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Loading, lengthening, healing.

Originally Posted by marinera

I missed this part when I read the article. Now I have about 100 needles in my penis while in my VacADS. What should I do? :D Just kidding!

Well, if you already did, don’t worry. Tell us how it’s working. Guinea pigs are always welcome ;) .

I do not have good links to proof, and the ones I have are in Russian..

I believe there could be a connection between Peyronie disease, over-conditioning from excess hanging, which leads to importance of decon breaks.

Information in this thread suggests that a long and intense load - an overload - on penis, would go past ‘normal’ plastic deformation, and into area of creation of scar (fibrous?) tissue.

Peyronie disease comes from bending of erect penis, which tears the tunica and creates - fibrous tissue! Which leads to ED, pains, and may cause severe bending of penis. Fibrous tissue is hard. Hovewer, in not too severe cases, it heals itself in about an year.

Now, my assumption is: Peyronie is a big lump fo fibrous tissue, from extreme local load. Overload from hanging etc, is distributed along the whole penis, and result is tiny amounts of fibrous tissue throughout the penis. It wouldn’t be paiful, but, as that tissue is very robust, gains slow down. But, these small lumps should not be hard to dissolve: and decon break does just that, it removes fibrous tissue and makes penis structure soft and malleable again.

I agree Nevod. Let’s add a little reference:

The underlying cause of Peyronie’s disease is thought to be trauma or injury to the penis usually through sexual activity. Most of the time, the patient is unaware of any traumatic event or injury. Without treatment, about 12-13% of patients will spontaneously improve over time, 40-50% will get worse and the rest will be relatively stable. Always consult a qualified physician before starting any treatment regimen. Anecdotal evidence supports use of a vacuum erection device to exert gentle longitudinal forces on the plaque, and to lead to remodeling; this too is now being studied in a clinical trial. Never attempt to bend or force the erect penis back to its former alignment as this could cause serious injury and significantly worsen the condition.

There is also an association that a class of anti-hypertensive drugs known as beta blockers may exacerbate or be a possible cause of PD, although it has not been proven. However, all beta blocker drugs list PD as a possible side effect.

That’s why I think rest-days are a good idea if one is using an high-load approach: adding trauma to trauma, without allowing your penis to recover, doesn’t make your penis bigger, I think, but make your penis harder to deform. That’s why the “don’t give your penis time to heal or it will be shorter” idea is a mistake to me (this was the original topic of this thread).

There are no warranties that, if a fibrous plaque develop in one’ penis, it will disappear spontaneously with time; maybe this could also explain why some guys seem enable to gain anything.

Of course, risks of thoughening the penis, instead that making it bigger, is linked not only with hanging, but also (and maybe even more) with manual exercises.

Thank for your input.

Very interesting. To put this information to practical application, is there some way besides a continuing lack of gains, to determine if one has reached a condition where it is time for a decon break?

How does one on a decon break determine when the break has achieved the needed refreshing of tissues?

Nevod, your idea is interesting.

I think that the connective tissue bocomes stronger by other means also. The tissue attempts to adapt in order to prevent further deformation. I don’t know what is actually occuring on the microscopic level. Still, I do remember reading that the collagen bundles begin to align themselves in a direction that is more effective at fighting the force or load, and therefore protecting against further deformation.

To be honest, I’ve confused myself over the years. I don’t know what aproach to take anymore.

Originally Posted by here2learn
Very interesting. To put this information to practical application, is there some way besides a continuing lack of gains, to determine if one has reached a condition where it is time for a decon break?

How does one on a decon break determine when the break has achieved the needed refreshing of tissues?

Unfortunately, I don’t think there isn’t other way that continued lack of gains; we can hope that if one has long and consistent PE experience, he can have some kind of “instinctive” feeling, like in athletic training, that can help him doing educated guesses.

How long a decon-break should last? I don’t know; I think alternating (low-loads)x(long-duration) and (high loads) x (short duration) stimuli, and/or girth and length focused routines could overcome the difficulty of guessing about. But rest is good also for your mind (roughly speaking). Any kind of penis enlargement technique hits your nervous system; I think we are often underestimating this point. Taking some days off in a week, and some weeks off after several weeks of continued penis enlargement work, is good for this reason also.

