Loading, lengthening, healing.

Yes, let me summarize what we have learn from studies here:

temporary residual lengthening (even lasting for many weeks) is produced with low/loads-long time stretching;

permanent residual lengthening is produced with high loads and recovery, as a result of repairing damages in CT.

Microfailures are repaired and/or cellular proliferation is the adaptive response to sub-failure damage. Maybe such last adaptive response is best activated by cyclic medium load (so, multiple ‘sets’ of applying the stretching for short time, but done at high frequency) than by low loads applied in a continuous way, for long time.

That’s all, since here.

So are you saying that elongation produced via traction or extender type devices (low loads, long time) is temporary in nature?

If you read previous studies posted here (see in example post #99), to have really permanent deformation you have to cause micro-failures. Micro-tears are not produced since very high tensions are used. Low tension/prolonged time are good to obtain long lasting temporary deformation; this deformation is based on changes in viscoelastic properties o the tissue.

So, what extenders do? I can see three options:

a) extenders are just causing viscoelastic changes based elongation; this means that gains will not be permanent;

b) at some point, the extender start to push with more force on the already relaxed tissue, causing a little amount of microfailures that will make gains permanent.

I accepted, previously in this thread, this second hypothesis, but I haven’t anything empiric to proof it’s true: we should ask to those who used extender and ceased using it for 1 year or more, to know if their gains were lost.

c) penile tissues can grow in a permanent way through a very specific adaptation, like cellular proliferation, without breakage of fibers.

Marinera
Maybe such last adaptive response is best activated by cyclic medium load (so, multiple 'sets' of applying the stretching for short time, but done at high frequency) than by low loads applied in a continuous way, for long time.

That seems to support my hypothesis of fast manual gainers, and the “Less is More” concept too. However, now we have to figure what exactly level of load causes subfailures, and not scar tissue growth. Plus, various augments, such as continuous heat appliance during loading, and pre-workout extender have to be considered.

Here’s something I found interesting. This study was an attempt to distinguish between Histogenesis (tissue lengthening by growth) and mechanical elongation (I’m assuming stretching.) I posted this in wad's thread but thought it fit well here also.

They studied 14 limbs undergoing lengthening by measuring the tensile force between the pins in the legs. They would increase the length .5 mm every 12 hours. The tension was measured continuously. Each time the length was increased the force on the tissue increased but then gradually decreased. What was interesting was that at night time the rate of decrease in the force was significantly higher than in daytime. If the tissues were simply stretching (a visoelastic response) this would not be the case. The rate should have been constant. But, as the study pointed out, this suggests that the tissue was lengthening by histogensis at night time.

What makes this more interesting is that studies also show that sleep deprivation can hinder wound healing.

If this is the case and the body grows and heals while at night, this might be a strong argument for PE while asleep. Unfortunately, this presents a dangerous situation as we are all aware. Maybe a break thorough lies somewhere here-in? Maybe a comfortable, safe, all night stretcher?

Thanks for your apport Iguana. Now, you do know that I’m going to be an a**hole, don’t you? ;)

We treated this topic before on this thread :
firegoat - Loading, lengthening, healing.

I’m on the very same line of thinking of firegoat.

Just in example, speaking about lengthening bones while sleeping: I don’t think you can extend this to penile tissues, at least if you don’t think your bones can have erections :) .

Now why in the world would you want to do that? I came in peace to join in the discussion… Very well then. You make me sad. Instead of writing a long drawn out explanation of why I think my penis tissues have more in common with my leg than a rat tail tendon. I will just take my studies and go home. :)

:d

I would still be interested to read the full copy, as abstracts can often be interpreted according to one’s expectation of content. But it’s another document on ‘pay per view’.

I would like to see if they have just assumed that viscoelastic response would be constant between day and night, and thus decided the presence of histogenesis may be suggested, or if they have researched nocturnal VE response separately to the leg lengthening (and if so how they did it).

I think there could be a high possibility that viscoelastic relaxation may accelerate at night when the nervous system is more relaxed than in the day.

It’s good to have more input Iguana. Thanks.

Yeah, of course keep helping here, Ig; there are (rare) days when I’m not so a bad guy :D .

Equivalence of single and incremental subfailure stretches of rabbit anterior cruciate ligament
Manohar M. Panjabi *, Russel C. Huang, Jacek Cholewicki
Biomechanics Laboratory, Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, Connecticut, U.S.A.

