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Microtears Result in Plastic Deformation

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Microtears Result in Plastic Deformation

Tonight while searching for the correct spelling of the “Blachoe Ring”, while replying to another thread, I came across the Penis Enlargement Wiki. I decided to look at the information on the Wiki. I noticed the “Growth Theories” link, one which I have looked at in the past. I then clicked on “microtears”, because that is what I am finding occurs in connective tissue in order for permanent elongation to happen, according to the science behind physical therapy. In many cases, the term Microtruama is used. As I read the description of “Microtears” is see that the author states that plastic deformation and microtears are not one in the same, and that the two are clearly different.

Well, that lead me to this point. I’ve been wanting to debate whether or not plastic deformation occurs here on the forums, even though it has been debated over and over again. You see, I believe that both parties are right, to an extent, and I will clarify what I mean by that.

What misleads people is that they refer “only” to engineering mechanics when considering the definition of plastic deformation. In that case, the molecules of a material are stretched, creating permanent added length, but no new or extra molecules are added/created.

I also held this same definition of plastic deformation when I first discovered the term and the theory as it applies to PE. I reasoned that if my penis had 1 billion cells, and it permanently lengthened, then there is no possible way that it would still have only 1 billion cells. So, by that analogy, I disagreed with plastic deformation PE theory. But, I was not 100% sure that it did not occur in the ligaments. So, I kept the term in mind, even though I suspected the body would add new cells (extra replacement cells/more than the original amount) in the long run over a years time or so.

Now, lets take a closer look at connective tissue. According to information that I have found, about 47% of the penis is made up of connective tissue. Connective tissue is made up of collagen, and is very much like a ligament/tendon. I’m not sure how many members agree with me, but I believe that the connective tissue in the penis is the LIMITING FACTOR to developing gains.

Permanent elongation of a ligament “as a whole” is known as Plastic Deformation in biomechanics. Biomechanics is the science that orthopedic doctors and physical therapist refer to. So, to say that a ligament, or other form of connective tissue has become plastically deformed, is to say that it has become permanently elongated. Plastic deformation is not meant to explain what occurs on the molecular level in biomechanics. In both engineering mechanics and biomechanics plastic deformation is a result of MICROTEARS. The difference in engineering mechanics, the mircotears are not healed, and new molecules are not placed in the stretched areas, while in biomechanics, the body heals itself. The end result is new tissue, or extra collagen, which occurs by the process of inflammation, proliferation, and remodelling.

Quote
The elastic region represents the response of the parallel-oriented collagen fibrils to elongation, once the crimp has been removed. Elongation in thisregion is within its physiological capability and recovery is completely reversible. Elongation in plastic range will result in a degree of permanent tissue lengthening or if extreme, complete failure. Clinically this is the region where tissue damage occurs.

Notice, tissue damage occurs in the region permanent lengthening is achieved.

Now with the next bit of info. Since tissue damage has been created, the body must now heal itself. When the microtear or microtruama occurs, the contents of the cell spill out into the extracellular matrix, known as the ECM. This signals to the body that healing is needed, and this is the onset of inflammation. If the injury is large enough, swelling and redness are symptoms (this is in injuries such as sprains, and such a large injury is not a goal of PE).

Quote
Healing of the most connective tissue except bone, epithelium and endothelium occur by tissue repair. Thisis often accompanied by fibrous scar, which is the typical patching material for wound repair. Repair responses varyconsiderably in different injured tissues. After an injury, the healed tissue is never same as it was before. Tissue repair starts at 48 hours after injury and lasts up to 6 to 8 weeks, fibroblasts begin wound repair and collagensynthesis. Collagen has the property of gradually shortening when it is truly formed. This contracture occurs fromthe third week to the sixth month. New scar tissue will always shorten unless it is repeatedly stretched.Remodelling, also known as maturation, involves increased collagen density and organization, resulting inincreased tensile strength. This process begins as early as 3 weeks following injury and continues for a year or longer.

In that quote we see that healing of connective tissue is done by tissue repair. Remodelling, the “R” in IPR is mentioned in this quote, but inflammation and so on are also mentioned on that page as the process is outlined.

