Reproductive dysfunction and associated pathology in women undergoing military training

Evidence from civilian athletes raises the question of whether reproductive dysfunction may be seen in female soldiers as a result of military training. Such reproductive dysfunction consists of impaired ovulation with or without long term subfertility. We critically review pertinent evidence, which points towards reduced energy availability as the most likely explanation for exercise-induced reproductive dysfunction. Evidence also suggests reproductive dysfunction is mediated by activation of the hypothalamic-pituitary-adrenal axis and suppression of the hypothalamic-pituitary-gonadal axis, with elevated ghrelin and reduced leptin likely to play an important role. The observed reproductive dysfunction exists as part of a female athletic triad, together with osteopenia and disordered eating. If this phenomenon was shown to exist with UK military training this would be of significant concern. We hypothesise that the nature of military training and possibly field exercises may contribute to greater risk of reproductive dysfunction among female military trainees compared with exercising civilian controls. We discuss the features of military training and its participants, such as energy availability, age at recruitment, body phenotype, type of physical training, psychogenic stressors, altered sleep pattern and elemental exposure as contributors to reproductive dysfunction. We identify lines of future research to more fully characterise reproductive dysfunction in military women, and suggest possible interventions which, if indicated, could improve their future wellbeing

Female reproductive, adrenal and metabolic changes during an Antarctic traverse

Purpose To explore the effects of the first all-female transantarctic expedition on hormonal axes pertinent to reproductive and metabolic function. Methods Six females (age, 28–36 yr; body mass index, 24.2 ± 0.97 kg·m−2) hauled 80-kg sledges 1700 km in 61 d. Estimated average energy intake was 20.8 ± 0.1 MJ·d−1 (4970 ± 25 kcal·d−1). Whole and regional body composition was measured by dual-energy x-ray absorptiometry 1 and 2 months before and 15 d after, the expedition. Body fat was also estimated by skinfold and bioimpedance immediately before and after the expedition. Basal metabolic and endocrine blood markers and, after 0.25 mg dexamethasone suppression, 1-h 10-μg gonadorelin and 1.0 μg adrenocortiocotrophin-(1–24) tests were completed, 39–38 d preexpedition and 4 to 5 d and 15 to 16 d postexpedition. Cortisol was assessed in hair (monthly average concentrations) and saliva (five-point day curves and two-point diurnal sampling). Results Average body mass loss was 9.37 ± 2.31 kg (P < 0.0001), comprising fat mass only; total lean mass was maintained. Basal sex steroids, corticosteroids, and metabolic markers were largely unaffected by the expedition except leptin, which decreased during the expedition and recovered after 15 d, a proportionately greater change than body fat. Luteinizing hormone reactivity was suppressed before and during the expedition, but recovered after 15 d, whereas follicle-stimulating hormone did not change during or after the expedition. Cortisol reactivity did not change during or after the expedition. Basal (suppressed) cortisol was 73.25 ± 45.23 mmol·L−1 before, 61.66 ± 33.11 mmol·L−1 5 d postexpedition and 54.43 ± 28.60 mmol·L−1 16 d postexpedition (P = 0.7). Hair cortisol was elevated during the expedition. Conclusions Maintenance of reproductive and hypothalamic-pituitary-adrenal axis function in women after an extreme physical endeavor, despite energy deficiency, suggests high female biological capacity for extreme endurance exercise

Efficacy of tibolone and raloxifene for the maintenance of skeletal muscle strength, bone mineral density, balance, body composition, cognitive function, mood/depression, anxiety and quality of life/well-being in late postmenopausal women ≥ 70 years: Study design of a randomized, double-blind, double-dummy, placebo-controlled, single-center trial

