Occam's Razor & PE

SteadyGains, you’re free to attach whatever “value” you want to my posts. But your implication that I “knowingly” deceive with my posts is unwarranted balony.

No, I’ve never used steroids.

I’m heavier than I was when my max was 180 (172 lbs BW), but lighter than when I hit 435.

Agreed. It’s possible to gain more size from bodybuilding-type training, and affect mostly sarcoplasmic hypertrophy. Conversely, lower-rep, lower-volume heavy training usually leads more to myofibrillar hypertrophy. I was merely using them in a decompensation paradigm.

While you’re correct about the extreme complexity of the Olympic lifts, I totally disagree with you regarding the bench - which is one of the most simple compound exercises there is - far simpler than power cleans (which football players routinely do), proper barbell squats, etc.

Iguana

I agree with your comments about vascular increases (for example, a person develops about 1/4 mile of extra capillaries for each additional lb of fat they gain). But I don’t believe you’re asserting that PE gains are merely the result of extra capillaries.

I did more searching about hyperplasia - as I’ve been away from the iron game for a long time. But, the consensus seems the same: muscular hyperplasia has not yet been “confirmed” in humans. There are various instances of other types of hyperplasia in humans, but theses are associated with pathological conditions (illnesses, tumors, disease, etc.).

Also, you wrote, “…Notice how shear stress (stress parallel to the vessel) can increase vessel diameter.”

Yes, I agree with you! In fact, that’s how I explain the EtP model of girth increases (tissue deformation via internally-invoked stressors). Increasing “vessel diameter” is not a model of mitosis, it’s more akin to the model of deformation.

Well fellas, I know that the connective tissue in my penis is the limiting factor for me. So that’s pretty much the only type of tissue that I research “outside” of thundersplace. I’m happy that others such as Iguana provide info about the characteristics of smooth muscle, so I don’t have to search for that myself. Nevertheless, I see the greatest challenge, at this point in PE, is to form the most accurate hypothesis as to what occurs in the connective tissue of the penis that yeilds gains in size.

As for the shoulder injury example, I believe that such an example can be used as evidence to support the idea that we “are not” creating microtears in the connective tissue of the penis. Yes, it does occur in shoulder injuries, and the ligament becomes permanently lengthened, which could be considered plastically deformed, but SCAR TISSUE is what makes this really permanent, and different from what “seems” to be experienced in PE.

Yes, I did promote microtear theory, but I’m considering all of the evidence. I’m not “sold out” against microtear theories, but I’m comparing and contrasting.

Ok, so back to Wads research.

I like what he has posted so far. Especially the way he has given examples of how the body recycles cells and decompensates. I must point out though, that in each of these cases, no scar tissue was produced.

I would like to mention that I dated a woman for 1.5 years who had very bad scars on her belly from her pregnancy, which was 1.5 years before I ment her. I was with her intimately till her child was just over 3 years old. The condition of the skin on her belly never improved. This was because the stretching was severe for her, and she had scars that looked like axe wounds. I believe that the scars will never go away completely, even if they improve slightly. Tears in the collagen of the skin occured. If indeed an enlarged penis can return to its previous size and condition as before PE, then scar tissue was not created, because microtears did not occur in the first place.

How does that sound? Do you guys believe:

1. If a penis returns to its pre PE size and condition after 3 or more years off of PE etc, then enlargement is not achieved by creating microtears in the connective tissue, because if gains were achieved by microtears, the scar tissue would make the gains (not counting erection quality) permanent.

It appears that sub-failure damages in connective tissue are repaired without formation of scars and without inflammation, but by fibillognenesis and extracellular matrix remodelling:

Healing?

That is a good bench with or without steroids, but really good without.

Off topic I know and I do agree with you about the complexity of the other lifts, but I see someone about once a month doing power cleans and usually they are in a sport (high school or college). I do see squatting more often, but most do not squat properly so I would not count it most of the time. Which leaves the bench, of guys that lift weights, 99% bench.

Kojack10, would you say that when using adequate heat, merely having a good erection would qualify as low-force on the tunica? And would 30mins qualify as long duration?

Believe it or not, it looks like we really only have one obvious point of contention. And, I think that can be resolved by some further clarification.

First, I whole heatedly agree with the EtP model applying to connective tissue. As I stated earlier, pretty much everything I have read on plastic
deformation applied to connective tissue. It seems most everyone else is in agreement with this also. This being said;

I think the hang up is EtP applying to soft tissues, such as smooth muscle. Being that the corpus cavernosa is composed of roughly 50% smooth muscle and 50% collagen. I do think that it is reasonable that a certain amount of deformation takes place in these chambers. But, we seem to disagree that there is actually growth here.

You stated:

As I mentioned in my previous post, this is correct when referring to “natural” skeletal muscular hyperplasis. When a person trains with weights muscle cells enlarge, they do not multiply. Growth hormone therapy is another issue.

