[remek]

Iguana: Interesting find on the Angiotensin. Do you by any chance know how it creates a growth response?

[Iguana]

remek, from my understanding, angiotensin is a type of peptide vasoconstrictor that elevates blood pressure. It's not really the presence of angiotensin that causes new tissue growth but a biochemical reaction from the elevated blood pressure. Meaning that angiogenesis can occur from elevated blood pressure/volume from any catalyst including angiotensin. The reason for my citing it, is it's prevailing use in angiogenesis studies. It's the increased blood volume and or pressure promotes remodeling of the vascular system.

[Iguana]

Remek, got me rethinking Smooth Muscle in this most awesome thread. I had been recording and compiling some research and working on some new ideas and this seemed to be a good time to try to put it together to share with you guys. First, I can’t say for sure that there is anything new here as far as components, ideas or concepts but as a whole, I think this may be a new perspective on the process of how and why growth takes place and why it ceases. I may be way off base. But, this is what makes sense in my mind. Feel free to share your thoughts, critiques and input.


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.


Enlarging the Erectile Chambers: I wholeheartedly agree with remek. I believe 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

I think that is what happens with jelqing and clamping. It seems to be the same process (angiogenesis) observed in patients with blocked arteries; increased blood pressure puts stress loads on the vascular cavities and natural arterial bypasses are formed as a result (although they are not usually able to fully compensate for the blockage.) In our case, when the stress load from exercise exceeds what the tissue is accustomed to a growth response is the result.

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.

• Enlarging the Tunica Albuginea

Here is where I diverge from the accepted beliefs regarding growth. First off, we must realize we are dealing with a tough fibrous structure that is difficult (but not impossible) to injure. The tunica has the ability to stretch to approximately 150% of its size. I believe initial gains (Newbie gains) are simply nothing more that maximizing the elastic capacity of the tunica (with minimal plastic deformation.) If a person is only utilizing say 90%, 110% or even 120% of his EQ potential there is room for some very quick elastic gains. This seems to be the case since the first noted benefit after starting PE is better erection quality. Once the elasticity is exhausted gains retard. From this point it would have to be pretty much plastic deformation. (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1464-410X.1997.26511.x)

Coupled with that point, this article states; healthy tissue itself adapts (to stress) by reorganizing the direction of collagen fibrils increasing the tissue's tensile strength. Evidence seems to support this: “Self-assembled collagen fibers were stretched 0-50% before cross-linking and then characterized by microscopy and mechanical testing. Results of these studies indicate that fibrillar orientation, packing, and ultimate tensile strength can be increased by stretching.” Self-assembly of collagen fibers. Influence of fibrillar alignment and decorin on mechanical properties., as we train the elasticity is exhausted and the tissue gains strength so more force is needed to achieve the same results.

It may be that the stretching of the tunica not only allows for greater expansion of the CC and CS chambers but also provides addition room for new tissue growth. If this is correct then this would greatly impact the way we train and could explain some observed odd PE phenomenon. For instance, once the tunica elasticity is maximized a routine with heavy jelqing would not be advantageous due to the fact there would be very limited room for tissue growth. It would make more sense to focus on stretching out the tunica and then fill the added room with new smooth muscle growth.

BPFSL and BPEL comparisons may be an indicator as to the elastic composition of an individual -
This could also explain why some have a BPFSL much greater than their BPEL. Meaning, the CC/CS tissue volume is not adequate enough to “fill in the gap.” It’s like not having enough air to fill your balloon. So, if your BPFSL and BPEL are close together, you would focus on a stretch intensive routine. If not, focus on a jelq, pump, and/or clamp routine.


This could also explain why gains disappear during a break. It is documented that smooth muscle can atrophy. One cause is decreased blood pressure from venous leakage in patients with ED. Meaning, increased stress/blood pressure = increased smooth muscle volume. Decreased stress/blood pressure = decreased smooth muscle volume.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=16390736&d opt=AbstractPlus
It could be that the smooth muscle, like skeletal muscle, atrophies when not used. This would also explain why gains return rather quickly.
I believe once the maximum elasticity of the tunica is reached (end of newbie gains) then it becomes a whole new ball game – total plastic deformation. This is where most guys give up.


