The HPG axis governs reproductive processes. In the male, the hypothalamus releases gonadotropin-releasing hormone (GnRH), which stimulates the pituit

The HPG axis governs reproductive processes. In the male, the hypothalamus releases gonadotropin-releasing hormone (GnRH), which stimulates the pituitary to secrete the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH acts primarily on Leydig cells in the interstitial tissue of the testes to stimulate the production of androgens, mainly testosterone. FSH acts on Sertoli cells within the seminiferous tubules, supporting spermatogenesis and other Sertoli cell functions. Testosterone provides negative feedback to both the pituitary and hypothalamus, helping regulate the axis. Although there is brief activity during fetal life and around birth, the HPG axis is largely quiescent until puberty, when its reactivation resumes spermatogenesis and continuous sperm production. The male is thus sexually mature once this axis is active.

LH and FSH release patterns differ markedly between the sexes. In females, LH shows high-amplitude preovulatory surges roughly every few weeks, with basal pulsatile LH release between surges. In males, LH is released in continuous, small episodes roughly every two to six hours. The hypothalamus of the male does not develop a surge center as in females; GnRH is released in frequent, intermittent bursts around the clock. These GnRH bursts last only a few minutes and are quickly followed by LH release (as indicated by a dotted LH trace in the figure referenced). Each LH episode lasts about ten to twenty minutes, and the Leydig cells respond to LH by releasing testosterone within less than about thirty minutes after the onset of an LH episode. Consequently, testosterone release is pulsatile and continuous.

The functional arrangement in the testes includes Leydig cells in the interstitium and Sertoli cells in the seminiferous tubules, with a nearby blood supply. LH binds to receptors on Leydig cells, triggering the production of progesterone, most of which is subsequently converted to testosterone. Testosterone can be secreted into systemic circulation, and it is also transported into Sertoli cells where it exerts critical actions for spermatogenesis. Sertoli cell function is largely driven by FSH; FSH binding to its receptors on Sertoli cells initiates a cascade of intracellular effects, including the induction of androgen-binding protein (ABP), also known as sex hormone-binding globulin (SHBG).

A key outcome of ABP expression is the binding of testosterone, forming a testosterone–ABP complex that is secreted into the lumen of the seminiferous tubules. ABP-bound testosterone is less lipophilic, enabling higher local concentrations of androgens in the luminal fluid. Elevated intraluminal androgen levels promote spermatogenesis within the seminiferous tubules and the maturation of sperm in the epididymis. Beyond supporting gametogenesis, testosterone, starting at puberty, also stimulates the development of male secondary sexual characteristics and influences sexual behavior.

Male secondary sex characteristics refer to features that enhance reproduction indirectly beyond genitalia and internal reproductive organs. Examples include the manes of male lions, cheek flanges in dominant male orangutans, antlers in male deer, and larger horns in rams. Testosterone levels rise, for instance, in deer during the mating season, paralleling the development of antlers; higher testosterone is associated with territorial aggression and mating-related behaviors. Testosterone also promotes anabolism and muscle growth, contributing to the generally greater muscle mass observed in male mammals.

This anabolic action underpins the practice of hormonal growth promotants in the beef industry in certain countries such as Australia and the United States. These interventions typically involve estrogenic and/or androgenic hormones administered via implants. In some cases, a combination of an estrogenic compound with an androgen—either testosterone or trenbolone acetate (an androgen with eight- to tenfold greater anabolic activity than testosterone)—is used. Anabolic steroid use in humans, including athletes, similarly aims to enhance muscle growth but is associated with serious health risks. Potential adverse effects include kidney failure, liver damage, increased risk of stroke and heart attack, and shrinking of the testicles.

The discussion of testosterone’s broader effects also covers behavior and reproductive strategies in wildlife. For example, in deer, testosterone drives antler development in the mating season, and its increase is correlated with territorial aggression and mating behavior, which are typically not exhibited outside the breeding period. Testosterone promotes anabolic processes that contribute to muscle development and overall physical vigor, reinforcing a link between endocrine regulation, physical traits, and behavioral patterns.

Ethical and practical implications arise from the use of hormonal growth promotants and anabolic steroids, including welfare concerns for animals, potential long-term health risks for humans, and the broader societal considerations around performance enhancement. The material concludes by noting that the next video will focus on reproductive cyclicity in female mammals, contrasting the male’s pulsatile pattern with the female’s cyclic (and surge-driven) regulation of GnRH, LH, and ovulation.

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ext{Testosterone rise after LH onset: } t_{ ext{rise}} < 30 ext{ minutes}
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extFSHaction:extFSHoextSertolicellsoextABPexpressionext{FSH action: } ext{FSH} o ext{Sertoli cells} o ext{ABP expression}