Physical changes of puberty

In North America and Europe, puberty in males visibly begins with testes enlargement between ages 9 and 14. Secondary sexual characteristics progressively appear over the ensuing 2–2.5 years, and facial hair, the last to appear, will not be fully mature until 20–25 years.

The physical changes of male puberty have been divided into five stages using a system developed by Marshall and Tanner, who examined groups of English boys as they went through sexual maturation (Fig. 11.1). They then classified the relative and absolute changes in the sexual characteristics of the participants. Although they did not regard their findings as universal, their system has been widely used to describe the timing and progression of typical pubertal changes. Their descriptions must be recognized as specific to the demographics of their study population and to the years covered by the study. Patterns persist, but the characteristics and timing of these changes are affected by race, nutrition and other genetic and environmental factors.

Adrenarche

This describes the contribution of the adrenal gland to puberty. It is characterized by an increase in adrenal synthesis and secretion of the relatively weak androgens: androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S). Although the adrenal gland contributes only 5% of the total circulating androgen pool in boys, these adrenal androgens are responsible for initiating axillary and pubic hair growth. They are converted in the periphery to the more potent androgens: testosterone and dihydrotestosterone (DHT). Testosterone and DHT then stimulate pubic and axillary hair growth as well as growth of, and secretion by, the axillary sebaceous glands. Axillary and pubic hair typically appear in parallel with increasing testicular size and visibly mark the onset of puberty.

The exact trigger for adrenarche is unknown. The best evidence indicates it is an intrinsic, programmed event within the adrenal gland independent of adrenocorticotropic hormone (ACTH). Adrenarche is distinct from pubarche and either may occur in the absence of its counterpart.

Testicular maturation

Testicular maturation at puberty involves initiation of androgen production by the Leydig cells, growth of the seminiferous tubules and initiation of spermatogenesis. The gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) control all three events.

Throughout childhood, FSH and LH concentrations in both the pituitary gland and plasma are low. Pulse amplitude and frequency of both hormones are also low, suggesting that the gonadotropin-releasing hormone (GnRH) pulse generator is cycling slowly. This characteristic of the gonadotropin–pituitary axis has been called the juvenile pause. About a year before testicular enlargement occurs, the release of pulsatile FSH and LH begins to increase in both amplitude and concentration. When this begins, it is most notable during sleep. This marked diurnal rhythm in FSH and LH secretion is the first endocrinologic manifestation of puberty. While these diurnal variations may be striking during early and mid-puberty, they are almost obliterated by the end of puberty.

The initiation of puberty is thought to reflect the release of the hypothalamic GnRH pulse generator from CNS inhibition. The site and exact mechanism of this inhibitory release are unknown. While much evidence indicates that the source of the trigger also resides in the CNS, there is growing interest in the role of leptin, a hormone produced by fat cells, in the initiation and progression of puberty. Leptin has been shown to be one of the many factors that influence the maturation of the GnRH pulse generator. Individuals who lack the hypothalamic GnRH pulse generator do not undergo puberty (Kallmann syndrome; Chapter 29) and tumors or surgery in the region of the median basal hypothalamus can be linked with delayed or absent puberty.

The increase in size of the testes with onset of puberty is largely the result of increasing mass of the seminiferous tubules and initiation of spermatogenesis. Leydig cell stimulation results in a 10-fold increase in testosterone production over the course of puberty but accounts for only a small proportion of the change in testicular size. The Leydig cells occupy less than 10% of the total testicular mass.