The rest of the penis is made of smooth muscle within the corpus cavernosa, and corpus spongiosum. This smooth muscle accounts for about 48% to 50% of the penis. The remaining 3% - 5% must account for the skin, veins, arteries, nerves, and capillaries. The structures of the penis mentioned in this paragraph or the ones that can be overworked. This is why high intensity routines require rest days. These structures are “more” responsible for engorgement of the penis during erection than the connective tissue is. This is the basis for negative PI’s occurring when these tissues are overworked. I am not sure of the process by which these tissues become permanently elongated. The skin, and the walls of veins and arteries are also made of of collagen, but I believe that mitosis may happen in the skin.

In closing, we now have evidence that plastic deformation is merely interchangeable with the words permanent elongation, and it is not used to describe what is occurring on the molecular level. Microtears/microtruama occurs on the cellular level in connective tissue, which is healed by the process of IPR, and results in permanent elongation, which is plastic deformation of the connective tissue.

The link to the site is: http://www.physiobd.info/articles/1…nflammation.pdf


Last edited by Kojack10 : 10-15-2007 at .

Here is another link. This link has presented me with the most scientific information that “I believe” explains PE theory.

In this information, the letters “CT” stand for connective tissue.

Quote
The physiologic loading region of the stress-strain curve shown in Figure 5 represents the range of forces that usually act on CT in vivo and implies that primarily elastic deformation occurs at these loads. The region of microfailure overlaps the end of the physiologic loading zone. Microfailure represents the breakage of the individual collagen fibers and fiber bundles that are placed under the greatest tension during progressive deformation. The remaining intact fibers and bundles that may have not been directly aligned with the force or those that had more intrinsic length absorb a greater proportion of the load. The result is progressive, permanent (plastic) deformation of the CT structure. If the force is released, the broken fibers will not contribute to the recoil of the tissue. A new length of the CT structure is established that reflects the balance between the elastic recoil of the remaining intact collagen and the resistance of the intrinsic tissue water and glycosaminoglycans to compression. Microfailure is a desired outcome of some manual stretching techniques that are intended to produce permanent elongation of CT structures. It is important to note that a low level of CT damage must occur in order to produce permanent elongation. The collagen breakage will be followed by a classical cycle of tissue inflammation, repair, and remodeling that should be therapeutically managed in order to maintain the desired tissue elongation. The use of modalities, compression, elevation, and directed—but limited—application of force may improve the final results through modulation of the inflammatory cycle.

Here the term “microfailure” is used instead of microtears or microtruama.

Also, notice that here we also see more evidence that the process of IPR occurs as connective tissue heals.

This astounding link is: http://www.thefreelibrary.com/The+e…ue -a013309993

The article is entitled, The Effects of Manual Therapy on Connective Tissue. This article is under the category of physical therapy at thefreelibrary dot com. I believe that were are merely practising physical therapy on our penis.

This thread has turned out to be more of a PE theory thread than I expected. I guess that I always draw things out and get into detail.

Generally, I would attempt to avoid posting back to back, but since I’m providing more information, I’m going to post again.

Here’s more information from a different website.

This is the best article/link that I’ve found yet. I’ve saved the information to notepad on my computer, and will likely copy it to a disk.

Quote
Microfailure represents the breakage of the individual collagen fibers and fiber bundles that are placed under the greatest tension during progressive deformation. The remaining intact fibers and bundles that may have not been directly aligned with the force or those that had more intrinsic length absorb a greater proportion of the load. The result is progressive, permanent (plastic) deformation of the CT structure. If the force is released, the broken fibers will not contribute to the recoil of the tissue. A new length of the CT structure is established that reflects the balance between the elastic recoil of the remaining intact collagen and the resistance of the intrinsic tissue water and glycosaminoglycans to compression. Microfailure is a desired outcome of some manual stretching techniques that are intended to produce permanent elongation of CT structures. It is important to note that a low level of CT damage must occur in order to produce permanent elongation. The collagen breakage will be followed by a classical cycle of tissue inflammation, repair, and remodeling that should be therapeutically managed in order to maintain the desired tissue elongation. The use of modalities, compression, elevation, and directed—but limited—application of force may improve the final results through modulation of the inflammatory cycle.

