Workpieces, collapsing structures, sharp edges, burrs, roughness on the surface of any workpieces, lifting and transport equipment, falling objects from a height. These same dangerous sources include corrosion of metals, weakening the strength of structures, improper operation of vessels under pressure, possible falls on slippery surfaces, etc. The most typical are risks, burrs, protrusions on rotating mechanisms and tools.

They are most often located in the following places:

1. At the site of surgery. This is the point at which work is carried out on the material such as cutting, forming, stamping, drilling, forming blanks, etc.;
2. In any component of a mechanical system that transfers energy to the machine or its parts that perform work. These can be flywheels, pulleys, belts, couplings, chains, gears, spindles, etc.;
3. Moving parts of machines during operation.

In principle, there are a huge number and variety of types of mechanical movement and actions, and all of them can pose a serious danger to workers. Any mechanical movement can hit, push or cause other dynamic effects, so the first step to protecting yourself from danger is to understand this. In addition to the main sources of mechanical impact, there are also other reasons.

These include:

1. Slippery floor. Especially if there is oil spilled on the floor that has leaked from the equipment;
2. An unstable, oscillating foundation on which a person stands while performing this or that work. A fall from a height can lead to irreparable consequences;
3. Technological transport moving in the work area - trolleys, loaders, electric vehicles;
4. Entry of a person into the range of action of industrial robots and manipulators.

If there is a danger of mechanical injury, then, of course, there are ways to protect yourself:

1. Inaccessibility of dangerous objects to humans;
2. Use of human protective devices;
3. Use of personal protective equipment.

Note 2

This particular equipment and tool has specific manufacturing requirements and limitations to help protect the worker. Requirements and limitations come from the type of work, the shape of the material being processed, the processing method, and the location of the work area. Most often, protective, safety, and braking devices are used for protection. Automatic control and alarm devices and remote control are also used.

Mechanical injuries

Definition 1

Trauma is called an external effect on the body that leads to some kind of damage.

Injuries can be different:

1. Mechanical – bruise, blow;
2. Thermal – cold and heat;
3. Electrical;
4. Chemical;
5. Injuries caused by X-rays;
6. Mental – fear, shock, etc.

In a narrow sense, this term is usually used to refer to mechanical damage. Mechanical damage can be obtained as a result of bruise, wound, or infliction by any object - blunt, sharp, gunshot, etc.

Consequence mechanical impact is stretching, compression, bruise, crushing of tissues, damage to blood vessels, damage to nerve endings, etc. Traumatic injuries can be either open or closed. With closed injuries, the integrity of the skin is not compromised. Open injuries, of course, have these violations - lacerations, incised wounds, open bone fractures, etc.

Characteristic sign of injury is painful sensation. Microbes may well enter damaged surface tissue and cause an inflammatory process in deeper tissues. Very often, a serious condition of the body can occur if the traumatic injuries are significant, for example, a wound to the stomach, chest, injuries to the limbs. This serious condition is called traumatic shock, characteristic the signs of which are:

1. At the initial stage, the heart rate increases;
2. Increased breathing;
3. Increased blood pressure;
4. The content of sugar and adrenaline increases in the blood;
5. The next stage is a decrease in blood pressure;
6. The amount of circulating blood decreases;
7. Body temperature decreases;
8. Reflex activity is weakened;
9. There is indifference to others;
10. There is a decrease in alkaline blood reserves;
11. The pain sensitivity threshold decreases;
12. Alkaline blood reserves decrease;
13. There is a decrease in electrophysiological activity;
14. The excitability of the cerebral cortex and autonomic centers decreases.

Shock may be primary and occur at the time of injury or shortly after it. Secondary or late sho occurs within $4$-$6$ hours after injury.

Note 3

Thus, short period Excitation during traumatic shock ends with a sharp inhibition of the basic physiological functions of the body.

Industrial injuries

Definition 2

An accident at work can lead to sudden damage to the body and loss of a person's ability to work. Repeated occupational accidents are called " industrial injuries».

The following industrial injuries are distinguished:

1. Mechanical, thermal, chemical, electrical - type of impact;
2. Individual, group from $2$ to $15$ and more people – number of injured;
3. Injuries incompatible with life, with a disabling outcome, with long-term treatment - degree of severity;
4. Moderate injuries – rehabilitation from $3$ to $30$ days;
5. Minor injuries – restoration of working capacity within $3$ days.

