Editors note: This post is a brief summary of what we have come up with so far. It is a collection of posts by remek and Iguana taken from posts both previous to this one and after it.
Tissue Growth Indicators (TGIs)
Tissue Growth Indicators refer to certain observable conditions that might lend clues to what is happening in the penis pertaining to growth or the lack of growth. These points are just some ideas, and in the future it may be found that certain TGIs don't belong in a certain category (similarly some TGIs may be found in the future).
The core of this theory is that PE is about enlarging
two key tissue types
Anatomy There are two main central components involved in enlargement: 1. The Corpus Cavernosa/Corpus Spongiosum - erectile sinusoids - composed of about 50% smooth muscle and 50% collagen. 2. The tunica albuginea – a dense outer lining surrounding the erectile chambers - composed of elastin and collagen.
From through research of this topic, we have found that these tissues do not enlarge from the same mechanisms. Conventional Natural PE seems to purport a "one-size-fits-all" approach when it comes to penile exercises. Meaning, there is little advocation for targeting or isolating the differing tissue types to elicit growth from each respective tissue. Given the differing composition (tough collagen vs smooth muscle) and structure of the two focal tissues involved in PE, we are advocating a more diametric approach.
We believe that the evidence supports differing growth mechanisms therefore requiring differing stress/stimulus approaches.
Enlarging the Erectile Chambers:The evidence here points to tissue regeneration: (Growth comes from added smooth muscle tissue and cell regeneration)
It is well documented that several factors can elicit a growth response in smooth muscle cells, including, but not limited to, stretching, injury and increased blood pressure. The following are excellent articles which support this. http://ajpregu.physiology.org/cgi/content/abstract/262/5/R895 http://www.ionchannels.org/showabstract.php?pmid=10666084 http://physrev.physiology.org/cgi/content/full/81/3/999 Quote:
C. Remodeling
Vascular remodeling is a physiological response to alterations in flow, pressure, and atherosclerosis. Remodeling involves changes in VSMC growth and migration as well as alterations in vessel matrix (214). Remodeling may be classified as proposed by Mulvany based on the nature of changes in vessel diameter (inward or outward) and by changes in mass (increased = hypertrophic, decreased = atrophic, no change = eutrophic) (214). As an example "eutrophic outward" remodeling would be an increase in lumen diameter without change in amount or characteristics of the vessel such as may occur with increased flow and atherosclerosis. In contrast, "hypertrophic inward" remodeling would be defined as a decrease in lumen diameter with increased wall thickness such as may occur with increased pressure. It has been best studied in resistance vessels during hypertension. During chronic hypertension, there is an increase in vessel wall thickness hypothesized to normalize wall stress. Physical forces (wall stress and cell stretch), autocrine growth mechanisms, and paracrine growth mechanisms (EC actions on VSMC) stimulated by the hypertensive environment appear causative. |
Enlarging the Tunica Albuginea: The evidence here points to a restructuring of the tissue through healing processes.
It is possible some cell growth takes place but most evidence points more toward plastic deformation.
Quote:
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Collagen has viscous properties which allow a residual elongation after a load is applied then released. This phenomenon is known as plastic deformation. Furthermore, its elastic properties allow for recoverable deformation which is a return to its original length after stretch is applied then released. As mentioned above, elevated temperatures increase the extensibility of collagen. Therefore, when a load is applied to heated tissue then released, greater plastic deformation results (increased residual length) and thus permanent elongation of the connective tissue.9
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Heat Application in Physiotherapy Growth process stages: A. Catalyst (Injury, Exercise, Force, etc.) B. Inflammation, Repair, Healing, C. Healing, Rest, Deconditioning Call it IPR or whatever you want but this seems to be the body's natural healing cycle regardless of the tissue type involved. Summary: According to this theory, if your tunica is not actively being stretched properly, but
you are continuing to build smooth muscle, your erections will get rock hard. The added smooth muscle tissue, tightly constricted by tunica, increases the penile density and rigidity. Now, if we refocus our attention on the tunica and stretch it out, length gains occur. But, because the smooth muscle is no longer tightly constricted it flows easily into the new tunica space giving us new length. But at the same time, because it is no longer tightly condensed, we loose EQ. The erection, although longer, is now softer and much less firm. The goal now would be to refocus on SM to regain the original density and thereby cement the added length. I think if we continue to stay focused on the tunica we may gain a little more length but here is where some guys think they need a break due to poor EQ. They assume the poor EQ means they're over-training, they start decon and loose some length due to atrophy, both SM & tunica. I think if we are giving equal attention
and getting results from both tissue types we avoid this situation. But, after we exhaust newbie gains, this seems very difficult to do.
