Possible reason for PE induced growth
I know many of you guy’s eyes glaze over when someone presents a “science-based” posts. Well, unfortunately (or fortunately depending on your perspective), I’ve got another one.
After posting on other threads regarding the theories of why we grow and by what proposed mechanism, I find that my 2¢ tended to be disorganized and almost contradictory. I believe it was because we continue to dance around the theories of micro injury (IPR) vs. sustained stretch growth.
I have done some research both on the forum to investigate what has already been posted and have dug into the medical literature regarding connective tissue remodeling in response to stress (tension/stretch).
I want to layer onto the thoughts of Bib (re: microtears), Hobby (re: sustained stretch growth) and others.
I believe that the evidence I will present from studies on connective tissue response to stress will add to our understanding as to why this whole process works on a cellular/fiber basis.
As has been noted many places elsewhere, connective tissue varies throughout the body.
Connective tissue is composed of the cells (fibroblasts) that make all of the substances outside the fibroblasts that make up this tissue (Extracellular Matrix; abbreviated ECM). Fibroblasts play a central role in tissue remodeling and wound healing processes
The ECM consists of collagen fibers (several kinds), elastic fibers (elastin), and ground substance (the other components are not important for this discussion). The fibers are arranged from very random to more organized orientation (depending on the connective tissue type).
The quantity of the fibers in the connective tissue determines the type; few (loose connective tissue; under skin for example) to many fibers (dense connective tissue; tunica, ligaments, tendons, for example).
Sustained stretch or intermittent stretch? Consider this:
“With any given stretching force, the resulting proportion of plastic to elastic response depends primarily upon two stretching force variables: time and intensity. Research on these variables has produced three significant findings:
1) Short duration stretching of high intensity favors the elastic response, while prolonged duration stretching of low intensity favors the plastic response.
2) There is a direct correlation between the duration of a stretch and the resulting proportion of plastic, permanent elongation.
3) There is a direct correlation between the intensity of a stretch and the degree of either trauma or weakening of the stretched tissues.”
“To summarize, the longest period of low force stretch produces the greatest amount of permanent elongation, with the least amount of trauma and structural weakening of the connective tissues. Consequently, permanent elongation of connective tissue results in range of motion increases for the patient.”
Hepburn GR. Case Studies: Contracture and Stiff Joint Management with Dynasplint. The Journal of Orthopaedic and Sports Physical Therapy 8 (1987) 498-504.
The principle is that short connective tissue fibers restrict stretch and must be broken and longer fibers allow stretch and can be elongated (quoted by Hobby in past):
“When stretched, the connective tissue appears to be viscoelastic in nature. When a force is applied against the tissue and then removed, the tissue behaves as if it has both plastic and elastic properties. The elastic response is shown by recovery of the tissue to its original shortened position, while the plastic response is characterized by permanent elongation. Optimal plastic deformation of the tissue results with applications of long periods of low force stretch. The tissue slowly remodels because a biochemical response, triggered by constant force, results in a loosening and shifting of the fibers’ connecting points within the tissue. By contrast, elongation of shortened connective tissue, through short periods of forceful stretching, relies upon attempt to mechanically break or tear the connecting points. Typically, with short periods of high force stretching, the result is a higher proportion of elastic response, less remodeling, and greater trauma and weakening of the tissue.”
And so goes the debate for injury-induced vs. non-injuring sustained stress-induced growth. As ModestoMan suggested several years ago, these theories are not mutually exclusive. Recent evidence in numerous medical articles supports this.
Fibroblast (like all other cells) talk to one another through what is known as cell signaling. Substances from other cells (growth factors and substances released by cells of the immune system known as cytokines) attach to specific proteins (receptors) on the cell surface. This binding causes changes inside the cell. It may turn on biochemical reactions or turn on special genes to make new substances in the cell. It is by this process that a mechanical load, either by prolonged or intermittent (cyclic) tension affects connective tissue.
“On the one hand, connective tissues have a major function in sustaining mechanical stresses; on the other hand, they require these stresses for their maintenance. Thus, connective tissue cells must sense strains [deformations] in the ECM caused by mechanical stresses (forces per area), and translate this information into an adaptive response, e.g. an increase or decrease in ECM production.”