To take the information one step further, I’ll tell you that we have to enter the plastic range in order to create permanent elongation. In order to enter the plastic range connective tissues must be stretched to about a strain of 3%. In other test, the yield point has been established to be at 5.14% which I covered on another thread. Here’s the information about that 3% strain.

Quote
Noyes estimated that macrofailure of CT occurs at approximately 8% elongation of the CT structure but that microfailure begins at approximately 3% elongation.

Also, it is important to distinguish stretching in the plastic range from stretching in the elastic range. The amount of force will determine which range you are in, or the amount of weight. I need to mention this information on the pound per minute theory thread. Now, we know that a minimum threshold of weight/force is required to create plastic deformation. Nonetheless, using an ads or golf weights can be supported by this information. If ADS’ing works in the elastic range all the time, it may make it easier for us to reach that 3% strain. In other words, for a rough example, we may be able to gain from less weight than would have been required without the extra use of an ads. Pre-exhaustion is a good term for working in the elastic range. This is just a theory of how ADS’ing works, but here’s the info.

Quote
Plastic deformation should not be confused with the phenomenon of creep. When a load is applied to a viscoelastic tissue over a prolonged period, the tissue will progressively deform until a new resting length is achieved. if the load was within the elastic limits of the tissue, the tissue will gradually return to the original resting length after the load is removed. in biological tissues, this phenomenon primarily represents the redistribution of water from the tissue to the anatomical spaces surrounding the tissue. Some of the elongation of tissues that results from manual stretching and massage techniques may reflect nonpermanent creep deformation. Clinical research designs examining manual therapy techniques should incorporate several repeated measurements of elongation up to 24 hours after the application of the technique in order to detect this phenomenon.

While all of this information supports PE theory behind intense moderately intense work, it does not seem to represent what occurs when using a stretcher for long periods. What about the few guys that gained from only ADS’ing? Yet, after thinking about it for a while, and putting together some other information from other articles, I can see how this still applies.

From another article I learned that a strain in the elastic range takes 10 times the amount of “loading time” for it to revert back to normal. So, if you wore a stretcher for 10 hours, the very slight strain or small increase in you FSBPL would take 100 hours to disapear. If you again used the stretcher before the 100 hours was up, possibly about 16 hours after removing it on the previous day, you may be able to pile the very small amount of strain from one day on top of the next day. Eventually the additional stretch in the connective tissue will pass the 3% mark, and would likely be best to continue till passing the 5% threshold over days/months.

The link to this wonderful article is: http://www.thefreelibrary.com/The+e…ue -a013309993

Here is a graph corresponding with the information. I did not create this graph.

Kojak, that’s a very interesting read, thanks. And although it was long, it provided some great info into what we’re doing here on the scientific level. Now, after reading that, I have a question for you. The article states that repair of the tissue takes place within the 48 hours after stress. Would this then be evidence that you should only PE 3-4 times a week or every other day? Back to back days would not be wise cause you would be preventing the tissue from healing, increasing in size and thus possibly hurting your gains?

Most of the veterans I think suggest every other day or 3-4 times a week anyway.

I feel that this PE theory is compatible with many, if not all aspects of PE.

I mentioned how overworking all of the other tissues in the penis besides the connective tissue results in negative PI’s. I believe that extremely overworking the connective tissue could also result in negative PI’s, but this is rarely done. This would be similar to a bad sprain.

Also, this information is compatible with our findings in the PE community that many different types exercises and schedules result in gains. Because it is merely that we stretch the connective tissue far enough, jelqing, stretching, hanging, etc… have all yielded gains for different individuals. Even enlargement from priapism (megalophalus) fits in these findings. I’ve gotta say that I believe clamping really fits this info well.