I hope this makes sense. After reading back through it I'm not so sure : )

[Dicko]

It makes sense Iguana, good findings and thoughts! I share your thoughts on the tunica, especially the "whole new ball game" part. That's pretty much where I'm at right now and have been for quite some time. I'm not so sure about the approach you suggest though. What do you think about the "SM creating PD on the tunica" concept?

Originally Posted by Iguana

Or.. we could simply be pushing the elasticity of the tunica.

Yes, that's pretty much what I meant.

Originally Posted by Iguana

It's not really the presence of angiotensin that causes new tissue growth but a biochemical reaction from the elevated blood pressure.

Priapism has the same effect. It elevates blood pressure, to say the least, and then maintains it for hours. This has been known to cause penis enlargement, in some cases extreme enlargement (megalophallus). This fits with your findings.

[remek]

Iguana: Amazing post! You've provided several new, unique concepts here.

I agree that enlarging the SM and enlarging the tunica might require different exercise strategies. As we know, the tunica is a tough tendon-like tissue. The CC/CS is, well, muscle. Stretching tendons and enlarging muscle probably needs two different approaches.

That said, I have a few questions:

1. Why is it that you believe jelqing/clamping/pumping works out the smooth muscle and not the tunica?

• Jelqing, in one form, is akin to a light stretch (that's why I think it provides length gains too)
• Doesn't clamping and pumping stretches the penis as well - only outward?

2. Similarly, why doesn't stretching/hanging workout the SM? Doesn't stretching put stress loads on the vascular cavities as well?
3. Why can't you focus on doing both at the same time? (i.e. stretching and jelqing, hanging and clamping, etc)

This isn't to say I don't agree with your theory. I think you have some very interesting thoughts going on. At the very least, you've provided an attempt to tie everything together. At the very best, you might have just found out a completely new way to PE, and - most importantly - gain

Your post reminds me a lot of the way Big Girtha use to train. He didn't really split things up, but he focused heavily on both hanging and clamping. Or, according to your theory, he focused on enlarging both the SM and the tunica - which is no doubt needed for big gains.

If I recall correctly, Big Girtha would use cable clamps on and off for 40 minutes to an hour, and then he would hang or 20 or so minutes. He did this for several sets, as he worked from home. It worked for him, as he fulfilled his the prophecy of his name by gaining over 2 inches in girth and 1.5 inches in length.

[Iguana]

Originally Posted by remek

Iguana: Amazing post! You've provided several new, unique concepts here.
Thanks remek! I hope some of these can be tested and verified. I think we have enough PE related experiences to start intelligently putting some of the pieces together.

I agree that enlarging the SM and enlarging the tunica might require different exercise strategies. As we know, the tunica is a tough tendon-like tissue. The CC/CS is, well, muscle. Stretching tendons and enlarging muscle probably needs two different approaches.





That said, I have a few questions:

1. Why is it that you believe jelqing/clamping/pumping works out the smooth muscle and not the tunica?

Sorry, I may have not been very clear on this. I think any stress force will get a growth response with both tissue types. I was just emphasizing that certain exercises seem to be more effective at targeting the differing tissue.

Jelqing, in one form, is akin to a light stretch (that's why I think it provides length gains too)

I agree totally. Light being the key word here. If you think about it. During jelqing, the hand really never firmly grips the tunica but slides repeatedly over it in a tugging motion. I think as the tunica tissue toughens this becomes less and less effective.

• Doesn't clamping and pumping stretches the penis as well - only outward?

Yes, I agree, they most certainly do stretch the penis. I just think it lessens the effectiveness for length. With manual stretching the force is concentrated on one axis. With pumping and clamping the force is distributed outwardly also. Which is fine if you are looking for girth gains.

2. Similarly, why doesn't stretching/hanging workout the SM? Doesn't stretching put stress loads on the vascular cavities as well?

Absolutely! You may have missed it, but I stated: "It is well documented that several factors can elicit a growth response in smooth muscle cells, including, but not limited to, stretching..." One article has great support for this. Here is another case where concentrated force may be the key. With stretching (at least for me) the tunica (and sometimes the ligs) seem to absorb most of the stress, while with jelqing, pumping and clamping I seem to feel it more in the tissue.

