Women have become increasingly physically active in recent decades. While e
xercise provides substantial health benefits, intensive exercise is also as
sociated with a unique set of risks for the female athlete, Hypothalamic dy
sfunction associated with strenuous exercise, and the resulting disturbance
of GnRH pulsatility, can result in delayed menarche and disruption of mens
trual cyclicity.
Specific mechanisms triggering reproductive dysfunction may vary across ath
letic disciplines. An energy drain incurred by women whose energy expenditu
re exceeds dietary energy intake appears to be the primary factor effecting
GnRH suppression in athletes engaged in sports emphasizing leanness; nutri
tional restriction may be an important causal factor in the hypoestrogenism
observed in these athletes. A distinct hormonal profile characterized by h
yperandrogenism rather than hypoestrogenism is associated with athletes eng
aged in sports emphasizing strength over leanness, Complications associated
with suppression of GnRH include infertility and compromised bone density.
Failure to attain peak bone mass and bone loss predispose hypoestrogenic a
thletes to osteopenia and osteoporosis.
Metabolic aberrations associated with nutritional insult may be the primary
factors effecting low bone density in hypoestrogenic athletes, thus diagno
sis should include careful screening for abnormal eating behavior. Increasi
ng caloric intake to offset high energy demand may be sufficient to reverse
menstrual dysfunction and stimulate bone accretion. Treatment with exogeno
us estrogen may help to curb further bone loss in the hypoestrogenic amenor
rheic athlete, but may not be sufficient to stimulate bone growth. Treatmen
t aimed at correcting metabolic abnormalities may in fact prove more effect
ive than that aimed at correcting estrogen deficiencies.