Last edited by iamaru : 01-12-2012 at .
Last edited by iamaru : 01-12-2012 at .
What do you think? I know it’s not a penis lig they’re discussing, but for the most part, a ligs a lig, right?
In house back up of Lengthening The Transverse Carpal Ligament Under Static Loads
The penis is largely composed of cavernous and connective tissues, so obviously the principles do apply. Note that the experiments were done on cadavers.
Check it out guys, no need to have a big dick if you ain't gonna use it!!
Would you expect the results on “live” ligs to be less or more?
Also, any idea what 2N and 4N denote?
Good link, RB.
2N = .45 lb.
The forces used seem quite low, but I don’t know how strong these ligs are to begin with. They said the 4N loads produced more lengthening than 2N. But what if they had piled on some real weight? Could they have obtained the same length increases in greatly reduced time? I wish they would have taken some ligs to failure so we’d have a better idea of how stressful these loads really were.
Does anyone have some spare arms in the freezer to experiment with?
hobby, you might check with that dude in Germany… Wait, it’s probably too late :)
Unless I missed it, they didn’t say if the length gain was permanent. I wonder if the ligs later retracted…
According to this article deformation over 5.14% is permanent
This article adds more insighr into the deformation/healing/re-deformation cycle..
Really good links. I learned a lot. Thanks.
Ditto. Great find, rakishly. The page covering repeated loading is very interesting. I wonder if this is why JAI’s and Blasters are effective.
Given limited time to hang, should we perhaps be hanging more, but shorter sets? Or is the extra creep and stress relaxation provided by longer sets more beneficial? Maybe we should alternate the two approaches. Those who can hang 10 sets a day can combine them. :)
This article would seem to support anecdotal evidence that PE gains are easier the older one is. Greater elongation at reduced stress with repeated load application is of particular interest.
I read both of those pages yesterday, but had a headache from a cold so they didn’t sink in. My head hurts worse today. Anyone care to summarize what they learned in laymen’s terms?
OK, I don’t have a cold or anything, but I can’t figure out the conclusions I should be drawing from those articles.
Can you science geniuses help me out please?
RB and Huge,
First, you have to realize that most of these pages, and in fact most information in general concerning human connective tissues are related to how to repair them, or how to keep them in good shape. IOW, most of the time, researchers or doctors are concerned with the relative tightness of joints and the problem associated with that is connective tissue failure. Much information has to be interpreted for the context of PE. Therefore, the information has to be extrapolated and assumptions made. Some assumptions may be correct, and others incorrect.
In association with the above, our bodies are constructed the way they are for a reason. In general, it is for whatever traits are the best to advance the species. It is easy to realize that the structures which are the hindrance to PE, are there for protection of the male reproductive organs. The ability for the penis to retract, to keep it sturdy during wild sex on the savannah or in the caves, etc. The structures were not evolved for our current, less hostile environments.
We, as opposed to researches and orthopedists are interested in how to safely make the tissues fail, either allowing more penis to extend out of the body, or, in the case of the tunica, to allow for more actual length and girth. The connective tissues of the penis, rather than holding joints in place, hold in the soft tissues of the penis, and hold the penis within the body.
In the pdf paper, selected passages:
>Microtrauma or sub-failure injury in tendon and ligament may occur either as the result of overuse or a single traumatic event. ………<
>Tendon and ligament microtrauma and partial tears may
accumulate damage to the point where load bearing is compromised and complete rupture occurs. <
>This leaves more than 85% of the sprains where sub-failure
damage is the dominant issue. <
Soreness vs pain. You have to find the correct amount of stress/time for gradual, controlled damage.
>Results indicate that tissue stretch induced laxity and cell death are fundamentally different in their behaviors when analyzed as a function of applied strain. Qualitatively, cellular damage can be seen to increase with strain by examination of the confocal microscopic images and damage to individual cells is seen in TEM images at 3.2% tissue strain (not shown).<
They actually see the cellular damage and cell death due to stresses.
>Results from this study indicate that rat medial collateral ligaments strained above 5.14% do not regain their original
length after significant recovery time and hence remain .stretched.. <
A definitive declaration of the amount of deformation required. You can have cell damage without lengthening. Soreness with no gains.
>The authors speculate that this increase in elongation is the result of fiber damage in the form of torn or plastically deformed fibers. The resulting increase in tissue length represents tissue laxity and can be hypothesized to increase joint laxity<
>….In addition, it is reasonable to hypothesize that a grade I tissue sprain occurs at strains just prior to this onset of tissue
damage (5.14%). Here, some cellular damage has occurred but no macroscopic laxity can be detected. <
Cellular damage without laxity is possible below the 5.14 threshold. You have to push beyond the primary stress levels.
