Spermatogenesis

Spermatogenesis happens inside the seminiferous tubules, where Sertoli cells form the blood-testis barrier and scaffold the germ cell line. Two signals sustain it: FSH acts on the Sertoli cell, while LH acts on interstitial Leydig cells to make testosterone, which reaches intratesticular concentrations on the order of a hundred times those in serum. A full cycle from spermatogonium to spermatozoon takes roughly 74 days, plus about two weeks of epididymal transit and maturation.

Sertoli cells also close a feedback loop by secreting inhibin B, which selectively suppresses FSH, so inhibin B tracks Sertoli function and sperm output more closely than FSH alone. Semen analysis is judged against World Health Organization reference limits, whose sixth edition puts the lower fifth-centile values near 16 million sperm per millilitre, 39 million total, 30 percent progressive motility and 4 percent normal forms. Those are population percentiles, not a line dividing fertile from infertile.

The timing has direct consequences. Any insult - a febrile illness, chemotherapy, a change in hormonal exposure - appears in the ejaculate two to three months later, so a semen analysis reflects the previous quarter and an abnormal result is repeated rather than acted on immediately. It also means no intervention can improve sperm parameters faster than one spermatogenic cycle, whatever timescale a product claims.

The consequential misunderstanding is that a normal serum testosterone implies normal spermatogenesis. It does not. Exogenous testosterone raises the serum concentration while suppressing LH, which collapses intratesticular testosterone and can drive sperm counts to zero. Men on androgen replacement are routinely surprised by this; it is the mechanism male hormonal contraceptive trials were built on, the same effect sought deliberately.