Originally Posted by Kyrpa
Hello Tutt,No experience on this. Yes there are studies showing results you suggested. The pulse frequency should be the key. Every study I have looked used frequencies which would need some kind of pulsating apparatus. You need to build one first.
Maybe I look deeper on it the day my gains start to show signs of diminishing permanently.
Which studies are you referring?
Unfortunately, I don’t have the full study citations handy. I know there were 1 or 2 rat tail studies testing cyclic straining and residual tendon elongation without heat. One of them might have been;
Elongation of rat tail tendon: effect of load and temperature.
Warren CG, et al. Arch Phys Med Rehabil. 1971.
I don’t have the full text study available right now. I seem to recall an assertion that a cyclical repeat of strain and relaxation produced the greatest residual elongation without rupture. This is also indicated in the study by Rigby et al 1959. Looking at figure 6, there is a dramatic decay in the load necessary to produce significantly greater extensions, ultimately reaching an impressive 35%.
Gustav et al 1951 show that the first strain curve (if less than 1%/min) can be taken to as much as 20%, but requires a constant or increased load depending on time, albeit the load increase required to produce an incremental increase in strain decreases as both time and extention increase. This, combined with the study above and others, suggest that it is the cyclical nature of the strain that allows the extreme plasticity without reaching the point of failure.
Keeping in mind that these are in vitro studies and that in vivo there would undoubtedly be severe pain at slightly beyond the elastic limit. But the evidence also suggests that cyclic strain changes the actual arrangement of collagen tissue, resulting in less damage and consequently less discomfort and arguably reduced healing times.
There are also additional considerations in vivo as it pertains to PE. The ‘I’ phase of IPR cannot be overemphasized at the expense of ‘P’ and ‘R’. Specifically, several studies suggest that internally produced Hyaluronic Acid, critical protein kinases, and Nitric Oxide each play a key role in cell proliferation and avoidance of “wound” type collagen formation (scarring and adhesions) in favor of repair via normal tissue growth. Additionally, they determine the type, shape, and orientation of collagen production. I’ve come across a couple specific references to these factors reaching peak production and concentration at 30min of strain and was dependent on the magnitude of the strain (I.e. Higher strain equals higher production). Obviously there were limits, as at a certain point the strain exceeded the limits of cell viability. One of the studies went on to suggest that strains in excess of 60 minutes resulted in a significant increase in cell apoptosis over time. Also, the Ribgy study asserts that strains in excess of 60 minutes are “deleterious” to the tissue. Although, in the case of PE this deleterious result might be desirable within moderation.
Some here focus very heavily on how to get the maximum residual extension of the collagen structures, while it is probably more advisable long term to find the optimal balance between residual extension and healthy cell proliferation. The latter would necessitate a commitment to retaining the viability of existing tissue and simultaneously triggering peak production of “scarless” healing agents.
Consequently, the most optimal regime would seem to include a very controlled strain cycle with the following characteristics. I will use the term baseline length to denote the transition point at the toe of the load strain curve. Roughly, this would correspond to the completely flaccid penis in a fully relaxed state and a light load (about 1lbs) over a period of several minutes. The term ‘elastic limit’ will refer to what we normally probably consider BPFSL under a modest load (about 3-5lbs depending on the conditioning).
STEP 1.. No heat if not at least partially loaded and within elastic zone, as anything above 37C results in collagen tissue contraction when not under load.
STEP 2.. Within elastic zone heat collagen to about 41-42C. Below 40C is repeatedly shown to leave the tissue unaltered, while above 43C risks tissue necrosis over prolonged periods. Keep in mind for next steps that studies experienced repeated tendon rupture at around 4% strain when temps were increased above 40C.
STEP 3.. Set strain rate of about 0.5-1.0%/minute, to avoid tissue damage/pain.
STEP 4.. Start 1st strain to about 2.5% beyond baseline length (should be no discomfort as we will still be within elastic range), followed by a 5 minute ambient cool down at static strain (notice I said static strain not constant load) and another 5 minutes relaxation under zero load. This is theoretically within the full elastic recovery safe zone but will get the tissue ready for a stretch.
STEP 5.. Under light load reheat to 41-42C then strain at 0.5%/min to 3% beyond baseline (should feel a stretch but not pain). 5 min ambient cool down under static strain and 5 min additional rest at no load. This should be just barely past the recovery zone and fundamentally weaken the collagen secondary bonds triggering a healing response. My assumption is that this step corresponds to about 1mm beyond the elastic limit referred to above.
STEP 6.. Under light load reheat to 41-42C and strain at 0.5%/min to about 4% beyond baseline (stop if any pain). Hold at this static strain under constant heat for 30min. 10-15min ambient cool down at this static strain, assuming no pain during cooling. This should be about 2.5mm past the elastic limit.
STEP 7.. Reduce load to near zero while maintaining new baseline length for 3-6 hours. The previous steps should’ve resulted in a stress-relaxation already taking the load back near zero, so this sort of ADS is mostly preventing the muscles from getting involved or contribution from other tissues that didn’t reach the plastic flow region.
What to do after that is very debatable. The half life of the HA and NO in collagen tissue is 1-3 weeks which follows more of a macro IPR timeline. Arguably, this procedure could be followed once every 3-4 days with some minor daily manuals or periodic light ADS (in both cases not exceeding the new elastic limit) to maintain the tissue memory of the extended state during initial cell proliferation. My assumption would be an ADS routine of 60min light stretch 4 times a day. After about 14 days switching into a macro P phase for 2-3 weeks with continued periodic ADS use but no more plastic strain, and then a Macro R phase for about 2-3 months with nothing like more than Kegels and light jelqs to massage the tissue.