Occupational statistics show that the most common injuries are:

1. For head, face, neck – $17.8$%;
2. For the body – $15.0$ %;
3. Upper extremities – $28.7$%;
4. Lower extremities – $38.5$%.

According to external factors of injury:

1. Mechanical impact – $92.5$%;
2. Burns from thermal exposure – $6.5$%;
3. Chemical poisoning and burns – $0.47$%;
4. Burns from electric shocks and electric shocks themselves – $0.28$%;
5. Gas poisoning – $0.25$%.

From the above data it is clearly seen that the main industrial injuries are mechanical injuries.

All industrial injuries are classified according to the types of traumatic factors:

1. Cause of injury;
2. What type of work contributed to the injury;
3. What was the source of injury, etc.

Common causes of industrial injuries:

1. Defects in the design of machines, equipment, mechanisms, etc.;
2. Malfunctions of technological equipment, transport vehicles;
3. Lack of protective equipment for working parts and gears;
4. Inadequate technical condition of buildings, structures, communications, engineering networks;
5. Weak technological discipline;
6. Failure to comply with the rules for the movement of vehicles, both on the territory of the enterprise and inside buildings;
7. Poor organization of work;
8. Unsatisfactory maintenance of workplaces, failure to comply with work safety rules;
9. Failure to comply with safety regulations;
10. Failure to comply with workplace lighting requirements;
11. Failure to use personal protective equipment;
12. Use of workers not in their specialty;
13. Insufficient training of workers in safe work practices;
14. Insufficient instruction.

Mechanical growth factor (MGF), Mechano growth factor (MGF) is a structural modification of insulin-like growth factor (IGF-1), a variation in the form of IGF-IEs. The production of MGF is observed as a result of physical activity or injury to muscle tissue, because MGF is a restorative substance for muscles.

IGF-I has a number of unique isomers (proteins that are structurally and functionally similar). MGF serves as a local variation of the IGF-1 compound, and is produced by muscles as a response to injury or overexertion. MFR is quite sensitive to any mechanical signals, especially to overload of the muscular system. As a matter of fact, this is why MGF is called a mechanical growth factor.

MFR is synthesized during muscle activity in the muscles themselves and performs the function of regenerating muscle tissue. MGF serves as one of the main factors whose task is to control the recovery and rate of muscle growth. MGF produces the synthesis of myoblasts (muscle growth cells), which accelerates muscle growth and regeneration after training. The physiological role of MGF has been well studied in in vitro cell models and in experiments with mice. Mechanical growth factor, unlike IGF-1, stimulates, for the most part, the processes of division of dormant muscle tissue cells (myoblasts), due to the activation of various receptors. A decrease in the level of MGF production is the main reason why muscle contractions are observed in patients with dystrophy and the elderly.

The entire chain of biomechanical influence of GH can be divided into 3 links:

• first – GH synthesis in the pituitary gland (the main effect of growth hormone is the destruction of excess fat)
• second - Changing growth hormone to the IGF-1 type directly in the liver (the main effect of IGF-1 is the regeneration of tissues and organs, etc.)
• third - Synthesis of MPPs in muscle tissue (muscles grow and recover, adapt to loads).

It follows that the MGF serves as the final link. In addition, in terms of stimulation of muscle growth, MGF is one of the main intermediaries between GH and IGF-1.

How to use MGF medicinal product at first it was limited, because this substance disintegrated within a couple of minutes after injection. The production of MGF in the body occurs continuously, so the concentration remains at a high level for a long time. It is quite difficult to give injections every half hour. Then scientists found a simple and at the same time ingenious solution - pegylation. As a result, the MGF molecule was combined with a polyethylene glycol molecule, which serves as protection against its destruction, and at the same time does not reduce biological activity and effectiveness. Hence the conclusion - almost all modern drugs are pegylated with Peg-MGF, and pure MGF is useless.

The PEGylation process creates a protein with an artificial protective binding that protects the underlying protein from enzymes and inhibitors, making the protein molecule much more stable and durable. Molecules after pegelation are absolutely safe and give the same effect on the body as their predecessors. The protective PEG binding is inert and does not bind to other substances in the body, and does not affect the quality of metabolism (non-toxic) and is quickly excreted in the urine. PEG is approved for use in dosage forms in Russia, the USA and some other developed countries, and it is also approved as a food additive. PEG is widely used as a filler and as a binding agent for food products and cosmetics.

