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Originally Posted by remek  Iguana: For the record, I just want to let you know that I intuitively agree that jelqing/clamping/pumping probably works out the smooth muscle more than it does the tunica (and stretching/hanging works out the tunica more). I've actually believed this for some time, yet I don't have any substantial evidence for this. Just a theory. I was hoping you could provide something  |
remek, keep in mind, this is somewhat based on speculation, but I think the evidence is supportive at the very least. I based my conclusions mostly on what I had read in a few smooth muscle related articles. This one in particular:
Vascular Smooth Muscle Growth: Autocrine Growth Mechanisms -- Berk 81 (3): 999 -- Physiological Reviews
I copied a particularly interesting excerpt and highlighted the statements (in red) that are especially applicable to PE.
II. PHYSIOLOGICAL PROCESSES THAT REQUIRE VASCULAR SMOOTH MUSCLE CELL GROWTH C. Remodeling Vascular remodeling (Fig. <A href="http://physrev.physiology.org/cgi/content/full/81/3/999#F1">
1) is a physiological response to alterations in flow, pressure, and atherosclerosis. Remodeling involves changes in VSMC growth and migration as well as alterations in vessel matrix (214). Remodeling may be classified as proposed by Mulvany based on the nature of changes in vessel diameter (inward or outward) and by changes in mass (increased = hypertrophic, decreased = atrophic, no change = eutrophic) (214). As an example "eutrophic outward" remodeling would be an increase in lumen diameter without change in amount or characteristics of the vessel such as may occur with increased flow and atherosclerosis. In contrast, "hypertrophic inward" remodeling would be defined as a decrease in lumen diameter with increased wall thickness such as may occur with increased pressure. It has been best studied in resistance vessels during hypertension. During chronic hypertension, there is an increase in vessel wall thickness hypothesized to normalize wall stress. Physical forces (wall stress and cell stretch), autocrine growth mechanisms, and paracrine growth mechanisms (EC actions on VSMC) stimulated by the hypertensive environment appear causative. 
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[in this window] Fig. 1. Vascular remodeling.
In response to changes in blood flow, remodeling appears to be fundamentally dependent on the presence of an intact endothelium as shown by Langille and co-workers (173, 174) and by Kohler et al. (155). Because flow-induced remodeling would be expected teleologically to be mediated by changes in vessel tone and hence diameter, candidate mediators are vasoactive molecules. Among these, nitric oxide [produced by endothelial nitric oxide synthase (eNOS)] appears to play a predominant role. Recent studies show that ~70% of flow-dependent outward remodeling is due to EC nitric oxide production as determined by inhibiting production of nitric oxide with eNOS inhibitors (317). During inward remodeling in response to decreased flow, there is a coordination of increased VSMC apoptosis and decreased VSMC proliferation to effect the decrease in vessel wall mass that occurs (47). An important role for monocytes has been elucidated in remodeling, especially in response to ischemia such as occurs after occlusion of a supply artery (277). In response to increases in flow, EC express monocyte chemotactic peptide-1 (MCP-1) and monocyte adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1). The monocytes are recruited to the vessel and infiltrate and digest the media. The EC are activated by monocytes and express basic FGF (bFGF), PDGF-BB, and TGF-
. These growth factors then lead to VSMC growth and vessel enlargement. In response to increased pressure, remodeling appears to be due to activation of autocrine mechanisms that stimulate VSMC growth and changes in vessel wall matrix (
123,
213,
215).
As discussed in greater detail in section IV, many VSMC growth factors have been implicated in the growth and remodeling of hypertensive vessels including PDGF (227, 274), TGF-, insulin-like growth factor I (IGF-I) and the IGF-I binding proteins (7), and hepatocyte growth factor (221). Paracrine mechanisms that are important in hypertension include increased production of ET-1 and angiotensin II by the endothelium.
Notice how increased pressure and flow stimulates an increase in mass and vessel diameter. Isn't this exactly what we are doing with jelqing, clamping and pumping, altering the blood flow and pressure?
Notice how shear stress (stress parallel to the vessel) can increase vessel diameter.
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Originally Posted by remek; So where do we go from here? Do you have a demo-routine in mind that we can put to the test? I know that we should always increase the intensity as time goes on (like you said, less is more goes out the window at some point), but if you had to take this information and set it into a routine, what would that be? |
Boy, that's the million dollar question. This is going to require a lot of thought. I was hoping we could put our heads together here and formulate some type of test routine. We need to assume this will be geared for those who are out of newbie gains. There would possibly be two routine types. One for those needing smooth muscle mass and one for those needing to focus on tunica elongation (based on BPEL to BPFSL ratio.) Or, maybe a routine that focuses a few weeks on one then switches to the other. Maybe, two weeks stretch based and then two weeks jelq, clamp, pump?
Any thoughts?