Mechanical growth factor. Part 3. Comparison of MPR and AAS.

Mechanical growth factor. Part 3. Comparison of MPR and AAS.

hypertrophy and hyperplasia

Now that some of the information we have gathered, perhaps it is useful to try to draw parallels between the mechanical factor in the growth and androgenic-anabolic steroids. But to carry out this comparison of non-standard (to completely confuse you) I will be a non-standard way, namely by comparing the two concepts to increase the size of skeletal muscle -gipertrofii and hyperplasia. The increase is achieved in two ways: by increasing the number and volume of myofibrils (myofibrillar hypertrophy) and by increasing the sarcoplasmic (sarcoplasmic hypertrophy). The theory myofibrillar hypertrophy is the principle of longitudinal splitting myofibrils and increase the contractile proteins, namely myosin since its volume is greatest {25% of the total number of contractile proteins) (about actin and do not forget, t. To. Without any myosin not help). What exactly is happening? It is under sufficient stress, actin filament break and myofibril split lengthwise into several fragments. In the cavity between these fragments invade sarcoplasm (sarcotubules) and transverse tubular system (T-Systems), which, together with new fragments myofibrils and can increase in volume of muscle fiber. Sarcoplasmic hypertrophy is characterized by an increase in sarcoplasmic (sarcoplasm an interior environment (many call it «liquid»), filling the space around myofibrils), which is carried out by increasing the amount of liquid interfibrillar, mitochondria and, as a result, glycogen, ATP and creatine. The muscles increases capillarization. In fact, muscle fiber increasing in volume, but the density is not increased myofibrils.

From the point of view of the «longevity» (minimize recoil after the «Course») to be the most interesting is myofibrillar hypertrophy, as those myofibrils, which «grew», in contrast to the sarcoplasmic have nowhere to go. But in fact it turns out that we observe abundant sarcoplasmic hypertrophy and only somewhere far away (we hope very much to it) — myofibrillar. This is due to the fact that for myofibrillar hypertrophy is characterized by a particular load («lifterskie protocols», ie. E. Work out with weights in the range of 90-100% of the maximum), and myofibril must reach their «ultimate strength» with progressively increasing load.

«But we have a secret weapon androgenic!» — You exclaim. Yes there is. But it looks nice and smooth only in theory. In fact, in our «exaggerated» the equation, there are several significant variables, without which the testosterone will not be able to help. This androgen receptors. By itself, the muscular activity that requires intense muscle contractions, stimulates an increase in androgen receptors in place of the load. Due to this property, after binding to testosterone «rodnymgt; receptor and protein synthesis occurs in the binding site. Not biting deep into the granite of science (the more, and so many know it almost by heart), try a basic «classical» theory of the effect of testosterone on muscle nucleus present in the following, very simplified sequence:

— LOAD;

-Deformation of the muscle fibers;

— EXPRESSION OF CORE muscle cell androgen receptors;

— TESTOSTERONE enters the cell and binds to a receptor;

— Benchmark suite receptor into the nucleus;

-Core through DNA that recognize this complex and releases the corresponding mRNA;

— MRNA gets into the cytoplasm and there from amino acid residues (which circulates at the time) to create the appropriate protein (myosin, actin and TD);

— This protein has its place in the structure of deformed reuse by myofibrils.

