Question

What happens during male pubertal growth?

Male-female sexual differentiation is completed by the late second trimester of prenatal gestation (Gluckman, et al., 1980; Grumbach & Styne, 1992). Between the 11th and 24th weeks of fetal life, a higher concentration of circulatory testosterone occurs in males in response to (1) placental gonadotropins (Greek: gone = seed; trope = nourishment for growth) and (2) release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland into the circulatory system. The testosterone is released from the fetal testes and it interacts with bodywide physicochemical processes to further develop uniquely male characteristics. In females, gonadotropins, LH, and FSH trigger the circulatory release of estradiol from the fetal ovaries, and estradiol interacts with bodywide physicochemical processes to further develop uniquely female characteristics.

The greater concentration of testosterone in males continues until just before birth when it is temporarily suppressed. Within just a few minutes following the birth of males, however, the concentration of peripheral circulatory luteinizing hormone (LH) increases by about ten times the level that was present before and during birth. LH levels then recede, but the spurt triggers the release of circulatory testosterone that lasts about 12 hours or more. LH levels then become more moderate, but greater LH pulsatility and more elevated testosterone levels continue for about six months, after which their levels are biochemically suppressed (not eliminated) until puberty (Grumbach & Kaplan, 1990; Grumbach & Styne, 1992).

The greater concentration of estradiol in females continues until just before birth when it is temporarily suppressed. No post-birth surge of LH release occurs in females. There is, however, a rise in levels of circulatory FSH and LH and it is irregularly pulsatile during the first few post-birth months. FSH pulsatility is then greater in females than in males for the first few years of life, resulting in greater levels of circulating estrogens. In general, greater FSH pulsatility and estrogen levels continue for about one to two years, after which their levels are biochemically suppressed (not eliminated) until puberty (Grumbach & Kaplan, 1990; Grumbach & Styne, 1992).

All of the anatomic components that produce voice are formed during prenatal gestation, and most begin functioning in some way before birth. The macro-architecture of voice-related anatomy is significantly smaller at birth compared to adult dimension; proportional relationships are significantly different; and anatomic micro-architecture is in very early stages of maturation. Middle and inner ear structures, however, are comparable to adults by about five months gestation (see later details). Physical growth of vocal anatomy progresses throughout childhood, but is notably extensive during the first 3 to 5 years and during puberty.

Puberty (Latin: pubertas = age of maturity) is one macro-growth phase in the continuum of human physical development. On average, it begins in females at about age 10 years and extends to about 16 years. In boys, it begins at about age 12 years and extends to about 18 years (Grumbach & Styne, 1992). During puberty there is observable growth in (1) standing and sitting height, (2) gross body weight, (3) lean body tissue (muscles and organs) and fat body tissue, (4) body hair, and (5) various anatomic and organ areas of the body such as feet, hands, gonads, pulmonary system, larynx, vocal folds, vocal tract, and various areas of the central nervous system (notably in the prefrontal cortex).

The initiation of puberty is triggered by: (1) cessation of biochemical suppression of the hormones of growth, and (2) elevated synthesis and release—from the hypothalamus into the anterior pituitary—of gonadotropin-releasing hormone (GnRH) [formerly known as luteinizing hormone-releasing hormone (LHRH)]. GnRH triggers the synthesis of luteinizing hormone (LH) and follicle stimulating hormone (FSH) and they are then released from the anterior pituitary into the circulatory system. An increase in both the frequency and amount of these hormones occurs. Elevated LH and FSH stimulate the release into the bloodstream of the anabolic (growth) steroids: (1) primarily testosterone in males with some estradiol, and (2) primarily estradiol in females with some progesterone. These events, plus many others, result in the anatomical growth spurts in height, weight, tissue and organ size, cognitive-emotional behavior changes (Warren & Brooks-Gunn, 1989; Michael & Zumpke, 1990), and so forth.

The years-long time scale release of these hormones and steroids produce the years-long pubertal macro growth phase. Within the pubertal macro-growth phase, however, there are shorter time-scale growth episodes that span multiple weeks to multiple months. During those growth episodes, the triggering hormones enter the circulatory system in pulsatile spurts that last anywhere from 5 to 10 minutes to one hour or more, and they occur mostly during the earlier stages of nightly sleep (Grumbach & Styne, 1992; O'Dell, 1995).

The growth episodes occur in sequential stages within the various anatomical areas of the body, but the time of initiation and the duration of each stage is different in each individual (Nielsen, et al., 1986; Wennick, et al., 1988; Martha, et al., 1989; Dunkel, et al., 1990; Hassing, et al., 1990; Grumbach & Styne, 1992; Lampl, et al., 1993; Vander, et al., 1994, pp. 627-629; O'Dell, 1995). For instance, the end-areas of both limbs (hands and feet) grow larger first, and then the bones and soft tissues of the arms and legs grow longer and larger. Increases in glove and shoe sizes, therefore, "announce" increases in general clothes sizes. Tanner (1972, 1984) devised five-stage evaluative scales of breast development in females and genital development in males to assist pediatricians in assessing normal versus abnormal pubertal development. Tanner's episodic stages of genital development in male adolescents have been correlated with their voice transformation stages (Harries, et al., 1996).

