Loading, lengthening, healing.

Lol this again has made my night please don’t stop them it’s funny and if I have a bad day I can all ways find a smart ass on here that brightens my day lol.

I agree with firegoat, as I said before science post are some what good but in the end if lots of guys grow from hang weights off there dick you will find me in that circle if the wheel ant broke don’t fix it my dad all ways said.

I am sure we will find out why hanging works some day but hay it works so do it. Don’t try to explain to me why a bumble bee shouldn’t fly in the laws of physics just watch it fly.

I think this is were we are having such a problem here because you will never convince guys who have grown big cocks with the us of hanging or extender work by saying that is illogical because this science report say so, the guy looks down at his 7.5 dick or in Monty’s case over 8 and say yea ok. This is the problem.

Until some one say hay here is a double blind penis enlargement study done my top urologist in the country and they tested every method of PE for over a year and found out these result and this is how you will get the best result by using this much weight or jelq only this much, then I think when we put stuff down. We should never say stuff like they are just illogical or don’t you see your theory is flawed.

This will only fuel the fire of the guys who have grown big dicks doing the exact opposite thigh you speak of you are almost calling them liars on what they say they have grown from and saying you have seen much more pics from jelqers then hangers and this cause doubt about if these are true gains is not fair some guys wife’s would freak if they did that this is what causes the tension if you just word it like, this is my way of doing it I find it to be the best method that has worked for me no one will fight you on that merinera. You can state all the facts you want and pot up tons of science post and you won’t here much from hangers. Maybe some stuff but what can we really say if your growing from it right only great gains keep it up.

Oh my God!!

Another story:

TGC Theory: One Month Results.

So, 1" EL gains and .25" - 0.5" EG gains in 6 months of work, 2-3 hours PE work weekly.

How this gains are possible according to the theory I’m critizing here?

And hear this:

One more:

My gain and a question

Again, why this guy’ penis has not shortened taking rest days?

Sorry, marinera; I’ll put the stick away; I hope I didn’t put out an eye or anything.

Both these ‘cases’ you’ve posted are focused on girth. For me, girth exercises, including jelqing, seriously affect my ability to get and maintain a good strong erection. So, extended periods of rest is somewhat mandatory for me. With that being said, I also seem to gain girth very, very easily, even with a very light, inconsistent routine.

Check this out: It’s a happy day!

I’ve also never experienced a loss in length when I’ve stopped a routine. And, I start and stop regularly in order to revert to skin stretching. In other words, I’ve never had to ‘cement’ my gains.

I’m not pointing this out to be argumentative. I’m just trying to point out that everyone seems respond to PE differently. I don’t think you can neatly package a routine that will apply to everyone. I have to work very, very hard in order to gain length. On the other hand, my dick gets a little fatter every time I sneeze.

Well, I examined here 4 cases (or five? Well doesn’t really matter). The first two were to see how not resting adequately can lead to counter-productive consequences.

The last two were to point out how good results are not explicable with the theory this thread is focused on.

It’s true that those routines were incorporating girth exercises, but : fresnillo gained 1.5” in length with 1 on - 1 off; and Springer 1” length or such with a minimal routine - (1” is a bit too much to be called “better EQ/newbie” gains). This disproof the theory on this basic point: “if you rest, your penis will shorten”.

You’re right that girth exercises require more rest (for most persons, at least), being involved other things (smooth muscles etc.) than connective tissue; but in those cases this really doesn’t matter, if you ask me.

Length and girth, on the other hand, seem quite analogous things: girth is circular length (wasn’t pudendum to coin this expression or similar?).
But since this is a topic that my friends Iguana and Remek are studying, I don’t want to go deeper on that (oh, what a fair man I am!!)

Starting and stopping regularly is a form of rest; you should add some more detail about your PE regimen, to see how it is fitting with the “mantra” I’m critiquing here.

Is there something bad in being argumentative? I don’t think so - I think there is something bad in arguing a priori (“just for the sake” should be the right translation), or using unrelated or malicious arguments.

The goal of this thread is not inventing any kind of universal routine. I’m not a Prophet or a Master of anything.

That theory, as I said many times, can’t be accepted in that form because (at least to me) has logical falls.
I know that many have an emotional reaction when that theory is critiqued - I was expecting that. But to grow as better humans, we have to kill Totems. Sad but true.

This has nothing to do with what worked for many: I’m searching for clear, enlightening “success stories” with the “never stop working” approach, exactly to figure out how and why some guys have better gains with that kind of routine. If you have similar links, post here, please (this wasn’t the original purpose of this thread, but I think there is nothing bad in that).

We could brainstorming on that - and saying We I mean me, you, and all guys that want to have a fair debate.

