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How ATI works (biologically)

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    Tendons respond to load (why bodybuilders, etc can move huge weights). Tendons adapt microscopically to load. They slowly remodel. If you progressively load a tendon and allow adequate recovery and growth (at least 36 hours between) they will slowly strengthen. You are literally microscopically breaking down collagen and then it remodels a little each time getting minutely stronger.


    Image result for collagen synthesis cycle"

    As you can see from the above, if you intensely train a tendon and don't allow adequate time between exercise, you just degrade the tissue and it never gets time to recover. This is how you get overuse injuries - chronic tendinopathy injuries/cycles. The principle is similar for injury recovery. At the later stages you have to load the tendon to encourage adaptation to the load so it strengthens. But you have the added issue of the weak collagen composition. When you overload a tendon you get microscopic tears that tend to fill in initially with weaker type 3 collagen, which is then prone to tearing again when over-loaded and the sufferer might fall into a tendinopathy cycle:

    Image result for tendinoptay cycle"

    The only way to escape is very slowly raising the load without aggravating the weaker collagen - this is all going on a massive scale cellularly - which is what traditional physiotherapy essentially does.

    The same can be said with more acute injuries. Tenocytes are crucial in the process and encouraging remodelling of collagen matrix (simplified, as changing weak type 3 to strong type 1) within tendons.

    To paraphrase:

    The three main stages of tendon healing are inflammation, repair or proliferation, and remodeling, which can be further divided into consolidation and maturation. These stages can overlap with each other. In the first stage, inflammatory and repair cells are recruited to the injury site. After the release of very crucial biological repair factors, the proliferation of tenocytes are initiated and start to synthesize collagen III. After about six weeks, the remodelling stage begins. The first part of this stage is consolidation, which lasts from about six to ten weeks after the injury. During this time, the synthesis of collagen is decreased, and the tissue becomes more fibrous as a result of increased production of collagen I and the fibrils become aligned in the direction of mechanical load (beginnings of normal functionality). The final maturation stage occurs after ten weeks, and during this time there is an increase in crosslinking of the collagen fibrils, which causes the tissue to become stiffer. Gradually, over about one year, the tissue will turn from fibrous to scar-like i.e. NOT malleable and inferior to the original.

    The problem is that the tendon is very weak until the remodelling begins (6-10 weeks) and remains weak until you can slowly progressively strengthen (perhaps as long as a year if you want to do heavy/explosive loads and that is if you get there without tearing on the way). Hence on a microscopic level, you often have this battle of the repair vs the tendinopathy cycle. Acute injuries don't repair properly and become chronic. Even when they do, the final tissue is less malleable and strong than the original.

    The problem also is as we get older we have less tenocyte cells in the tendon and less ability to produce them. This is where ATI steps in cultivating literally millions of these tendon stem cells and injecting them into the injury site - a proliferation that your tendon cannot begin to replicate on its own even in youth. Massively amplified. These tenocyte cells have already evolved somewhat so you literally have this mass of stem cells ready to form type 1 collagen - the strong stuff. The repair and adaptation process is massively expanded, intensified and sped up, thus improving the whole recovery process AND the final tissue (i.e. less scar tissue and more like normal tissue). Perhaps a misnomer, but its literally giving your naturally occurring tendons stem cells a massive (massive) boost in number.

    This is why I bang on about the merits of ATI. It literally mimics the bodies normal repair process, but massively amplifies it. Before you worry about messing with nature, unlike mesenchymal stem cells, tenocyte stem cells can only become tendon cells - many antagonists of stem cells cite cancer cell growth encouragement. Tenocytes literally lack the ability.

    It will be a travesty to society if this procedure does not become mainstay in tendon injury treatment. Hopefully the J&J trials will be the start.
 
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