Steroid hormones

Steroid hormones – a group of hormones with a similar structure, based on a cholesterol hydrocarbon ring with various biological functions. Steroid hormones are small-molecule hormones that easily penetrate the cell membrane and for which receptors are found in the nucleus of the cells they affect.

The steroid hormones also include vitamin D, which is the only one of these types of hormones not based on the structure of cholesterol.

The synthesis of steroid hormones in the cell corresponds to a smooth endoplasmic reticulum.

There are several dozen different steroid hormones that meet the most diverse regulatory functions in animal organisms and the human body. The most well-known steroid hormones include male sex hormones (androgens), such as testosterone and female hormones (estrogens and gestagens), among others estradiol and progesterone. They are synthesized in the testes or ovaries and adrenal glands.

Testosterone production is directed by the hypothalamic – pituitary – nucleus axis, later referred to as HPTA (hypothalamus – pituary – testis – axis). HPTA balances the action of all serum-dependent (liquid part of the blood containing active hormones that circulate in the body) hormones and prohormones. If testosterone production is too low, the testicles affect the hypothalamus to trigger more hypothalamic Luteinizing Hormone Release Factor (LHRH). Circulating LHRH tells the pituitary to release more luteinizing hormone (LH) and follicle stimulating hormone. When circulating FHS and LH reach the testicles, they signal Leyding cells to produce more sperm and testosterone.

When testosterone levels are too high, the testes signal the hypothalamus to release less LHRH and … then the production of “father-in-law” falls or ceases. It is quite interesting that elevated estrogen levels can affect the production of androgens such as testosterone, much more significantly than any other androgen. It’s good to read this one more time to make sure you understand the basics of HPTA. It refers significantly to its effects and effectiveness to exogenous (emerging from outside the body) SAA used by athletes. IT’S ANOTHER FUNCTION TO PROTECT!


SAA have a positive effect on fat management and storage. There are three reasons.

First of all,  they reduce the amount of insulin released in response to the ingestion of nutrients and improve the sensitivity to it. This is partly due to the improvement of the CP synthesis rate and other metabolic factors resulting from the muscle cells of athletes better absorbing nutrients such as carbohydrates in the form of glucose and glycogen as well as proteins in the form of amino acids. Insulin is also an anti-catabolic and anabolic. It works great on muscle cells, however, it also causes the transformation of glucose into glycerol, and the latter into triglycerides. Insulin can therefore increase fat stores and cause the growth of fat cells. The decrease in insulin release and the increase in insulin sensitivity mean better nutrient utilization for muscle growth.

regarding the effect of SAA on fat is that testosterone blocks the activity of a fat-synthesizing hormone called lipoprotein lipase. Because lipoprotein lipase is blocked, less can be produced and deposited. The same operation has also GH.

The third way in which testosterone affects fat synthesis is not positive. When testosterone levels are elevated, most of it is converted to estrogens with the help of the conversion enzyme, called aromatase. This is called aromatization, an important term, the meaning of which must be understood before the user becomes familiar with the next portion of the information contained on the page! Estrogens, in turn, increase the deposition of fat in places typical for women and inhibit the action of HPTA. It’s good that estrogens increase at least GH production.

Anyone who used SAA in the past noticed an increase in the effect of “inflating muscles”. This is partly due to the elevation of the previously explained phosphocreatine (CP) synthesis, but also due to the increase in blood volume. Testosterone increases production and the number of red blood cells by stimulating red bone marrow. It also increases hemoglobin production. Hemoglobin is an iron-containing compound that carries oxygen from the lungs to tissues such as muscles. It gives a result in the form of bigger, more blooded, harder muscles that receive more oxygen and nutrients. This is a potentially positive aspect to a certain place, because the result is increased training capacity and improved tissue regeneration. Unfortunately, a significant increase in the number of red blood cells can lead to the accumulation of platelets and thrombosis.