Another point that I’d like to cover is that many members believe that we are all different, and that what works for one may not work for another. To address this, I’d like to say that gains are established by the same processes on the cellular level as everyone else. The things that will vary are the amount of force required, the amount of time the the force is applied, and the amount of recovery time needed. These things will vary from individual to individual.

The fact that we are each more proficient at different exercises or routines makes some more effective for us than others. Also, some members require that more force be applied to their penis than others, so certain methods are more effective for each individual.

Age also plays a role. The amount of force required for an older individual to cause plastic deformation in their connective tissues is lower than the amount of force required for a younger individual to do the same. This is due to the fact that younger people have more elasticity in their connective tissues. Genetics may also affect this, and for example, not all 35 year old guys will have the same amount of elasticity. Less elasticity would mean that a guy would need less force to enter the plastic range. Older individuals generally require more recovery time, but that is a general estimation. That covers my opinion on how we vary from one member to the next.

I don’t that we will ever be able to identify an exact amount of weight/force or amount of time that is perfect for everyone. This would be wonderful, but the amount of force required for John to reach the 3% strain may be more than is required for Bill. Nonetheless, both will have to reach the 3% mark for permanent change to be occurring.

We have been able to give ranges and estimations of force required, time of applying the force, and recovery time. I believe that we will be able to narrow the ranges down some in the future, but as I said before, there will always be a range.

Kevin12, I have not focused my efforts on determinig the optimal amount of rest days, yet. I would recommend that you follow what is commonly recommended on the board. Even though there is some variance, the vets here know their stuff.

Also, about the 48 hours, the information states that tissue repair begins within 48 hours. That has a different meanig from “the repair takes place within 48 hours”, which sounds like it may have been completed, but that is not the case.

I will be testing various schedules myself. I’m currently on a break.

Newbies, please follow the newbie routine. This theory even supports what goes on for newbies. Newbies don’t have to apply as much force to their penis in order to create microfailure or microtears. The tissues in your penis are fresh. Collagen has not yet alligned itself in the most optimal way to resist stretching.

Originally Posted by Kojack10
Another point that I’d like to cover is that many members believe that we are all different, and that what works for one may not work for another. To address this, I’d like to say that gains are established by the same processes on the cellular level as everyone else. The things that will vary are the amount of force required, the amount of time the the force is applied, and the amount of recovery time needed. These things will vary from individual to individual.

BINGO! In my opinion the most important factor is to determine work/rest ratio(how much to PE and how long to rest-on micro and macro scales) for each of us. Moreover-I suspect that such ratio is not ‘once given’ and it changes throughout our PE journey…it is like chasing the rabbit with eyes closed…but here is the secret in my opinion and here lays the key to gains.

So Kojak would you say that newbies should take is easier cause it will be better for them in the long run? Meaning that if you start slow you have a better chance of gaining over a long period of time cause your penis will take longer to build up an immunity to the various exercises and greater force that you give over said period of time. I hope that makes sense.

BTW, I’m currently doing a one on/one off routine.

Just wanted to bump this. Kojak have you discovered any new information or support in your findings since you last reported on this?

I’d like to see a more clear definition of “plastic deformation” as it applies to the penis.

And point out that we are all different, on both a chemical and molecular level. Is the process the same for all ages/strength of force? I am not at all sure it is.


_______________

avocet8

Kojak10…

Very interesting stuff. Wonderful contribution. Thanks.

I have two questions:.

Your documents say that “micro-failure begins at 3% elongation.”

My normal flacid approaches 6” or 152.4 mm, but a static stretch gives me 8.5” or 215.9 mm

My first question is this: 3% elongation … of which value? 152.4 or 215.9

I assume that it must be the latter.

On that assumption, my second question is this: it takes a bit of force to stretch my 152.4 mm to 215.9 mm,

more than a typical ADS provides.

3% elongation of 215.9 = 6.48 mm, or just a hair over 1/4”.

The force to get that last 1/4” in order to have 3% elongation is quite large.

I don’t think one could get that with any type of ADS, yet

your analysis (if I am reading it correctly) suggests it should.

Am I reading you correctly?

