BMJ  2007;334:164-165 (27 January), doi:10.1136/bmj.39043.625498.80

Editorials

Exercise and menstrual function

Up to four fifths of women who exercise vigorously may have some form of menstrual dysfunction

The risks to sportswomen of exercise related menstrual dysfunction and impaired bone health are important and under-recognised. Exercise related menstrual dysfunction may include any abnormality along the continuum of luteal phase deficiency, annovulation, oligomenorrhoea, amenorrhoea, and delayed menarche. Such dysfunction is multifactorial in origin, with a high degree of individual variation, but its main underlying mechanism is hypothalamic inhibition with suppression of gonadotrophin releasing hormone pulsatility (the frequency at which pulses of the hormone are released by the hypothalamus).¹

This hypothalamic suppression has a variety of causes in sportswomen, including the physical and psychological stress of training and competition, caloric deficiency, low body mass, low body fat,^{1 2} inadequate leptin values,³ and altered peripheral hormone metabolism.¹ Relative hyperandrogenism and genetic influences may also have a role.¹ The consequences can include musculoskeletal injuries (in particular stress fractures), infertility, and the general medical consequences of hypo-oestrogenism.

When menstrual dysfunction (in particular amenorrhoea) occurs in sportswomen in combination with low bone mass and energy deficit, the syndrome is termed the "female athletic triad." This is a complex and poorly understood disorder seen in females who exercise intensively.^{2 w1} Athletes in lightweight sports (distance running, gymnastics, lightweight rowing) are at high risk, although the syndrome can arise in relation to any sport. The energy deficit is usually related to eating disorders and is partly influenced by peer pressure. Genetic, neurochemical, and psychodevelopmental factors may also contribute, along with the physical and psychological effects of training and competition. The long term effects tend to be greatest in young girls who start intense exercise before menarche. These girls have an increased chance of delayed menarche, impairment of growth and pubertal progression, subsequent menstrual dysfunction, and suboptimal bone health.^{1 4}

Secondary amenorrhoea occurs in up to 44% of women who exercise vigorously, compared with 2-5% of the general population.^{1 5 6} Athletes who present with amenorrhoea are at the severe end of the spectrum of exercise related menstrual dysfunction. Subtle menstrual disturbances are more common, occurring in nearly four fifths of very active women.⁷ The impact of this on bone mineral density is unclear,^{8 9} and there is no evidence that women whose menstrual function recovers develop chronic infertility.

No specific threshold at which exercise leads to menstrual dysfunction has been defined because contributing physiological and psychological factors produce considerable individual variation. However, women who run more than 50 miles each week have a significantly increased incidence of amenorrhoea.¹⁰

Screening may be useful in women who exercise vigorously. Dietary, medical, and training histories should be taken from any apparently physically fit woman presenting with recurrent or resistant injuries to soft tissue or bone (in particular stress fractures). Women with eating disorders are often reluctant to describe their diet, however. Urinalysis to detect ketonuria will suggest inadequate caloric intake, and thyroid function tests (yielding normal or raised thyroid stimulating hormone and reduced free thyroxine) will indicate a hypometabolic state.

Women who are amenorrhoeic will need the standard investigations. In women with suspected luteal phase deficiency basal body temperature should be monitored, surges in luteinising hormone measured with ovulation predictor kits, multiple samplings of serum progesterone taken, and ideally, endometrial biopsy carried out. Women with suspected bone loss may need a DEXA (dual energy x ray absorptiometry) scan, preferably including peripheral sites such as the tibia and forearm.^w2

Management of exercise related menstrual dysfunction aims primarily to restore normal menstrual cycles. Education of patients, coaches, peers, and parents about the risks of excessive exercise in girls and women is of paramount importance. Dietary counselling to ensure a positive energy balance and adequate calcium and vitamin D intake,^w3 and advice on altering the volume and intensity of training programmes and reducing the stressors of competition, may be effective.¹ Supplementation with combined oestrogen and progesterone should help maintain bone mass, although it will not rebuild what has already been lost.¹¹ Treatment with recombinant leptin may have a role in the future but evidence is preliminary.¹²

¹ Rheumatology, Sports, and Exercise Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ

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Extra references w1-w3 are on bmj.com

Competing interests: None declared.

References

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9. De Souza MJ, Miller BE, Sequenzia LC, Luciano AA, Ulreich S, Stier S, et al. Bone health is not affected by luteal phase abnormalities and decreased ovarian progesterone production in female runners. J Clin Endocrinol Metab 1997;82:2867-76.[Abstract/Free Full Text]
10. Cumming DC, Rebar DW. Exercise and reproductive function in women: a review. Am J Ind Med 1983;4:113.[ISI][Medline]
11. Hergenroeder AC. Bone mineralization, hypothalamic amenorrhea, and sex steroid therapy in female adolescents and young adults. J Pediatr 1995;126:683-9.[CrossRef][ISI][Medline]
12. Welt CK, Chan JL, Bullen J, Murphy R, Smith P, DePaoli AM, et al. Recombinant human leptin in women with hypothalamic amenorrhea. N Engl J Med 2004;351:987-97.[Abstract/Free Full Text]

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