The example I gave earlier of angiogenesis is proof positive that smooth muscle hyperplasia does indeed occur in humans. Otherwise, how could new blood vessels form without smooth muscle mytosis? It would be impossible.

Also, the articles on smooth muscle I referenced support this. Note this excerpt:

I have other supportive information. I would be happy to post, if requested.

So, in summation, what I think we have as possible growth models thus far is:

EtP = Connective Tissue (tunica, fascia), and CT portion of Corpus Cavernosa
GvM = Smooth Muscle, vascular system, extracellular matrix, and some soft tissues.

(I actually think the GvM model should be relabled GvM/Hp (Growth via Mitosis/Hypertrophy) as smooth muscle cells actually enlarge as well as multiply.)

Something I think we really need to qualify going forward (which has already been touched on several times), is what the process of plastic deformation actually entails. I will try to post what my understanding is. Others please jump in also.

wad, I believe your work on understanding this is a very important step. As kojack10 correctly pointed out, as far as size limitations go, the connective tissue is the enemy. Smooth muscle growth can always follow. But, it’s the CT that ultimately defines the limits. I believe this is the key to the next major PE break through. Thanks for starting this thread.

Excellent post!

I must say I agree with pretty much everything you said. My wife also has some pretty bad scarring from pregnancy. It’s been 9 years since the birth of our last child. Some of the scars still look fresh. It’s obvious they will never completely fade.

This brings up an important point that I mentioned at the end of my last post regarding what actually qualifies as plastic deformation vs injury that produces scarring.

man-of-10, I don’t think “having a good erection” would be sufficient enough force to cause changes to occur in the connective tissue.

marinera, thanks for that link. I will take a look at it.

Nothing to mention, sir :) .

Iguana,

Newer muscular growth theories account for cell division, and fibre type conversion (from fast twitch to slow twitch and vice-versa ).

It pretty much says that the body has a huge amount of adaptation within it, most will not deliver the punishment necessary to cause the conversion.

Any links? (Just asking).

Well, after reading the information on the link that marinera provided here on this thread, in post # 63, it seems that subfailure damage is not out of the question, even if gains are not infinitely permanent.

The information states that subfailure damage does occur, but scar tissue is not formed. The is in a grade II sprain.

When contemplating all of this, it does seem that we would have to go beyond the elastic range and into the plastic range, just as we have always imagined with the microtear theory. Possibly no real tears, or gaps or created in the tissue (read the info on the link in post #63), even though subfailure damage occurs. Yes, more collagen is then applied to the CT.

Still, as in an earlier post, it seems that if gains are not permanent, we are not creating tears/gaps in the CT, because Imflammation, scar tissue, etc… would occur.

So, is Wads theory in line with this newinformation about grade II sprains? Deos he believe that we have to develop a level of strain in the CT that goes beyond the elastic range and into the plastic range?

I’m looking forward to more input from everyone. As Iguana posted somewheres, this is a team effort.

Thank you kojack, excellent resuming of complex stuff.

Once again muscle type shoud be noted. We are dealing with smooth muscle not skeletal muscle. Smooth muscle does not contian slow twitch and fast twitch fibers.

Great post. This is the kind of shit I like to read. But I have a few questions.

(1) You spoke of smooth muscle hyperplasia, do you have any links about smooth muscle hypertrophy?

(2) I know that hypertrophy is an enlargement of the fibers, while hyperplasia is a dividing of the fibers - but even if we could affect hyperplasia in the penis, would not a 3-year absence from stressors still result in the shrinkage of those additional fibers?

In other words, this is the hurdle than I can’t get over: It took me so much damn intense effort to enlarge my wang, then I stopped cold turkey…and held my size for 3+ years….so, even if we have this model:

EtP = Connective Tissue (tunica, fascia), and CT portion of Corpus Cavernosa
GvM = Smooth Muscle, vascular system, extracellular matrix, and some soft tissues.

(I actually think the GvM model should be relabled GvM/Hp (Growth via Mitosis/Hypertrophy) as smooth muscle cells actually enlarge as well as multiply.)

How do you explain that the stressor-induced adaptions remained for so long, YET WERE NOT PERMANENT?

If the cells not only enlarge, but actually multiply, 2 things could’ve/should’ve happened during so lengthy a time from stressors:

(1) AT LEAST a shrinkage of the size of those cells,

(2) Possibly even a reduction of numbers, since the stressors that caused the splitting are no longer present AND we have (DNA-guided) cellular recycling occurring.

I remember reading some excellent posts along the lines of PE theory by hobby, shiver and others.

Maybe some of the vets can remember a lengthy, detailed post here (quite some time ago - and I can’t remember the title or the author!), it was about research on human stretching…very detailed, going into percentages of overstretching required, times, even optimum heating temperatures (something like 106°F or so).

Damn! I recall it being a great post. I downloaded the page offline, but I can’t find the old CD. Nor can I even remember enough to do an effective search of the forum.

Help anyone?????