DIMINISHED PULSATILE LUTEINIZING HORMONE SECRETION AND SUPERSENSITIVITY TO GONADOTROPIN RELEASING HORMONE IN AMENORRHEIC RUNNERS

Abstract

Menstrual irregularity is common in endurance-training women, although precise pathophysiological mechanism(s) remain unknown. To evaluate possible disturbances in the pulsatile mode of LH release, we sampled blood at 20 min intervals for 24 h in 10 am-enorrheic long-distance runners. LH pulse frequency and amplitude were calculated using a computerized algorithm, and pituitary responsiveness evaluated by infusing graded submaximal doses of gonadotropin releasing hormone [(GnRH); 2.5,5,10 and 25 μg)] at 2 h intervals for 8 h. We observed that 6 women had very low frequency LH pulsations (5,1,3,4,2,6 pulses/24 h), and 4 others maintained normal LH pulse frequency (11,12,13 and 15 pulses/24 h). Reduced LH pulse frequency occurred despite normal mean and 24 h integrated serum LH concentrations, and normal early follicular phase levels of estradiol, testosterone and progesterone. Spontaneous LH pulse amplitude (% or absolute) was normal or accentuated and administration of submaximal doses of GnRH promoted greater release of LH in runners than in controls (P<0.001). We conclude that the women athletes exhibit normal or increased responsiveness of gonadotrophs to endogenous or exogenous GnRH. Thus, the decreased frequency of LH pulsations seems to reflect a defect in the hypothalamic GnRH pulse generator rather than the pituitary gland. These observations provide clear evidence for a brain defect in the regulation of LH secretion in certain long-distance runners.