It’s unlikely that we’ll discover anything of much value, but knowledge has to start somewhere - and, in the worst of cases, we’ll have had some sort of funny.

Another pill of Med’ views :

Soft Tissue Manipulation

Soft tissue is often manipulated for a variety of effects (33,34). Soft tissues display both viscoelastic and viscoplastic mechanical properties. The stress-strain curve depicted in Figure 1.5 describes the behavior of soft tissues under varying loads. The area of tissue microfailure is located just beyond the linear portion of the stress-strain curve, where the curve falls away from its elastic modulus. Tissue microfailure is the destruction of individual tissue fibrils that occurs as a tissue is loaded beyond its physiologic limit but before gross tissue failure. Figure 1.5 displays a typical stress-strain curve and demonstrates the region of microfailure. Microfailure can be exploited for several therapeutic effects.

Permanent elongation of contracted tissues depends on tissue microfailure and is necessary for permanent tissue reorganization to occur (35). Following micro-failure, phases of tissue inflammation, edema, repair, and remodeling ensue.

…………
Although conditioning is a recognized creep-related phenomenon, its importance with respect to human, in vivo, conditions has, until recently, not been investigated, and mechanical testing of isolated tendon may not necessarily represent human in vivo conditions, where concerns regarding tissue storage, clamping technique, perfusion and pressure can be avoided.
……….
Because of the viscous, time-dependant properties of tendon, it is likely that the duration of each repeated tensile loading event will in some way influence the load–deformation properties of the tendon. The issue of history dependency in the mechanical behaviour of human tendons in vivo was addressed by Maganaris
……………………………..
The loading pattern caused tendon elongation to increase by 5 mm from the first to the fifth contraction, without any significant changes thereafter. A similar pattern and magnitude of changes were found in the tendon residual deformation after relaxation. These changes clearly demonstrate a ‘conditioning’ effect.
…………….
Adaptations of tendons to chronic regimes of loading, unloading and ageing, new findings and perspectives
In contrast to previous beliefs, it has recently been shown that human tendinous tissue is metabolically rather active in response to activity. In fact, using the microdialysis technique it has been shown that an acute bout of exercise immediately reduces human tendinous collagen synthesis followed by a dramatic increase in the subsequent days (Langberg et al. 1999b). Chronic loading appears to increase synthesis and degradation, although the latter occurs primarily in the initial phase of a period in persons subjected to increased physical activity (Langberg et al. 2001).
………………….
However, the influence of the various components of the extracellular matrix or the collagen fibril size, number or density, on the mechanical properties of tendon has not been established. Moreover, up to recently, whether the influence of various forms of physical activity, ageing and a combination of these, would influence the mechanical properties of human tendons was mostly unknown. However, new findings, based on the above-described ultrasound techniques, show that the mechanical properties of human tendons, assessed in vivo, undergo substantial changes both with ageing and disuse. In both conditions, a decrease in tendon stiffness has been found (Fig. 5) (Reeves et al. 2003a; Karamanidis & Arampatzis, 2005; Narici et al. 2005; Reeves et al. 2005b; Maganaris et al. 2006).

…………..
As a matter of fact, in vitro studies have shown that older tendon tissue displays: (1) an increase in collagen cross-linking; (2) a reduction in collagen fibril crimp angle; (3) an increase in elastin content; (4) a reduction in extracellular water and mucopolysacharide content; and (5) an increase in type V collagen (Kjaer, 2004). Despite the reduction in tendon stiffness with ageing, resistive loading has been shown to significantly reverse/mitigate these alterations (Reeves et al. 2003a,b, 2005a).

……………………….
Animal data show that tendon may undergo either qualitative (Buchanan & Marsh, 2001; Viidik, 1967) or hypertrophic changes (Woo et al. 1982; Birch et al. 1999), or both (Woo et al. 1982)
…………………..
Surpisingly, however, a total training stimulus of 9 months of running in previously untrained subjects did not result in tendon hypertrophy of the Achilles tendon (Hansen et al. 2003). At the same time it has been shown that resistance training for 3 months induced marked changes in the material properties of human tendon in the absence of any tendon hypertrophy (Reeves et al. 2003a,b). It is possible that these apparent discrepancies may be explained by the training mode, namely endurance versus resistance training. On the other hand, perhaps qualitative changes in the extracellular components preceed any hypertrophic response since metabolic activity increases with an acute bout of loading (Langberg et al. 1999b; Kalliokoski et al. 2005; Miller et al. 2005; Bojsen-Moller et al. 2006), and there is a lack of hypertrophy with loading for months, while the material changes (Young\’s modulus) are apparent fairly soon (Reeves et al. 2003a,b). Furthermore, what remains to be established is whether the tendon hypertrophy induced by chronic training represents a physiological response to reduce tissue stress or a tissue repair response to damage induced by repeated loading (Rosager et al. 2002).

