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 .
Evidence for a causal role of low energy availability in the induction of menstrual cycle disturbances during strenuous exercise training.
Cross-sectional and short-term prospect i ve studies in humans support the concept that low energy availability , and not other factors associated with exercise , causes the development of exercise-induced reproductive dysfunction . To rigorously test this hypothesis , we performed a longitudinal study , examining the role of low energy availability on both the development and the reversal of exercise-induced amenorrhea , using a monkey model ( Macaca fascicularis ) . Eight adult female monkeys developed amenorrhea ( defined as absence of menses for at least 100 d , with low and unchanging concentrations of LH , FSH , E2 , and P4 ) after gradually increasing their daily exercise to 12.3 + /- 0.9 km/d of running over a 7- to 24-month period . Food intake remained constant during exercise training . To test whether amenorrhea is caused by low energy availability , four of the eight amenorrheic monkeys were provided with supplemental calories ( 138 - 181 % of calorie intake during amenorrhea ) while they maintained their daily training . All four monkeys exhibited increased reproductive hormone levels and reestablished ovulatory cycles , with recovery times for circulating gonadotropin levels ranging from 12 - 57 d from the initiation of supplemental feeding . The rapidity of recovery within the reproductive axis in a given monkey was directly related to the amount of energy that was consumed during the period of supplemental feeding ( r = -0.97 ; P < 0.05 ) . Repeated measurements of plasma T3 concentrations , a marker of cellular energy availability , revealed a tight correlation between the changes in reproductive function and T3 levels , such that T3 significantly decreased ( 27 % ) with the induction and significantly increased ( 18 % ) with the reversal of amenorrhea ( P < 0.05 ) . These data provide strong evidence that low energy availability plays a causal role in the development of exercise-induced amenorrhea
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 .