I have to interject here with my own experience and some noted history. 1st congrats on your progress. You are a unique case because in my experience with pumping it produced virtually no gains, just fluid build up which dissipated rather quickly. Note also that there was a new member that moved here some years ago that testified that he had been pumping for some 3 years and experienced no gains.
So your accomplishment is although admirable but I must agree with Marinara that it is off topic in this tread and could easily be considered misleading as well. 1 inch in 3 months? Let’s face it some guys dicks are made of taffy. :D
11-2004 BPEL:8.25x6.25 . . 9+ by Spring is the goal AIR CLAMP
Sorry if I am not on subject. I was just vehemently objecting to your claim Originally Posted by marinera and follows:
” I don’t see many pumpers gaining at all, frankly. A lot of fluid build up and bad measurement. If there is any permanent gains from pumping, has to come through sub-failure damage”
I just can’t agree based upon my (although limited) experience.
But how your experience disproves my statement? If you are realtively new to this, sub-failure damage could be caused even with relatively low force (by the way, I think the bathmate can reach pretty high pressure); beside that, you are also jelqing and stretching, so how you know what is causing the gains?
Old But Interesting
MECHANICAL BEHAVIOUR OF TENDON IN VITRO* A PRELIMINARY REPORT MICHAEL ABRAHAMS Biomechanics Laboratory, University of California School of Medicine, San Francisco, California 94122, U.S.A.
Abstract—The mechanical behaviour of horse and human tendon, as cbaracterised by the stress-strain curve, has been examined withrespect to load-strain cycling and strain rate. It was found that the tendon stress-strain curve forsuccessive cycles was reproducible provided that strain on the specimen did not exceed 2.0—4.0~. If this strain level was exceeded, a permanent deformation occurred. This phenomenon was verifiedby histological studies on strained tendon which showed that some ofthe collagen fibres did not return to their original orientation. Variation in the rate of strain was found to affect both the magnitude and the shape of the stress-strain curve. Additionally, it was found that the stress relaxation phe- nomenon for tendon was essentially the same as that found for other connective tissues.
2. GENERAL METHODS OF PROCEDURE All tests on human tendon were carried out at 37~ within 36 hr of autopsy; horse tendon was tested at 38~ within 48 hr of autopsy. All specimens were refrigerated in Ringer’s solution from time of detachment until time of testing. Each specimen was immersed in Ringer’s solution at the temperature used for testing for 15 min before the start of each test, unless otherwise indicated.
All experimental testing was carried out on a floor model Instron Testor, Type T.C., which is shown in Fig. 1.
The machine was modified slightly so that the tendon specimens could be tested in Ringer’s solution at body temperature. The immersion tank (shown in detail in Fig. 2) is mounted on the stool below the large crosshead. Experimental load and specimen strain can be recorded continuously on a time-base chart by the two-pen recorder which is contained in the control console shown on the left side of Fig. 1. In Fig. 2, a specimen of horse extensor tendon is held in the specially designed grips Each grip is made from stainless steel and consists of a block which encloses two self-tightening springloaded wedge-shaped jaws.
The grips were successful up to the 4-0-5.0% strain level; thereafter, damage to the tendon fibres within the jaw faces occurred, and in some cases the specimen slipped from the grips. ……..
Effects of cycling and determination of “elastic limit”
RIGBY et al. (1959), PARTINGTONand WOOD (1963), and RIGBY (1964) all found that if rat-tail tendon was strained beyond a 2.0—4.0~ level, is suffered a permanent deformation. Partington and Wood also observed that load extension curves for successive cycles beyond the 2.0~ level were displaced along the extension axis. To see if this overstrain phenomenon 9 occurred in horse and in human tendon, and to ascertain the effects of repeated cycling, the following experimental procedure was adopted.