Applying this to PE, can we quantify the amount of stretch of the entire penis that is required? This figure should not be a 5.14% stretch of the entire penis. This should refer to individual fibers being affected at stretches greater than 5.14.
Interesting though, for a five inch penis, this would equate to only about a 1/4 inch stretch.
>The threshold of cellular damage was found to be at 0% strain in the rat MCL. That is, statistically, cellular damage begins with the application of tissue strain. It should be noted that physically one would not expect an increase in cellular damage at infinitesimal strains as our statistical analysis implies. However, necrotic cells are present in the control tissues (e = 0) and are present after very small strains. This behavior did not allow the authors. to identify any threshold other than zero. While 0% strain may not be the exact physical threshold of
cellular damage, our analysis shows it is significantly different than structural damage.<
Cellular damage begins with any strain. An actual increase in the length of tissues requires more stress.
In the htm page:
>The crimp is the waviness of the fibril; we will see that this contributes significantly to the nonlinear stress strain relationship for ligaments and tendons and indeed for bascially all soft collagenous tissues.<
I like the term “crimp”. This could explain much of the phenomenon of fast gainers. Also, relates to the ablility for more fibers to resist in concert over time. This entire section is very interesting.
>There are three major regions of the stress strain curve: 1) the toe or toe-in region, 2) the linear region and 3) the yield and failure region. In physiologic activity, most ligaments and tendons exist in the toe and somewhat in the linear region. These constitute a nonlinear stress strain curve, since the slope of the toe-in region is different from that of the linear region. <
For our purposes, this could be telling between the hard and easy gainers. The amount of crimp of the fibers between individuals, and the level of strains reached, over time, whether in the 1,2 or 3 category.
>In terms of structure function relationships, the toe-in region represents “un-crimping” of the crimp in the collagen fibrils. Since it is easier to stretch out the crimp of the collagen fibrils, this part of the stress strain curve shows a relatively low stiffness. As the collagen fibrils become uncrimped, then we see that the collagen fibril backbone itself is being stretched, which gives rise to a stiffer material. As individual fibrils within the ligament or tendon begin to fail damage accumulates, stiffness is reduced and the ligament/tendons begins to fail. Thus a key concept is that the overall behavior of ligaments and tendons depends on the individual crimp structure and failure of the collagen fibrils. <
This could have many different implications. The uncrimping would indicate fast, easy gains. After uncrimping, the increased stiffness could be a reason for early plateaus. Then later, with reduced stiffness, gains resume as the tissues approach lig failure. Or for those who apply the perfect amount of stress/time, plateaus may never be an issue.
>In this case, as a spring is stretched to its limit its stiffness increases. This can easily be seen if the effective ligament stiffness is modeled using the Voight model, with each fibril contributing a small part to the overall stiffness. As a fibril becomes uncrimped, its stiffness increases, increasing the overall ligament/tendon stiffness.<
A very clear analogy.
>Another important aspect of ligament/tendon behavior is viscoelasticity. Viscoelasticity indicates time dependent mechanical behavior. Thus, the relationship between stress and strain is not constant but depends on the time of displacement or load. There are two major types of behavior characteristic of viscoelasticity. The first is creep. Creep is increasing deformation under constant load. This contrasts with an elastic material which does not exhibit increase deformation no matter how long the load is applied. Creep is illustrated schematically below:<
This is the first time I have read of the actual mechanical properties of connective tissue. How the tissues actually respond under stress, over time. It is very illuminating to realize the non-linear elasticity of ligaments.
Also, the declaration of the importance of time in the relationship with stress: ” Thus, the relationship between stress and strain is not constant but depends on the time of displacement or load.”
You really need to refer to the graphs to understand the relationships in this entire section.
>The second significant behavior is stress relaxation. This means that the stress will be reduced or will relax under a constant deformation. This behavior is illustrated below:<
This may not apply to us since we are able to constantly increase the stresses, up to a point. The tissues affecting a joint can only be stressed up to a certain point within the joint. The lengthening and following relaxation of the tissues lower the amount of stress that can be placed on the tissues.
>The two figures above show that the amount of hysteresis under cyclic loading is reduced and eventually the stress-strain curve becomes reproducible. This gives rise to the use of pseudo-elasticity to represent the nonlinearity of ligament/tendon stress strain behavior.<
This is a very clear, two steps forward, one back.
>While increasing age from child to adult also increases the mechanical properties of ligaments and tendons, further increasing age from young adulthood decreases the properties of ligaments and tendons.<
Bad for the knees of older guys, but good for PE>
>Excercise and increased load on tendons and ligaments is believed to alter their structural makeup and lead to increased mechanical properties, although experimental data is far from conclusive.<
A possible explanation of the strengthening of the penis through PE, and a possible explanation of the benefits of an extended rest break to get through a plateau.
