Thunder's Place

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Loading, lengthening, healing.

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

09-2003 BPEL:6.0x5.5

11-2004 BPEL:8.25x6.25 . . 9+ by Spring is the goal AIR CLAMP

Now BPEL:8 5/8 x 6 5/8 PE Weights

Originally Posted by Idoforyou
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

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.


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”.

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.

09-2003 BPEL:6.0x5.5

11-2004 BPEL:8.25x6.25 . . 9+ by Spring is the goal AIR CLAMP

Now BPEL:8 5/8 x 6 5/8 PE Weights

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
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.

As you say though just another theory.

About Strain And Stress Relaxation

In a recent threads the topic of stress relaxation came out; this is the thread
My Stress Relaxation-based Traction Device in Action (p. 8)

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…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. 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 . Reason: grammar

Stress Relaxation And Creep

Ligament and tendon biomechanics:
Nonlinear non-QLV ligament viscoelasticity, tendon viscoelasticity, creep, relaxation

Provenzano, P., Lakes, R. S., Keenan, T, Vanderby, R. Jr., “Non-linear ligament viscoelasticity”, Annals of Biomedical Engineering, 29, 908-914, Nov. (2001)
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.


This study was already posted here but reading it again I rememberd something I had to have forgot (or maybe not noticed before):

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…”

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.


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