I feel the need of starting this posting with the closing paragraph of the personal, now favorite of mine article, which is the basis of my hypothesis regarding the plateau and the scheduling for de-conditioning breaks.
“Several major outstanding questions remain: How do tissues maintain normal matrix organization and tissue stiffness? What pathways mediate the negative feedback loop that prevents progression toward stiffer matrix and higher cell contractility?
What governs the switch between these two states, the homeostatic one that maintains health versus the fibrotic one that compromises the function of many tissues? Lastly, can we devise treatments to break the fibrotic cycle and restore the homeostatic state?
Understanding the regulatory pathways in detail and the factors that govern switching between these states is likely to be the best route forward.”
1) Mechanotransduction and extracellular matrix homeostasis - PMC
Mechanical stimulation is an important modulator of cell function and plays a critical role during tissue development and repair. Mechanical stimuli are transmitted to cells via the extracellular matrix (ECM), which provides an adhesive surface for cells and structural organization to tissue.
Cells sensing mechanical strains will then reciprocate by remodeling their surrounding ECM.
The role of mechanical stimuli was described first in bone remodeling studies and applications, is now being actively investigated for many tissue types, including soft tissues we are working out.
This is the line of studies we should follow closely if we were to continue gaining after we have plateaued. Best case scenario should the controlling the process by taking precautionary de-conditioning breaks avoiding plateauing to happen in the first place.
That said we can start to digest it by taking a look on the hypothesis of how we might be plateauing.
We reach the plateau and some of us keep on hammering being not able to break through despite any efforts. Some of us take another path going for de-conditioning breaks.
Newest knowledge on mechanotransduction and the extracellular matrix (ECM) homeostasis suggest latter being the way.
Cells senses the mechanical loading via ECM and ECM actively regulates multiple functions including the cell functions and growth response. ECM is primarily responsible for adaptation for mechanical stresses.
It regulates the elongation due collagen expression and the stiffening of the ECM.
ECM subjected for external stresses has to respond to strain by increasing internal stress. The internal stress should correspond to the external stresses applied for reaching the ECM homeostasis.
Same mechanism is responsible for adaptation for workout loads in the long run. TheECm adjusts itself against the external forces.
Unfortunately there remain residual stresses which are proportional to the residual elongation of the tissues achieved due the intensive PE.
Individuals gaining fast will and not taking enough time off from PE duties between growth bursts expose their units for the state of plateauing due the accumulating internal residual ECM stress.
I have been largely promoting the use of stress relaxation stretch for the elongation.
There is hypotheses of the calculus for the internal ECM stress decay which suggest that in one hour the contracting force within cell-ECM mesh to be reduced 50% from the stress the initial strain has caused.
Continuing to keep the strain, let´s say with a longtime contraption for 24 hours the internal stress has reduced to 40% , after a continuous use of the whole one month the stress should be decline to 30%.
For the decline due the stress relaxation ,or the creep as well , behavior of the extracellular matrix leads to a continuous decline of the apparent stiffness. The power-law exponent of 0.08 is assumed for ECM Stress decay.(graph StressDecay).
The exponent for cellular stress is A power-law exponent of 0 is indicative of a purely elastic solid, and 1 is indicative of a purely viscous fluid. In cells, the power-law exponent usually falls in the range between 0.1 and 0.5.
Apart from their higher elastic modulus, extracellular matrix biopolymers exhibit power-law mechanical responses similar to cells [9], with power-law exponents typically below 0.1—closer than cells to an ideal elastic solid.
Consequently, tissue as a combination of cells and extracellular matrix also shows powerlaw stress relaxation and creep (2).
2) https://www.res earchgate.net/p … _cell_migration
Now what happens within the elongation due external forces apply to the residual elongation as well. Meaning the permanent gains.
Using the power law assumption introduced above I have managed to cumulatively build u the residual stress due 20% increase in BFSL by 12,9%.
Using the power law exponent -0.08 the calculation shows that to reduce it to 4,8% it takes three months of time. Which should be the minimum time needed for gaining with a significant rate.