With the help of PEGelation, PEG MGF (PEG MGF) is converted into a drug with a longer effect and becomes more accessible to a wider range of people. PEG MFR can be taken only 3 - 4 times a week to achieve the required results. The only negative factor of long-term use of PEG MGF is the occurrence of addiction, but this is not scary - you just need to take breaks from using the drug from time to time.

There is an opinion that pegylated peptides will soon be able to be detected during anti-doping control, and the time for their detection will be very significant. For example, the pegylated version of erythropoietin - Mircera - is determined over more than one month, in contrast to EPO itself, where we are talking about a matter of days. MGF is quickly destroyed in the gastrointestinal tract, and therefore is taken exclusively by injection subcutaneously or intramuscularly.

MGF COURSE

MFR continues to undergo clinical trials today, but this fact does not stop athletes. In the West, it is already widely used to accelerate muscle growth. Experience in taking this drug was formed by trial and error. The result was the following regimen:

The average dosage of Peg-MGF is 1000-4000 mcg per week. Significant dosage will not significantly improve results.

On training days, the injection of the drug is performed immediately after the end of training to maximum simulate physiological secretion, preferably locally intramuscularly, because natural MGF is produced precisely as a result of damage and stress on muscle tissue.

On rest days, both local and general (subcutaneous) injections are acceptable.

Occasionally, it is allowed to use MGF in mega-doses up to 1000 mcg with regularity 4-7 times a week, before training. However, reviews from athletes indicate a slight increase in results, so taking such dosages is considered inappropriate.

Effects

Tests on rats showed that muscle cross-sectional area increased by 25% in 3 weeks with just one injection of MPP. When testing a similar regimen with insulin-like growth factor, there was an increase in muscle cross-sectional area of ​​only 15%.

In addition, research has shown that MFR is most effective at a young age. The older the person, the lower the muscle response to the drug.

Based on the summary data on the use of MFR, the results were obtained that a 5-week course of the drug promotes:

1. Accelerated muscle growth due to an increase in the rate of cell division (hyperplasia), cell growth in volume (hypertrophy) and prolongation of their lifespan, at any age
2. Reduce fat content by approximately 5-6%
3. Increasing endurance
4. Muscle development
5. The appearance of pronounced venous delineation
6. Growth of new vessels in muscle and bone tissue (proven by Deng M, Wang Y. in 2012)

Additional effects:

• Growth of immunity
• Improvement appearance and skin properties
• Reducing cholesterol levels in the body
• Strong Bones
• Fast tissue repair process
• Protection nervous system(neuroprotective effect)

Side effects

To date, drugs of this kind are still undergoing a number of clinical trials, and therefore there is no comprehensive information about the presence of pronounced side effects. MFR affects the DNA of cells, which theoretically could have Negative consequences in future.

Side effects of mechanical growth factor (according to studies):

1. Myocardial (heart) hypertrophy - experimentally substantiated by van Dijk-Ottens M in 2009. In this case, there was a simultaneous demonstration of the drug’s dual effect on the heart: protective - without loads and damaging - during loads.
2. A 2010 study by Armakolas A, Philippou A. proved the participation of MPP in the biology of prostate cancer development in men.

Author: Dmitry Ustimenko
Published in the magazine " Iron World No. 7 2013"
Now that we have collected some information, perhaps it would not be amiss to try to draw parallels between mechanical growth factor and androgenic-anabolic steroids. But I will make this non-standard comparison (in order to completely confuse you) in a non-standard way, namely by comparing two concepts of increasing the size of skeletal muscle - hypertrophy and hyperplasia.

