A basic, unresolved mechanistic issue is whether aging causes a primary hypothalamic disturbance that enforces a high frequency of GnRH pulses and/or whether low bioavailable testosterone concentrations elevate LH pulse frequency via feedback withdrawal (27,35-37,40,55). This query is central to contemporary physiological assessments of aging, inasmuch as earlier investigations in healthy young men document that (1) infusion of testosterone or a nonaromatizable androgen suppresses LH pulse frequency and elevate LH peak amplitude (24,88,99,100) and (2) administration of ketoconazole (which depletes testosterone) or flutamide (which inhibits androgen-receptor binding) augments LH pulse frequency and reduces incremental LH peak (fractional) amplitude (79,80,101). In the human, monkey, sheep, and rat, a high frequency of GnRH stimuli reduces incremental (fractional) LH pulse amplitude (37,48). In view of this reciprocal control mechanism (albeit not fully understood), diminished androgen bioavailability in older men could contribute, in principle, to both more rapid and lower amplitude LH pulses. What remains unknown is whether hypoandrogenemia in aging fully accounts for the degree of observed neuroendocrine changes.
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