Puberty In Boys
Puberty is the
process by which the immature individual will acquire the physical and
behavioral attributes that allow him or her to repro- duce. In males, puberty
is largely the response of the body to the wide- spread actions of androgens.
These are secreted by the newly awakened testes, under the influence of
gonadotropins secreted by the anterior pituitary. While the progression of
pubertal changes is predictable, the age of their onset differs dramatically in
different areas of the world and even among children of different ethnic
backgrounds within a particular region. Economic disparities may also be reflected
in the age of onset.
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. Pat- terns 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.
Secondary sexual characteristics Testosterone and its metabolites cause the following somatic changes in
pubertal boys:
•
Increased
laryngeal size.
•
Deepening
of the voice.
•
Increased
bone mass.
•
Increased
mass and strength of skeletal muscle.
•
Thickened
skin.
•
Increased
and thickened hair on the trunk, pubis, axillae and face.
Somatic growth
Somatic growth at puberty is the
result of a complex interaction between gonadal sex steroids, growth hormone
(GH) and insulin-like growth factor 1 (IGF-1). Insulin and thyroxine are also
necessary for optimal growth. The absence of GH, IGF-1 or IGF-1 receptor will
lead to somatic dwarfism, even in the presence of normal plasma sex steroid
concentrations.
Concomitant with the changes in
the pulse frequency of LH that signal the beginning of puberty is a change in
the amplitude of GH secretion. This appears to be the result of estrogen
stimulation in both boys and girls. In boys, while the increase in GH can be
initiated and maintained by testosterone, it does not occur with the
administration of DHT. Further, GH secretion in the presence of testosterone
can be blocked by the administration of tamoxifen, which blocks the estrogen
receptor. In contrast, even miniscule doses of estrogen substantially increase
GH concentrations. These findings suggest that the effect of testosterone on
bone growth is indirect and probably secondary to aromatization of testosterone
to estradiol. This is in stark contrast to the action of testosterone on
muscle, where androgens act directly to increase muscle mass.
Bone growth occurs when
testosterone, aromatized to estradiol, increases GH levels. This causes a
parallel rise in IGF-1, a potent anabolic hormone that mediates many metabolic
actions of GH, including trabecular bone formation. Normally, GH stimulates
IGF-1 synthesis, and IGF-1 suppresses GH release in a negative feedback loop.
At puberty, however, GH continues to rise despite high levels of circulating
IGF-1. This allows for maximum linear bone growth during puberty. Outside of
puberty, this combination of an increase in both GH and IGF-1 is seen only in
acromegaly, a disease state characterized by autonomous GH secretion. Peak
growth velocity in boys occurs when plasma testosterone levels reach 50% of
adult male levels, and growth will continue until epiphyseal fusion occurs in
the long bones. The sex steroids (perhaps via estrogen activity) are
responsible for epiphyseal closure, which occurs at a median age of 21 in young
men. The determinants of final adult height are many and include genetic
predisposition, body mass index at the onset of puberty, nutrition and length
of puberty. Genetic determinants of bone growth appear to be carried on the
distal short arm of the X chromosome. This locus does not appear to undergo X
inactivation. Therefore, this locus, and any homologous loci on the Y
chromosome, will direct final adult height. The effects of this genetic control
pattern are apparent among men with the sex chromosome disorder Klinefelter
syndrome; they have a 47XXY karyotype and are unusually tall, presumably
because of the double dose of X-linked
stature determinants.
Higher body mass indices in late
childhood affect final height in both boys and girls. Children with increased
body fat tend to enter puberty earlier. They begin their growth spurt after a
shorter period of prepubertal growth and hence may not reach the full
genetically pre- determined adult height. Boys enter puberty later than girls
and so have a longer period of prepubertal growth. Boys also experience a
greater peak linear growth velocity during adolescence than girls. For both
reasons, men tend to be taller than women.
Androgens have a direct anabolic
effect on muscle mass. The increase in androgen secretion during puberty
increases muscle mass in both boys and girls. Reflecting the higher levels of
circulating
androgens, this effect is more
dramatic in boys.
