Although scarce , the data available to date suggest that hyper and rogenism , such as that observed in PCOS , may likely be associated with oligomenorrhoea in exercising women , and may not always represent hypothalamic inhibition secondary to an energy deficiency .
To date , the predominant mechanism underlying  menstrual disturbances in exercising women supports an underlying energy deficiency-related aetiology , in which a failure to compensate dietary intake for the energy cost of exercise suppresses reproductive function .
Increasing evidence demonstrates that energy deficiency plays a causal role in the induction of amenorrhoea in  exercising women , and consistent with this mechanism are findings of glucoregulatory perturbations such as low triiodothyronine , reduced insulin secretion and elevated cortisol , growth hormone and ghrelin levels .
The menstrual disturbance that may differ in its energetic characteristics and , perhaps in its and rogenic and ovarian steroid environment , is oligomenorrhoea .
We conducted a systematic review of the literature to begin to underst and whether oligomenorrhoea in  exercising women is a mild sub clinical phenotype of polycystic ovarian syndrome ( PCOS ) in which exercise is conferring beneficial effects in protecting women from the classic PCOS phenotype , or whether oligomenorrhoea is part of the spectrum of menstrual disturbances caused by an energy deficiency that is often reported in exercising women with menstrual disturbances .
The GnRH pulse generator.
The notion of an oscillator or signal generator in the central nervous system that controls the rhythmic release of GnRH and , thereby , the pulsatile secretion of the gonadotropic hormones , originated in the finding of strikingly abrupt and rhythmic fluctuations in the concentration of LH in the plasma of ovariectomized monkeys . These oscillations had a period of about one hour when blood sample s were obtained at 10 to 20 minute intervals . I These surprising observations were presaged by reports of seemingly r and om , major fluctuations in plasma gonadotropin concentrations in gonadectomized monkeys " and rats""1 as well as in women . ' In these earlier studies the sampling intervals employed were never less than one hour and unable , therefore , to reveal the orderly , rhythmic events that occur with frequencies of one event per hour , or more . In the original study describing pulsatile LH secretion in ovariectomized monkeys the possibility was considered that the circhoral discharges of LH may be initiated by autoregulatory mechanisms involving long or short feedback loops , but the more likely view that these discharges were due to intermittent signals from the central nervous system unrelated to circulating LH levels that result ed in putative increments in GnRH release was favored . Nevertheless , the possible role of autoregulatory mechanisms in the control of pulsatile LH secretion was repeatedly considered,6 but finally laid to rest in the relatively recent past.7 Conversely , the view that each pulse of LH released from the pituitary gl and is the consequence of a bolus of GnRH secreted into the pituitary portal system has been unequivocally upheld by the demonstration of synchronous increments ofGnRH assessed in the pituitary portal circulation and of LH measured in sample s of peripheral blood obtained simultaneously.s , 9 In any case , the phenomenon of pulsatile gonadotropic hormone secretion was rapidly extended to most vertebrate species studied in this regard , including our own ,
Although scarce , the data available to date suggest that hyper and rogenism , such as that observed in PCOS , may likely be associated with oligomenorrhoea in exercising women , and may not always represent hypothalamic inhibition secondary to an energy deficiency .
To date , the predominant mechanism underlying  menstrual disturbances in exercising women supports an underlying energy deficiency-related aetiology , in which a failure to compensate dietary intake for the energy cost of exercise suppresses reproductive function .
Increasing evidence demonstrates that energy deficiency plays a causal role in the induction of amenorrhoea in  exercising women , and consistent with this mechanism are findings of glucoregulatory perturbations such as low triiodothyronine , reduced insulin secretion and elevated cortisol , growth hormone and ghrelin levels .
The menstrual disturbance that may differ in its energetic characteristics and , perhaps in its and rogenic and ovarian steroid environment , is oligomenorrhoea .
We conducted a systematic review of the literature to begin to underst and whether oligomenorrhoea in  exercising women is a mild sub clinical phenotype of polycystic ovarian syndrome ( PCOS ) in which exercise is conferring beneficial effects in protecting women from the classic PCOS phenotype , or whether oligomenorrhoea is part of the spectrum of menstrual disturbances caused by an energy deficiency that is often reported in exercising women with menstrual disturbances .