Yowza. I had certainly read much of that information before - but never consolidated and organized for easy digestion. Thanks Modesto…and Hobby.
Facia (tunica) is Collagen Type I.
Smooth Muscle is Collagen Type III.
I spent a good bit of my lunch break yesterday discussing the nature of connective tissues like Collagen Types I & III. “Official science” offers us very little information that is directly helpful to PE…but most of you already know that.
“Synthesis of collagen involves a cascade of biochemical modifications of the original building blocks. Many enzymes, cofactors and growth promoters influence these modifications which are crucial to the structure and function of mature collagen. The most abundant form of collagen, Type I, consists of three units of polypeptide chains, which are comprised of subunits of amino acids. Differences in the chemical structure of the polypeptide chains determine the different collagen types. These chains intertwine in a triple helix to form molecules called procollagen. Procollagen is formed within the cell and subsequently transported outside of the cell into the extracellular matrix. Outside the cell, procollagen is altered to form tropocollagen, which is then able to form into microfibrils. Microfibrils form fibrils when they are packed together in an overlapping fashion. The microfibrils are held by hydrogen bonds, hydrophobic interactions and reinforced by cross-links between tropocollagen molecules. The characteristic types and amounts of their cross-links largely determine the mechanical properties of collagen fibers. As we shall see throughout this article, nutrient deficiencies and pharmaceuticals may influence synthesis or metabolism during the critical stages in development of collagen.”
Bingo. Now what?
“Ground substance: The ground substance fills the spaces in-between the cells and fibers. Its viscosity acts as a lubricant due to the high water content. Soluble precursors of the fibrous proteins, proteoglycans, glycoproteins and other molecules secreted by cells are abundant in the ground substance.”
Is this where our biomechanical growth starts? I’ll bet it is. Tensile forces such as those associated with PE trigger changes all along the collagen spectrum.
We should all be drinking plenty of water.
“Individual cells, such as the fibroblasts in connective tissue, rarely divide into new cells unless the tissue requires additional cells as when a tissue is damaged. During inflammation and repair, the numbers of fibroblasts increase within some connective tissues. The extracellular matrix greatly influences function and differentiation of the cells. Tensile forces may also influence cell function, as changes in cell shape may alter the responsiveness of the cell to hormones and growth factors (3). The discussions on inflammation and pharmaceuticals examine the influences of hormones and growth factors on cell function.”
Yup. Yup. Uh-huh. *Goon nods his greying head excitedly*
“Synthesis and degradation of tissues is a continual process and are integral parts of tissue remodeling and turnover.”
“Changes in gene transcription and in events after translation of macromolecules can alter distribution and deposition of tissue proteins and proteoglycans. For example, many pathological conditions are attributable to abnormal or insufficient collagen synthesis, such as scurvy and vitamin C deficiency.”
“Specific enzymes initiate degradation of macromolecules. Collagenases, which degrade collagen fibers, are synthesized by various cell types and stimulated by hormones, prostaglandins, and other substances secreted by lymphocytes and macrophages. Metal ions, such as calcium, also regulate collagenase activity. Enzymes within cellular lysosomes degrade proteoglycans. We will see how synthesis and degradation are an integral part of tissue turnover.”
“Proteoglycans in the extracellular matrix appear to regulate remodeling of connective tissue by influencing collagen formation during the repair process. Remodeling is also regulated by mechanical stimulation. Mechanical tension and compression modify bone and cartilage remodeling, where tissues such as these depend on diffusion of nutrients for maintenance since they have no direct blood supply.”
No direct blood supply? Hmmm. I’m thinking transdermal ointments…
“Turnover of connective tissue is the net balance between synthesis and degradation of the macromolecules. A turnover negative balance is characteristic of several inflammatory and joint diseases where degradation occurs at a higher rate than synthesis.”
That’s bad. It leads to Negative PI’s like shrinkage!!!
“The repair process in tissue injury involves managing macromolecule turnover so that synthesis equals degradation.”
And that is tissue maintenance or “the status quo” which, in my opinion, is also bad…er, NOT “desirable”. You understand.
“Turnover rate of various connective tissue components varies. Elastin may take months to years for renewal. Collagen is also a stable protein and renewal is slow. Replacement of mature collagen can require weeks to several months. Collagen turnover rates vary in different structures. Tendon collagen renewal is very slow, whereas the collagen of loose connective tissue that surrounds our organs is renewed more rapidly.”
THIS is where the IPR protocol shines the brightest. Rest gives the tissues the time they require to repair themselves. But How Much? What about BUILDING vs. just maintaining? Ugh.
“Acute inflammation phase: Immediately after injury, several vascular and cellular reactions initiate the response known as inflammation. The process begins with a release of chemical mediators from cells into the extracellular fluid. The initial tissue damage stimulates release of histamine from mast cells, which causes dilation of blood vessels in the local area and increases vascular permeability. Increased blood flow and fluids and proteins that leak from the permeable blood vessels cause edema in the tissue and consequent swelling. Cells migrate from nearby blood vessels and cause release of more inflammatory mediators, such as kinins and prostaglandins (PGs). Local tissue pressure and some of these mediators act on nearby nerves to cause pain. These events lead to the classical signs of inflammation: redness, swelling, pain and heat.”
“The primary purpose of inflammation is to rid the site of damaged tissue cells and set the stage for tissue repair. Acute inflammation generally lasts from 48 to 72 hours after an injury and gradually subsides as the repair process progresses. Many of the events that occur during this time initiate tissue repair. PGs are considered important mediators of inflammation and are often the target of intervention with anti-inflammatory agents. However, PGs may also have a significant role in tissue repair. Many immigrant cells also have significant roles in tissue remodeling. Leukocytes (white blood cells), such as neutrophils and monocytes, accumulate within the damaged tissue along with resident macrophages. Enzymes released from these cells help digest necrotic cells and degrade matrix molecules; neutrophils and macrophages engulf cell debris. Blood platelets release growth factors that stimulate new fiber and matrix molecule synthesis.”
Inflammation…good. Make it burn, baby.
“Matrix and cellular proliferation phase: Chemical mediators released by inflammatory cells stimulate migration and proliferation of fibroblasts, which participate in the repair process. Fibroblasts secrete fibronectin, proteoglycans and small diameter Type III collagen fibers. In addition to these fibers, newly formed capillary channels, clotting proteins, platelets and freshly synthesized matrix molecules form granulation tissue. However, this granulation tissue has little tensile strength.”
We NEED those fibroblasts. They create the new collagen tissues. Also, this may be the best time to apply a light tensile force, as the new tissues have little tensile strength and less force may lead to no new inflammation. (It could do more work.)
“Remodeling phase: Recall that remodeling reshapes and strengthen damaged tissue by removing and reforming the matrix and replacing cells. As repair progresses, inflammatory cells disappear, the number of blood vessels and the density of fibroblasts decrease. The proportion of Type I collagen to Type III collagen and the matrix organization increases. Collagen fibers are reoriented in the direction of loading, especially in ligament repair. Collagen matures and elastin forms; tensile strength increases. However, the remodeled tissue may not completely resemble the original and thus the mechanical capabilities of that tissue may be altered.”
But, the IPR protocol has already received much touting around here in the last year or so…the chemical manipulation of Collagen is what I am specifically after.
While it is CRUCIAL to get a better grip on the TIMING of IPR…I want to know more about how to increase the yields of the Proliferation phase.
If all we do is rebuild what was damaged…we have done nothing.
"Debate the idea..."