Hypertrophy in a number of various scientific and popular publications, it is defined as an increase in the individual cross-section of the muscle fiber. This increase is achieved in two ways: by increasing the number and volume of myofibrils (myofibrillar hypertrophy) and by increasing sarcoplasm (sarcoplasmic hypertrophy). The theory of myofibrillar hypertrophy is based on the principle of longitudinal splitting of the myofibril and an increase in contractile proteins, namely myosin, since its volume is the largest (25% of the total amount of all contractile proteins) (we also do not forget about actin, since without it no myosin will help). (picture of muscle - myosin)
What exactly is going on? When under sufficient tension, the actin filaments break and the myofibril splits lengthwise into several fragments. Sarcoplasm (sarcoplasmic reticulum) and transverse tubular systems (T-systems) invade the resulting cavity between these fragments, which, along with new fragments of myofibrils, allow the muscle fiber to increase in volume. Sarcoplasmic hypertrophy is characterized by an increase in the volume of sarcoplasm (sarcoplasm is the internal environment (many call it “liquid”) that fills the space around myofibrils), which is due to an increase in the amount of interfibrillar fluid, mitochondria and, as a consequence, reserves of glycogen, ATP and creatine phosphate. Capillarization increases in the muscles. Essentially, the muscle fiber increases in volume, but the myofibril density does not increase. From the point of view of “durability” (minimizing the rollback after the “course”), it is myofibrillar hypertrophy that is most interesting to us, since those myofibrils that have “grown”, unlike sarcoplasm, will not go anywhere. But in fact, it turns out that we are observing abundant sarcoplasmic hypertrophy and only somewhere far away (we really hope for it) – myofibrillar hypertrophy. This is due to the fact that myofibrillar hypertrophy is characterized by a specific load (“lifting protocols,” i.e., working with weights within 90–100% of the maximum), and the myofibril must reach its “breaking point” with the help of a progressively increasing load. “But we have a secret androgenic weapon!” - you exclaim. Yes, I have. But everything looks beautiful and smooth only in theory. In fact, there are several more significant variables in our “hypertrophied” equation, without which testosterone will not be able to help. These are androgen receptors. Muscle activity itself, which requires intense muscle contractions, stimulates an increase in androgen receptors at the site of exercise. Thanks to this property, after testosterone binds to the “native” receptor, protein synthesis occurs at the binding site. Without delving deeply into the granite of science (especially since many already know this practically by heart), I will try to present the main “classical” theory of the effect of testosterone on the muscle core in the following, very simplified, sequence:
-load;
- muscle fiber deformation;
-expression of the androgen receptor by the muscle cell nucleus;
- testosterone enters the cell and binds to the receptor;
-the testo-receptor complex penetrates the nucleus;
-the nucleus, thanks to DNA, recognizes this complex and releases the corresponding mRNA;
-mRNA enters the cytoplasm and there, from amino acid residues (which circulate at this time), creates the corresponding protein (myosin, actin, etc.);
-this protein takes its place in the structure of a deformed or newly created myofibril.

But why then is there a “rollback” after a course of androgens? But because it is mainly sarcoplasmic hypertrophy that predominates, which is observed in fast phasic fibers of the oxidative type and in fast phasic fibers with the glycolytic type of oxidation. Slow phasic fibers of the oxidative type are also affected by sarcoplasmic hypertrophy, but not so much. It is not possible to “break down” a large number of myofibrils, and androgens partly help with this by stimulating the synthesis of proteins, which, in turn, restore damaged areas of the same myofibril. Protein synthesis requires a lot of energy. And the muscles now do a much greater amount of work, and they also have to be supplied with a much larger amount of nutrients. Therefore, it turns out that the network of sarcoplasm, blood capillaries and vessels, as well as the number of mitochondria, increases. Thanks to supercompensation of glycogen, after each subsequent workout it (glycogen) is stored on a scale greater than it was before the previous workout. And all this leads to the proliferation of sarcoplasm. After the course (and the cessation of active bombardment of the muscle nuclei with androgens), the abundant production of contractile proteins ceases. The myofibril also loses the ability to actively recover, and loads are reduced. The need for nutrient substrates decreases, and the entire bloated “sarcoplasmic infrastructure” loses its meaning. The number of mitochondria is greatly reduced, and the network of blood vessels is reduced. And have you forgotten another serious factor? Cortisol, which was controlled by strong concentrations of androgens, returns to the arena. This is what “deepens” the rollback. And all this happens against the background of a decrease in the secretion of its androgens, which could help the cell nucleus in the synthesis of new proteins. But they can't. And what help, because the nucleus reduces the expression of androgen receptors. As a result, it is possible to save basically only what has been acquired by myofibrillar hypertrophy and a small amount of baggage from sarcoplasmic hypertrophy (after all, the infrastructure for a small number of new and old myofibrils is still needed).
This “classical” concept of hypertrophy has recently been subject to more and more revision, since it is believed that the influence of androgens on skeletal muscle is not limited only to the stimulation of protein synthesis. They have been developing this area for decades (I was able to familiarize myself with articles on this topic in the editorial office dating back to the 70s). But this “unconventional theory” received its impetus and concrete (scientifically based) development only in the 2000s, when research results began to appear demonstrating the effect of testosterone on myosatellite cells. In 2004, research revealed the presence of an androgen receptor in myosatellite cells. More precisely, it turned out that the myosatellite cell, in response to stimulation with superphysiological doses of testosterone with complete hormonal replacement (the studies used a “course” of 600 mg of testosterone enanthate per week + GnRH, which acted as a blocker of natural testosterone secretion) is capable of generating an androgen receptor. “Well, why do we need MFR in this case, if androgens already do all the work?” – you ask reasonably. And I will answer: for hyperplasia.