Test specimen. The results of repeated strain cycling to different strain levels on one sample of horse extensor tendon are shown in Fig. 4. This specimen was cycled 10 times to the 2.0~ strain level and then allowed to rest for 5 min while the strain cam was reset to produce a 3.0~ strain. It was then cycled 10 times to the 3”0~o strain level, allowed to rest and the cam reset to give a 4.0~ strain. No rest period was allowed between cycles of the same strain magnitude. Curves nos. 1 and 10 are, therefore, the first and last cycles to the 2”0~o strain level, plotted as nominal stress against percentage strain. The curves are, for practical purposes, identical, because complete recovery was obtained after each of the 10 cycles. The crosshead speed selected, 2 in./min, produced an average specimen strain rate of 45~o/min q-5~o/min. The total time for 1 cycle to the 2.0~ strain level was about 5.3 sec. The stress obtained at the maximum level was approximately 1600 Ib/in~ (110 kg/cm~). ….. The above results show that if tendon is strained beyond the 2.0-3.0~ level, permanent deformation will result. The tests also show that if tendon is not strained beyond the 2~0-2.5~ strain level, then test results from one sample are reproducible and, therefore, one sample can be used for a series of tests as long as this level is not exceeded. The point at which “residual” or permanent strain occurs is henceforth referred to as the “elastic limit”. …. http://homepages.cae.wisc.edu/~lakes/TendonHuman.pdf
What I have trouble with is the fact that cadaver tests are great except there is one significant flaw in the results in that they are incomplete.
If the tendons are stretched and there is deformation that is perceived as permanent, I believe this is incredibly misleading because there are no results that can be determined with the tendon out of the body which will act upon such damage with swift presentation of enzyme’s and proteins to heal and correct the condition.
To assume that the stretched condition would not be influenced and changed from the bodies processes to heal such damage is short sighted.
11-2004 BPEL:8.25x6.25 . . 9+ by Spring is the goal AIR CLAMP
I agree that those results can’t be utomatically transferred to our purposes. This kind of ‘permanent deformation’ in vitro could means ‘injury’ in vivo, tissue inflammation and lack of functionality for some span of time. Beside that, tunica is similar, but not identical to tendons; tendon have 3% of elastin, tunica albuginea 5%, so the strain rate could be noticeably different; tendon have a different function than TA too, the former has to transfer force, the latter has to provide a ‘skeleton’ for smooth tissue.
Also a good read, found this section particularly interesting.
The fraction of lengthening (change in length divided by initial length) is the definition of strain. When fascia has stress applied to it, it first lengthens elastically. If the force is removed at this point, the connective tissue returns to its original length. It’s thought that this elastic region occurs as the crimp, or natural physiological zigzagging in the tissue, is removed. This is analogous to pulling on a piece of the rickrack trim used in sewing. If greater force is applied to fascia, it begins to plastically deform, lengthening but creating microtears within the tissue. If the force is further increased to the tensile strength or shear strength of the tissue, a tear occurs, resulting in discernable injury. In combination, a conception model capturing both the initial elastic phase and the latter plastic or viscous phase is known as a viscoelastic model.2 If the amount of stress we incur increases gradually, to a great extent we adapt. Davis’s Law for soft tissue and Wolff ’s Law for bone state that tissue is laid down along lines of stress. 19 This is the key to both functional and dysfunctional adaptations. Tom Myers presents the theory that the mechanism for adaptation is not an increase in the rate at which tissue is actually deposited by fibroblasts and osteoblasts, but a reduction in the rate of resorption or removal. The reduction in removal is thought to be induced by a piezoelectric field resulting from the applied stress. 16 Since both deposition and removal occur continually, a piezoelectric suppression of removal changes the local balance toward more accumulation of tissue. Similarly, lack of regular applied stress changes the balance toward loss of tissue. This concept motivates the use of weight-bearing exercises.
So not so much more collagen being added but less being removed and recycled.
That is describing how the tissue strengthens, though, so it seems at least.
Originally Posted by marinera
That is describing how the tissue strengthens, though, so it seems at least.
