Academic journal article Women in Sport & Physical Activity Journal

Bone Turnover in Premenopausal Women with Exercise-Associated Menstrual Disorders

Academic journal article Women in Sport & Physical Activity Journal

Bone Turnover in Premenopausal Women with Exercise-Associated Menstrual Disorders

Article excerpt

Abstract

We compared bone mineral density and turnover in women with exercise-associated menstrual disorders (AMD, n=10; 0-9 [cycles.y.sup.1]), hormonal contraceptive users (AHC, n=16; 12 [cycks y.sup.1]), and regularly menstruating controls (AE, n=13; 10-13 [cycles.y.sup.1]). Thirty-nine active women ([greater than equal to] 5 h aerobic exercise/wk) participated in this cross-sectional study. BMD was lower in AMD vs. AHC and AE . Scrum hormone and bone turnover markers did not differ between AMD and AE. Cortisol was elevated (P=0.0002), progesterone suppressed (P=0.05), and bone alkaline phosphatase significantly lower (P=0.003) in AHC vs. AE. Lifetime missed menstrual cycles and body weight were significant, independent predictors of lumbar spine BMD, regardless of current menstrual status (adj [R.sup.2])=42.8%).Exercise-associated menstrual disorders have a negative effect on BMD.

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Before 1985, most female athletes viewed missing a menstrual cycle as a blessing. It was a sign of becoming "fit" and, if nothing else, it was convenient. Twenty years ago, however, physicians first reported low bone density in amenorrheic female athletes, and they noted that the more periods an athlete missed, the lower her bone density (Cann et al., 1984; Drinkwater et al., 1984). They also noticed something insidious about the bone loss: it was irreversible (Keen et al., 1997). In the 10 years since the authors of the American College of Sports Medicine's Position Stand called for research on the etiology, treatment, and prevention of the Female Athlete Triad (Otis et al., 1997), little progress has been made. As yet, we do not fully understand the mechanism of the bone loss; therefore current treatment practices may be suboptimal. We have limited evidence that exercise-associated bone loss is due to suppressed bone turnover rather than accelerated remodeling, as in postmenopausal osteoporosis (Ihle et al., 2004; Zanker et al, 1998a, 1998b). Evidence that hormonal contraceptives are effective for treating exercise-associated amenorrhea is modest (Liu et al., 2006).

The recommended treatment for women with exercise-associated amenorrhea is hormonal contraceptives after 6 months of amenorrhea (Birch, 2005). The rational for this recommendation is the demonstrated efficacy of hormone replacement therapy (HRT) for postmenopausal bone loss (Cauley et al., 2003). Estrogen withdrawl at menopause accelerates bone turnover; women with postmenopausal bone loss have abnormally high rates of bone formation and breakdown (Recker et al., 2004), leading to loss of bone mass. Thus, HRT is an effective treatment for postmenopausal bone loss in women with increased rates of bone turnover.

Because premenopausal women with oligomenor-rhea or amenorrhea also are hypoestrogenemic, the current treatment practice is based on the efficacy of hormone replacement therapy (HRT) in treating postmenopausal bone fragility. However, there is limited evidence that premenopausal women with exercise-associated hypothalamic amenorrhea (decreased secretion of gonadotropin-releasing hormone) may lose bone because of suppressed, rather than accelerated, bone turnover (Zanker et al., 1998a, 1998b). Precedent for this hypothesis comes from studies of premenopausal women with anorexia nervosa. Anorectics also are hypoestrogenemic, but in addition to suppression of the hypothalamus-pituitary-ovarian axis, the hypothalamus-pituitary-thyroid and hypothalamus-pituitary (growth hormone, GH)-insulin-like growth factor-I (IGF-I) axes also are down-regulated (Munoz et al., 2002). As a result, individuals with anorexia nervosa not only have low estrogen levels, but also altered production of thyroid hormone, GH and IGF-I. Thyroid hormone, GH, and IGF-I stimulate bone turnover; therefore, anorectics may lose bone because of decreased rates of bone turnover (Munoz et al., 2002). In contrast to postmenopausal women, estrogen treatment for bone loss in women with anorexia nervosa is ineffective (Grinspoon, Miller, Herzog, Clemmons, & Klibanski, 2003; Grinspoon, Thomas, Miller, Herzog, & Klibanski, 2002). …

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