For the really HARD GAINERS, I think the best message from these papers is that lengthening can occur given sufficient stress/time. In some cases, Krytonite may be required.
There is more good stuff within the papers. Some thoughts have to be developed through the sum of the information. I just picked out my favorites.
Wow, thanks!! I didn’t even realize how much I was missing… LOL.
Your assistance is greatly appreciated.
I still have a headache, but that helped a bunch, thanks for taking the time… :)
Excerpts from Too bad the diagrams aren’t included in the file. Interesting info about fluid content of the ligs, which I’d never read about before. Don’t worry, this doesn’t require an aspirin. ;)
Viscoelasticity is the Combination of Elastic and Viscous Properties of Materials in Response to Stress
The rate at which a stress is applied can be a particularly important determinant in the response of materials that exhibit a combination of both elastic and viscous behavior in response to an applied stress. Viscous behavior can be described as resistance to flow such as with cold syrup. Viscosity in biological materials arises largely, but not completely, from the resistance of their water content to flow into and out of the material with applied stress. For example, spaces between molecules of collagen in ligaments contain a large amount of water with salts and other small relatively mobile molecules. Tensile stress (stretching) of the ligament will decrease the available space between collagen molecules, forcing the fluid between them out of the ligament. This process is similar to stretching a wet sponge (Figure 6). If the structure is stretched rapidly, there is an increasing resistance to fluid to movement out of (and into) these spaces, since this requires time. The time required for fluids to move out of intermolecular spaces acts to slow the rate of deformation of an elastic material. This alters the elastic and plastic regions of the stress strain curve. In combination with the elastic properties of the material, this behavior is described as viscoelasticity. This property is usually modeled as a spring acting in parallel to a resistance provided by a fluid compartment (Figure 6).
Besides the flow of small molecules from intermolecular spaces, frictional resistance due to molecular movement and ionic interactions between molecules also contributes to the viscosity in a material. These molecular interactions, along with the elastic properties of the material, are important in the return of water and other small molecules back into the matrix, again much as a sponge reabsorbs fluid after being squeezed. This recovery process is important if the biomaterial properties of the tissue are to be maintained under repeated loading. Additionally, since viscoelastic behavior involves the movement of small molecules and the interaction between molecules, temperature can significantly affect this property.
Viscoelastic properties can produce significant alteration of material behavior when the rate of loading is too fast for the fluid exchange to occur. Under these conditions, a material may exhibit a higher elastic modulus (that is, appear stiffer or more brittle) under high loading rates as compared to the same load applied over a longer period of time. If a viscoelastic material is stretched rapidly and the load is sustained after the initial loading period, there will be a rapid initial deformation of the material followed by a slower deformation as the remaining fluid in the matrix reaches a new equilibrium at a slower rate (Figure 6). Two types of measurements are used to describe this property. First, if the material is subjected to an initial load, such as tensile stress (Figure 6), which is then maintained, the material will stretch to an initial length and then more slowly increase in length as the more resistant fluid in the matrix effuses. The slower phase after the initial stretch is called creep.
Another measurement looks at the load necessary to maintain a constant deformation or, in the case of Figure 6, the length of the material. As the matrix reaches equilibrium, the load necessary to maintain the length will decrease. This property is referred to as stress/relaxation.
Because of their high water and solute content, bone, muscle, ligament and tendon and other biological materials have viscoelastic properties that are important for their function. Due to the differences in the cellular structure and the matrix between cells in these materials, the actual viscoelastic properties of these tissues differ markedly.
LIGAMENTS AND TENDONS
Ligaments and Tendons are Dense Regular Connective Tissue with a High Resistance to Tensile Loading
Ligaments and tendons, along with joint capsules, surround the articulations of the skeletal system. Their functions are, in the case of ligaments and joint capsules, to structurally connect, stabilize and guide the bones forming the articulation (28). They may also act as a sensor for joint position and strain for the joint. Tendons connect muscle to bone and transmit forces from muscle to bone to produce motion. Both tendons and ligaments are classified as dense regular connective tissues. They have sparse cellular elements and abundant extracellular matrix in a highly organized array. The extracellular matrix is rich in collagen and water with a small amount of elastin, again producing a viscoelastic behavior under stress. The collagen molecules are linked together in lengthwise overlapping arrays to microfibrils, that are in turn combined in a similar overlapping arrays to form fibrils, then fibers, and bundles of fibers to form the macroscopic tendon (Figure 10). This successive parallel linkage down to the molecular level makes ligaments and tendons capable of handling high tensile loads. The arrangement of fibrils in ligament tissue is less parallel than tendon and accounts for its higher resistance to tensile loading in orientations other than along the tissue axis. The collagen molecules are also linked to each other by cross-links. While there are some important biomechanical differences between ligaments and tendons, most of their properties are basically similar and will described together here.
