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1 Department of Statistics, University of Virginia, Charlottesville, VA, USA
2 Department of Internal Medicine, Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: veldhuis.johannes{at}mayo.edu.
The present study extends a recent composite model of in vivo interglandular signaling to assess the impact of age on: (i) nonequilibrium exchange among diffusible and protein-bound testosterone (Te); (ii) elimination of total and free Te; (iii) basal and pulsatile Te secretion (sec); (iv) the implicit feedforward function mediating luteinizing hormone (LH) concentration (con) drive of instantaneous Te sec; and (v) possible stochastic variability of the predicted LH con-Te sec dose-response linkage. To this end, we measured LH and Te con every 10 min for 24 hr in healthy young (N = 13) and older men (N = 13). Statistical comparisons of analytical estimates revealed that elderly subjects manifest: (a) reduced maximal burst-like LH-stimulated Te sec (impaired stimulus efficacy); (b) depressed half-maximally LH-stimulated Te sec (lower Leydig-cell responsivity); (c) decreased pulsatile and total Te sec; (d) elevated basal Te sec; (e) a prolonged half-life of total but not free Te con; and (f) delayed time-evolution of LH and Te sec bursts. In contradistinction, age did not influence estimated LH-pulse potency (ED50); steroidogenic sensitivity (slope term); or stochastic variability of LH-Te coupling. Based on these data, we postulate that aging in the human male alters specific dose-response attributes linking LH con and Te sec and disrupts the time-waveform of LH and Te sec bursts.
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