It is the main androgen, the hormone that separates children from men.
It was manufactured right before World War II (1935) by Germans, who received the Nobel Prize later (1939).
Nazis used it extensively in order to sustain injuries and malnutrition, while aggressiveness was the main drawback of it.
Testosterone is produced during adolescence by the Leydig cells of testicles, being responsible for the male characteristics.
These include increase of the testicular size and scrotum (nut sack), hoarseness, hirsutism, alopecia (MPB), aggression and increase of libido-sex drive.
Testosterone’s effect on skeletal-striated-contractile muscles is based on hypertrophy.
This is something achieved by water and electrolyte retention, leading to edema.
The swelling caused by sodium and water retention in the cytoplasm-sarcoplasm, is most likely due to corticosteroids and their main representative, aldosterone.
Testosterone is not just anabolic, but androgenic as well.
It oxidises adipose tissue, thus making the body to look harder.
Testosterone becomes beneficial as an ergogenic agent during training, through the aggression stimulus that provides; especially in combination with other anabolic substances.
It has a balanced ratio between androgenic and anabolic index 1:1
This is why, it is used as a basis on each steroid cycle, in order to provide a ‘’pseudo HPTA’’.
The administration of testosterone consists of 50 % of an AAS cycle.
It enhances the ability of protein synthesis, through the assimilation of more animal protein (positive nitrogen balance).
It also reduces the abdominal fat (β-oxidation), as all androgens do anyway.
Testosterone’s concentration is proportional to that of somatomedin C, or Insulin like Growth Factor (IGF1), released from liver.
This practically translates into their synergistic action.
Testosterone has no benefits to connective tissue growth (cartilage, ligaments, tendons), unlike growth hormone.
Abuse of testosterone results in tendons’ rupture, since there’s no proportional development between muscles and connective tissue.
All AAS have an inverse relationship with glucocorticoids, of which the main representative is cortisol, thus they create an anabolic environment.
Steroids also act as anti-inflammatory agents in certain diseases such as angioedema (stanozolol).
However, the presence of glucocorticoids and cortisol has positive effect against inflammations of the musculoskeletal system.
Although the injection of cortisone in the tendon bears the risk of rupture, joint pains can be suppressed only by the presence of (hydro) cortisone.
Furthermore, the suppression of inflammation is a phenomenon that acts negatively on the muscle development process, since it is based on the presence of inflammation in the muscle fiber.
ARA (omega 6 UFA) plays a significant role on that, through the increase of prostaglandins (inflammatory cytokines).
The reduction of glucocorticoids during a steroid cycle lowers their anti-inflammatory effect in tendons and enhances the appearance of tendon ruptures.
It is well known, that if excessive muscle development is not followed by proportional connective tissue development (something that GH-IGF1 do), detachments and ruptures of tendons and ligaments occur.
Testosterone circulates in the blood in two forms.
The total testosterone (TT) which is bound to a protein, the sex hormone binding globulin (SHBG) and the free testosterone (FT) which is essentially the active form in tissues.
Total testosterone is not able to penetrate the cell membrane and join the androgen receptor.
The majority of testosterone is bound to the SHGB protein, which transports it into the blood serum.
A very small percentage (2%) remains free-detached from sex hormone binding globulin.
The higher the rate of free testosterone, the better our libido and strength.
Therefore, the values of free testosterone and SHBG are inversely proportional.
As we age, the value of SHGB increases and this is also one of the reasons of andropause.
Also, the increase of beta estradiol (E2) will increase the SHGB and reduce the FT.
Obesity and metabolic syndrome are diseases that elevate estrogens and beta estradiol concentration.
One way to increase the value of free testosterone, is to use a synthetic form of DHT (mesterolone, drostanolone), or even danazol.
This way we improve the libido, since the SHGB is reduced.
Free testosterone enters the cytoplasm of cells and joins the androgen receptor (AR).