What are your thoughts?

DD.


Nov 2006 bpel: 7.88 eg: 5.19

Mar 2007 bpel: 8.25 eg 5.38

Shooting for 9 x 6 Ddog.

Originally Posted by Kojack10

Quote:
Healing of the most connective tissue except bone, epithelium and endothelium occur by tissue repair. Thisis often accompanied by fibrous scar, which is the typical patching material for wound repair. Repair responses varyconsiderably in different injured tissues. After an injury, the healed tissue is never same as it was before. Tissue repair starts at 48 hours after injury and lasts up to 6 to 8 weeks, fibroblasts begin wound repair and collagensynthesis. Collagen has the property of gradually shortening when it is truly formed. This contracture occurs from the third week to the sixth month. New scar tissue will always shorten unless it is repeatedly stretched.Remodelling, also known as maturation, involves increased collagen density and organization, resulting inincreased tensile strength. This process begins as early as 3 weeks following injury and continues for a year or longer.

In that quote we see that healing of connective tissue is done by tissue repair. Remodelling, the “R” in IPR is mentioned in this quote, but inflammation and so on are also mentioned on that page as the process is outlined.

That quote you include….tearing, healing, scar tissue, etc….has, I believe, nothing to do with actual PE growth:

(1) If collagen actually “has the property of gradually shortening when it is truly formed,” then PE is an exercise in futility….OR….collagen has little to do with PE gains.

(2) If “new scar tissue will always shorten unless it is repeatedly stretched,” then my gains have had nothing to do with scar tissue formation (read: I’ve gone an entire YEAR, cold turkey, with no PE whatsoever - and only lost about 1/8” of the approx 2” of length gains I’d achieved; and, only about 1/8” or so of girth).

If our gains are about scar tissue formation, and I’ve more than doubled my erect size (volumetrically), then - according to your theory - my penis must be a mass of scar tissue. But it’s not. My penis looks the same (except a lot bigger!), it feels the same to the touch, and my sensitivity seems the same it always was [none of those qualities should be present if my penis were a mass of scar tissue].

The article was packed with info, I just don’t think it addresses the unique situation that we are involved with.

I second wadzilla : scar tissue = non functional tissue, so, according this theory, we all had to be impotent.

It is a bout cell replication. Are all the components there to grow dick cells. The stem cells that are formed in the bone marrow that will eventually become penis cells go to replace dead cells. The object is to have more cells grow than die. Now how do we encourage that?

So genetics designed a certain length and shape to the penis. But we have proved over and over again that we can grow and thicken it. Cell hypertrophy, how do we encourage this?

First we stretch the ligaments and then we work their tunica for growth. Growth slows how do we speed that up again?

Constant rotating and changing PE may be the answer. Dick gets bored of the same ol same ol. The key to this how to find the right flavor of the week. The right PE routine that will spur new growth.

I think the key is telemeres, telemeres shorten become frazzed from distress. Exercise rebuilds the telemeres in the body. PE renews the telemeres in the penis.

Good nutrition must be present. Good diet high in anti oxidants to kill off free radicals. Zinc and vitamin “C” to to normalize the hormone testosteron. “A” and “E” for skin and “B” vitamins for metabolism. Minerals are necessary to in the right amounts. Magnesium, calcium, potassium, sodium, Chloride, don’t forget phosphorus or vitamins are useless without minerals.

Protein in adequate amounts for hypertrophy is needed. Not just enough to get by but enough to encourage cell replication,repair and cell health.

Biblically speaking we should be living to 120-130 years. To have the issue of donkeys and the flesh of horses like in the Bible we must be missing something what is it?


Speak softly carry a big dick, I'm mean stick!

Hypertrophy isn’t the multiplication of cells, but the growth of existing cells.

New cells born in a tissue in four cases, by what I know:

1) when cancer developes;
2) when scar tissue is formed;
3) when tissue is broken (ex. bones);
4) when hyperplasia developes: but hyperplasia phenomenon never has been observed in humans.

So, I’m pretty skeptics that PE is related in someway with those studies.

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