Introduction

The association of physical activity with the suppression of reproductive function in women has been recognized for a number of years. The relationship seems clearest in the association of strenuous exercise and amenorrhea (the absence of menstrual cycling owing to complete ovarian suppression). However, we now recognize that exercise in recreational, as well as competitive athletes, is associated with reproductive dysfunction along a continuum, ranging from normal ovulatory cycles to subtle luteal phase defects (LPD), anovulatory cycles, and finally to amenorrhea (De Souza, 2003; Prior & Vigna, 1985). The most common menstrual cycle anomaly associated with exercise is LPD (De Souza et al., 1998), although amenorrhea is the most dramatic and best known.

There is a growing consensus that the primary cause of these menstrual cycle abnormalities is a deficit of dietary energy intake (EI) (Loucks, 2005), which can lead to a temporary state of negative energy balance, the most obvious consequence of which is the loss of body weight, as tissues (both protein and fat) are catabolised for fuel. Less obvious consequences are the decreases in metabolic rate per kg FFM (fat-free mass, i.e. muscle and organs), the differential loss of tissues with different metabolic rates, and the accompanying reduction in core temperature (Elia, 1997). Behavioural changes also occur, such as reductions in the duration and intensity of physical activities and the adoption of more resting postures (Keys, 1950).