Note- any number of various other factors could also cause the above observations. If this theory is correct multiple indicators should be present in either instance.
Signs SM tissue is limiting gains. - Weak or soft Erections The theory: According to some studies, the lower the percentage of SM in the penis, the softer the erections.
"In recent electron microscopic studies, it could be shown that, in the case of many patients, a degeneration of the cavernous smooth muscles is present as cause of the erectile dysfunction (11-13)." Therapy apparatus for the functional electromyostimulation of smooth muscle cells - US Patent 6128536 "It has been shown that decreased smooth muscle content is associated with an impaired erection." Sexology 2005
In theory, if everything else is working properly, then the percentage of the SM in the penis could be low compared to the other tissues (e.g. the tunica). That said, this sign is the hardest to interpret, as several things can affect erection strength, including overtraining, stress, an unhealthy lifestyle, and much much more.
- BPFSL is .25" or greater than BPEL The theory: When the BPFSL is greater than the BPEL, it essentially means that the length of the penis can extend further than an erection is allowing it to. The cause of an erection is the smooth muscle, so it is probably the limiting factor here. Also, the tunica is no doubt the part of the penis that determines how far the penis can be stretched. So, with this in mind, the tunica is stretched further than an erection, so it can't be the limiting factor to BPEL gains (and the SM probably is).
- Loss of gains when combined with weaker erections, especially loss of girth. The theory: Let's go through the motions here. If the erection is hard, then that means their is enough smooth muscle (volume wise) and it is relaxed enough to press against the tunica. This, in turn, will essentially create a suction so blood can't leave the penis.
If the erection is weak, a few things could be happening . . . but it most often means the smooth muscle is either not relaxed enough to press against the tunica (which might be caused by the smooth muscle being fatigued, constriction of the blood vessels, stress, etc) or there not being enough smooth muscle volumetrically to press against the tunica. The later is where this theory comes into play. If there is not enough smooth muscle to press against the tunica, then essentially there is a "gap," and blood can't be held in the penis efficiently. So if everything else is right - i.e. the smooth muscle isn't overtrained, the blood flow is optimal, testosterone level is good, and you're living a healthy lifestyle (physically and emotionally) - then it would suggest that you might not have enough smooth muscle to press against the tunica, creating a gap and causing the weaker erections. (
The Penis as a Vascular Organ).
According to this new theory, when gains are made, two things can happen:
- Both the tunica and the smooth muscle have to be pushed to a new limit
- Either the tunica or the smooth muscle was already pushed to a new limit, and the other one "catches up" causing the gain
Similarly, when gains are lost, either both fall from their previous limit or just one does (either the tunica or the smooth muscle). If a loss of gains occurs in conjunction with weaker erections, then hypothetically the smooth muscle volume has decreased while the tunica has stayed the same - and thus the smooth muscle volume isn't enough to effectively expand the tunica. A loss of gains can occur in either short-term or long-term.
- A short term loss of gains is a negative PI. It's caused by overtraining. We can assume that similar to skeletal muscle, when the smooth muscle is overtrained, it experiences fatigue and can't be pushed to the fullest - and thus can't sustain maximum erections.
