Male reproductive function entails complex processes, involving coordinated interactions between molecular structures within the gonadal and hormonal pathways, tightly regulated by the hypothalamic–pituitary gonadal axis. Studies in men and animal models continue to unravel these processes from embryonic urogenital development to gonadal and urogenital ducts function.
The hypothalamic decapeptide gonadotropin-releasing hormone is released into the hypophyseal portal circulation in a pulsatile fashion. It acts on the gonadotropes to produce the gonadotropins, the main trophic hormones acting on the testis to regulate sperm production. This endocrine control is complemented by paracrine and autocrine regulation arising from the testis, where germ cells originate, modulated by growth factors and local regulators arising within the testis. The process of spermatogenesis, originating in seminiferous tubules, is characterized by stem cell proliferation and differentiation, meiotic divisions, expression of transcriptional regulators, through to morphological changes which include cytoplasm reorganization and flagellum development. Metabolic processes and signal transduction pathways facilitate the functional motion and transport of sperm to the site of fertilization. The normal sperm structure or morphology acquired during spermatogenesis, epididymal maturation, sperm capacitation including motility, and subsequent acrosome reaction are all critical events in the acquisition of sperm fertilizing ability. Generation of the male gamete is assured through adequate gonadal function, involving complex differentiation processes and regulation, during spermiogenesis and spermatogenesis. Sperm functional changes are acquired during epididymal transit, and functional motion is maintained in the female reproductive tract, involving activation of signaling processes and transduction pathways. Infertility can arise in the male, from spermatogenic failure, sperm functional quality, obstruction and other factors, but causes remain unknown in a large proportion of affected men. Semen analysis, complemented by the clinical picture, remains the mainstay of male infertility investigation. Assisted reproductive technology has proved useful in instances where the cause is not treatable. Complications from sexually transmitted infections could lead to male infertility, by impairing sperm quality, production, or transport through the reproductive tract.
Male fecundity denotes the biological capacity of men to reproduce, based on ability to ejaculate normal sperm. Lifestyle, environmental, and endocrine disruptors have been implicated in reduced male fecundity.
Interactions between vascular, neurological, hormonal, and psychological factors confer normal sexual function in men. Nocturnal erections begin in early puberty, occurring with REM sleep. Sexual health is an integral part of sexual and reproductive health, while sexual dysfunction, in various forms, is also experienced by some men.
Methods of contraception available to men are few, and underused. They include condoms and vasectomy.
Enhanced knowledge of male reproductive function and underlying physiological mechanisms, including sperm transit to fertilization, can be catalytic in improvements in assisted reproductive technologies, male infertility diagnosis and treatment, and development of contraceptives for men.
The article reviews the processes associated with male reproductive function, dysfunction, physiological processes and infertility, fecundity, approaches to male contraception, and sexual health. It further alludes to knowledge gaps, with a view to spur further research impetus towards advancing sexual and reproductive health in the human male.
Increased FOXL2 expression alters uterine structures and functions†