I believe the ideas from this site on bodybuilding can be used for PE http://www.hypertrophy-specific.com/hst_index.html I hope you can find these excerpts useful.
“Acute vs. Chronic Stimuli
In order for the loading to result in significant hypertrophy, the stimulus must be applied with sufficient frequency to create a new “environment”, as opposed to seemingly random and acute assaults on the mechanical integrity of the tissue.
Over time, the tissue adapts and becomes resistant to the damaging effects of mechanical load. This adaptation (resistance to the stimulus) can happen in as little as 48 hours (Repeated Bout Effect or Rapid Training Effect). As this happens, hypertrophy will stop
At this point, it is necessary to either increase the load (Progressive load), or decrease the degree of conditioning to the load (Strategic Deconditioning). The muscle is sensitive not only to the absolute load, but also to the change in load (up or down). Therefore, you can get a hypertrophic effect from increasing the load from a previous load, even if the absolute load is not maximum, assuming conditioning (resistance to exercise induced micro-damage) is not to extensive. There is a limit to the number of increments you can add to increase the load. You simply reach your maximum voluntary strength eventually. This is why Strategic Deconditioning is required for continued growth once growth has stopped (all things remaining equal).”
I also found this about wound/tissue repair on that site.
“Hunt TK, Hussain MZ.
Can wound healing be a paradigm for tissue repair?
Med Sci Sports Exerc. 1994 Jun;26(6):755-8..
This paper is written in the hope, if not the conviction, that it will be helpful to investigators of muscle physiology and development. Its thesis is that cell growth, connective tissue matrix deposition, and angiogenesis are stimulated in wounds in response to NAD+ depletion caused by a burst in lactate generation. We surmise that muscle development may also involve this metabolic control.
Hunt TK, Knighton DR, Thakral KK, Goodson WH 3rd, Andrews WS
Studies on inflammation and wound healing: angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages.
Surgery. 1984 Jul;96(1):48-54.
Hunt TK, Conolly WB, Aronson SB, Goldstein P.
Anaerobic metabolism and wound healing: an hypothesis for the initiation and cessation of collagen synthesis in wounds.
Am J Surg. 1978 Mar;135(3):328-32.
Total LDH activity corresponded directly to lactic acid concentration and inversely to oxygen availability. LDH isoenzymes in wound fluid were in an anaerobic pattern soon after injury and evolved toward the aerotic pattern as oxygen supply more nearly matched metabolic capacity. Lactate levels in the wound space are elevated soon after wounding and remain elevated far above those in blood. These data again indicate that wound metabolism is characterized by a relatively poor oxygen supply. Current data from several sources indicate that lactate found in the hypoxic area of the wound may stimulate collagen synthesis in fibroblasts lying in the high lactate environment. We postulate that elevated concentration of lactate in wounds is a major signal for collagen synthesis and repair.”
My guess is kegel holds may help flush the area with lactic acid?
Info about stretching I found.
“Passive stretch puts the strain of the load on “structural” proteins (both collagenous and otherwise) and the cell membranes. When the fibers contract, it shifts the load to the contractile proteins (myosin, actin, z-discs, etc). This appears to be crucial for activation of p38, which of course leads to significant fiber hypertrophy.
Long term modulation of protein synthesis involves the activation of myogenic stem cells or satellite cells. This is how existing muscle cells increase the number of nuclei they contain. If you recall, when a muscle is stretched it not only produces mechano growth factor (MGF), but also PGF2α and PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications for hypertrophy. This helps shed light on the ability of prostaglandin inhibitors such as ibuprofen and other NSAIDs to prevent training induced muscle growth.
Is this possibly what is going on when we PE?