- Long term lost of gains due to taking a break or not cementing gains. If erections are weak, then presumably more tunica gains were cemented than smooth muscle gains (thus causing a gap and weaker erections).
Note: According to this theory, weak erections can get tricky real quick. If the tunica enlarges and the smooth muscle doesn't, this creates a "gap" that needs to be filled. This is where the theory gets tricky - are you experiencing weak erection because of muscle fatigue or because you need to catch your smooth muscle limit up to your tunica limit?
Further note: Perhaps a way to test this would be that if your penis is the same size when it's at its peak, then your smooth muscle didn't decrease (or become fatigued) and thus the tunica just enlarged. This might be hard to test, as if the smooth muscle can't relax enough to cut off blood from leaving the penis, then there is no way to reach the "peak."
Maybes - Poor Veinage The theory: The reasoning here is 2-fold.
- Within the veins and arteries, there are also smooth muscles cells (these are slightly different than the smooth muscle cells found in the corpus chambers within the penis). If the smooth muscle is poor in the veins and arteries, then the smooth muscle in the penis is most likely poor as well.
- Blood flows into the penis through the arteries. The arteries take the blood into spongy-like spaces called "sinusoidal spaces" which lead to an erection. Inside the spongy spaces is where the corporal smooth muscle is (the stuff were presumably trying to make bigger). When there is more blood flowing to the penis, there is more blood flowing to the smooth muscle. If not enough blood is flowing to the corporal smooth muscle, then it is most likely not being pushed to its limit. Moreover, by actually focusing on exercising the smooth muscle within the penis, you're presumably exercising the smooth muscle in the arteries, which will increase blood flow.
- Good flaccid hang - but erections are weak or soft - Good expansion when clamping or pumping (beyond typical erect size)
-Signs Tunica is limiting gains- - BPFSL is .25" or less than that of BPEL The theory: As mentioned, the tunica is most likely the part of the penis that determines how far the penis can be stretched. When the BPFSL is equal to or shorter than the BPEL, then the tunica is being stretched to its limit when erect. Thus, the tunica is limiting the gains.
- Rock hard, firm erections The theory: When the penis feels very strong and firm it's as if the smooth muscle is trying to buldge out of the tunica - almost like when a bike tire is pushed to it's complete maximum. In this case, the tunica is the bicycle tire and the air inside is the smooth muscle. Just like a bigger tire can take more air, a bigger tunica (once enlarged) can take more smooth muscle.
- Loss of gains when combined with harder erections The theory: Again, if the erection is hard, then that means the smooth muscle is relaxed enough to press against the tunica (and essentially create a suction so blood can't leave the penis). If a loss of gains occurs, and firm erections are taking place, then the tunica fell from its previous limit.
Maybes: - Good Veinage The Theory: If good veinage occurs, presumably erections are hard and the smooth muscle is being pushed to its limit. . . Thus making the major limit the tunica.
- Poor expansion when clamping or pumping Targeting the Tunica or the Smooth Muscle Targeting the tunica: When we are stretching/hanging/or using an ADS, we are stretching
both the SM and the tunica. However, it would appear that the tunica is probably taking the blunt of the stress, as it is the tissues closest to the point of origin. In other words, the tunica is on the outer layers of the penis, the smooth muscle is on the inner layers, and hanging/stretching is generated closer towards the outer layers. Meaning, the hanger is on the outside of the penis, pulling the tunica. (Physics) For girth, it's possible you can focus on the tunica with certain exercises like the O-bend/flaccid bend.
Targeting the smooth muscle: Conversely, when we are clamping/pumping/or squeezing presure from the inside, we are also providing pressure on both the SM and the tunica. However, the smooth muscle is probably taking the blunt of the stress as it is the tissue closest to the point of origin. In this case, the pressure is coming from the inside (from a rapid influx of blood flow), and
directly causing smooth muscle to expand, which
indirectly causes the tunica to expand.