Loading, lengthening, healing.

Even if we could get 1/2 a mm in a day consistently in PE - we’d all be very happy. Its obvious from the leg lengthening, that tissues, fascias, nerves and blood vessels must be able to support the 1mm per day rate of extension.

Marinera,

1) the tissues such as skin, veins, nerves, and collagen fibers are in both the leg and the penis.
2) I’m sure that the bone was cut (is that what you mean by dissected?), but thankfully we have no bone in our penis.
3) yes, it does support the same methods of applying a load to tissue.

I believe that this extra post, which restated earlier posted information, was worth posting because:

1) elongating at a faster rate, 2mm per day, created more damage, and a much higher percent of type III collagen became present. What if that “extra damage” was microtears, that would not have occured at the slower rate of 1mm per day. Again, “what if” this type III collagen is doing the bridging and covering the gaps created in connective tissue that many people talk about.

If that were the case, we can also see that creating gains at that rate causes the tissues to adapt quickly to prevent more microtears from occuring.

Ok, so I’m just reinforcing the low-load/long-duration methods, but I believe that we should gather all of the evidence that we can, both in favor, and against certain theories.

I’m trying not to be biased. I know that I’ve done so in the past. I like Iguana’s perspectives on putting theories to the test.

Ok, so we can’t just monitor how many millimeters a day we stretch our penises, but we can start off with a very light routine (possibly daily), then very gradually intensify it until we reach a level of intensity that delivers gains.

Another couple of “what if’s”. What if pudendum’s thread that describes what goes on in connective tissue when it attempts to adapt was an account of how CT elongates without the incidence of microtears. What if that was a model of how CT becomes longer with histogenesis.

I’d like to discuss this more, but I’ve got to get to work now.

I write “what if”, because I don’t want to misslead anyone to state any of this as fact, but as something that we should continue to explore.

That’s ok, I was asking just to be sure that I had correctly understood this study.

It seems that histogenesis is a kind or hyperplasia. And this study seems to fit exactly on what this thread was suggesting since when it was started, and with firegoat views on this topic as well : maybe the advise (suggested by anecdotal evidence) we always give to newbies :”Don’t start too hard or your tissues will be harder and you’ll have trouble getting future gains” has some scientific support. All is pointing to one direction, right ?:) .

An interesting immediate question to me, right now, is : how long is a New Zealand white rabbits leg? This study regards rabbits; knowing how much is, in %, 1 mm on the leg of a rabbit could be interesting.

So, I were not biasing you, Kojack, quite the contrary: I agree on the points you raised and on the fact that this study is very interesting. :)

The holy grail of PE could be : at what degree of stress (load, % of elongation, cycles of stretching…whatever) we can have new tissue growth without strengthening tissue?

Another major question: if we have a tissue that has become stronger, what we should do to allow it to return to a state where it’s more easy to elongate?

There has been some really great post by members concerning the amount of time necessary for tissue to return to its pre-trained state, or for it to weaken if no longer used.

You’re right marinera, you and firegoat have been discussing low force methods, and warning others about toughening there tissues.

Maybe my interest, or understanding of the low intensity methods is just starting to come together, even though I’ve read quite a bit on this thread, and others. I’m a little behind the curve, I guess.

firegoat has stated that the CT adapts. Even though he knows what he is talking about, in my limited understanding, I wanted more explanation of what was happening within the CT.

Really, I’m still excited to see that histogenesis is the likely explanation for the extra skin, and the extra length in the nerves and veins. I first discovered PE on the Internet back in 1997, when I stumbled across the JES extender website. A process like histogenesis is what I “assumed” was a possible explanation for additional length in “all” of the penile tissues. I did not know that an explanation like “distraction histogenesis” even existed back then. Since those early years I’ve changed my views back and forth, and even became confused at times.

In fact, I still feel confused, but like others I desire to see the science of PE narrowed down, to the most plausible possibilities.

So, that’s why I persist.

Speaking about narrowing things down, marinera, firegoat, and others, do you guys think that histogenesis is a good explanation for the gains in skin, nerve length, and vein length?

That leaves out the connective tissue and the smooth muscle, but possibly we could narrow things down by answering this question.

Modestoman stated in a post concerning histogenesis, on a different thread, that this “MIGHT” be a likely explanation for the skin, veins, and nerves. In a round about way, he stated that once the connective tissue was permanently elongated, that it would provide the traction forces for the skin etc… to then grow by histogenesis. This would of course be in very small non-visible increments. His words were actually that these soft tissues were possibly “along for the ride”.

What do you guys think of that? In other words, even “IF” we are only deforming the connective tissue (and we may be doing way more than simply deforming it), do you think that the other soft tissues are then growing around it in order to adapt?