We are a complex whole, and each parts of our body/mind is inter-acting with some other part.

Beautiful response Marinera. Thanks.

Thanks for the thanks :) .

“The only constant is change.” Heraclitus

I think this quote relates to PE pretty well, lol.

I posted these excerpts here the first time
My Loss of Gains is Nearly Complete :(

I think it’s well worth repeating here:

Memory Encoded Throughout Our Bodies: Molecular and Cellular Basis of Tissue Regeneration.

Pediatric Research. 63(5):502-512, May 2008.

This article postulates the existence of tissue structural memory as a complex distributed homeostatic mechanism. We support such an idea by referring to an extremely fragmented literature base, trying to synthesize a broad picture of important principles of how tissues and organs may store information about their own structure for the purposes of regeneration. Selected developmental, surgical, and tissue engineering aspects are presented and discussed in the light of recent findings in the field.

Tissue memory 1

Somatic Recall
Part 1 — Soft Tissue Memory

By James L. Oschman, Ph.d. and Nora H. Oschman

Young states that the structure of any tissue depends both on how it developed and on the forces exerted on it by other tissues and by the environment. Collagen is deposited along the lines of tension in connective tissues, such as fascia, tendons, bones, ligaments, and cartilage.

Paul Weiss studied tissue cultures and healing wounds, and documented the phenomenon Young described. Wound repair begins with the formation of a clot containing fibrin filaments. At first, the fibers are oriented randomly. As the clot dissolves, fibers that are not under tension are dissolved first, leaving behind a web of oriented fibrin fibers. Fibroblast cells migrate into this web, become oriented along the fibers, and deposit collagen, primarily along tension lines. Any collagen fibers that are not oriented along tension lines are removed by a process similar to the readjustment that took place in the clot. The result is a tissue composed of fibers oriented in the direction that is appropriate to the tensional forces produced by normal movements.

From Young’s work we can see these as examples of the way the organism makes predictions or “forecasts” that promote future survival. Genetic information programs the fibroblasts to deposit collagen in the direction of tensions, and forces from the environment generate those tensions.

Connective tissue structure is therefore a record or memory of the forces imposed on the organism. This historical record has two components. The genetic part recapitulates the story of how our ancestors successfully adapted to the gravitational field of the earth. The acquired component is a record of the choices, habits, and traumas we have experienced during our individual lifetime. The collagen fibers orient in a way that can best support future stresses, assuming that the organism will continue the same patterns of movement or disuse.
It is widely thought that the phenomena Young described are not confined to healing wounds (reviewed by Bassett). Readjustment of collagen deposition takes place in all portions of the living matrix all of the time. This readjustment is the primary method by which body structure adapts to the loads imposed on it and the ways the body is used ……….
Young stated that memories are stored not only in the collagen network, but in the elastin fibers and even in the various cells found throughout the connective tissue: histocytes, fibroblasts, osteoblasts, plasma cells, mast cells, fat cells, etc.

Young’s concept of memory in connective tissues and cells provides a physiological basis for the way the stresses of life, injuries, diseases, muscular holding patterns, emotional attitudes, and repeated unbalanced movements can influence the form of the body.
One has the impression that every movement of the body is recorded in the living matrix. Repeated or habitual movements result in a particular connective tissue architecture. Any change in those habits, no matter how slight, will forever alter that architecture.

Tissue memory 2

I have to thanks Kojack10 for this reference:…e_dynamique.pdf

It’s an advertising of a orthopedic device, backed-up with scientific studies. It resume many of the things posted here; just among the most interesting points:

1) TERT priniciple: the increase in rom of a given joints is directly proportionated to the length of time the joint is held at its end range of motion.
2) optimal time for TERT is the 6-12 hours/daily range.
3) a guide to the use of device (basically, an hand-stretcher) :
- for days 1-2, one should wear the device for no more that 3 hours daily;
-then, the device should be worn for 6-12h/day;
-never wear the device for more than 12 hours daily;
-never sacrifize time at benefit of intensity;
-if the device is worn in the 100 hours after the trauma occured, gains are in the range of 3-6 degree per week, if after the 100 hours gains will be of 1-3 degrees/week.

