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

Gene expression of the liver in response to chronic hypoxia

Hypoxia is an important ecological, evolutionary, and biomedical stressor. While physiological acclimatization of mammals to hypoxia is well studied, the variation in gene expression that underlies acclimatization is not well studied. We acclimatized inbred mice for 32 days to hypoxic conditions that simulated altitudes of 1400, 3000, and 4500 m. We used oligonucleotide microarrays to measure changes in steady-state abundance of mRNA in the livers of these mice. Mice exposed to more severe hypoxia (simulated altitude of 4500 m) were smaller in mass and had higher hematocrit than mice exposed to less severe hypoxia. ANOVA and false discovery rate tests indicated that 580 genes were significantly differentially expressed in response to chronic hypoxia. Few of these 580 genes have previously been reported to respond to hypoxia. In contrast, many of these 580 genes belonged to same functional groups typically respond to acute hypoxia. That is, both chronic and acute hypoxia elicit changes in transcript abundance for genes involved in angiogenesis, glycolysis, lipid metabolism, carbohydrate metabolism, and protein amino acid phosphorylation, but the particular genes affected by the two types of hypoxia were mostly different. Numerous genes affecting the immune system were differentially expressed in response to chronic hypoxia, which supports recently proposed hypotheses that link immune function and hypoxia. Furthermore, our results discovered novel elevated mRNA abundance of genes involved in hematopoiesis and oxygen transport not reported previously, but consistent with extreme hematocrits found in hypoxic mice