The Primary Biomaterial Characteristics of Ligaments and Tendons are Described by Elastic Modulus and Viscoelastic Properties
The primary stress response characteristics of ligaments and tendons are described by their modulus of elasticity properties. Under tensile loading (stretch), ligaments and tendons exhibit a modulus of elasticity that is variable with load (Figure 10). Under low loading, there is a relatively large increase in length in response to the load applied (low elastic modulus). This is attributed to lengthening as the result of macromolecular “slack” within the collagen fiber structure that offers less resistance to an imposed load. As the slack is taken up, fibers slide relative to each other and fluid is extruded from the matrix. The elastic modulus then increases (stiffness increases) gradually with increasing load and shows a linear response up to the point where failure begins. The behavior of tendons and ligaments is similar except for ligament tissue such as the ligamentum flavum of the spinal column, where a high elastic content produces a different pattern of the elastic modulus.
[Hobby’s note: I’ve read several places that the penile ligs have characteristics similar to spinal column ligs. For PE purposes, we may be dealing with that “different pattern of the elastic modulus.” Anyone have info about how these ligs differ?]
The extracellular matrix of tendons and ligaments between the collagen fibrils has proteoglycans, a high water content and other small ionically charged molecules that can interact with structural elements. This matrix is comparatively more porous than cartilage or bone, and is structured to resist tensile rather than compressive stresses. The viscoelastic properties be come evident at high loading rates, where the tissue will demonstrate increased stiffness and offer increased resistance to tensile stress (stretch). As with cartilage, repeated tensile loading in cycles, can result in a slow increase in elastic stiffness due to plastic deformation (29;30). This plastic deformation is presumably due to molecular deformation in the fibrous structural elements of the tendon or ligament, and also to the inability of fluid and small charged molecules to re-equilibrate within the molecular structure.
Ligaments and tendons also demonstrate the viscoelastic properties of stress or load relaxation and creep. To characterize these properties, the tissue is placed under a tensile load (stretch) within the linear region of the elastic modulus and maintained at a constant length (stress relaxation) or a constant load (creep). Ligament and tendon tissue adjusts its molecular structure and fluid distribution to the load primarily within the first 6 to 8 hours, but will continue over a period of months. The creep phenomenon is used clinically as plaster casts or braces are employed to place a constant load to correct a soft tissue deformity such as some spinal curvatures (31).
Material Failure of Ligaments and Tendons is Preceded by Microfailure of the Molecular Structural Elements
Overall failure of the ligament or tendon is usually sudden and preceded by the microfailure of the attachments between collagen fibers within the tissue and loss of the ability of the tendon or ligament to recover its length. With tendon and ligament, it is also important to distinguish eventual failure due to a sustained load (creep failure) from sustained cyclic loading and unloading (fatigue failure). Both are important biomaterial properties for tendon and ligament. As with bone, a smaller degree of microfailure may occur within the range of physiologic loading, suggesting that repeated stress may lead to declining strength or fatigue over time (32). There may be a range of damage depending upon the total deformation and extent of partial failure. Inflammation resulting from such damage is associated with tendonitis (32).
Failure of both tendons and ligaments may also occur at the bone interface. The site of failure may depend upon the loading rate (33). Tendons, with their attached muscles, typically have a higher tensile strength than muscle, and rupture of muscle is more common than tendon. The instability of the joint that may result from tendon or especially ligament damage, and can contribute to and be complicated by damage to the joint capsule. This damage and associated abnormal loading patterns may contribute to osteoarthritis (31).
Ligaments and Tendons Can Adapt to Stresses
Like other tissue, ligament and tendon structurally remodel in response to the stresses placed upon them within the limits of damage (32). They become stronger and stiffer with increased stress and weaker and less stiff with a reduction in stress (34). Physical training can increase the strength of tendons and ligaments along with the ligament-bone interface (35;36). Immobilization (such as from casting) can decrease the strength and stiffness of ligaments. While reconditioning can occur, it can require a considerable length of time (34;37).
The Properties and Structure of Ligaments and Tendons Change with Age
During maturation, the number and quality of crosslinks increases in the collagen of ligaments and tendons and fibril diameter increases (38) producing increased tensile strength. The mechanical properties of collagen reach a maximum with maturation and begin to decrease with progressing age (39) and the collagen content of ligaments and tendons decreases. This results in a decrease in strength, stiffness and deformation to failure (40). However, the overall biomechanical properties of tendon remain reasonably constant with age (41) The amount of time require for tissue repair and reconditioning (see above) will also increase. Other physiological factors such as pregnancy can also affect the biomechanical properties of ligaments and tendons (31; 40).
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