Thunder's Place

The big penis and mens' sexual health source, increasing penis size around the world.

Loading, lengthening, healing.

Originally Posted by dongalong
…………….
Extender wearing isn’t any faster than any other PE technique judging by some members’ results.
The routines linked in my thread - Design The Ultimate Fast Gains Routine
are all different but the results are equally as fast.
It would seem that manual stretches held for a few minutes are long enough to get beyond creep into the microfailure zone for some men - for example, Wadzilla’s Big gainer friend.
This makes me think that wearing the extender before a PE routine, although beneficial, probably isn’t as efficient as long manual stretches.
………….

The problem is: if you have a large and/or conditioned penis, causing microfailures is really hard; you have to soften tissue with a low load-prolonged time approach. Consider this: manual stretches work good for some guys, but don’t work at all for many others, where extenders, used for long time (1000+ h), seem to work for near everybody.

The article you mentioned in post 99 describes what might have occured in a overly-conditioned tunica which makes further gains extremely difficult:

“Effect of Injury and lmmobilization on Connective Tissue

The classic sequence of inflammation, repair, and remodeling follows CT injurys. The long-term effects of reduced stress (immobilization) on CT structures are similar to acute injury, although the process is prolonged and the acute inflammation stage is absent The end result of the
healing reorganization process in CT is that the tissue has a more irregular arrangement; contains proportions of collagen types that are different from normal; has a lower water content; and contains more random cross-links between fibers, fiber bundles, and adjacent tissues. Periarticular CT that has been removed from immobilized limbs has been described as “woody.” As the collagen fibers are more randomly arranged with respect to the testing force, the fibers must resist forces that are not aligned with their long axes (shearing forces)-a task for which collagen is not structurally prepared, as reflected by reduced ultimate strength. In addition, the loss of water diminishes the ease with which the collagen bundles might slide past one another, which has the effect of reducing the ability of the various collagen bundles to align and equilibrate with the applied stress.The end result of both inflammation and immobilization is a remodeled CT with lower tensile stiffess and a lower ultimate strength than normal tissue .This weakening is caused by the more randomized collagen fiber direction, by the inability of collagen bundles to easily slide past one another (cross-linking and loss of water), and possibly by the substitution of collagen types that are less strong than the original collagen.”

It is probable that the toughened tunica has been over-stressed and injured, which has resulted in irregular collagen fibres that don’t react in the ideal way for growth.
The purpose of a deconditioning break is to allow the irregular fibres to be realigned by natural cell renewal into a more orderly arrangement which will react better to the PE forces that will be applied.
Since tension applied by the extender stimulates the realignment of the crosslinks (as mentioned in my first post) I think that you are probably right Marinera, your suggestion could be a superior alternative to a deconditioning break.

Thank you for your views, dongalong, your posts are always based on lectures and well meditated. I really appreciate your contributes in this thread :up: .

Our theories may be psuedoscience but as mentioned in that article (post 99) there is very little scientific knowledge about Connecting tissue (collagen fibre) growth and treatment, let alone penis enlargement.

This site really is at the cutting edge and I hope that some day it will inspire real scientists to work out the optimum time/force needed to enlarge the penis.

We know what works but there is such a fine line between too little or too much.

Healing?

Intrinsic fibroblast-mediated remodeling of damaged collagenous matrices in vivo

Paolo P. Provenzanoa, b, , , Adriana L. Alejandro-Osoriob, c, Wilmot B. Valhmub, Kristina T. Jensena, b and Ray Vanderby, Jr.a, b

aDepartment of Biomedical Engineering, University of Wisconsin, Madison, WI, United States bDepartment of Orthopedics and Rehabilitation, University of Wisconsin, Madison, WI, United States cDepartment of Biomolecular Chemistry, University of Wisconsin, Madison, WI, United States

Abstract

Numerous studies have examined wound healing and tissue repair after a complete tissue rupture and reported provisional matrix and scar tissue formation in the injury gap. The initial phases of the repair are largely mediated by the coagulation response and a principally extrinsic inflammatory response followed by type III collagen deposition to form scar tissue that may be later remodeled.In this study, we examine subfailure (Grade II sprain) damage to collagenous matrices in which no gross tissue gap is present and a localized concentration of provisional matrix or scar tissue does not form. .This results in extracellular matrix remodeling that relies heavily upon type I collagen, and associated proteoglycans, and less heavily on type III scar tissue collagen. For instance, following subfailure tissue damage, collagen I and III expression was suppressed after 1 day, but by day 7 expression of both genes was significantly increased over controls, with collagen I expression significantly larger than type III expression. Concurrent with increased collagen expression were significantly increased expression of the collagen fibrillogenesis supporting [urlproteoglycans fibromodulin, lumican, decorin, the large aggregating proteoglycan versican, and proteases cathepsin K and L. Interestingly, this remodeling process appears intrinsic with little or no inflammation response as damaged tissues show no changes in macrophage or neutrophils levels following injury and expression of the inflammatory markers, tumor necrosis factor-α and tartrate-resistant acid phosphatase were unchanged. Hence, since inflammation plays a large role in wound healing by inducing cell migration and proliferation, and controlling extracellular matrix scar formation, its absence leaves fibroblasts to principally direct tissue remodeling. Therefore, following a Grade II subfailure injury to the collagen matrix, we conclude that tissue remodeling is fibroblast-mediated and occurs without scar tissue formation, but instead with type I collagen fibrillogenesis to repair the tissue. As such, this system provides unique insight into acute tissue damage and offers a potentially powerful model to examine fibroblast behavior.

