Loading, lengthening, healing.

I think that we may be able to deduct that higher intensity induces more damage and type III collagen becomes more prevelent in the tissues. While lower intensity (smaller increments), the balance between type I and type III collagen stays the same.

What if type III collagen expression is related to a connective tissues ability to adapt and resist further elongation?

It’s just an idea.

I agree on that, it is consistent with studies cited earlier - see post #230, in example.

marinera, post #230 is an excellent post! I did read it last week, but it was nice to go back and read it again.

Some very interesting terms were used in the text by the original author of the study. A couple of them were new to me, like “fibroblast-mediated”, and “fibrilogenesis”.

There’s another genesis word again. Could it be that new fibrils are generated, to replace older fibrils (that may have been short/tight while under tension)? Could the new fibrils be longer, since the connective tissue is attempting to adapt, to the tension forces at that particular point in time?

Continuing on this track:

What if the older fibrils that were under the most tension were dissolved by collagenase?

From the little bit that I’ve read about collagenase, this could explain why applying tension-stress for a longer duration leads to more residual elongation. Is the release of collagenase time dependent?

If this were all true, it would fit very nicely with a “fibroblast-mediated” mode of tissue repair. The fibroblast would then “generate” new collagen fibrils that were more suitable to the conditions forced upon the connective tissue.

I’ve searched the forums for mention of the biochemical collagenase over the last two days. Some of the information that I was able to find about collagenase was on this thread in earlier posts. I need to learn more about the biochemical.

At this point in this thread, I would like to admit that I did not understand the true definition of the term “extra cellular matrix” (sometimes abbreviated ECM) until this last week. I always read quickly over the term and assumed that it was just the cell wall of the collagen cells, or that it was sort of a covering, much like the fascia of the body. I know, shame on me, especially after going so far as to debate issues about the connective tissue in the body.

Well, for anyone who doesn’t have a clear picture of what the ECM is, it is all of the tissue that makes up the connective tissue that is not a cell, or within a cell. It is tissue that is outside of the cells, and which spans from one cell to the next. Sure, there are some cells in the connective tissue, and in the case of connective tissue, they are called fibroblast. I had mistakenly overlooked the importance of the definition of fibroblast also. I do have a bad habit of reading quickly, and that has caught up with me apparently.

It may have been obvious to many readers here, but I had long overlooked this. You see, I foolishly presumed that connective tissue was made up of cells that all touched each other, much like the magnified pictures of plant cells in textbooks, or like the pieces of a puzzle. I know, connective tissue is far from being similar to a plant cell, and that was a mistake out of laziness on my part.

Hopefully my explanation of the ECM and FIBROBLAST in layman’s terms were worth the forum space. I’m sure there are many members that have been quickly skimming over this information without knowing what the terms actually meant. Actually, I do hope that most of you go and search for the real definitions to these terms.

I know that I shouldn’t make back to back posts, but I would like to ad that post #216 written by dongalong is where I learned that collagenase may dissolve collagen fibers. #216 is a great post to reread.

Don’t be too severe with yourself, Kojack, we are treating stuff not easy to understand, and I’ve putted even too many studies here without a really systematic exposition.

So, if there is somebody to be biased here, that’s me.

Fatigue is More Damaging than Creep in Ligament Revealed by Modulus Reduction and Residual Strength Gail M. Thornton1, 2, 3 , Timothy D. Schwab2 and Thomas R. Oxland2

Journal Annals of Biomedical Engineering
Publisher Springer Netherlands
ISSN 0090-6964 (Print) 1573-9686 (Online)
Issue Volume 35, Number 10 / October, 2007
DOI 10.1007/s10439-007-9349-z
Pages 1713-1721
Subject Collection Biomedical and Life Sciences
SpringerLink Date Saturday, July 14, 2007