But why, then it turns «roll back» after a course of androgens? And because it is mainly dominated by the sarcoplasmic hypertrophy that occurs in fast oxidative fibers type phasic and phasic fast glycolytic fibers with a type of oxidation. Phasic slow oxidative fibers type sarcoplasmic hypertrophy is also affected, but not so much. «Split» a large number of myofibrils is not possible, and help in this part, and androgens stimulate the synthesis of proteins, which in turn, restore damaged areas of the myofibrils. Protein synthesis requires a large amount of energy. And the muscles now do much more work, and they also have to provide far more nutrients. So it turns out that a network of sarcoplasmic increases, blood capillaries and vessels, as well as the number of mitochondria. Due to glycogen supercompensation he (glycogen) after each subsequent workout is stored in large scale than it was before the previous workout. And all this leads to a proliferation of sarcoplasmic. After the course (and termination of active androgens bombarding the muscle nuclei) stops excessive production of contractile proteins. Myofibrils loses the ability to actively recover, load reduced. It reduces the need for nutrient substrates, and all hyped «sarcoplasmic infrastructure» loses its meaning. Greatly reduces the number of mitochondria decreases network of vessels. And you do not forget another major factor? Cortisol, which managed to contain a strong concentration of androgens, returns to the arena. It’s the «deepening» rollback. And it’s all happening on the background of reducing their androgen secretion, which could help the cell nucleus in the synthesis of new proteins. But can not. Yes, and that help some, because the core reduces the expression of androgen receptors. As a result, manage to keep basically just acquired myofibrillar hypertrophy and a small luggage from sarcoplasmic hypertrophy (because the infrastructure for a small number of new and old myofibrils still needed).

This «classic» concept hypertrophy lately lends itself to more and more revision, t. To. It is believed that the effect of androgen on skeletal muscle is not limited to the stimulation of protein synthesis. Development of this area are engaged in more than a dozen years (I was able to read the articles on this subject in the wording of another 70-ies). But this «alternative theory» received its impetus and concrete (science-based) develop only in the 2000s, when they began to appear the results of studies showing the effect of testosterone on miosatellitotsity. In 2004, the research it has been found the presence of androgen receptor in miosatellitotsita. Rather, it appears that miosatellitotsit in response to stimulation sverhfiziologichnymi doses of testosterone in full hormone replacement (used in studies of the course of 600 mg of testosterone enanthate per week + GnRH, which acts as a natural blocker testosterone secretion) is capable of generating androgen receptor. «Well, why do we in this case, MPR if androgens and so do all the work?» You ask -rezonno. And I answer: for hyperplasia.

The fact that the consensus that promotes the expression of the androgen receptor whether cell division satellites or testosterone helps satellite cells to become a full myoblasts, there is still no. Scientists working in this direction, in one voice say that some effect is, t. To. «Steroid users» with extensive experience in using AAS number of nuclei in the muscle cells and the size of the muscle fibers is several times higher than in athletes (powerlifting), not to resort to using exogenous androgens. On the other hand, there is evidence that testosterone is able to inhibit the formation of myoblasts miotrubochek, and as a consequence, there is no formation of new myofibrils. As you can see, the situation is a little hazy. But it broke through the fog still a ray of truth, which was born out of the theory of the indirect effect of androgens on miosatellitotsit by the isoforms of IGF-1, and it is through the effect on IGF-1 Her (aka MFR) and IGF-1Ea.