<p>Abstract</p> <p>Background</p> <p>Postmenopausal women are prone to develop functional disabilities as a result of reduction in muscle strength and muscle mass caused by diminished levels of female sex hormones. While hormone replacement therapy may counteract these changes, conventional hormone replacement therapy is associated with potential harmful effects, such as an increased risk of breast cancer, and its prescription is not recommended. For this reason newer alternative drugs, such as tibolone, a synthetic steroid with estrogenic, progestogenic and androgenic activity, and raloxifene, a selective estrogen receptor modulator, may be more appropriate. This trial investigates the effect of tibolone and raloxifene on muscle strength.</p> <p>Methods</p> <p>We recruited 318 elderly women in our single-center randomized, double-blind, double-dummy, placebo-controlled trial. Participants were randomized to tibolone 1.25 mg (Org OD 14, Organon NV, the Netherlands) plus placebo, raloxifene 60 mg (Evista^®, Eli Lilly, United States) plus placebo or two placebo tablets daily for 24 months.</p> <p>The primary aim is to determine if there is a difference between tibolone and placebo or if there is a difference between raloxifene and placebo. Primary endpoints are muscle strength and bone mineral density. The secondary endpoints are postural balance, body composition, cognitive function, anxiety, mood and quality of life. The secondary aim is to determine if there is a difference between tibolone and raloxifene.</p> <p>The measure of effect is the change from the baseline visit to the visits after 3 months, 6 months, 12 months, and 24 months. A follow-up measurement is planned at 30 months to determine whether any effects are sustained after cessation of the study. By December 2007 the blind will be broken and the data analyzed.</p> <p>Trial registration number</p> <p>NTR: 1232</p

Cytokine response to acute running in recreationally-active and endurance-trained men

To compare the cytokine response to exhaustive running in recreationally-active (RA) and endurance-trained (ET) men. Eleven RA men (VO 55 ± 7 mL·min·kg ) and 10 ET men (VO 68 ± 7 mL·min ·kg) followed a controlled diet and refrained from volitional exercise for 8 days. On the fourth day, participants completed 60 min of treadmill running (65 % VO), followed by intermittent running to exhaustion (70 % VO). Fasting blood was obtained at baseline, after 20, 40 and 60 min of exercise, at the end of intermittent exercise, during 2 h of recovery and on four follow-up days (FU1-FU4). Tumour necrosis factor-alpha (TNF-a), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra) and creatine kinase (CK) were measured. Exercise increased the concentrations of all cytokines and CK, but there were no significant differences between groups. IL-1ß increased (2.2-2.5-fold, P <0.001) during exercise, while TNF-a was increased (1.6-2.0-fold, P <0.001) during exercise and for 2 h post-exercise. IL-6 (71-84-fold, P <0.001) and IL-1ra (52-64-fold, P <0.001) were increased throughout exercise and up to FU1, peaking immediately after exercise and at 1.5-2 h post-exercise, respectively. CK concentrations were increased (P <0.001) throughout exercise and up to FU4, peaking at FU1, but were not associated with changes in any cytokines. Exhaustive running resulted in modest and transient increases in TNF-a and IL-1ß, and more marked and prolonged increases in IL-6 and IL-1ra, but improved training status did not affect this response. Increased CK might indicate either exercise-induced muscle cell disruption or increased cell permeability, although neither appears to have contributed to the increased cytokine concentrations

Resistance exercise-induced changes of inflammatory gene expression within human skeletal muscle

Aberrant local inXammatory signaling within skeletal muscle is now considered a contributing factor to the development of sarcopenia. Recent evidence indicates that chronic resistance training contributes to the control of locally derived inXammation via adaptations to repeated, acute increases in pro-inXammatory mRNA within muscle. However, only a limited number of gene transcripts related to the inXammatory process have been examined in the literature. The present study utilized an acute bout to examine the eVects of resistance exercise on several inXammatoryrelated genes in 24 physically active, post-menopausal women not currently undergoing hormone replacement therapy. Following a standard warm-up, participants completed a lower-body resistance exercise bout consisting of 3 sets of 10 repetitions on machine squat, leg press, and leg extension exercises (80% intensity). Muscle biopsies were obtained from the vastus lateralis of the dominant leg at baseline and 3 h following exercise. SigniWcant (p < 0.05) up-regulation in mRNA content was observed for TNF-alpha, IL1-beta, IL6, IL8, SOCS2, COX2, SAA1, SAA2, IKKB, cfos, and junB. Muscle mRNA content was not signiWcantly altered at the 0.05 level for IL2, IL5, IL10, or IL12 (p35). Venous blood samples were also obtained at baseline as well as at 3, 24, and 48 h post-exercise. Serum was analyzed for circulating TNF-alpha, IL1-beta, IL6, IL8, COX2, and SAA with no signiWcant changes observed. These results indicate that resistance exercise is capable of up-regulating transcription of numerous inXammatory mediators within skeletal muscle, and these appear to be worthy of future examination in chronic studies