That is the science behind wearing a penis extender for hours at a time. Possibly an ads works this way also, since it is very similiar, but do not take my word for it.

Something we are doing to our dicks is causing cell replication. Division and destruction at an alarming rate. Maybe it is the milking direction. To get it to go out further by stretching it. This must cause a chemical reaction that causes rapid cell replication. Grip to hard growth stops.

Grip to soft starts the growth again. It is by gradually adding stress for a period of time that somehow gently coaches new growth. Applying heat softens the tunica enough to allow for deformation. Proper heat allows the ligs to soften a bit so than they stretch easier without much trauma.

Rest following a routine is the beginning point of cell replication.

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

Anti-Inflammatory Drugs And Collagen

The Effects of Common Anti-Inflammatory Drugs on the Healing Rat Patellar Tendon

  1. Scott T. Ferry, MD,
  2. Laurence E. Dahners, MD,
  3. Hessam M. Afshari, and
  4. Paul S. Weinhold, PhD*

Background: Tendon injuries that occur at the osteotendinous junction are commonly seen in clinical practice and range from acute strain to rupture. Nonsteroidal anti-inflammatory drugs are often prescribed in the treatment of these conditions, but the effect that these agents may have on the healing response at the bone-tendon junction is unclear.


Study Design: Controlled laboratory study.

Methods: A total of 215 Sprague-Dawley rats underwent transection of the patellar tendon at the inferior pole of the patella, which was subsequently stabilized with a cerclage suture. The animals were then randomized into 7 groups and administered 1 of the following analgesics for 14 days: ibuprofen, acetaminophen, naproxen, piroxicam, celecoxib, valdecoxib, or control. At 14 days, all animals were sacrificed, and the extensor mechanism was isolated and loaded to failure. Biochemical analysis of the repair site tissue was performed. Animal activity throughout the study was monitored using a photoelectric sensor system.

Results: The control group demonstrated greater maximum load compared with the celecoxib, valdecoxib, and piroxicam groups (P < .05). The acetaminophen and ibuprofen groups were also significantly stronger than the celecoxib group (P < .05) but not statistically different than the control group. A total of 23 specimens had failure of the cerclage suture with the following distribution: control (0/23), ibuprofen (0/23), acetaminophen (0/24), naproxen (3/24), piroxicam (4/24), celecoxib (6/22), and valdecoxib (10/24). The difference in distribution of the failures was significant (P < .001).

Conclusions: Anti-inflammatory drugs, with the exception of ibuprofen, had a detrimental effect on healing strength at the bone-tendon junction as demonstrated by decreased failure loads and increased failures of the cerclage suture. Acetaminophen had no effect on healing strength. The biomechanical properties paralleled closely with the total collagen content at the injury site, suggesting that these agents may alter healing strength by decreasing collagen content.


An In Vitro Investigation Into the Effects of Repetitive Motion and Nonsteroidal Antiinflammatory Medication on Human Tendon Fibroblasts

  1. Louis C. Almekinders, MD
  1. Division of Orthopaedic Surgery, Sports Medicine Section, University of North Carolina School of Medicine, Chapel Hill, North Carolina
  1. Albert J. Baynes, PhD
  1. Division of Orthopaedic Surgery, Sports Medicine Section, University of North Carolina School of Medicine, Chapel Hill, North Carolina
  1. Lynette W. Bracey
  1. Division of Orthopaedic Surgery, Sports Medicine Section, University of North Carolina School of Medicine, Chapel Hill, North Carolina

Soft tissue injuries due to repetitive motion are common sports injuries and are often treated with antiinflamma tory therapies. We investigated the in vitro effects of repetitive motion and nonsteroidal antiinflammatory medication on human tendon fibroblasts. In addition, we studied the effects related to the presence of inflam matory cells………

Our results ……….suggest that nonsteroidal antiinflammatory medication may have potentially negative effects during the proliferative phase of a healing since it was associated with decreased DNA synthesis. However, it may be beneficial in the maturation and remodeling phase since it stimulated protein synthesis.



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