Abstract
Following injury of a complementary joint restraint, ligaments can be subjected to higher than normal stresses. Normal ligaments are exposed to static (creep) and cyclic (fatigue) loading from which damage can accumulate at these higher than normal stresses. This study tracked damage accumulation during creep and fatigue loading of normal rabbit medial collateral ligaments (MCLs) over a range of stresses, using modulus reduction as a marker of damage. Creep tests were interrupted occasionally with unloading/reloading cycles to measure modulus. Test stresses were normalized to ultimate tensile strength (UTS): 60%, 30%, and 15% UTS. Not all creep and fatigues tests progressed until rupture but were stopped and followed by an assessment of the residual strength of that partially damaged ligament using a monotonic failure test. Fatigue loading caused earlier modulus reduction than creep. Modulus reduction occurred at lower increases in strain (strain relative to initial strain) for fatigue than creep. In other words, at the same time or increase in strain, fatigue is more damaging than creep because the modulus ratio reduction is greater. These findings suggest that creep and fatigue have different strain and damage mechanisms. Ligaments exposed to creep or fatigue loading which produced a modulus reduction had decreased residual strength and increased toe-region strain in a subsequent monotonic failure test.This finding confirmed that modulus reduction during creep and fatigue is a suitable marker of partial damage in ligament. Cyclic loading caused damage earlier than static loading, likely an important consideration when ligaments are loaded to higher than normal magnitudes following injury of a complementary joint restraint.

fatigue

Does this suggest the idea that cyclic and static stretching should both be used (at the same time or alternating the two kinds of stimuli)?

I think that judging by newbie routine results, the answer is yes. Manual stretches are static and jelquing is cyclic.

It depends on the frequence. If you consider ADS and manual stretches, the first is static where the second are cyclic.

I purchased an X4 labs extender about 3 months ago.
I use it for about 2 hrs daily, and have yet to see any positive results.

I read in some of these posts where stretcheing too much can actually cause it to shrink in length. Is that true?

I’m lost here.

Extenders start showing gains after at least 600-800 hours of wearing (on average). It’s unlikely that you can have shrinking by extenders, because they really use a very low tension; on the other hand, using too much tension will not allow you to wear it for the required time.

As you could have read somewhere else, for PE beginners the newbie routine (that is just a model, however) is the way to go.

Let’s see; I gonna start an experiement soon, I want to wear an extender (phallosan) 24/7 or at least 22 hours a day I hope to be mental strong enough to do that for at least 10 Months..

I think the key is low tension but long duration.

No form of PE is safe when sleeping.

He’s going to have to wake up every 2hrs or so. I would to readjust, allow blood flow, and re connect.

Sleeping with the Phallosan is no problem; I have done this many Times and no Problem.

Connective Tissue Mechanotransduction Responses To Stretch and Acupuncture: From Ex Vivo Fibroblast Cytoskeletal Morphology to In Vivo Ultrasound Elasticity Imaging
Helene Langevin, M.D., L.Ac., Research Assistant Professor, University of Vermont, Department of Neurology, Burlington, Vermont

A common feature of manual therapies is the therapeutic application of mechanical forces (e.g. stretching, pressure) on either “dense” (tendons, ligaments, joint capsules) or “loose” (fasciae, subcutaneous, interstitial) connective tissues. Tissue viscoelastic responses to mechanical forces are determined by their connective tissue matrix composition (collagen, glycosaminoglycans (GAGs), water content) and architecture.
……………….

The effect of mechanical forces on connective tissue fibroblasts may be key to the therapeutic mechanism of manual therapies by causing important cellular effects both immediate (activation of signaling mechanisms) and delayed (gene expression, modification of extracellular matrix composition) which may affect future biomechanical tissue behavior during movement.

Ex vivo and in vivo animal models can be used to study the effect of mechanical forces on fibroblasts in whole tissue. Using histochemistry and confocal microscopy, we found that both tissue stretch and acupuncture induced a dynamic, reversible change in fibroblast morphology within 30 minutes. During acupuncture, connective tissue mechanical stimulation is caused by winding and pulling of collagen during needle manipulation. With both types of mechanical stimulation, fibroblasts cell bodies became large, flat and “sheet-like” in contrast to the small cell bodies and long branching processes seen without stretch. These changes in cell shape required the presence of both intact microtubules and microfilaments, implying an active, cytoskeletal-dependent mechanism.
…………….
Further studies will be needed to examine the effects of varying force amplitude, frequency and duration on these mechanisms, and how these effects may differ across treatment modalities.
……………..
Using a combination of ultrasound elasticity imaging and robotic acupuncture needling, we quantified spatial and temporal tissue displacement and strain patterns during acupuncture needling in humans. We found that rotation of the acupuncture needle preconditioned the tissue and modified its biomechanical behavior during subsequent axial needle motion.
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Combined approached using these ex vivo and in vivo techniques may ultimately allow translation of findings from animal models leading to mechanistic studies of therapeutic mechanisms in humans.

DON’T TRY THIS AT HOME!