Abstract
Experimental models are often used in the laboratory to produce incomplete soft-tissue injuries simulating those observed clinically. Single and incremental stretch protocols have been utilized. The latter has many advantages over the former. This study was designed to determine if incremental and single ligamentous stretches are biomechanically equivalent. Eleven paired fresh rabbit bone-anterior cruciate ligamentbone preparations were used. One of each pair (single-stretch protocol) was stretched to 88% of the average failure deformation and then stretched to failure. The other ligament (incremental-stretch protocol) was stretched to 55, 66, 77, and 88% of the average failure deformation and then stretched to failure. All stretches were performed at 1.2 m/sec. Stress-relaxation tests were performed before and after the 88% stretch for both stretch protocols. Relaxation curves were parameterized as forces at six time points and were also fitted to a three-element model. Load-deformation curves recorded during stretch to failure were characterized by eight parameters. Each incremental stretch step produced a significant increase in deformation, indicating alteration in the mechanical properties of the ligament. Both groups of ligaments, when intact, exhibited no differences in relaxation curves (p > 0.2). The 88% stretches, produced by each of the two stretch protocols, significantly altered the viscoelastic behavior of the ligaments (p < 0.002). However, after the 88% stretch, there were no differences in either viscoelastic (p > 0.1) or load-deformation (p > 0.1) paramters of the two stretch protocols. In conclusion, the 88% subfailure stretch significantly altered the mechanical properties of ligament, and the incremental and single stretches were biomechanically equivalent.

Single And Incremental Sub-failure stretches

Modulation of cell functions of human tendon fibroblasts by different repetitive cyclic mechanical stress patterns

Tanja Barkhausena, , , Martijn van Griensvena, Johannes Zeichena and Ulrich Boscha

aDepartment of Trauma Surgery, Hannover Medical School, Hannover, Germany

Summary
Mechanical stress is a factor that is thought to play an essential role in tissue generation and reparation processes. The aim of the present study was to investigate the influence of different repetitive cyclic longitudinal stress patterns on proliferation, apoptosis and expression of heat shock protein (HSP) 72. To perform this study, human tendon fibroblasts were seeded on flexible silicone dishes. After adherence to the dish, cells were longitudinally stressed with three different repetitive stress patterns having a frequency of 1 Hz and an amplitude of 5%. The proliferation and apoptosis rates were investigated 0, 6, 12 and 24 hours after application of cyclic mechanical longitudinal strain. Expression of HSP 72 was tested after 0, 2, 4 and 8 hours. Control cells were also grown on silicone dishes, but did not receive any stress. Stress patterns applied during one day resulted in a significant increase in proliferation and a slight increase in apoptosis. HSP 72 expression was rather unchanged. A stress pattern applied during two days resulted in a reduced proliferation and apoptosis rate whereas the expression of HSP 72 showed a significant increase. This study shows that different stress patterns result in different cellular reactions dependent on the strength of applied stress. Repetitive stress applied during one day stimulated proliferation and apoptosis in contrast to an extended stress duration. The latter induced an inhibition of proliferation and apoptosis probably through an increased HSP 72 activity. This may be related to an excess of applied stress.

Differet patterns of cyclic stretching

Fibroblast orientation to stretch begins within three hours
C. Neidlinger-Wilke 1, E. Grood 2, L. Claes 1, R. Brand 3 *

Abstract
Most connective tissue cells align in response to stretch. Previous studies have shown these responses occur within 12-14 h of initiation of stretch, but do not identify the time at which this orientation occurs, nor whether the orientation continues after cessation of stretch. To ascertain the earliest times at which fibroblast orientation occurs, we cultured primary human fibroblasts on deformable culture dishes and stretched (1 Hz, 8% uniaxial strain) them for up to 24 h. We photographed the cells at 0.5, 1-6, 8, 10, 12, 14, 16, and 24 h. Similarly cells were photographed at 1-3, or 4 h after cessation of stretch for stretch durations of 1, 2, and 3 h. Orientation of cells were ascertained by an interactive computer program. The fibroblasts began to orient by 2-3 h and orientation appeared nearly complete by 24 h. Cultures stretched for 2 or 3 h continued to exhibit greater degrees of orientation (compared to controls) for 2 or 3 h respectively after cessation of stretch. We conclude fibroblasts begin to orient within 3 h of initiation of stretch, and that they continue to orient for several hours after cessation of stretch.

