TGC theory made some good sense to me. I also fit the other indicator of the “smooth muscle” situation, my EQ is around 7.5 to 8, sometimes a little better after consecutive rest days. Point is, at this time my elasticity is pretty good. I am gaining. It is hard to guage what my previous elasticity was back in ‘03 when I peaked in size and quit PE, but I know my EQ was much better then. I bet my flaccid stretch had become less, I just can’t prove that for sure.

I think it is likely that as we get larger, elasticity decreases. Makes sense based on what limited memory I have regarding my experience. As far as permanent loss of elasticity? Not for me yet, but it seems more likely to happen as we get older?

The megalophallus case is very interesting and potentially relevant to understanding PE, even with all the caveats about the patient’s medical issues. Thanks for posting that, Wad, I had forgotten about it :up:

Originally Posted by Beretta92
I appreciate the time and effort Wad is putting into trying to figure this out. I am not at all interested in the arguing and shit-slinging that happened in the other thread. I am here to offer my experience to the mix, in hopes that it helps to ultimately draw some solid conclusions.

Regarding elasticity; I never really payed much attention to my BP flaccid stretch during my first round of PE years ago (2002/2003). Checked it a couple times (early into PE) back then, it was at about 1/2 inch longer than my real BPEL.

Now, having got back into full-time PE and started getting gains again, I have been keeping a closer eye on it. This, especially after reading the TGC theory thread from March 2008. My BP flaccid stretch is exactly 1/2” more than my true BPEL at this point. I will be keeping a closer eye on it now, as the TGC theory made some good sense to me. I also fit the other indicator of the “smooth muscle” situation, my EQ is around 7.5 to 8, sometimes a little better after consecutive rest days. Point is, at this time my elasticity is pretty good. I am gaining. It is hard to guage what my previous elasticity was back in ‘03 when I peaked in size and quit PE, but I know my EQ was much better then. I bet my flaccid stretch had become less, I just can’t prove that for sure.

I think it is likely that as we get larger, elasticity decreases. Makes sense based on what limited memory I have regarding my experience. As far as permanent loss of elasticity? Not for me yet, but it seems more likely to happen as we get older?

I appreciate your input, man. Regarding BPFSL, I’m not so sure if that has as much to do with “elasticity” as it does with tissue conditioning. In the past, my BPFSL always shot up after a decon break, and I would get excited about it - but that never “translated” into anything.

I’ve come to believe that “tissue conditioning” is different from elasticity. Consider how a newbie usually gets petichiae (I know I did). But that stops relatively soon - long before any gains or changes in flaccid size. Even a vet can get this if he returns to PE vigorously after a long break.

I would recommend that you try to pay attention to your “typical flaccid” (regarding elasticity), and you might want to track BPFSL regarding the condition of your tissues.

Originally Posted by Para-Goomba
The megalophallus case is very interesting and potentially relevant to understanding PE, even with all the caveats about the patient’s medical issues. Thanks for posting that, Wad, I had forgotten about it :up:

I think I actually got it from YOU, lol.

Why is the Glans so Resistant to PE?

As I cover this in “EtP Deformation Theory.pdf” (VII. THE DILEMMA OF THE GLANS, p. 13-14), I won’t belabor the point.

The gist of the argument is that the glans is especially elastic – more so than the tissues of the shaft. While that might, in theory, suggest that the glans is capable of extreme enlargement, there’s simply too much elasticity to attempt to overcome (in practical terms). The shaft of the penis would suffer catastrophic injury before you could impart sufficient forces to induce much plasticity within the glans.

In the previous thread regarding the megalophallus of the sickle cell anemia patient, it’s worth noting that – despite his massive enlargement (7.67” of semi-flaccid girth) - his glans remained unchanged.

While the mechanism of his megalophallus was several severe bouts of priapism (brought on by his sickle cell anemia), I’m more interested in the explanation of what happened to his penis: “…a sudden and permanent loss of elasticity of the tunica albuginea, brought about by a particularly intense priapism and a very engorged organ.”

A dramatic loss of tunica elasticity led to his massive enlargement; yet, his glans was not enlarged.

Why are Girth Increases so tough for many guys?