Chiquet M, et al. How do fibroblasts translate mechanical signals into changes in extracellular matrix production? Matrix Biology 22 (2003) 73–80.
“…there is ample reason to believe that the amount and composition of ECM are controlled not only by endogenous cellular programs [normal processes in the cell itself] and growth factors, but also by the kind and magnitude of mechanical stress acting on a tissue.”
Chiquet M. Regulation of extracellular matrix gene expression by mechanical stress. Matrix Biology 18 (1999).417-26.
To understand the studies, the following information is important. Tension on a connective tissue can be uniaxial (along its long axis, while it shortens in its perpendicular direction) or biaxial (both direction). Studies have been performed with either of these types of tension loading. This tension can be static or dynamic.
Fibroblasts are embedded in ECM and subjected to tension, compression, and shear stress. Tension loading is most common, especially for fibroblasts in tendons and ligaments.
The maximum stretch of a ligament or tendon depends on its type and location. This tension is generally beyond between 5 – 12% of its no-tension stretch length (that would be equivalent to BPFSL without tension with regards to at least the suspensory ligaments). Most of the studies looking at the effect of tension on fibroblasts and ECM were done at about 10%, stretch which is considered to be well within what would be seen in normal physiology.
Mechanical loading of cells has been shown to affect fibroblast division, and the turning on of genes and the production of proteins needed for ECM production. The extent of this production depends on the connective tissue location and loading conditions.
There are substances on the surface of fibroblasts (known as side groups) that make them sticky to the different portions of the ECM. These sticky projections make the fibroblast stick to ECM over the entire cell surface. An individual cell can attach to numerous surrounding fibers. When the connective tissue is stretched, these “glued” groups are tugged on by the moving fibers causing the cell to distort.
“The mechanical properties of the cells also influence how they respond to mechanical stress because how the cell deforms under mechanical forces depends on their mechanical properties. [Influencing whether the fibroblast is just deformed, damaged or killed.]”
KJÆR M. Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading. Physiology Reviews 84 (2004) 649-698.
The deformed fibroblast and/or the stretched sticky side groups causes the activation of very specific proteins known as enzymes. These enzymes act as a catalyst to speed up a chemical reaction to produce special chemicals that act as messengers inside the cells (intracellular messengers). These messengers travel to very specific areas on chromosomes to turn on particular genes. The DNA of these genes make RNA which are then used to make specific proteins.
Multiple fibroblasts are connected together by small fused areas called gap junctions. Any deformation in one cell appears to signal other connected cells through these junctions to respond in a similar way.
Some of the genes turned on make many of the subunits making up collagen, elastic fibers and ground substances. These are then packaged, transported and released outside the cell to make replacement (for injured connective tissue) or new fibers and ground substance.
Other genes are turned on. There are classes of substances called Connective Tissue Growth Factors (CTGF). There are more than one. These CTGFs are also released outside the cell where they diffuse to other fibroblast to make them divide to increase fibroblast numbers (fibroplasias) and for them to also make more subunits for fibers and ground substance.
“Upregulation [increase] of collagen synthesis [production] may be a part of the repair process but may also occur without any evidence of muscle damage. Acceleration of collagen biosynthesis after exercise may thus reflect both physiological adaptation and repair of damage.”
“…intensity and loading pattern including recovery periods between training bouts likely
play an important role in adaptation of ECM.”
KJÆR M. Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading. Physiology Reviews 84 (2004) 649-698.
Even though this statement talks about tendons, it is likely to be true for ligaments and other connective tissues as well. The suspensory ligaments and tunica do not have the fixed attachments (both ends) and stretch length restrictions that tendons have. Tendons respond by increasing the mass of the tendon to deal with the increases in stress caused by repeating muscle contractions (particularly during training). Their “goal’ is to reduce the chance of rupture, tears or complete severing from bone. Penis connective tissue would not necessarily respond by increasing fibers to the degree as with tendons. However, does this explain the plateaus in PE?
Studies have shown the same mechanisms in skin and blood vessels in response to tension.