It’s past my bed time and I have a busy weekend, but I’ll stick that somewhere in my subconscious and get back to it. For now, here are the dictionary definitions of histogenesis and hyperplasia, as sometimes I’m reading one, but the question seems to be more relative to the other. That could get confusing if we are thinking of different, but related, concepts.

http://dictiona ry.reference.co … se/histogenesis

http://dictiona ry.reference.co … wse/hyperplasia

So the theory suggests that without constant stretching or hanging that the penis will ultimately lose length and girth?

Thanks fg.
I found this definitions, also :

Histogenesis is the formations of different tissues from undifferentiated cells.
http://en.wikip … ki/Histogenesis

Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue beyond that which is ordinarily seen in e.g. constantly dividing cells. Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor, or may be visible only under a microscope. Hyperplasia is considered to be a physiological response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and some benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.[1]

Hyperplasia - Wikipedia

However, maybe is beneficial adding some more details about the article cited by Kojack:

The concept of distraction histogenesis was introduced by G.A.Ilizarov and classic papers were published in the English literature in 1989[1,2]. Gradual traction on living tissues creates stresses that can stimulate regeneration and maintain active growth of certain tissue structures. Ilizarov designated this principle the Law of Tension-Stress [1]. The clinical applications of this principle in orthopaedics include limb lengthens discrepancy or short stature [3,4], delayed unions and nonunions of fractures [5], limb deformities correction [6], congenital pseudoarthrosis [7], and the treatment of bone defect [8]. The basic research of limb lengthening falls into two aspects. One is the responses of various tissues under tension stress during limb lengthening, including new bone formatted in the distraction gap, muscles, tendons, vessels and nerves [9-11].
……….
In 24 adult New Zealand white rabbits (License number SCXK 2002–005, lab animal center of the Fourth Military Medical University), the fascia of the leg was distracted by a unilateral external fixator applied with four pins to the medial surface of the tibia. Adult rather than immature rabbits were used to eliminate the factors of growth and development which may affect the accuracy of the study.
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Leg lengthening
Seven days after operation [17,18], axial distraction was conducted at 2 different rates, 1 and 2 mm per day, respectively. Lengthening was performed twice daily until 10% and 20% increases in the initial length of the tibia had been achieved. The initial length of the tibia varied between each rabbit with an average length of 9 centimeters. Thus the lengthening values were correspondingly 0.9 and 1.8 centimeters.
…..

The effect on the extracellular matrix of the deep fascia in response to leg lengthening
Hai-Qiang Wang , Xin-Kui Li , Zi-Xiang Wu , Yi-Yong Wei and Zhuo-Jing Luo

Institute of Orthopaedics, Xijing Hospital, Fourth Military Medical University, Xi’an, People’s Republic of China, 710032

BMC Musculoskeletal Disorders 2008, 9:101doi:10.1186/1471-2474-9-101

The effect on the extracellular matrix of the deep fascia in response to leg lengthening | BMC Musculoskeletal Disorders | Full Text

So, in this study there isn’t a multiplication of cells, but the generation of new collagen (especially type III collagen) - so changes in the extracellular matrix. So there isn’t hyperplasia involved in this study, right?

Quite the contrary, if you read the thread from it’s beginning :) .

…………….
There are several kinds of connective tissue. All are variations on a common theme, in that they are combinations of cells and extracellular fibers and fluids that are strong, resilient, and capable of repairing themselves.
………
The most common type of cell found in connective tissue is the Fibroblast. A cell that can adopt many shapes, depending on its activity, the Fibroblast produces the two major classes of extracellular material found in connective tissue: fibers and Ground Substance. Fibers are strands of proteinaceous macromolecules that make connective tissues strong, resilient, and elastic; ground substance is a complex, viscous fluid that makes up the Matrix in which the fibers and cells are embedded.

The three main types of fibers in connective tissue are Collagenous Fibers, reticular fibers, and elastic fibers. Of these, Collagenous Fibers are the strongest and also the most common. While the strength and durability of leather is well established, few realize that leather consists of interwoven Collagenous Fibers - fibers that originate from the Dermis of the skin of large mammals. Strong though leather is, the Collagenous Fibers from which it is made are even stronger in the living animal. Collagenous Fibers possess a formidable tensile strength; they can withstand pulling forces of up to 300 kg/cm ? ? ? without rupturing. Under those conditions, the Collagenous Fibers will stretch very little - 3% at most. The properties of Collagenous Fibers are derived from the fibrous protein Collagen from which they are assembled.