The fact is that there is still no consensus on whether the expression of the androgen receptor promotes the division of satellite cells or whether testosterone helps the satellite cell become a full-fledged myoblast. Scientists working in this direction unanimously claim that there is some effect, because “steroid users” with extensive experience in using AAS have several times more nuclei in muscle cells and the size of muscle fibers than athletes (powerlifters) who did not resort to the help of exogenous androgens. On the other hand, there is evidence that testosterone is able to suppress the formation of myotubes from myoblasts and, as a result, the formation of new myofibril does not occur. As you can see, the situation is a little foggy. But out of this fog, a ray of truth still broke through, which was born from the theory of the indirect influence of androgens on myosatellite cells through IGF-1 isoforms, namely through the influence on IGF-1Ec (aka MGF) and IGF-1Ea.
But let's take it in order, or rather, we smoothly move on to the next way of influencing muscle growth - hyperplasia.

Hyperplasia , as you know, is an increase in the number of muscle fibers. In principle, myofibrillar hypertrophy can also be included under this definition, since it can also lead to an increase in the number of fibers, but the hyperplasia that will be discussed in this section is of a slightly different origin. This hyperplasia is the result of activation and “transformation” of myosatellite cells into full-fledged myofibrils. In principle, this idea runs as a “red line” through the entire narrative about MFR, therefore, in order to emphasize the difference between AAS and MFR, I will allow myself to repeat myself a little. Satellite cells are derivatives of myoblasts that did not coalesce during embryonic development to form myotubes and thus muscle fibers. When a muscle is damaged (due to mechanical stress), satellite cells undergo division, migrate along the fiber to the site of injury, and then unite to form a multinucleated myotube. This myotube eventually develops into muscle fiber, as in embryonic development. Thus, a new muscle fiber is formed to replace the necrotic muscle fiber. This process is triggered by a mechanical growth factor, which causes myosatellite cells to divide. “But this is “repairing the muscle,” not increasing it!” - you will notice. That's right. Increasing muscle volume through hyperplasia is impossible without activating myosatellite cells in quantities greater than those required for muscle repair. That is, satellite cells should “produce” much more than were required to “treat” the damaged muscle. What is needed for this? For this we need more MFRs. We need to maintain the division, division, division of the myosatellite cell for a long time, without transforming it into a myoblast, since the myoblast will no longer divide. And so it turns out that MPR binds to the myosatellite cell, triggers division, and the MPR molecule is no longer there, but two myosatellite cells appear. Not bad in principle, but we want to grow and we need more myosatellite cells before they become myoblasts. Therefore, we launch two MPR molecules to these two myosatellite cells. We get four myosatellite cells. It's already better. Shall we add four more MPP molecules? Of course, let's add and get 16 myosatellite cells. In general, we maintain a constant progression, which under normal conditions (without exogenous MFR) reaches its peak by the end of the first day after muscle damage. If we add synthetic MFR to this system, we get much more fission, which also declines 30 hours after damage (if we add longer forms (peg MFR or pMGF720), we make this process take longer). A large number of myosatellites is, of course, cool, but what should we do with them next? As it turns out, our long-suffering body knows the answer to this question. IGF-1 appears on the scene, or rather, its isoform IGF-1Ea, which is present in small concentrations from the onset of muscle damage and reaches maximum activity somewhere between 48 and 72 hours after injury. This isoform triggers the differentiation of myosatellite cells into full-fledged myoblasts. In other words, MGF increases the number of satellite cells, and IGF-1 makes myoblasts out of them. Next, the myoblasts form a myotube, which takes its place in the place of the damaged fiber, and after all the damage is “repaired,” the myotubes form a new muscle fiber (and in the new muscle fiber nuclei are formed, the number of which, according to some data, corresponds to the number of those that formed myoblast fiber). This process is inseparably linked with the synthesis of proteins, of which we need a lot (both for restoration and for additional growth). This is where androgens and GH come in handy. What do we get as a result? We get restored muscle fiber and “weak”, newly formed fiber, which is relatively fragile (with the contractile apparatus just forming) and which still needs to develop before it can withstand the workload without the risk of being completely destroyed. This completes the hyperplasia.