After year of absence if I was supposed to keep the BPFL gains it would be at the 3 % residual stress rate etc.(Graph Residual Stress)
What is the primary mechanism behind the reduction of the residual stress is harder to call.
It should be a mix of collagen turnover, and the cellular contraction diminishing due the cell migration and ECM turnover.
Computational models suggest that mechanical homeostasis in soft connective tissue depends primarily on four key factors, rates of ECM production, rates of ECM removal, the mechanical properties of the ECM constituents,
and the degree of prestress that is built into these constituents when deposited. (1)
Now we need to take a look only for the collagen maturation stage as well, the remodeling phase of the collagenous matrix restructuring for the new homeostatic state in elongated frame.
The complete maturation of the collagen remodeling should take up two years for complete turnover.
Tutt suggested in our private conversations that the stage of the remodeling should minimum of 80 % complete if we aspire the newly fresh setup for the gains to come.
Quote:
“I think we can fairly safely use a Pareto assumption here. If your assertions are correct that via US heated stretching we have not created an injury or fibrotic response at all, then we might assume that the return of the penis to ECM homeostasis would primarily be the result of collagen turnover. A properly executed rest environment should result in a general collagen half life of 90 days as this is not musculoskeletal or cardiovascular ECM. As such, using the Pareto in saying that we are waiting for 80% collagen turnover before starting a new growth cycle, we can assume a 210 day rest requirement.” TUTT
Studying some individual taking years of some of the still not able to duplicate the gain rate at their peak despite the long resting period allowing the matrix complete turnover to happen.
What I suggest is to use a method to break this equilibrium and accelerate the natural collagen degradation with stress induced degradation. I am talking about ESWT here.
There a interesting study available on treating healthy tendon tissues of the Shetland ponies legs with ESWT aka shockwaves. Surprisingly the ESWT highly accelerates the degradation of the collagen to that extend that the researchers recommend limited use of the treated parts for sometime after treatments. After six of treatment the markers were still shown but the healing had started and the rate of degraded collagen was decreased.(3)
"In a pony model study6, increased glycosaminoglycan and total ECM protein syntheses – 3 hours after shock waves exposure – were detected. Such results may be considered indicative for an early stimulating
ESWT effect on cell metabolism, which may accelerate the healing process in injured tendons. Moreover, these authors described – 3 hours following exposure – disorganisation of matrix structure with degradation of normal collagen fiber, which were detectable up to 6 weeks. In a more recent report
18, the same group observed –6 weeks after ESWT exposure – an up-regulation of
MMP14 and COL1 gene expression, probably ascribable to a shock waves-induced repair phenomenon. In fact, MMP-14 should play an important role duringthe remodelling phase of tendon healing, generally occurring several weeks after the original trauma.
However, considering the early collagen-degradationeffects on exposed tissues, the shock wave exposure on non injured tissue is matter of debate, and the authors stated that it may be advisable to consider a temporary restriction of the physical activities in recently treated patients."(3)
(3) https://www.ncb i.nlm.nih.gov/p … pdf/357-361.pdf
I suggest that using ESWT at the start of the decon we might significantly alter the stage of collagenous tissues. Allowing the maturation process progress more towards the original structure than the elongated stressed ECM structure. Rebooting the ECM .
More from my educated friend ,QUOTE: “However, I believe that your flirtation with ESWT is on the right track. The biological half life seems to be driven by stress induced degradation. The body will regenerate ECM as needed to maintain homeostasis. ESWT accelerates the degradation of collagen fibrils and triggers the neo-collagenesis. I would still suggest that with effective use of ESWT the process would still take at least 90-120 days, but even then you would’ve effectively halved the rest period.” TUTT
So what I am after is with the rebooting the ECM we should be able to significantly reduce the time needed for the a) homeostasis with a reduced residual stress b) the collagenous matrix turnover to be completed more as a reminiscent of the original structure than elongated state stronger build structure.
Therefor I am planning take four weeks of intensive ESWT treatment period followed by 8 weeks of total rest before I start the new chapter on PE.
The total decon will be 4 months long and if I am lucky and my predictions are thereabout, I will come back gaining at decent rate. If the impact turns to be negligible I have still had a great break from PE and happy to continue as it happens.