Because Collagenous Fibers stretch so little and connective tissue so often needs to be elastic, the elastic Fiber has evolved. When stretched, an Elastic Fiber can return to its original length. Elastic fibers, which are also made by fibroblasts, have two components-a fibrous core and an amorphous covering. The amorphous covering, made of the protein Elastin, is thought to be responsible for the capacity of elastic fibers to recoil after being stretched. It is no accident, then, that connective tissues subjected to deformation often contain both kinds of fibers, Collagenous Fibers for strength and elastic fibers for elasticity.
………..
The third class of connective tissue Fiber, the reticular Fiber,
………
often distributed in a spiderweb or “reticular” fashion, were called reticular fibers after their configuration. They are common to organs of the immune system, in which they form the connective tissue framework for the spleen and lymph nodes. More recently, electron microscopists have shown that reticular fibers are actually made of Collagen fibrils. (A Fibril is a tiny structure, visible by electron microscopy but too small to be seen by light microscopy. Many fibrils, when packed together, make up a Fiber). Within a given reticular Fiber, the Collagen fibrils that compose its core are covered by a Glycoprotein coat that resembles material of the Basement Membrane. In organs such as the spleen and lymph node, the reticular fibers are surrounded by thin cytoplasmic extensions of reticular cells - cells, quite similar (perhaps identical) to fibroblasts, that are thought to elaborate the reticular fibers. In ordinary histologic preparations not specially stained to detect them, reticular fibers are impossible to distinguish from Collagenous Fibers.

Connective tissue has been classified into several categories based on the manner of packing of the fibers and the ratio of cells to fibers. Connective tissue that features many densely packed fibers going in many different directions is known as dense irregular connective tissue. Found in such places as the Dermis of the skin and the Submucosa of the gut, dense connective tissue is well suited to binding epithelial sheets to underlying tissues.

Connective tissues that are subjected to the exertion of heavy forces in one direction, such as the forces that pull on tendons and ligaments, are quite different. They have densely packed Collagenous Fibers oriented parallel to one another. This type of connective tissue, known as Dense Regular Connective Tissue, has many fibers and relatively few cells. The paucity of cells, most of which are fibroblasts, may account for the slow healing of torn tendons.
……….
Connective tissue cells are varied. Most abundant is the Fibroblast, which seems to be capable of secreting all of the types of fibers. Mesenchyme cells, too, are abundant. Mesenchyme is embryonic connective tissue; Mesenchyme cells, therefore, are embryonic connective tissue cells. Despite their embryonic nature, Mesenchyme cells persist in the connective tissues of the adult. Similar in appearance to undifferentiated fibroblasts, these Mesenchyme cells are capable of developing into whatever type of connective tissue cell is required at the moment. They are thought to be multipotent and can differentiate into fibroblasts, cartilage cells, bone cells, and, on occasion, smooth muscle cells.
………………..
I
…………….
Dense Regular Connective Tissue: The Tendon
…………….
Tendons and related ligaments, which hold bones together, are made of Dense Regular Connective Tissue that consists of a small population of fibroblasts in a field of parallel Collagenous Fibers.
…………………….

I’m going to have to read the study later because my wireless connection is very slow right now, but if I remember correctly, the balance between type I and type III collagen stayed the same within the tissues that were distracted at the lesser rate of 1 mm per day. In the rabbits that experienced the faster rate of distraction, 2 mm per day, more type III was present. I would guess that the faster rate of 2 mm per day creates more microtears, and those are covered by type III collagen. That is only a guess.

In the rabbits that experienced the slower distraction rate of 1 mm per day, the balance of type I and type III collagen was said to be similiar to normal connective tissue that was not experiencing tension stress.

Creating an imbalance and having more type III collagen may explain why more intense routines reach plateaus sooner. This is just an idea of my own that I will explore.

firegoat, thanks for those definitions.

Is interesting to note (just as a curiosity) that 1 mm on 9 cm (average length of rabbits leg in the study) is about 1.5 mm per day elongation on the average penis.

There is obviously a link between thickness, tension and speed of growth. The thinner rabbit’s leg will grow much faster than a penis.

The fastest penis growth I have seen is one guy mentioned in the Phallosan study:
http://www.phal … /resultate.html

1.9" (48mm) in 6 months, 8 hours per day, 6 days per week = 8mm per month or 0.26mm growth per day with a starting EG of 3.75"

It makes me wonder whether 8mm per month is possible with a thicker penis and more force.

Today I experimented with ADS , I measured before and after. I measure quite accurately (bone pressed) by attaching a 2" long piece of tape onto the ruler at right angles to my measurement goal, which was set at 199mm. At my first measurement, I was maybe 1mm short of the tape but at my second I touched the tape no problem. A notable difference which I haven’t seen before. I will see if it wasn’t just temporary swelling by measuring tomorrow.

I totalled 6 hours of ADS during the day and an extra 3.5 hours during my PE routine with Far infra red heating.

8+ hours of ADS per day is my future goal, however comfort is the biggest problem, wearing ADS causes lots of irritating little pains and needs to be removed regularly.

Still I doubt we can deduct anything by that study. 1 mm is the lengthening of the leg, not of the tendon/ligament - that is the kind of tissue we are interested on. I’d like to hear firegoat opinion on that study.