I hope that my “empirical-metaphysical” explanation of the above processes allowed you to grasp the difference in hypertrophy and hyperplasia and, as a consequence, the difference between AAS and MFR. But if we try to simplify even more and characterize the difference in simple and understandable words for every athlete, then the difference lies in the “kickbacks” after the course. If the “rollback” after a course of (average) AAS sometimes amounts to 40–70% of the achieved result, which largely depends on the volume of sarcoplasm developed during the course, then the “rollback” after a course of MFR, if possible, is extremely minimal (no more than 20– 30%), since MPR mainly works locally, and also because MPR does not lead to a significant increase in sarcoplasm. Although you may notice that hypertrophy and hyperplasia are closely related, and, in fact, one without the other is practically impossible, but this does not mean that it is impossible to progress without combining MFR and AAS.

In addition, our comparison of MFR and AAS would not be entirely complete if we had not paid attention to such important elements of the course as negative side effects, influence on strength indicators, influence on joints and ligaments, PCT, doping control. I will not test your patience and instead of a detailed analysis of the MFR and AAS for each of the indicated “nominations”, I will simply briefly go through these aspects.

Possible negative side effects
AAS: gynecomastia, increased cholesterol, liver damage, seborrhea, testicular atrophy, decreased sperm production, decreased libido, suppression of the HPA axis, decreased concentration of IGF binding protein type 3, stimulation of the development of cancer.
MFR: stimulation of the development of existing oncological diseases, possible decrease in bone tissue strength.

Impact on strength indicators
AAS: increase in overall “tonnage” within one workout; increasing maximum weight when performing one repetition at 100% of maximum power. MFR: increase in total “tonnage” within one workout; temporary reduction in maximum weight when performing one repetition at 100% of maximum power.

Effect on joints and ligaments
AAS: mostly positive.
MFR: does not affect joints and ligaments.

Post cycle therapy
AAS: in some cases mandatory.
MFR: not needed.

Doping control
AAS: the probability of being detected (without “preparatory measures”) is 100%.
MFR: can only be detected if mass spectrometry is used after liquid chromatography of blood samples.

In the next part we will finish our story by covering the following topics:

• the role of ifr in the mfr system (proliferation/differentiation)
• combining MFR with other types of pharmacological products.

Mechano Growth Factor (MGF) or Mechanical Growth Factor is one of the modifications of Insulin-like Growth Factor. The production of this hormone occurs mainly during physical activity or when muscles are damaged, since its main task is recovery.

Structure and effect on the body

MFR in its education goes through three levels:

• Formation of growth hormone in the pituitary gland;
• Synthesis of IGF-1 (Insulin-like growth factor) from GH in the liver;
• Synthesis of MPPs in muscles.

As you can see, Mechanical Growth Factor is a local hormone (that is, it is formed in a certain part of the body and acts only on it). Powerful production of this hormone occurs during muscle ruptures and microtears, their overload and during the recovery period. In general, MFR is an essential part of this recovery - it activates regeneration and controls muscle growth through accelerating the synthesis of myoblasts (muscle growth cells). Basically, this MGF activates the growth of dormant myoblasts, and the lack of this hormone causes muscle contractions in people suffering from dystrophy.

Thanks to its powerful anabolic properties, MFR has become actively used in sports and medicine. Initially, they began to administer it in its pure form, but after a couple of seconds the hormone disintegrated and, accordingly, did not bring any benefit. Another problem is that the process of our body’s production of this hormone occurs continuously, which means that the concentration remains constantly at a high level. This means that you would have to inject pure MFR every half hour. Of course, no one needs this. Scientists have found a way out of these problems - pegylation - the MPP molecule is combined with a polyethylene glycol molecule, which prevents the substance from decomposing. This is why you can only find PEG-MGF on sale now.

