What Is the Effect of Testosterone on Male Enhancement?

Testosterone, the primary male hormone, regulates spermatogenesis, male sexual characteristics, sex differentiation, and fertility. The fetus is the first to experience testosterone's effects. During the first six weeks of development, the reproductive tissues of both males and females are identical. The SRY (sex-related gene on the Y chromosome) initiates testicular development around week 7 of gestation. Sertoli cells in the testis cords (fetal testicles) eventually differentiate into seminiferous tubules.

As a result of a Mullerian-inhibiting substance (MIS) generated by Sertoli cells, the typical female Mullerian structures, including the Fallopian tubes, uterus, and upper vaginal section, regress. Wolffian duct (mesonephric duct) structures, which subsequently develop into the male urogenital tract, are supported in their development by fetal Leydig cell migration and endothelial cell production within the gonad. The peripheral conversion of testosterone to dihydrotestosterone (DHT) is responsible for the development of the prostate and male external genitalia 

In the final two months of fetal development, testosterone also facilitates the descent of the testicles through the inguinal canal. An embryo without a Y chromosome and, consequently, the SRY gene develops ovaries. Due to insufficient testosterone production by the fetal ovaries, the Wolffian ducts do not form. These individuals also lack MIS, which promotes the growth of the Mullerian ducts and other female reproductive systems.

FunctionTestosterone is responsible for fundamental sexual development, including spermatogenesis, growth of the penis and testes, and an increase in libido. Around the seventh month of pregnancy, when the testes begin to secrete a significant amount of testosterone, they typically begin to descend toward the scrotum. Male neonates who are born with undescended but otherwise healthy testes that do not descend through the inguinal canals by the time they are 4 to 6 months of age may benefit from testosterone therapy. 

In addition, testosterone regulates secondary male characteristics, which lend men their masculinity. Testosterone's anabolic effects include growth spurts in puberty (testosterone increases tissue growth at the epiphyseal plate early in puberty and ultimately causes the plate to close later in puberty) and skeletal muscle growth (testosterone stimulates protein synthesis).

MechanismDuring puberty, the hypothalamic-pituitary-gonadal axis is essential for regulating gonadal function and testosterone levels. The hypothalamus secretes GnRH, which travels via the hypothalamohypophyseal portal system to the anterior pituitary, which then secretes LH and FSH. LH and FSH, two gonadotropic hormones, act on gonad receptors as they circulate in the circulation. Particularly in response to LH, the Leydig cells produce more testosterone. Negative feedback is used by testosterone to regulate its own secretion. Both elevated blood testosterone levels and the anterior pituitary provide feedback to the anterior pituitary.

Every three to four hours, the hypothalamus pulse releases GnRH throughout a man's reproductive existence. Despite this pulsatile release, the average plasma levels of FSH and LH remain relatively constant from the beginning of puberty, when levels rise, until the third decade of life, when levels peak and begin to progressively decline. Low testosterone levels before puberty are a result of insufficient synthesis of gonadotropin and GnRH. Puberty causes a significant increase in GnRH secretion due to alterations in brain activity and neuronal input to the hypothalamus.

Leydig cells in the testes execute their activity to convert cholesterol into testosterone. LH regulates the earliest stage of this process. Dehydroepiandrosterone (DHEA) and androstenedione are key intermediates in this process. Androstenedione is converted to testosterone by 17-beta-hydroxysteroid dehydrogenase. The preponderance of testosterone is bound to plasma proteins including albumin and sex hormone-binding globulin. This predominant source of protein-bound testosterone provides an excess of testosterone hormone to the body.

Similar TestingThe first steps in diagnosing male hypogonadism require a thorough medical history and physical examination, as the symptoms of testosterone deficiency can be quite apparent. Male hypogonadism has prepubertal and postpubertal characteristics that can be distinguished. Pre-pubertal development is characterized by small testes (less than 20 mL in volume), a small phallus, fewer secondary sex traits (such as facial or axillary hair), gynecomastia, difficulty developing muscle mass, eunuchoid proportions, low sperm count, and low energy/libido. Post-pubescent characteristics include osteoporosis, hot flushes, and severe hypogonadism, in addition to phallus size and eunuchoid proportions.

If a physician suspects hypogonadism based on a patient's medical history and physical examination, he or she should order a total blood testosterone test between 8 and 10 a.m. Normal testosterone levels may indicate eugonadal low testosterone levels. In the event that FSH and LH levels are insufficient, a repeat level should also be obtained. Secondary hypogonadism is present when FSH/LH levels are normal, but testosterone levels are insufficient. Prolactin, T4, 8 AM cortisol, iron, ferritin, and an MRI of the brain would be the subsequent steps. Primary hypogonadism was indicated by high FSH/LH and low testosterone levels. In the event of primary hypogonadism, a karyotype should be determined.

Clinical RelevanceOverproduction, underproduction, receptor insensitivity, and inefficient testosterone metabolism are all examples of testosterone-related pathology. The conditions outlined below are among the more prevalent and thoroughly studied testosterone diseases.The overproduction of androgens can be caused by polycystic ovarian syndrome (PCOS), adrenal virilization/adrenal tumors, ovarian or testicular tumors, Cushing syndrome, and the use of exogenous steroids. It is essential to understand the differences between testosterone and dehydroepiandrosterone (DHEA) in order to comprehend these diseases. DHEA is produced by the adrenal glands and ovaries/testes and is a relatively modest androgen. DHEA functions as a precursor for a variety of hormones, including estrogen and testosterone. DHEA is only present in its sulfated form, DHEAS, in the adrenal glands. In polycystic ovarian syndrome (PCOS), abnormal gonadotropin-releasing hormone (GnRH) secretion causes an increase in LH secretion.

LH increases androgen secretion by ovarian theca cells in women with PCOS, resulting in hirsutism, masculine escutcheon, acne, and androgenic alopecia.[6] In ovarian and adrenal malignancies, androgenic symptoms (hirsutism, virilization) typically progress swiftly. When DHEAS levels are normal and testosterone levels are elevated, the most probable cause is an ovarian tumor. If DHEAS is elevated and testosterone levels are ordinarily normal, this is likely an adrenal tumor. Age, certain medications, chemotherapy, diseases of the hypothalamus-pituitary axis, intrinsic hypogonadism, cryptorchidism, orchitis, and inherited conditions such as Klinefelter and Kallmann syndrome can all lead to a decrease in testosterone production. Klinefelter syndrome is the most common congenital disorder that causes primary hypogonadism. In Klinefelter, Seminiferous tubule dysgenesis and Sertoli cell loss decrease inhibin levels and increase FSH levels.

URL: https://ssjournals.com/health-guide/testosterone-and-its-impact-on-male-enhancement/