But let’s order, or rather, we will gradually move to the next method of influence on the growth of muscle — hyperplasia. Hyperplasia, as you know — this increase in the number of muscle fibers. Basically, this definition can be summed and myofibrillar hypertrophy, because it, too, can lead to an increase in the number of fibers, but hyperplasia, which will be discussed in this section is of a different origin. This hyperplasia is the result of activation and «transformation» in full miosatellitotsitov myofibrils. In principle, this idea passes the «red line» through the story of the MPR, therefore, to emphasize is the difference between the AAS and MPR, I allow myself a little bit again. Runs the process mechanical growth factor, which makes sharing miosatellitotsit. «But this is "Muscle Recovery"And not increase it! «- You’ll notice. That’s right. Increased muscle hyperplasia through impossible without activation miosatellitotsitov in excess of the amount needed to restore muscle. E. Satellite cells should «spawn» much more than they were required to «treat» the affected muscles. What do you need? For this need to IFR. We need over time to maintain the division, division, division miosatellitotsita, without converting it into a myoblast, because myoblast will not be shared. And so it turns out that MPR associated with miosatellitotsitom, runs the division, and the molecule has no IRF, and there are two miosatellitotsita. In principle, a good idea, but we want to grow and we need more miosatellitotsitov until they become myoblasts. Therefore, these two miosatellitotsitam launch two molecules IFR. We get four miosatellitotsita. Even better. Add another four molecules MPR? Of course, we add and get 16 miosatellitotsitov. In general, we support continued progress, which in normal conditions (without exogenous MPR) reaches its peak at the end of the first day after muscle damage. If we add to this a system of synthetic MPR, we get a much larger division, which also starts to decline 30 hours after injury (if you add the longer form (pegylated or MPR pMGF720), we will make the process take longer). A large number of myosatellites — this is certainly cool, but what we do with them now? As it turned out, our long-suffering body knows the answer to this question. In the arena appears IGF-1, or rather its isoform of IGF-1 Ea, which is present at low concentrations from the beginning of muscle damage and reaches maximum activity somewhere between 48 and 72 hours after injury. This isoform and triggers differentiation of myoblasts miosatellitotsitov in full. In other words, the MFR increases the number of satellite cells, and IGF-1 does have myoblasts. Next myoblasts form myo tube that takes its place at the site of the damaged fiber, well, after all the damage, «refurbished», myo tubes form new muscle fibers (and the new muscle fibers form the nucleus, the number of which, according to some reports, correspondence number of educated fiber myoblasts). This process is inseparably linked with the synthesis of proteins, which we need a lot (both for recovery and for additional growth). Here’s the handy androgens and growth hormone. What do we get as a result? We get reduced muscle fiber and «weak», the newly formed fiber, which is relatively fragile (just emerging from the contractile apparatus) and that you want to develop further, so that it can withstand the workload without the risk of being completely destroyed. This hyperplasia is completed.

I hope my «empirical-metaphysical» explanation of the above processes has allowed you to tell the difference in hypertrophy and hyperplasia and as a result, the difference between the AAS and the MPR. But if you try to further simplify and describe the difference simple and understandable to everyone sporty words, the difference lies in the «rollback» after the course. If the «rollback» after the course (average) AAS often is 40-70% of the achieved results, which largely depends on the amount advanced to the sarcoplasmic course, the «rollback» after a course of MPR if possible, it is extremely minimal (no more than 20 30%) as MPR basically operates locally, and also because the MFR does not significantly increase the sarcoplasm. Although you may notice that the hypertrophy and hyperplasia are closely related and, in fact, the one without the other is almost impossible, but that does not mean that progress is impossible without combining MPR and AAS.

In addition, our comparison of MPR and AAS would not quite be complete if we have not paid attention to such important elements of the course as the negative side effects, the impact on power rates, the impact on the joints and ligaments, FCT, doping control. Testing your patience, I will not, and instead of a detailed analysis of the MPR and AAS for each of these «nominations» tezisno just go over these aspects.

POSSIBLE ADVERSE SIDE EFFECTS

AAS: gynecomastia, high cholesterol, liver disease, seborrhea, testicular atrophy, decreased sperm production, decreased libido, suppression of the HPTA, reducing the concentration of IGF binding protein type 3, the stimulation of the development of cancer.

MPR: the stimulation of existing cancer, possible reduction in bone strength.

IMPACT ON POWER PERFORMANCE

AAS: increase in total «tonnage» in one workout, increasing the maximum weight when one repetition with 100% of maximum power. MPR: increase in the total «tonnage» in a single workout; a temporary reduction of the maximum weight when one repetition with 100% of maximum power.

Effect on joints and ligaments

AAS: mainly positive.

MFR: no impact on joints and ligaments.

Post-cycle therapy

AAS: in some cases required. MPR: not necessary.

DOPING CONTROL

AAS: the likelihood of being discovered (not «preparatory activities») is 100%.

MPR: Is it possible to reveal only in the case of mass spectrometry, liquid chromatography, after blood samples. In the next issue we finish our story, highlighting the following topics:

ROLE OF FMI IN THE MPR (proliferation / differentiation)

COMBINING MPR with other species PHARMACOLOGICAL PRODUCTS.

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