Matrix Biology, Volume 23, issue 8, January 2005, pag. 543-555

Subfailure damage repairing in ligaments


Last edited by marinera : 07-29-2009 at .

Originally Posted by marinera

Intrinsic fibroblast-mediated remodeling of damaged collagenous matrices in vivo

Abstract….

Numerous studies have examined wound healing and tissue repair after a complete tissue rupture and reported provisional matrix and scar tissue formation in the injury gap. The initial phases of the repair are largely mediated by the coagulation response and a principally extrinsic inflammatory response followed by type III collagen deposition to form scar tissue that may be later remodeled.In this study, we examine subfailure (Grade II sprain) damage to collagenous matrices in which no gross tissue gap is present and a localized concentration of provisional matrix or scar tissue does not form.

This results in extracellular matrix remodeling that relies heavily upon type I collagen, and associated proteoglycans, and less heavily on type III scar tissue collagen.

For instance, following subfailure tissue damage, collagen I and III expression was suppressed after 1 day, but by day 7 expression of both genes was significantly increased over controls, with collagen I expression significantly larger than type III expression. Concurrent with increased collagen expression were significantly increased expression of the collagen fibrillogenesis supporting [urlproteoglycans fibromodulin, lumican, decorin, the large aggregating proteoglycan versican, and proteases cathepsin K and L. Interestingly, this remodeling process appears intrinsic with little or no inflammation response as damaged tissues show no changes in macrophage or neutrophils levels following injury and expression of the inflammatory markers, tumor necrosis factor-α and tartrate-resistant acid phosphatase were unchanged. Hence, since inflammation plays a large role in wound healing by inducing cell migration and proliferation, and controlling extracellular matrix scar formation, its absence leaves fibroblasts to principally direct tissue remodeling. Therefore, following a Grade II subfailure injury to the collagen matrix, we conclude that tissue remodeling is fibroblast-mediated and occurs without scar tissue formation, but instead with type I collagen fibrillogenesis to repair the tissue. As such, this system provides unique insight into acute tissue damage and offers a potentially powerful model to examine fibroblast behavior.

Matrix Biology, Volume 23, issue 8, January 2005, pag. 543-555

Subfailure damage repairing in ligaments

I have changed the bold emphases, but this sub-failure model research fits very neatly with my model of how growth occurs, as linked in post 15 of this thread. More thoughts on how Growth occurs

I much prefer the theory of fibroblastically mediated type I collagen fibrillogenesis tissue remodelling, without inflammation and scar tissue, over the theory of complete tissue rupture/failure, with inflammation, followed by type III collagen deposited to form scar tissue in the injury gap.

Also the statement “following subfailure tissue damage, collagen I and III expression was suppressed after 1 day, but by day 7 expression of both genes was significantly increased over controls, with collagen I expression significantly larger than type III expression. Concurrent with increased collagen expression were significantly increased expression of the collagen fibrillogenesis” also serves to illustrate why recovery time is needed between PE sessions.


Heat makes the difference between gaining quickly or slowly for some guys, or between gaining slowly instead of not at all for others. And the ideal penis size is 7.6" BPEL x 5.6" Mid Girth.

Basics.... firegoat roll How to use the Search button for best results

Thank you firegoat, your inputs are always very appreciated. This article seems really validate your thougths.

Sorry to interrupt, but I have a feeling that most theory threads need some practical summarizing in layman’s terms.
After (a not-so-thorough) reading this thread I came to next conclusions about a practical routine:
A routine has to include rest days. There doesn’t seem to be enough information here to derive figures, but I guess that 2on,1off is okay.
Then, an workout may be subdivided into next parts:
1) Preparation
2) Workout - the only really necessary part. Others are supplemental.
3) Post-workout part.

Preparation’s role is to pre-stretch the penis so that there is no more elastic deformation reserve, and that the collagen tissue is weakened by enzymes.
Workout uses a much heavier load for less time, to reach plastic deformation zone. Constant application of heat also helps by relaxing collagen and easifying deformation.
Post-workout consists of applying low temperature to penis for a short time, to counter inflammatory reaction and “fix”, to some extent, tissues in elongated state.