Additional information

The additional point here is that the chemical compound contained in the bloodstream, called fibrinogen, causes the formation of blood clots. There is a lot of evidence supporting the thesis that beer and red wine inhibit this relationship. Of course, this is not an excuse to drink, but moderate consumption can be taken into account. A popular drug used as a so-called “diluter” of blood is aspirin. Aspirin is a non-specific COX inhibitor (info: “Prostaglandins”), which can also have a negative effect on PGE-1 and PGF-2. Prostaglandins are an important growth factor in the process of building muscle tissue. Those who have used creatine products such as monohydrate or phosphate are aware of the effects that more creatine can provide. When anabolic-androgenic steroids (SAAs) are delivered, they increase the phosphocreatine (CP) synthesis. Let me explain why moron is such a nice thing. ATP (adenosine triphosphate) is the fuel that your muscles use to stimulate contractions. For this to happen, ATP must be converted into ADP (adenosine diphosphate) so that energy can be released. This in turn allows muscle contraction. To convert ADP back into the energy source, or ATP, you need phosphocreatine (CP). Thus, the more CP available, the more ADP to ATP regeneration and greater muscle performance. There was once a view that the elevated cellular level of CP adds strength, but not magnitude. Of course, this belief was refuted as soon as the creatine supplements conquered the market. Increased CP levels simultaneously increase glycogen levels and protein (amino acid) stores in muscle tissue. This SAA role as well as creatine products perform very well. CP also increases the size of cells by increasing the level of intercellular nutrients. Phosphocreatine is an endogenously produced form of creatine and is often referred to as creatine phosphate or CP.STERYDY A GROWTH: Myths about steroid increments how does this really apply? Just a few years ago, scientists they claimed that the overall muscle growth achieved thanks to SAA was only due to increased water retention. Part of the support of this idiotic view were the obvious declines in weight and strength that appeared after SAA discontinuation. Muscle growth is based on two mechanisms.

Enlargement of individual muscle cells and fibers through protein synthesis induced by anabolic compounds.

This is the first mechanism of growth called hypertrophy. Androgens such as testosterone (endogenous or exogenous) and all SAA give the highest result at this level. The second mechanism is called hyperplasia, which involves the formation of new muscle cells and fibers. Although hyperplasia has not been proven for humans, there is a lot of research on doubts that is not. As an example … a study covering a group of non-school students and a group of bodybuilders competing in the competition. Of course, bodybuilders have a larger arm size, but in the case of a muscle biopsy performed in both groups, the individual muscle fibers were identical. Because the bodybuilders had much more fibers, the researchers adopted the theory that they had to experience hyperplasia. The next study conducted on people exercising with force is much more clear. Two groups of well-trained strength exercisers were divided in two. One group exercised throughout their lives without using steroids, while in the second group the average period of steroid use oscillated around 9 years. The group using steroids at that time had cycles based on Anadrol-50, Winstrol-V, Primobolan, Deca Durabolin, Masteron and Proviron in various combinations. It showed a significant increase in the “number” of muscle fibers compared to the group of people training without support. In the steroid group, the researchers also noted an increase in the number of muscle cell nuclei and an increase in the percentage of newly formed muscle fibers. These new fibers with an increased number of cell nuclei were created from satellite cells. Satellite cells are uneducated muscle cells. This is HIPERPLASIA. Another finding that is equally amazing is that satellite cells have been shown to have a larger number of androgenic receptors. This means that new cells or fibers have a greater ability to use androgens such as SAA. This study showed that the size of muscle cells reflects the number of cell nuclei.

The experiment also showed that there was an increase in the number of satellite cells in the steroid group, and it was much larger compared to the steroid-free group. So what does all this mean? Intensive training with heavy weights creates pressure on fibers and muscle cells strong enough to induce hyperplasia and cell growth. Those who use steroids as part of the training plan, accelerate these responses to stimulus, like training. Newly formed muscle cells and fibers have more androgenic receptors, hence SAA work better on these cells. Because SAA contribute to the growth of muscle cell DNA and hence increase protein synthesis without increasing catabolism (currently SAA decreases the normal rate of catabolism), the formation of new cells and muscle fibers is accelerated. Bigger muscles! An important point to add is that years of intense training can pay back to those who do not stop training without SAA. New fibers added to existing ones mean more fibers to grow. In theory, it is assumed that SAAs, which are highly anabolic (protein synthesis), could be beneficial to those that have highly androgenic properties. This is because, partly, more lean muscle mass can be preserved after the cycle, if highly anabolic / low to mediumandrogenic steroids have been used.