This study suggests that approximately half of exercising women experience subtle menstrual disturbances, i.e. LPD and anovulation, and that one third of exercising women may be amenorrheic. Estimates of the prevalence of subtle menstrual disturbances in exercising women determined by the presence or absence of short or long cycles does not identify these disturbances. In light of known clinical consequences of menstrual disturbances, these findings underscore the lack of reliability of normal menstrual intervals and self report to infer menstrual status.

Recent findings support a role for ghrelin in the regulation of energy homeostasis and possibly reproductive function. The primary purpose of this study was to test whether differences in fasting ghrelin levels exist in exercising women with differing menstrual and metabolic status. Menstrual cycle status was defined as sedentary ovulatory (SedOvul; n = 10, cycles = 26), exercising ovulatory (ExOvul; n = 11, cycles = 22), exercising luteal phase defect/anovulatory (ExLPD/Anov; n = 11, cycle = 27), and exercising amenorrheic (ExAmen; n = 8, cycle = 16). Subjects were 27.7 +/- 1.2 yr of age, weighed 60.2 +/- 3.3 kg, and had menstrual cycle lengths of 28.4 +/- 0.9 d. Blood was collected during the follicular phase (d 2-9) of each menstrual cycle and analyzed for total ghrelin, insulin, total T(3), and leptin. Ghrelin was significantly elevated by approximately 85% in the ExAmen category (725.5 +/- 40.8 pmol/liter) when compared with all other categories (P < 0.001; SedOvul = 393.6 +/- 32.0 pmol/liter, ExOvul = 418.9 +/- 34.8 pmol/liter, and ExLPD/Anov = 381.1 +/- 314 pmol/liter). Leptin levels were lower in all groups vs. SedOvul (P < 0.001). Insulin was lower in both the ExLPD/Anov and ExAmen categories vs. SedOvul and ExOvul (P < 0.018), and total T(3) was lower in ExAmen compared with all other groups (P < 0.001), with concentrations in ExLPD/Anov and ExOvul exceeding those in SedOvul (P < 0.05). These data clearly indicate a metabolic hormonal profile consistent with chronic energy deficiency in exercising women across a range in menstrual status and introduces ghrelin as a potential supplementary indicator that uniquely discriminates amenorrheic athletes from athletes with other menstrual disturbances.

ObjectivesWe systemically reviewed the literature to assess how long-term testosterone suppressing gender-affirming hormone therapy influenced lean body mass (LBM), muscular area, muscular strength and haemoglobin (Hgb)/haematocrit (HCT).DesignSystematic review.Data sourcesFour databases (BioMed Central, PubMed, Scopus and Web of Science) were searched in April 2020 for papers from 1999 to 2020.Eligibility criteria for selecting studiesEligible studies were those that measured at least one of the variables of interest, included transwomen and were written in English.ResultsTwenty-four studies were identified and reviewed. Transwomen experienced significant decreases in all parameters measured, with different time courses noted. After 4 months of hormone therapy, transwomen have Hgb/HCT levels equivalent to those of cisgender women. After 12 months of hormone therapy, significant decreases in measures of strength, LBM and muscle area are observed. The effects of longer duration therapy (36 months) in eliciting further decrements in these measures are unclear due to paucity of data. Notwithstanding, values for strength, LBM and muscle area in transwomen remain above those of cisgender women, even after 36 months of hormone therapy.ConclusionIn transwomen, hormone therapy rapidly reduces Hgb to levels seen in cisgender women. In contrast, hormone therapy decreases strength, LBM and muscle area, yet values remain above that observed in cisgender women, even after 36 months. These findings suggest that strength may be well preserved in transwomen during the first 3 years of hormone therapy.

The renin-angiotensin-aldosterone system (RAAS) is integrally involved in multiple cardiovascular physiological processes including arterial blood pressure (BP) regulation. Over activity of the RAAS has been implicated in the pathogenesis of a number of cardiovascular disease entities, including hypertension. Several lines of evidence suggest estrogen favorably modulates the RAAS. Conversely, estrogen deficiency due to menopause may contribute to over activity of the RAAS. Of importance, estrogen deficiency in women is not exclusive to the postmenopausal period. Functional hypothalamic amenorrhea is a reversible cause of premenopausal hypoestrogenemia. In contrast to postmenopausal women (PMW), premenopausal women with exercise-associated functional hypothalamic amenorrhea demonstrate decreased, not increased, resting BP compared with their estrogen-replete eumenorrheic counterpart. In this review we briefly examine the effects of estrogen status on the RAAS and present the hypothesis that the RAAS is altered in physically active women with functional hypothalamic amenorrhea.