At the beginning there has to be some impulse/stimulus that triggers the desired response (adaptation) in the form of e.g. muscle hypertrophy, increase in strength etc. Depending on how we want the body to adapt, we must also choose the appropriate form of stimulation (training style).
Specific stimuli to stimulate hypertrophy and strength growth are:
- innervation of muscle fibers (neural aspect)
- damage to muscle structures and fatigue (physical and metabolic side)
Let’s stop at the first point. By exercising we make the muscles work and this is the neural stimulation. Thanks to the CNS (central nervous system), you transmit a signal from the brain that you want to lift the barbell from your chest and the muscles comply with your request. We’ll get into more detail on muscle engagement in another article.
As for the second point, it has more to do with the way you train. Due to the load used (dumbbells), microtraumas are formed in the muscle fibers, damage to various muscle organelles, metabolic fatigue and the subsequent secretion of growth factors.
Recovery is next. The body tries to return everything to its optimal state so that it is better prepared next time, both neurally (CNS) and physically (tissues). Other factors involved in regeneration are hormones and substances of an anabolic nature. Their secretion is conditioned by load.
These include androgens (male sex hormones) and estrogens (female sex hormones), growth hormone, etc. All of these have a certain effect on increasing the volume of the muscle.
When do muscles grow?
Let’s say you go to exercise in the morning, from the moment you finish, under optimal conditions, anabolic processes start to multiply. So muscles grow all day, not just at night.
As for the time they show increased proteosynthesis, that is, tissue repair (hypertrophy). We can say quite accurately that it is 24 hours for small muscle groups and 48 hours for large ones. The biggest growth wave is only about 36 hours after training. The fact that your muscles are still sore on the 4th day after training is a sign that they have not yet regenerated to 100%, but their growth potential is at the bottom! So why train a bunch just once a week! We’ll look at the training system in more detail next time.
Maximum muscle hypertrophy requires the interplay of at least a few of the factors and mechanisms listed below.
The accumulation of protein in muscle fibers, either by increasing its synthesis or by suppressing proteolysis.
Increased activity of growth factors such as GH, HGF, IGF-1, FGF
Increased proliferation and differentiation of myogenic stem cells or satellite cells, dependent either on the above growth factors or on exogenous administration of anabolic steroids or other natural stimulants, including training.
New myofibril formation, known as hyperplasia.
Suppression of post-training increases in certain catabolic cytokines, especially interleukin-6.
Modulation of the gene producing the protein myostatin, a negative modulator of muscle growth.
So these are the basic criteria you’ll need to focus on in your bodybuilding endeavors, especially if you want to progress naturally, but in the case of doping, it’s not a bad thing either.
Satellite cells, also referred to as myoblasts, are mononuclear (single-nucleated) cells of the myogenic or muscle-forming lineage. Resting (dormant) satellite muscle cells are located between the outer basal lamina and the plasmalemma of the adult skeletal muscle fiber. Although their activation and involvement in the cell cycle allows muscle regeneration and adaptation, the activation signal is far from known. In this study, for example, the role of nitric oxide (NO) on satellite cell activation was investigated.
After injury to skeletal muscle, for example by training or anabolic steroids, new fibers are formed or repaired from resident satellite cells, which restore the fiber composition of the original muscle. In injured human muscle, satellite cells play an important role in muscle regeneration, both as a source of reinforcement of failing metabolism and as potential replacement parts for necrotic segments of the original cell. These cells are further responsible for providing additional nuclei with DNA to growing and regenerating muscle cells. Muscle satellite cells have long been considered a specific myogenic (muscle-forming) lineage responsible for postnatal growth, repair, and maintenance of skeletal muscle. This is not the case; satellite cells have yet to differentiate and thus acquire the specificity and characteristics of the various tissue cells they are intended to replace or fuse with. Recent studies in mice, for example, have revealed that bone marrow haematopoietic (haematopoietic) cells also have the potential for muscle regeneration.
Activation of satellite cells after injury is essential for muscle repair, and hepatic growth factor was the first to be shown to stimulate this activation. Do not be misled by the name of this growth factor, which would lead one to conclude that it is found only in the liver. Experiments show that HGF is also present in muscle, can be released after injury, and is capable of activating dormant satellite cells. The satellite cells are quiescent when exposed to serum in culture, but proliferate when exposed to mitogens from crushed muscle extract. Basic fibroblast growth factor or bFGF also has these properties. At least as far as proliferation is concerned.
I probably won’t surprise anyone if I reveal that certain anabolic steroids activate satellite cell proliferation and differentiation. For example, in an experiment in rats, the anabolic steroid trenbolone was found to exert anabolic effects by stimulating the proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to the action of IGF-1 and FGF.
The role of insulin-like growth factor-1 or IGF-1
Among those factors that stimulate both the proliferation and differentiation of satellite cells, we cannot miss the well-known insulin-like growth factor-1 or IGF-1. On the other hand, the increase in the concentrations of the binding protein-2 (IGFBP-2) for this factor decreases the proliferation and differentiation of satellite cells induced by IGF-1. Type I receptors for IGF-1 have been found on the surface of satellite cells from turkey.
This raises the question of how satellite cells can be activated. The natural way to do this is by various training that disrupts the integrity of the cell membrane to allow the cell contents to leak into the environment. In fact, with this content leaks the described and other growth factors which will induce proliferation and differentiation of the satellite cells, thus providing new nuclei with DN to allow further growth of the muscle fibers and thus the muscle overall.
The important role of the newly discovered myostatin protein
Recently, news broke in the press that scientists have finished discovering and mapping the human genome. Among those genes that have recently been discovered is a gene that produces a protein known as ‘myostatin’. The first report on myostatin appeared in the scientific literature only in September 1997 and concerned cattle. Myostatin or GDF-8 (growth and differentiation factor-8) is a member of the large family of transforming growth factor-ß (TGFß). Exceptional muscle development, referred to as ‘double muscling’, has been observed in several breeds of beef cattle and has attracted considerable attention from meat producers. Double-muscled animals are characterized by a 20% increase in muscle mass, which is thought to be mainly due to muscle fiber hyperplasia. At least that is what is reported in this study. Further research has shown that this extra muscle gain is due to a mutation in the relevant gene that produces the inactive protein myostatin. A similar mutation was found in mice that also showed excessive muscle growth. This has given rise to various speculations about the possibility of targeted genetic manipulation of other breeding animals, thus creating double-muscled breeds. The benefit to the food industry, and thus to humanity, is obvious. However, it will not be that simple. Research in this area is in its infancy, but myostatin undoubtedly has a role in tissue growth. For example, increased expression of myostatin during prenatal development in pigs results in low birth weight piglets.
Recent research has also disrupted the existing dogma that muscle hypertrophy in non-functioning myostatin is caused predominantly or solely by muscle fibre hyperplasia. Transgenic (the artificial introduction of an altered gene into the cells of the test organism) mice expressing mutant negative myostatin showed a significant 20-35% increase in muscle mass, which was due to muscle fiber hypertrophy, not muscle fiber hyperplasia.
What does this all mean? Postnatal muscle growth is controlled by different mechanisms than the bodybuilding literature tries to tell us, promoting, without any scruples, dopey muscles. Do you know any other magazines that promote dope? I don’t. This is also why Bill Philips, editor-in-chief of Muscle Media, does not include any bodybuilding sports in the pages of this magazine. You can’t promote nutrients with doping muscles and vice versa. It’s a scam on potential customers who may conflate the two.