Stimulation of Sperm Production by Human Luteinizing Hormone in Gonadotropin-Suppressed Normal Men*

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Abstract
The relative roles of FSH and LH in the control of human spermatogenesis are not well established. We previously reported that supraphysiological doses of hCG can stimulate sperm production in gonadotropin-suppressed normal men despite prepubertal FSH levels. To determine whether more nearly physiological levels of human LH (hLH) also can stimulate spermatogenesis when FSH levels are suppressed, we administered hLH to normal men whose endogenous gonadotropin levels and sperm production were suppressed by exogenous testosterone enanthate (T). After a 3-month control period, 11 normal men received 200 mg T, im, weekly to suppress LH and FSH. T administration alone was continued for 3–4 months until 3 successive sperm concentrations (performed twice monthly) revealed azoospermia or severe oligospermia (sperm concentrations, P < 0.001). However, none of the men achieved sperm concentrations consistently in their own pretreatment range. Sperm motilities and morphologies were normal normal in all four subjects by the end of hLH plus T administration. In contrast, sperm concentrations in the seven control subjects remained suppressed (in vitro mouse Leydig cell bioassay in all four experimental subjects, was markedly suppressed during T administration alone (120 ± 10 ng/ml) compared to that during the control period (390 ± 20 ng/ml; P < 0.001). With the addition of hLH to T, LH bioactivity returned to control levels (400 ± 40 ng/ml; P = NS compared to control value). Serum FSH levels determined monthly by RIA were reduced from 98 ± 12 ng/ml during the control period to undetectable levels (P < 0.01). Urinary FSH excretion was in the normal adult range at the end of the control period (353 ± 117 mlU/h) and was markedly suppressed to prepubertal levels with T alone (62 ± 14 mlU/h) and hLH plus T (48 ± 17 mlU/h). We conclude that dosages of hLH that result in LH levels in the physiological range can reinitiate sperm production in gonadotropin-suppressed normal men despite markedly suppressed FSH levels. Therefore, normal levels of FSH are not an absolute requirement for the stimulation of spermatogenesis after short term gonadotropin suppression. Since hLH was not able to return sperm counts to fully normal levels during selective FSH deficiency, we hypothesize that normal levels of FSH may be necessary for quantitatively normal spermatogenesis in man.