An adolescent does not go to bed one night and wake up the next morning with mature breasts and genitals, nor do their feet need shoes that are one or two sizes larger than the shoes they wore the previous day. These growth processes do not literally happen "overnight". Over many nights, specified recipes of growth hormones interact with their biochemical receptor sites on the cells of specified target tissues and organs. Intracellular physicochemical processes are then triggered in the cells of those tissues and organs so that some cells within just hands, or feet, or legs, or arms, or larynges start dividing into more cells faster than they did before. So, elevated growth hormone, testosterone, and estradiol levels are followed by physical growth processes which activate for a period of time, then subside, then activate, then subside, and so on in an evolving, longer-term, episodic pattern (Grumbach & Styne, 1992; O'Dell, 1995). The "choreography" of these complex pubertal growth processes is unique in each person.

The continuum of human growth in prenatal, childhood, and pubertal age spans are reflected in the growth patterns of the respiratory system, the larynx, and the vocal tract. The end-age parameter of the "young" voice is established by the Hirano, et al., finding (1981) that nearly all of the macro- and micro-architecture characteristics of adult laryngeal anatomy have been completed by about age 20-21. One important evolution of micro-architecture is not substantial until ages 28 through 32, that is, calcification and ossification of the hyaline laryngeal cartilages. This change usually proceeds earlier in males than females (Hately, et al., 1965; Kahane 1983).

REFERENCES

Dunkel, L., Alfthan, H., Stenman, U., et al. (1990). Pulsatile secretion of LH and FSH in prepubertal and early pubertal boys revealed by ultrasensitive time-resolved immunofluorometric assays. Pediatric Research, 27, 215-219.

Gluckman, P.D., Grumbach, M.M., & Kaplan, S.L. (1980). The human fetal hypothalamus and pituitary gland: The maturation of neuroendocrine mechanisms controlling the secretion of fetal pituitary growth hormone, prolactin, gonadotropin, and adrenocorticotropin-related peptides. In D. Tulchinsky, & K. Ryan (Eds.), Maternal-Fetal Endocrinology (pp. 196-232). Philadelphia: W.B. Saunders.

Grumbach, M.M., & Kaplan, S.L. (1990). The neuroendocrinology of human puberty: An ontogenetic perspective. In M.M. Grumbach, P.C. Sizonenko, & M.L. Aubert, (Eds.), Control of the Onset of Puberty (pp. 1-68). Baltimore: Williams & Wilkins.

Grumbach, M.M., & Styne, D.M. (1992). Puberty: Ontogeny, neuroendocrinology, physiology, and disorders. In Wilson, J.D., & Foster, D.W. (Eds.), Williams Textbook of Endocrinology (8th Ed., pp. 1139-1221). Philadelphia: W.B.Saunders.

Harries, M.L.L., Griffin, M., Walker, J., & Hawkins, S. (1996). Changes in the male voice during puberty: Speaking and singing voice parameters. Logopedics Phoniatrics Vocology, 21(2), 95-100.

Hassing, J.M., Padmanabhan, V., Kelch, R.P., et al. (1990). Differential regulation of serum immunoreactive luteinizing hormone and bioactive follicle-stimulating hormone by testosterone in early pubertal boys. Journal of Clinical Endocrinology and Metabolism, 70, 1082-1089.

Hateby, B.W., Evison, G., & Samuel, E. (1965). The pattern of ossification in the laryngeal cartilages: A radiological study. British Journal of Radiology, 38, 585-591.

Hirano, M., Kurita, S., & Nasashima, T. (1981). The structure of the vocal folds. In M. Hirano (Ed), Vocal Fold Physiology. Tokyo: University of Tokyo Press.

Kahane, J.C. (1983). Postnatal development and aging of the human larynx. Seminar in Speech and Language, 4, 189-203.

Lampl, M., Veldhuis, J.D., & Johnson, M.L. (1993). Saltation and stasis: A model of human growth. Science, 258, 801-803.

Martha, P.M., Rogol, A.D., & Veldhuis, J.D. (1989). Alterations in the pulsatile properties of circulating growth hormone concentrations during puberty in boys. Journal of Clinical Endocrinology and Metabolism, 69, 563-570.

Michael, R.P., & Zumpke, D. (1990). Behavioral changes associated with puberty in higher primates and the human. In M.M. Grumbach, P.C. Sizonenko, & M.L. Aubert (Eds.), Control of the Onset of Puberty. Baltimore: Williams & Wilkins.

Nielsen, C.T., Skakkebaek, N.E., Darling, J.A., et al. (1986). Longitudinal study of testosterone and luteinizing hormone (LH) in relation to spermarche, pubic hair, height and sitting height in normal boys. Acta Endocrinologica [Suppl], 279, 98-106.

O'Dell, W.D. (1995). Endocrinology of sexual maturation. In DeGroot, L., et al., Endocrinology (3rd Ed., Vol. 2, pp. 1938-1952). Philadelphia: W.B. Saunders.

Vander, A.J., Sherman, J.H., & Luciano, D.S. (1994). Human Physiology: The Mechanisms of Body Functions (6th Ed.). New York: McGraw-Hill.

Warren, M.P., & Brooks-Gunn, J. (1989). Mood and behavior at adolescence: Evidence for hormonal factors. Journal of Clinical Endocrinology and Metabolism, 69, 77-83.

Wennick, J.M., Delemarre-Van de Waal, H.A., van Kessel, H., et al. (1988). Luteinizing hormone secretion patterns in boys at the onset of puberty, measured using a highly sensitive immunoradiometric assay. Journal of Clinical Endocrinology and Metabolism, 67, 924-928.

Recent published resources.

Topics

0 / 0  ·  0 Answers  ·  202 Views

Contributors

Question Followers (2)