Stretch orientation

Ok, so distraction histogenesis has been discussed before on this thread, and in others, but I believe that we need to examine it further and read the results of more studies on it.

While reading Wad’s thread, EtP theory, I read posts where histogenesis was mentioned. I remembered reading the term before on the forums, but I had always wrote it off as something that "might" happen in smooth muscle, and since I don’t see smooth muscle as being the toughest limiting factor, I didn’t read into it. Anyway, some of the statements mentioned on Wad’s thread caused me to look further into histogenesis. I’m impressed with what I’ve read. I found studies and definitions of the term stating that all of the soft tissues grow. This includes the skin, veins, nerves, fascia, tendons, and ligaments.

Now, I’m not suggesting that we look into attempting some method of applying traction to the penis for 24 hours, or at night, but I do think that we should explore what is the minimum amount of "time under tension" necessary to elicit the response of histogenesis.

I did find some very interesting study results that I’d like to post regarding histogenesis.

The study is titled: The effect on the extracellular matrix of the deep fascia in response to leg lengthening

"The distribution and composition of extracellular matrix in tissues play important roles in the etiology, pathology and mechanism of diseases. In particular, the abundance alterations of collagens are closely related to the injury and repairing of tissues, fibrosis pathology and the physiologic process of tissue regeneration. The total amount of collagen type I is approximately equal to that of collagen type III under normal conditions in most organs and tissues. Total collagens increases from 4% in normal liver to 10% in cirrhosis, and the levels of collagen type I reaches 4 times collagen type III as cirrhosis occurs [20]. Similarly, collagen type I increases dramatically while collagen type III decreases in the fibrosis of lung [21]. In contrast, collagen type III but not collagen type I level increases during tissue repair, suggesting a prior role of collagen type III in the regeneration of related tissues."

"In this study, a distraction rate of 2 mm/d led to injuries of fascia and increasing amount of collagen type III in the matrix, which represents a repairing process of related tissues. The closest abundance of collagen to that of normal fascia was detected in the matrix of fascia that had been distracted at a rate of 1 mm/d until 20% increase in tibia length was achieved. Combined with our previous findings of increased amount of reticular fibers and ribosome, a nuclear split, the activation of endotheliocyte and newly formed young collagenous fibrils in the same scheme [14], these data indicate that the regeneration of multi-tissues involving deep fascia occurs in animals subjected to distraction-forced leg lengthening. While the distraction rates represent a certain load exerted on legs, the increments in tibia length (10% and 20%) may reflect the duration time of the load. As a result, efficient fascia regeneration is initiated only in certain combinations of the leg load parameters including appropriate intensity and duration time, e.g., either low density distraction that persist a relatively short time or high distraction rates. This may explain why 20% lengthening at a rate of 1 mm per day causes less collagen damage than 10%. Whereas GAGs are essential components of the extracellular matrix in normal, embryonic, or tumor tissues, in our study, a strong staining with Alcian blue in both control and distracted fascias indicated the presence of chondroitin sulphate and heparin sulphate, but not of keratan sulphate. However, the accurate detection of GAGs in biological samples has been precluded by the lack of sensitive methods [22]."

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

Regardless of whether or not you believe that penis enlargement does, or CAN occur by histogenesis, I believe that some of the information provided in the study is very important.

The study tells us that type III colagen becomes more prevalent when damage occurs to connective tissue. The study also gives an example of the balances between type I and type III staying the same, just as in normal CT, even though the CT is being permanently lengthened. This more natural balance of collagen types, as well as less damage, occurs when the lenthening is done at a slower rate.

I believe that this explains how enlargement is achieved through high intensity IPR type routines, with planned decon breaks, and it also explains how gains are made with low intensity, unscheduled decon breaks, and little addaptation (reaching plateaus very slowly).

Ok, I shouldn’t use the word "believe", but I think that this information is a good "lead" for us to follow up on.

Thank you Kojack10. Interesting. Three points:

1) this study refers to leg-lengthening, so a structure composed of different kind of tissues;
2) the “structure” was dissected, so cut (correct me if I’m wrong);
3) it seems to sustain, as many others studies reported in this thread, that [low-load/long-time/slow-rate-increase of stress] lead to best functional elongation, right?