S. Peter Magnusson, Marco V. Narici, Constantinos N. Maganaris, Michael Kjaer (2008) Human tendon behaviour and adaptation, in vivo
The Journal of Physiology 586 (1) , 71–81 doi:10.1113/jphysiol.2007.139105

(Published)

I find this article extremly interesting. It suggest that repairing and growth of connective tissue is even more complex than we figured.

In this thread was discussed if the growth of TA could happens with hypertrophy or hyperplasia:

Yet another theory of how we grow

pudendum in this thread:

Possible reason for PE induced growth

reached some evidence that hyperplasia, or cellular proliferation, was a mechanism used to make connective tissue heal and grow.

Now, the article cited suggest that there are (at least) 4 kinds of response to a stress :

1) elastic reaction;
2) viscoelastic response;
3) hypertrophy;
4) hyperplasia.

Any of this adaptive response could be triggered by a given stimulus (either acute, repeated or chronic).

The preceding studies reported in this thread suggest that there isn’t a distinct plastic deformation phase and micro-tears repairing phase, if I’m not reading them wrong: micro-tears are produced at the same time plastic deformation occurs.

Further: after the very few stretches, plastic deformation is less pronounced or un-existent, while micro-tears are increasing.

Finally, we have that high loads, repeated over time, could lead to a delayed hypertrophy adaptation in connective tissue.

I think that this point is causing a bit of confusion to many readers. Some of them are assuming that I’m saying a thing that has no meaning, and some others are suggesting that my poor English is the cause why I’ve misunderstood things I’ve read.

It’s all ok, I know that this point is a bit difficult to understand. So, I want add a better explanation of the phenomenon I’m supposing is happening in that case:

Plastic deformation should not be confused with the phenomenon of creep (Fig. 6). 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.
……………..
One of the components of manual thrust techniques is to preload a tissue by "taking out the slack prior to
beginning therapeutic movement. This component is often referred to as "reaching the first point at which
resistance is felt," a point sometimes called "Rl" in the manual therapy literature.
……………………….
The end result should allow the collagen fiber crimping to be removed from the CT and for some amount of creep deformation to occur. These are temporary lengthening phenomena demonstrating a damped elastic response and can easily be misinterpreted as permanent lengthening. Plastic deformation does not take place untll the forces within the tissue reach a higher level.
……………
The ligament deforms considerably at first. Elongation tends to plateau after 6 to 8 hours, although vely
gradual deformation can continue for months if the load is continued. The creep phenomenon is characteristic of viscoelastic materials and occurs at load well below those of the linear region of a stress strain curve. Creep deformation is not permanent, and the tendon will slowly resume its original length after the load is remove this response is called a "damped elastic response."

http://www.ptjo urnal.org/cgi/r … t/72/12/893.pdf

Marinera - I’m interested in how you’d translate all this into some pragmatism.

In other words, how does this theory translate into a hanging or stretching routine that someone could follow?

Can we conclude any rules from this? Such as maximum/minimum hanging times? The use of an ADS afterwards?

Your theories may well be the key why guys like Bib have looked back and thought they may have done too much, or taken an ill-informed approach when they could have been gaining more and smarter.

~L

I think if you want some pratical translation of the references I’m posting, you should ask to firegoat: he already knows any article/book on the subject of connective tissue, has pratical experience in applying that theoric knowledge, is a more experienced PEer than I am. He posted basic points in this thread and in the one he linked; maybe he’ll like to go further on this subject, we can just hope, but that would be like a teacher finishing his daily work and teaching in the night to 100,000 guys basic things, answering 1 billion time to the same question - like (the worse of the “newbie forum”)^1000.

I’m trying to accumulate some references in this thread, alternating them with some “case-study” just to avoid to annoy the reader, and brainstorming about that (even incomplete) theoric knowledge and his application in the PE world.

Basing on your feedback and help, I think we can get some minimal results.

The first thing to note, I think, is this:

The creep phenomenon is characteristic of viscoelastic materials and occurs at load well below those of the linear region of a stress strain curve..

(from #99)

If we think to a PE technique that, without reasonable doubts, works by "load well below etc.", extenders come in mind. I’m speaking of the "old-school" extenders: JESS, Penimaster, Max-Xtender and similar. They apply 1/4"<= tension =< 4 lbs.

…….Elongation tends to plateau after 6 to 8 hours, although vely gradual deformation can continue for months if the load is continued.