An explanation for (fast) manual-only gainers may be as such: These people do not experience severe overloads, which can be caused by hanging excess weight, so their penis is in a healthy state and do not contain hardly deformable scar tissue. As such, manual loading is enough to overcome elastic deformation and enter plastic deformation zone. An extender may still help them, however, then, manual load timing probably should be reduced, in order not to cause overloads.

Another info found in this thread, recommends applying less than maximum withstand-able load, and not increase it till one reaches an plateau. Upon reaching, plateau can be overcome by applying significantly higher load for some time, just until gains start again, then one should decrease the load to just above than previous long-time load.

Thanks for your views, Nevod.
Traducing the big (or maybe huge) amount of information posted here in layman terms is really hard. Everyone is encouraged to help in this job.

It seems that you have read a lot here, and that’s good. Your observations also make sense.

cyclic loading and fatigue

Subrupture tendon fatigue damage
David T. Fung, Vincent M. Wang, Damien M. Laudier, Jean H. Shine, Jelena Basta-Pljakic, Karl J. Jepsen, Mitchell B. Schaffler, Evan L. Flatow *
Leni and Peter W. May Department of Orthopaedics, Mount Sinai School of Medicine, 5 East 98th Street, 9th Floor, New York, New York 10029


Abstract

The mechanical and microstructural bases of tendon fatigue, by which damage accumulates and contributes to degradation, are poorly understood. To investigate the tendon fatigue process, rat flexor digitorum longus tendons were cyclically loaded (1-16 N) until reaching one of three levels of fatigue damage, defined as peak clamp-to-clamp strain magnitudes representing key intervals in the fatigue life: i) Low (6.0%-7.0%); ii) Moderate (8.5%-9.5%); and iii) High (11.0%-12.0%). Stiffness, hysteresis, and clamp-to-clamp strain were assessed diagnostically (by cyclic loading at 1-8 N) before and after fatigue loading and following an unloaded recovery period to identify mechanical parameters as measures of damage. Results showed that tendon clamp-to-clamp strain increased from pre- to post-fatigue loading significantly and progressively with the fatigue damage level (p 0.010). In contrast, changes in both stiffness and hysteresis were significant only at the High fatigue level (p 0.043). Correlative microstructural analyses showed that Low level of fatigue was characterized by isolated, transverse patterns of kinked fiber deformations. At higher fatigue levels, tendons exhibited fiber dissociation and localized ruptures of the fibers. Histomorphometric analysis showed that damage area fraction increased significantly with fatigue level (p 0.048). The current findings characterized the sequential, microstructural events that underlie the tendon fatigue process and indicate that tendon deformation can be used to accurately assess the progression of damage accumulation in tendons .

Subrupture tendon fatigue damage

marinera, post #230 was excellent! Thanks for posting the link to it on Wad’s thread “Occam’s Razor”.

Well, I’m looking forward to reading more about grade II sprains now. It is also exciting to see that the information from that research fits neatly with Firegoat’s model of how growth occurs.

Thank you kojack10.

Now, I would like to hear yours (or anyone else’ have read something here) opinion on this doubt:
micro-failure in connective tissue is repaired with or without scar formation?

Originally Posted by marinera
In this study, we examine subfailure (Grade II sprain) damage to collagenous matrices in which no gross tissue gap is present and a localized concentration of provisional matrix or scar tissue does not form. .

Matrix Biology, Volume 23, issue 8, January 2005, pag. 543-555

Subfailure damage repairing in ligaments

marinera, I would say that this quote from your earlier post #230 answers your question. The quote above should give us some direction “IF” subfailure damage, and micro-failure damage are the same.

I don’t have specific knowledge about CT other than having access to the research that has been quoted here on this forum.

By looking at the root words in “micro-failure”, I would say that subfailure damage would include micro-failure. Wouldn’t micro-failure damage be: damage that has occured on the mircroscopic level.

The word “subfailure” simply means: the amount of damage that occured to the CT when the CT was stretched, but NOT to the point of failure (popping/breaking/or a large tear).

It seems that subfailure damage would include micro-failure, but that is just my opinion. I don’t believe that failure on the microscopic level should be assumed to include tears or gaps being created in the CT. Failure could happen in other ways.

Thank you, Kojack. So, if we are meaning the term microfailure as “breakage of few CT fibers”, we have : plastic (rectius : permanent) deformation can happens in sme kind of CT (like ligaments) without inflammation and without scar tissue formation.

It seem really not a small finding to me. We “just” have to know if what is true for ligaments is true also for tunica albuginea.

Research on CT such as ligaments/tendons says that residual elongation is due to changes that occur in the viscous properties of the connective tissue.

I know that similiar statements have been quoted many times on this forum, and possibly on this thread already, but that statement is still an example of the limits of my understanding of this process. Sure, I imagine various scenarios of what may happen in the viscous parts of the CT, but I just don’t know for sure.

We are still closer than we previously were.

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