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Female athletic activities have now achieved widespread social acceptance. Although one of the greatest public health problems is the lack of exercise, exercise induced menstrual abnormalities can produce serious life threatening abnormalities as well as subfertility. It is accepted that different levels of exercise as well as different types of exercise can cause different effects on the hypothalamic pituitary gonadal axis.
This paper by Ramsay and Wolman helps by providing another small piece of the jigsaw in this fascinating area. The authors do allude to body mass, but the role that this has is still under debate. There appears to be no critical fatness threshold for the maintenance of menses that is applicable to athletes in general.1 A popular theory has maintained that low body fat is the cause of amenorrhoea and 22% body fat is thought to be necessary to maintain regular menstrual cycles. This does need to be challenged as regular cycles are seen in athletes with less than 17% body fat, and amenorrhoeic and eumenorrhoeic runners have been found to have similar percentages of body fat. Leptin, a protein that is encoded in the obese gene and expressed in adipocytes, may have a role as a metabolic signal between body composition and reproductive maturation and regularity.
Protein, fat, total energy intake, and training regimens may also play a role in discipline specific menstrual irregularities. Immersion in water may also have a specific effect on prolactin levels, with breast support being given to prevent a simulated suckling response. This has been demonstrated in pregnancy.2
The authors do need to be congratulated on keeping this important debate going.
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