PEGylation made the hormone more stable and did not affect its properties. The PEGylation process creates an artificially tethered protein that is inert and does not bind to other substances in your body. It serves as a simple protection for the MFR molecule, and is then excreted in the urine, but thanks to it the hormone is able to act in the body much longer - you can inject only 3-4 times a week instead of every 30 minutes.

Application of MFR in sports

Today, MGF is actively used by athletes in the West to accelerate muscle growth (but it is worth noting that the hormone is still undergoing clinical trials). Since they are full scientific developments are not yet available, the method of reception was formed by trial and error and looks like this:

• Dosage: 1000-4000 mcg per week. On non-training days, injections can be administered both intramuscularly and subcutaneously;
• Dosage: 1000 mcg 4-7 times a week before each workout.

It is difficult to judge which of these methods is better, but it is better to stick to the first classical scheme.

As for the effects of MFR, in terms of anabolism it showed itself to be even better than IGF - the cross-section of muscles with 1 injection per week for 3 weeks increased by 25% (compared to IGF - 15%). It was also noted that this hormone is more effective for young people; with age, sensitivity to it decreases.

MFR effects:

• Hyperplasia and muscle hypertrophy;
• Reduction of body fat by 5-6%;
• Increased endurance;
• Improving vascularity and the formation of new vessels in muscles and bones;
• Increasing immunity and accelerating recovery;
• Protects the nervous system and improves the appearance of the skin.

Totally talk about side effects It is still early days for this drug, as studies have not yet been completed. So far, only what is known is the possibility of myocardial hypertrophy (MFR simultaneously performed a protective function of the heart without exercise, but damaged it during exercise), and the participation of MFR in the development of prostate cancer in men.

In general, MGF is a very promising hormone in sports, along with IGF and Growth Hormone. While there are no full-fledged studies, it is better to stick to the classic regimen, which has already been tested and worked out.

Fans healthy image Lifetime bodybuilders work in the gym mainly for increase in muscle volume. Muscle growth occurs due to both hypertrophy (increase in muscle fiber volume) and hyperplasia (increase in the number of muscle fibers).

Mechanical growth factor and its role in fitness

The process of increasing the number of structural muscle elements, or hyperplasia, is triggered by a peptide called insulin-like growth factor-1. Its main variety (isoform) is mechanical growth factor(MGF). This compound begins to be synthesized after intense physical activity. Its production is caused by mechanical damage to the muscles.

The formation of microtears in muscle tissue is a natural reaction to excessive loads in the process of working with heavy weights. The body must heal these injuries as quickly as possible. The signal for the start of muscle recovery and restructuring is the production of MGF. It activates stem cells, which actively divide and replace damaged muscle areas. In their normal state, such cells are inert; they begin to divide and form new mature muscle cells only under the influence of a growth factor.

Growth factors are needed to make the process of tissue regeneration controllable. They influence different types cells, because not only muscles, but also blood, intestinal epithelium, liver tissue, kidneys, etc. need periodic renewal. The mechanism of action of various MGF the same: they bring cells capable of division and further specialization out of a state of rest.

Of particular interest to athletes is growth factor, which affects the precursor cells of muscle fibers. MGF comes into play after physical activity and triggers the following chain of events: activation of stem cells and acceleration of protein synthesis, muscle fiber hyperplasia, muscle mass gain.

MGF as part of a sports nutrition system

Mechanical growth factor can be taken in the form of a pharmacological drug. But this substance breaks down very quickly, literally in a few minutes. To extend its duration, the MGF molecule was combined with a polyethylene glycol molecule. After pegylation, the concentration of MGF in the body remains at a high level for a long time.

It makes no sense to release pure MGF, sports supplement always sold as a bundle PEG-MGF. And since the drug is destroyed when it enters the digestive tract, fitness enthusiasts introduce it into the body through injections.

By consuming synthetic MGF in addition to what the body produces, bodybuilders strive to maximize muscle recovery and enhance muscle growth. Since the body begins to produce MGF in response to muscle damage, the optimal time for injections is immediately after training. This coincides with natural MGF production and mimics natural secretion.