3. Why can't you focus on doing both at the same time? (i.e. stretching and jelqing, hanging and clamping, etc)

I think as long as your FSL stays far enough ahead of your EL you should be able to work both effectively.

This isn't to say I don't agree with your theory. I think you have some very interesting thoughts going on. At the very least, you've provided an attempt to tie everything together. At the very best, you might have just found out a completely new way to PE, and - most importantly - gain

Your post reminds me a lot of the way Big Girtha use to train. He didn't really split things up, but he focused heavily on both hanging and clamping. Or, according to your theory, he focused on enlarging both the SM and the tunica - which is no doubt needed for big gains.

If I recall correctly, Big Girtha would use cable clamps on and off for 40 minutes to an hour, and then he would hang or 20 or so minutes. He did this for several sets, as he worked from home. It worked for him, as he fulfilled his the prophecy of his name by gaining over 2 inches in girth and 1.5 inches in length.

You are right on! That seems to be an underlying factor in almost all big gainers (bib, girtha, aristocane, etc.) They push the limits after the newbie gains are gone. I think once you hit the plastic deformation stage you better be prepared to pull out the big guns. I think by this time the "less is more" approach goes out the window. Tissue at this point is VERY tough. It is used to you tugging and yanking on it. You need to push the envelope to make headway. I'm not advocating strapping an anvil to your penis but I think new approaches are absolutely necessary to get results, be it with time, weight, angle, heat, or whatever.

Speaking of, I think we still undervalue/under use the resource of heat. I was reading an scientific article on what makes meat tough and how scientist are trying to engineer leaner softer beef. It stated that heat was the most valuable tool for breaking down collagen into a soft pliable substance. Collagen becomes a soft gel at 140 degrees Fahrenheit. I wouldn't recommend applying that to your penis although. : )

I may be the eternal optimist but I can't help but feel PE is approaching a major breakthrough.

[quik4life]

Originally Posted by Iguana

I may be the eternal optimist but I can't help but feel PE is approaching a major breakthrough.

Dido!!!

This is one of the most interesting threads of I've ever read.

I'm going to have to re-read it a couple more times before I fully grasp it though. There is a lot of useful information - both for newbies and advanced PEers.

Good work guys....seriously.

[remek]

Iguana: For the record, I just want to let you know that I intuitiavely agree that jelqing/clamping/pumping probably works out the smooth muscle more than it does the tunica (and stretching/hanging works out the tunica more). I've actually believed this for some time, yet I don't have any substantial evidence for this. Just a theory. I was hoping you could provide something

So where do we go from here? Do you have a demo-routine in mind that we can put to the test? I know that we should always increase the intensity as time goes on (like you said, less is more goes out the window at some point), but if you had to take this information and set it into a routine, what would that be?

[Iguana]

Originally Posted by remek

Iguana: For the record, I just want to let you know that I intuitively agree that jelqing/clamping/pumping probably works out the smooth muscle more than it does the tunica (and stretching/hanging works out the tunica more). I've actually believed this for some time, yet I don't have any substantial evidence for this. Just a theory. I was hoping you could provide something

remek, keep in mind, this is somewhat based on speculation, but I think the evidence is supportive at the very least. I based my conclusions mostly on what I had read in a few smooth muscle related articles. This one in particular: Vascular Smooth Muscle Growth: Autocrine Growth Mechanisms -- Berk 81 (3): 999 -- Physiological Reviews

I copied a particularly interesting excerpt and highlighted the statements (in red) that are especially applicable to PE.

II. PHYSIOLOGICAL PROCESSES THAT REQUIRE VASCULAR SMOOTH MUSCLE CELL GROWTH



C. Remodeling
Vascular remodeling (Fig. <A href="http://physrev.physiology.org/cgi/content/full/81/3/999#F1">1) 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.


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Fig. 1. Vascular remodeling.

