The onset of male sexual development begins around the ages of 11 or 12 and is completed by ages 15 to 17. The mechanisms initiating the onset of puberty are not well understood, but the sequence of events is known. Hormones of the hypothalamus, anterior lobe of the pituitary gland, and testes are involved. Melatonin from the pineal gland may also be involved.
Puberty begins when unknown stimuli trigger the hypothalamus to secrete gonadotropin-releasing hormone (GnRH), which is carried to the anterior lobe of the pituitary gland by the blood. GnRH activates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior lobe of the pituitary gland. LH promotes growth of the interstitial cells of the testes and stimulates their secretion of testosterone, the primary male sex hormone. FSH and testosterone in combination act on the seminiferous tubules, stimulating spermatogenesis.
Action of Testosterone
Male sex hormones are collectively called androgens, and testosterone is the most important one. They are produced primarily by the testes. Testosterone secretion starts in fetal development, continues for a brief time after birth, and then nearly ceases until puberty.
At puberty, testosterone stimulates the maturation of the male reproductive organs, the continuation of spermatogenesis, and the development of the male secondary sex characteristics. Secondary sex characteristics are the physical features that distinguish sexes from each other. Male secondary sex characteristics include (1) growth of body hair, especially on the face, axillary, and pubic regions; (2) increased muscular development; (3) development of heavy bones, broad shoulders, and narrow pelvis; and (4) deepening of the voice due to enlargement of the larynx and thickening of the vocal folds. Less obvious effects are increases in the rate of cellular metabolism and RBC production. Both metabolic rate and the concentration of RBCs in the blood are greater in males than in females. Testosterone production starts to decline at about 40 years of age, resulting in a gradual decline in the functions of reproductive organs and secondary sex characteristics.
Like many other hormones, testosterone production is controlled by a negative-feedback mechanism. Note that the secretion of GnRH starts the feedback mechanism. After puberty, this mechanism maintains the testosterone level in the blood within normal limits.
As testosterone concentration increases in the blood, it inhibits the production of GnRH by the hypothalamus, which, in turn, reduces the release of LH and FSH from the anterior lobe of the pituitary gland. The decrease in LH production causes a decrease in testosterone secretion by the interstitial cells of the testes, which reduces testosterone concentration in the blood. The reduction in FSH decreases sperm production.
Conversely, as testosterone concentration in the blood declines, the hypothalamus is stimulated to secrete GnRH, which, in turn, promotes the release of LH and FSH by the anterior lobe of the pituitary. The increase in LH production causes an increase in testosterone secretion by the testes, which increases the testosterone concentration in the blood. The increase in FSH increases sperm production.
Testosterone maintains the male reproductive organs and spermatogenesis. However, sperm production is fine-tuned by the hormone inhibin, which is secreted by supporting cells within the seminiferous tubules. When the sperm count is high, secretion of inhibin is increased, which decreases sperm production by decreasing FSH secretion by the anterior lobe of the pituitary. When the sperm count is low, inhibin secretion decreases, and sperm production is increased by an increase in FSH secretion. Thus, inhibin works to keep sperm concentration in semen within normal limits without altering the secretion of LH and testosterone.