Deformation continuing for months: fit it?

So extenders, we can suppose, are working along the "creep deformation". You use them for many minutes daily for several months and the penis should elongate. But: why are length gains with extenders permanent?

These are temporary lengthening phenomena demonstrating a damped elastic response and can easily be misinterpreted as permanent lengthening. Plastic deformation does not take place untll the forces within the tissue reach a higher level. .

Something is wrong, agree?

But, let’s look at what happens using an extender, basing on "happy buyer" posts (people like Westsidetoni*):

for the initial 600-800 hours of wearing, no erect gains are seen. FL gains, yes. We have to remember, also, that in that initial period the extender is applying a so little tension that the penis is not extended over the BPL.
I think that, reading the preceeding reference, we can say that what is happening is : the penis is loosing elaticity.

When the user starts having more BPFL, being able to stay at that lenght for hours, we could guess that some kind of deformation is happened. What kind of deformation? Not "plastic deformation", I think, for two reasons:

1) because the users has not applied high load (AKA - load NOT below the strain-stress curve);
2) because he’s has not yet gotted BPEL gains.

I speculate that there is a link between overstretced tissue and "erectible" tissue: if that tissue is temporarily deformed to a given Max length, doesn’t spontaneously stretch to that Max.

Let’s go on : extenders users start to see gains (about 1/4") when the 600-800 h x wear is touched. In the next 500 h they have their first BPEL gains AND the most gain of the total : 1/2" in 400-600 h, when the first portion gave 1/4" EL gains. What’s happening? Permanent deformation? But: with low loads? Doens’t it counteradict the load-strain relation?

I think in the previous period of use, "elastic deformation phase", the extender was acting (foremost) on the collagenous tissue, extending it slowly, with minimal tension, so to cause the minimal degree of scars and/or hypertrophy (or whatever adaptations that would thougthen tissue) .

After that, when "elastic deformation" adaptation is stalling, "micro-tears healing" adaptation is happening. At a given length, some fibers are damaged more than others, because the same load is less counter-acted by collagen-resistence. So, even if the load is low, the basic process that lead to permanent deformation is happening. I think what books are seeing is that you don’t have plastic deformation when the collagenous tissue is not yet temporarily deformed to a given length; a low load cannot create permanent deformation - that’s because the collagen is resisting.

I would like also to note this:

Elongation tends to plateau after 6 to 8 hours

This suggest that wearing an ADS 24/24 does not allows a better (temporarily) deformation than wearing it 6/24, or maybe 8/24 - there is always an optimal amount of time even with a very low tension, and more than that is, in the best of cases, unuseful.

*My gains (start 1-1-2007)

To better understand the previous post, a bit more reading could help:

Connective Tissue Structure
The basic constituents of most biologic tissues are cells, fibers, and ground substance. Dense regular CT
is a histologic category of CT that includes ligaments, tendons, fasciae,and aponeuroses.
…………………….
Ligaments and tendons are similar because most of their collagen content is aligned in roughly parallel
bundles, with a few fine elastic fibers between the bundles.
……….
bundles in both structures may have some undulations or “crimping” when not under tensile loading .Tendons and ligaments have sparse, flattened fibroblasts that are scattered throughouttheir structure and have little
ground substance.

………
The presence of waviness or crimping in the normal collagen bundles represents a variable amount of slack. This
slack must be taken out by a tensile force before any individual bundle of collagen is placed on stretch. The
result of the crimping in conjunction with the variability in bundle alignment is a collagenous structure with subunits that are loaded asynchronously. ‘The bundles that are most closely aligned parallel to the direction
of tensile stress and have the least slack (crimping) will be the first to resist tensile loading. The remaining
bundles of collagen will come into play as further deformation takes out additional slack. Only after
many of the bundles are placed on stretch does the CT structure as a whole begin to provide significant
resistance to the tensile force.

The resistance of a tissue to deformation.

The physiologic loading region of the stress-strain curve 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.

[Threlkeld AJ. The effects of manual therapy on connective tissue. Phys
Ther. 1992; 72:893-902]

(Published)

You mean to say you don’t KNOW a way to apply it?

OK, OK, sorry..

That’s interesting about the 6-8 hour plateau.

I think a good routine would be hang high weights for 2 hours or so until you reach fatigue, then ADS it for 8. Rinse and repeat.

~L

I mean : anyone doing a semplicistic transposition of these findings in PE is doing a guess. I also mean that many that are speaking like Truth Owner don’t really know so much.

As I see things, we should see if this notions can fit in someway with anedotical evidence, to understand something more about how PE works, wich tissues are more or less affected, which are ideal variable involved - rest, load, time etc..