In response to changes in blood flow, remodeling appears to be fundamentally dependent on the presence of an intact endothelium as shown by Langille and co-workers (173, 174) and by Kohler et al. (155). Because flow-induced remodeling would be expected teleologically to be mediated by changes in vessel tone and hence diameter, candidate mediators are vasoactive molecules. Among these, nitric oxide [produced by endothelial nitric oxide synthase (eNOS)] appears to play a predominant role. Recent studies show that ~70% of flow-dependent outward remodeling is due to EC nitric oxide production as determined by inhibiting production of nitric oxide with eNOS inhibitors (317). During inward remodeling in response to decreased flow, there is a coordination of increased VSMC apoptosis and decreased VSMC proliferation to effect the decrease in vessel wall mass that occurs (47). An important role for monocytes has been elucidated in remodeling, especially in response to ischemia such as occurs after occlusion of a supply artery (277). In response to increases in flow, EC express monocyte chemotactic peptide-1 (MCP-1) and monocyte adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1). The monocytes are recruited to the vessel and infiltrate and digest the media. The EC are activated by monocytes and express basic FGF (bFGF), PDGF-BB, and TGF-. These growth factors then lead to VSMC growth and vessel enlargement. In response to increased pressure, remodeling appears to be due to activation of autocrine mechanisms that stimulate VSMC growth and changes in vessel wall matrix (123, 213, 215). As discussed in greater detail in section IV, many VSMC growth factors have been implicated in the growth and remodeling of hypertensive vessels including PDGF (227, 274), TGF-, insulin-like growth factor I (IGF-I) and the IGF-I binding proteins (7), and hepatocyte growth factor (221). Paracrine mechanisms that are important in hypertension include increased production of ET-1 and angiotensin II by the endothelium.

Notice how increased pressure and flow stimulates an increase in mass and vessel diameter. Isn't this exactly what we are doing with jelqing, clamping and pumping, altering the blood flow and pressure?
Notice how shear stress (stress parallel to the vessel) can increase vessel diameter.

Originally Posted by remek;

So where do we go from here? Do you have a demo-routine in mind that we can put to the test? I know that we should always increase the intensity as time goes on (like you said, less is more goes out the window at some point), but if you had to take this information and set it into a routine, what would that be?

Boy, that's the million dollar question. This is going to require a lot of thought. I was hoping we could put our heads together here and formulate some type of test routine. We need to assume this will be geared for those who are out of newbie gains. There would possibly be two routine types. One for those needing smooth muscle mass and one for those needing to focus on tunica elongation (based on BPEL to BPFSL ratio.) Or, maybe a routine that focuses a few weeks on one then switches to the other. Maybe, two weeks stretch based and then two weeks jelq, clamp, pump?

Any thoughts?

[remek]

Great finds, Iguana! The scientific journals you referenced go along with what I've been assuming all along (yet had no scientific backing for) - the smooth muscle grows with increased pressure. This also explains why veins get bigger due to PE, and why it might be a healthy sign that the SM is growing.

These growth factors then lead to VSMC growth and vessel enlargement. In response to increased pressure, remodeling appears to be due to activation of autocrine mechanisms that stimulate VSMC growth and changes in vessel wall matrix

This also builds a little evidence for something I've believed in for a long time - to keep the gains coming, you have to increase the intensity as time goes on (albeit healthfully).

There would possibly be two routine types. One for those needing smooth muscle mass and one for those needing to focus on tunica elongation (based on BPEL to BPFSL ratio.) Or, maybe a routine that focuses a few weeks on one then switches to the other. Maybe, two weeks stretch based and then two weeks jelq, clamp, pump?

You know what would really help is if we could build a list of signs to help people know when they need to focus on one or the other. If the theory is sound, then this would be a completely new way to PE - and it would almost be akin to the importance of following the PIs.

Didn't you mention earlier that you think an increased BPFSL means the tunica is stretched and thus it would be a good time to focus on the SM?

Perhaps another one is increased flaccid hang. The tunica is stretched, so the penis stays in a bigger flaccid state. In this case, what would be the best to focus on?

Or what about the firmness of the penis? Have you ever noticed that sometimes the penis feels very strong and firm - almost like when a bike tire is pushed to it's complete maximum? It's almost as if the SM is trying to buldge out of the tunica. It doesn't always happen - or at least for me - rather every once in a while. Perhaps it's a sign?

These are just some ideas. I could be going out a limb here, but feel free to scrutinize