The stronger the bonding between AAS-AR is, the greater the suppression of HPTA.
Moreover, the stronger the attachment between AAS-SHGB, the more FT circulated free, therefore libido increases.
Testosterone is one of the safest injectable AAS, since it is a natural hormone that is daily produced.
Unlike the plethora of synthetic derivatives (AAS).
It is not hepatotoxic, but has a negative effect under chronic abuse (supraphysiological doses) on the atheromatic index and the HDL/LDL ratio.
It also leads to left ventricular hypertrophy– LVH (thickening of the left ventricular wall).
This is something based on a variety of reasons:
1) Myocardium posses has androgen receptors
2) Heart muscle also consists of striated-skeletal fibers
Testosterone also increases production of sebum and skin becomes more elastic, with heavier odor.
Sebum overproduction, traps microbes and infection within the hair follicles result in the form of acne (inflammation)
Testosterone abuse results in testicular shrinkage, as a result of homeostatic cessation in endogenous testosterone production and Leydig cells.
Testosterone’s chronic abuse, as all androgens, may lead to psychosis and manic behavior.
However, this is something depending on the genetic predisposition of each individual.
As all androgens, testosterone has a positive effect on the bone marrow, and the production of erythropoietin (EPO) by kidneys.
Erythrocytosis and polycytemia are extreme cases of red bone marrow over stimulation.
This results in the rise of hemoglobin and hematocrit.
The consequence of this is a greater blood viscosity and the risk of occlusive stroke and arterial hypertension.
Testosterone has the ability to improve insulin sensitivity (or decrease insulin resistance), by improving BMI and muscle mass.
Therefore, diabetic patients who will to use testosterone should have to reduce their dosage of exogenous insulin.
Another issue with testosterone use is the hypertrophy of the prostate, known as benign prostatic hyperplasia (BPH), which occurs after the age of 40.
As well known, the main androgens in reduced into dihydrotestosterone (DHT), by the presence of 5a reductase enzyme.
Dihydrotestosterone is a powerful androgen, a metabolite of testosterone.
That reduction takes place in different tissues, as the prostatic gland, scalp and epidermis (skin).
It is advised to those who receive testosterone replacement therapy (TRT) after the age of 40, to measure the prostate specific antigen (PSA) and undergo a digital rectal examination. It should be noticed, that the gland is also getting enlarged, under the dominance of estrogens over androgens.
Something that is mainly noticed in older people over 60.
The use of finasteride and dutasteride (inhibitors of the 5 alpha reductase enzyme) inhibit the activity of the enzyme in the I and II receptors, which correspond to the prostate gland and the scalp respectively.
Therefore, they deal with excessive hirsutism on the back as well as with androgenic alopecia (MPB).
5a reductase inhibitors drugs are first choice medication against prostatic cancer.
However, suppression of DHT, will have a negative impact on a man’s libido, gynecomastia (anti-estrogenic action of DHT), possible melancholia-moodiness (lack of DHT is associated with lower self-esteem).
DHT is an androgen with anti-estrogenic properties and five times more androgenic than testosterone.
However, there are no ergogenic benefits on muscle tissue.
In local application on the nipples, it acts against gynecomastia.
Interruption during night sleep for urination (nichtouria), difficulty during the start of urination and the leakage of a small amount of urine on the underwear, post urination are signs of a potential growth of the gland.
Something that could be the result of prostatitis (inflammation) and elevation of PSA.
In men of older age, the theory of benign hypertrophy of the prostate gland was based on dihydrotestosterone.
Metabolites of DHT are those AAS that do not aromatize, like mesterolone, methenolone, stanozolol, oxandrolone, drostanolone, oxymetholone.
They do not harm the prostate gland, as other AAS do.
This is something related to the activation of 5a reductase enzyme.
DHT derivatives have a less suppressive effect on HPTA, in less extend than the metabolites of testosterone (equipoise, fluoxymesterone).