Yes but it suggests that strengthening occurs due to a slow down in the recycling of tissue not an increase in tissue production. It’s a small distinction but an interesting one and if true could have some importance re the rest days/deconditioning debate.
Could also explain how some facial treatments that claim to increase collagen through piezoelectric charges work ?
In the recycling or removal. I can’t find the quoted text in your link; it’s not clear to me what the guy is saying; anyway it is a theory, right? I don’t see how the difference could be relevant for us either.
Tom Myers presents the theory that the mechanism for adaptation is not an increase in the rate at which tissue is actually deposited by fibroblasts and osteoblasts, but a reduction in the rate of resorption or removal. The reduction in removal is thought to be induced by a piezoelectric field resulting from the applied stress. 16 Since both deposition and removal occur continually, a piezoelectric suppression of removal changes the local balance toward more accumulation of tissue. Similarly, lack of regular applied stress changes the balance toward loss of tissue. This concept motivates the use of weight-bearing exercises.
I searched for something new (for me at least) and this two studies came out, this Stress relaxation and recovery in tendon and ligament: Experiment and modeling http://silver.neep.wisc.edu/~lakes/…onBiorheo10.pdf wich is quite interesting; among the other things it says that tendons and ligaments, considered interchangeable buy surgeons, have actually a completely different behavior under stress. In the case of ligaments, the higher the strain, the lower the stress relaxation rate; in the case of tendons, the higher the strain the higher the stress relaxation rate. The study examines how good three different equations are at predicting the stress, relaxation, and recovery cycle of both tendon and ligaments. It find outs that Schapery’ method is the best.
This is the other one: [Biomechanics of human tendons: connection between stress relaxation and stress recovery (author\’s transl)].
V Buss, H Lippert, M Zech, G Arnold Archiv fü Orthopädie Mechanotherapie und Unfallchirurgie 11/1976; 86(2):169-82. Source: PubMed ABSTRACT 108 tendons of the m. extensor hallucis longus were examined with a tensile testing machine within 36 h after death. The specimen were kept at a resting length of 20 mm. After the “steady state” was reached by cyclic loading, the tendons were stretched up to a maximum load of 18 kp, then deloaded to a certain level and after that the elongation was kept constant. At high loading level the tension of the tendon decreases with time (relaxation).
At medium and low loading level the tension increases slightly (mechanical recovery). Between that two regions there is a certain load, where the tension will not change with time (isorheological point). The position of the isorheological point depends on the velocity of the elongation. At low velocity (2 mm/min) the isorheological point is situated at 70%, at high velocity (12 mm/min) at 60% of the maximum load. One will find the maximum relaxation, when no deloading occurs. The mechanical recovery, however, has its maximum at 5—25% of the maximum load. But when the tendon is totally deloaded, there seems to occur no recovery.
The maximum relaxation is 5 to 6 times larger than the maximum recovery. Supposingly the relaxation- and recovery-processses will happen at the same time but with different intensity depending on the loading level. At least the relaxation-process consists of different relaxation components with different relaxation times. This will explain the phenomenon of a “secondary relaxation”: After a long time of registration the recovery will turn into a slight relaxation. http://www.researchgate.net/publication/22170159_Biomechanics_of_human_tendons_connection_ between_stress_relaxation_and_stress_recovery_(aut hor’s_transl))
Maybe somebody more brained than me could explain what it means.
Last edited by marinera : 01-04-2014 at .
………… Provenzano, P., Lakes, R. S., Keenan, T, Vanderby, R. Jr., “Non-linear ligament viscoelasticity”, Annals of Biomedical Engineering, 29, 908-914, Nov. (2001) Abstract Ligaments display time dependent behavior, characteristic of a viscoelastic solid, and are non-linear in their stress-strain response. Recent experiments (Thornton et al., 1997) reveal that stress relaxation proceeds faster than more rapidly than creep in medial collateral ligaments, a fact not explained by linear viscoelastic theory but consistent with non-linear theory by Lakes and Vanderby (1999). This study tests the following hypothesis. Non-linear viscoelasticity of ligament requires a description more general than the separable quasi-linear viscoelasticity (QLV) formulation commonly used. The experimental test for this hypothesis involves performing both ligament creep and ligament relaxation studies at various loading levels below the damage threshold. Freshly harvested, rat medial collateral ligaments were used as a model.