This process, of course, is not quite as simple and varies from connective tissue to connective tissue. The kinds of fibers and ground substance produced and CTGF may differ. The invasion of an area of connective tissue injury with other immune cells (white blood cells and macrophage) causes the production of other growth factors. This may alter the response and may explain why the repair of some moderate to severe injury might form abnormal amounts of collagen fibers. This thickening is known as fibrosis (which is abnormal or pathological). Peyronie’s disease?
Disuse of a connective tissue (bed rest, limb in a cast, for example) or aging causes the number of fibers (collagen, elastic) to decrease and in the case of tendons and ligaments (disuse atrophy). In regards to the penis this may explain the retraction of the penis with age (“hung like and acorn”). Does this mean that if PE is stopped, atrophy occurs? Does this mean that at least some stretching is necessary to maintain permanent success? Good questions, but at this time neither can be answered.
This may also explain the findings of the following report showing tunica changes in impotence, age and Peyronie’s Disease:
“The concentration of elastic fibres was lower in impotent than in potent patient and was also significantly less in patients with Peyronie’s disease. Furthermore, the concentration of elastic fibres decreased with age. Electron and light microscopy revealed the presence of distinct alterations in the tunica albuginea in impotent patients and patients with Peyronie’s disease that might interfere with function.”
Akkus E, et al. Structural alterations in the tunica albuginia in the penis: impact of Peyronies’s disease: Aging and impotence. British Journal of Urology 79 (1997) 47-53.
The authors suggest that the loss of elastic fibers cause these problems. However, they do not rule out the possibilities that the “disuse atrophy” in guys with these problems may in fact be the cause of this loss of these fibers. This study made an observation but did not prove the cause. I personally think this is classic chicken or the egg argument; does the fiber loss cause theses problems or do the problems cause decreased erections that lead to the loss of fibers.
Be aware androgenic and anabolic steroids have been shown to have a negative effect on this connective tissue mechanism at least in tendons:
“Anabolic-androgenic steroid treatment can impair tissue remodeling in the tendons of animals undergoing physical exercise by downregulating [decreasing] matrix metallopeptidase activity [an enzyme outside fibroblasts involved with assembling fibers], thus increasing the potential for tendon injury.”
Marqueti RC, et al. Androgenic-Anabolic Steroids Associated With Mechanical Loading Inhibit Matrix Metallopeptidase Activity and Affect the Remodeling of the Achilles Tendon in Rats. American Journal of Sports Medicine 34 (2006) 1274-80.
This is only one study and in tendons, but it deserves consideration by us.
None of the reports that I found have done studies on the suspensory ligament or the tunica. We can only infer that these came process occur in the penis. We all think our penis is special, but it is doubtful that the connective tissues in it are any different from any other.
This process could be used to explain the mechanism of the response to our PE efforts on a cellular level. Stretch of the suspensory ligaments and tunics along its long axis (hanging, extenders, manual) and circumferential stretch of the tunica with pressure by jelging and clamping (pumping?) both generate tension. This tension must have similar effects.
These studies were done with static and dynamic tension. How this relates to static stretches by hanging or with an extender, or with dynamic stretch with manual stretches or jelqing is a big unknown.
This information does not end the discussion on PE effect on penis connective tissue to cause enhancement. In fact, This will increase discussion. How much tension is necessary? Injury vs. stretch-induced growth? Does this explain plateaus? Deconditioning breaks? Is enhancement truly permanent over the long term? Is continuing PE necessary since tension generation may be necessary for normal connective tissue physiology (homeostasis)?
It is at least interesting.
Sorry this post is so long.
I have pdfs of all the references in this posts.
Schild C, Trueb T. Mechanical stress is required for high-level expression of connective tissue growth factor. Experimental Cell Research 274 (2002) 83–91.
Wang JHC, et al. Mechanoregulation of gene expression in fibroblasts. Gene 391 (2007) 1–15.
Wang JHC, Thampatty BP. An introductory review of cell mechanobiology. Biomechanics and Modeling in Mechanobiolology (2006) 5: 1–16.
Last edited by pudendum : 12-26-2007 at .