Though I’ve visited Thunder’s exclusively for the past few years, I’d been a member of 3 other forums (going back to 2002). Looking back, I couldn’t begin to count how many posts I’ve read of PE’ers lamenting the fact that they can’t gain one or the other (length or girth), no matter the routine, no matter the effort.

Some guys, content with length but desperate for girth, have done jelq-only routines….only to gain more length (and little if any girth). Other guys, seeking length like myself, have stretched & stretched & stretched….but seem to gain only more girth.

It’s possible that some guys do have certain variations in their technique which might (unknowingly) promote the gaining of one property over another, but there are just too many examples to chalk it up to mere “accident” of workout/gripping technique, etc.

By following the most generic “newbie routine” that’s been out there floating on the internet for years, I managed to gain ½” of EG in only 4-5 weeks. Sorry, but I can’t claim any “credit” for that – or reveal to you some mystical, esoteric knowledge. It is what it is.

Some guys gain 1 ½” EL in a matter of months or go over the 2” mark after a few years – but bitch that they’ve gained only 3/8” of girth. Others, like myself, have to fight a death match for every grueling mm of length that they’ve gained.

I have to believe that there’s more to this disparity of gains than meets the eye….

I believe that most PE’ers suspect that the tough coverings or “wraps” around inner spongy penile tissues – Tunica albuginea, Buck’s fascia & Dartos tunica – are the structures that most inhibit our efforts. It’s not the spongy structures themselves.

But when we closely study the Tunica albugina, we see that it’s not “one” layer, but that it’s actually comprised of two layers.

The 2-layered Tunica albuginea

(1) outer longitudinal layer
(2) inner circular layer

This absolutely cannot be a mere “accident” of nature – 2 distinct layers, each distinctly comprised. When you consider the purpose of the tunica (to control the engorging soft tissues in order to promote a uniform shape & hardness of the erection) and that these 2 layers are distinctly designed (one longitudinal, one circular), it becomes so clearly evident that each of those layers is, respectively, controlling a different aspect of erection: length or girth.

I believe they work antagonistically to create the “classic hard cylinder” of the erection – each of the layers being responsible for directing/shaping those forces (lateral & vertical, along the axis of the penis) to form the “cylinder.”

I do NOT know which layer is responsible for girth or length stabilization. I can only guess (my guess would be that the outer, longitudinal layer controls length; the inner, circular layer controls girth) – albeit, I might well have it backwards.

Nonetheless, I am convinced that the different layers control different aspects of tumescence. Two possible explanations:

(1) It might be that, in some men, one layer is “tougher” than the other. This layer would make whatever properties it controls (length or girth) tougher for the PE’er to develop.

(2) Or, it might be that in all men, one of the layers is always tougher (either the girth layer or the length layer). Yet, the difference in ease/difficulty of gains might be due to the disparity between the layers…coupled with the training approach one (often arbitrarily) employs.

Consider a set of antagonistic muscles in the body: abdominals & spinal erectors. While the latter are more powerful (I could always do a stiff-legged deadlift or a hyperextension with more weight that I could perform with weighted situps), weak abdominal muscles can actually cause pain to the (stronger) lower back. Why? Because the excessively weak ab muscles result in poor posture & will impose a constant, low-level strain on the lower back. Often, if one’s back pain isn’t too severe, it can be gradually eliminated by following a progressive abdominal workout (as well as weight loss).

So, even a stronger muscle group can be degraded by a weaker muscle group – if they work antagonistically. The same concept might apply to any pronounced disparities between the 2 layers of the tunica.

This could explain why some guys – regardless of routine – will be better gainers at girth (or length) than other guys.

Can anything be done about this? Maybe, maybe not. But I believe that a trainee’s best bet would be to do extensive damp heat wraps (before & after) and to focus on whatever property they seek (length or girth), but without totally neglecting the training of the other.

It’s also my opinion that you’ll have better chances of making girth gains by training an unloaded tunica. Some, in favor of extreme & dangerous girth routines, will heartily disagree with me. But I’ll say this, having gained about 1 ¼” of EG – without ever really focusing on girth – I never sustained an injury from any impaction exercise.

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