Results shown above consistently show a non-linear behavior in which the rate of creep is dependent upon stress level and the rate of relaxation is dependent upon strain level. Furthermore, ligament relaxation proceeds faster than ligament creep, as shown on the right, consistent with the experimental observations of Thornton et al., (1997). The above results are not consistent with a separable QLV theory. QLV fails to describe observed nonlinear creep or relaxation. Inclusion of these nonlinearities requires a more general formulation. … [/i] http://silver.neep.wisc.edu/~lakes/Biom.html
This study was already posted here but reading it again I rememberd something I had to have forgot (or maybe not noticed before):
Results from this study indicate that rat medial collateral ligaments strained above 5.14% from preload do not regain their original length after significant recovery time (3003 the time of test). This recovery is considerably longer than other studies showing that ligaments stretched below 5% completely recover in ,103 the time of test (30). Hence, we conclude that ligaments stretched beyond this threshold remain “stretched.” These findings are valuable to researchers performing multiple tests on the same ligament specimen because no change in length or properties is evident in the tissue below ;5% when testing under the methods described in this study for rat. We speculate that the increase in elongation after ;5% strain and change in mechanical properties are the result of fiber damage arising from two possible mechanisms. One mechanism would be torn or plastically deformed fibers. Torn fibers would be consistent with the fiber failure mode of Hurschler’s micromechanical model for ligament behavior (16), and plastically deformed fibers could be supported by experimental observations by Sasaki et al. (33, 34) and Kukreti and Belkoff (22) who observed that collagen fibrils, which make up collagen fibers, elongate during tendon loading. In addition, Yahia et al. (41), using scanning electron microscopy, reported damage to collagen fibers in subfailure strained ligaments. Another possible mechanism for the observed ligament laxity could be biochemical degradation of the ECM from protease release associated with the observed cellular necrosis. Regardless of the mechanism, the resulting increase in tissue length represents tissue laxity and can be hypothesized to increase joint laxity. ……….. The statistical threshold of cellular damage was found to be at 0% strain from preload 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 small strains as our statistical analysis implies. However, necrotic cells are present in the control tissues (e 5 0, i.e., preload) and are present after very small strains (above reference preload). This behavior did not allow the authors to identify any statistical threshold other than the preloaded value.
… Strain in fibroblasts during in vitro equibiaxial testing on membranes are often higher than the tissue strains at which we are reporting cell damage (e . 2% from a preloaded state). However, the relationship between reference (initial) strains used in these studies compared with the complex cell loading in an in vivo state is unknown. Furthermore, differences between the reference strain in our study and previously published in vitro cell deformation studies is also unknown. We propose that microstructural irregularities in ECM organization create local distortions in fibroblasts during ligament strain that result in the cellular damage reported in this study. …….. In summary, structural and cellular damage occur at different levels of tissue strain in a rat MCL. Subfailure strain above the damage threshold changed the mechanical properties of the ligament. Further investigations into loading rate, multiple loadings, ligament microstructural displacements and deformations, cell deformation, and cell biology need to be performed to understand the subfailure behavior of ligament and the role of cell death in the healing process…” http://silver.neep.wisc.edu/~lakes/LigSubFailDmg.pdf
Question: a) would the cellular damage at low strains happen in vivo too? b) where would it lead when a high number of low strains with low rest were applied? Structural damage? A longer tissue? c) How would laxity be felt in tunica albuginea of the penis if not as ED?
Marinera does stretching cause laxity and increase ED?
Prolonged stretching is known to cause a drop in EQ. If this is due to laxity of TA and so to plastic deformation, we don’t know. That’s my understanding.