Background: Previous studies to develop and validate bioelectrical impedance analysis (BIA) equations to predict body composition were limited by small sample sizes, sex specificity, and reliance on reference methods that use a 2-component model. Objective: This study was designed to develop sex-specific BIA equations to predict total body water (TBW) and fat-free mass (FFM) with the use of a multicomponent model for children and adults. Design: Data from 5 centers were pooled to create a sample of 1474 whites and 355 blacks aged 12–94 y. TBW was measured by dilution, and FFM was estimated with a multicomponent model based on densitometry, isotope dilution, and dual-energy X-ray absorptiometry. Results: The final race-combined TBW prediction equations included stature²/resistance and body weight (R² = 0.84 and 0.79 and root mean square errors of 3.8 and 2.6 L for males and females, respectively; CV: 8%) and tended to underpredict TBW in black males (2.0 L) and females (1.4 L) and to overpredict TBW in white males (0.5 L) and females (0.3 L). The race-combined FFM prediction equations contained the same independent variables (R² = 0.90 and 0.83 and root mean square errors of 3.9 and 2.9 kg for males and females, respectively; CV: ≈6%) and tended to underpredict FFM in black males (2.1 kg) and females (1.6 kg) and to overpredict FFM in white males (0.4 kg) and females (0.3 kg). Conclusion: These equations have excellent precision and are recommended for use in epidemiologic studies to describe normal levels of body composition.

Sex hormone-binding globulin (SHBG) production in humans has been thought to be stimulated by estrogens and thyroid hormone and inhibited by androgens. However, recent data indicate that SHBG production in vitro is stimulated by both androgens and estrogens. This study was designed to determine what other hormonal factors regulate SHBG production. Since hyperinsulinemia and hyperprolactinemia both occur in disease states in which low serum SHBG levels are found, the effects of insulin and PRL were compared to and/or studied in combination with estradiol (E2), T4, and testosterone (T) in a human hepatoma cell line (Hep G2). Hep G2 cells were grown to near confluence in medium including 10% fetal calf serum, and then 72-h experimental incubations were carried out which used only fetal calf serum-free medium. Compared to control incubations, both insulin (10(-8) mol/L) and PRL (10(-8) mol/L) decreased SHBG production from 65.0 +/- 0.6 (+/- SE) to 46.8 +/- 1.1 and 46.8 +/- 1.2 nmol/10(6) cells, respectively (P less than 0.01). Insulin also inhibited both E2 and T4-stimulated SHBG production. T stimulated SHBG production to the same degree as E2. Finally, both E2 and insulin significantly increased cell number, an important consideration when expressing the effect of a hormone on SHBG production in cultured cells. We conclude that insulin and PRL inhibit SHBG production and confirm that T4, T, and E2 stimulate SHBG production in vitro. These findings suggest that insulin and PRL may be important factors in the regulation of SHBG production in vivo.

To examine endogenous anabolic hormonal responses to two different types of heavy resistance exercise protocols (HREPs), eight male and eight female subjects performed two randomly assigned protocols (i. e. P-1 and P-2) on separate days. Each protocol consisted of eight identically ordered exercises carefully designed to control for load, rest period length, and total work (J) effects. P-1 utilized a 5 RM load, 3-min rest periods and had lower total work than P-2. P-2 utilized a 10 RM load, 1-min rest periods and had a higher total work than P-1. Whole blood lactate and serum glucose, human growth hormone (hGH), testosterone (T), and somatomedin-C [SM-C] (i. e. insulin-like growth factor 1, IGF-1) were determined pre-exercise, mid-exercise (i. e. after 4 of the 8 exercises), and at 0, 5, 15, 30, and 60 mm post-exercise. Males demonstrated significant (p < 0.05) increases above rest in serum T values, and all serum concentrations were greater than corresponding female values. Growth hormone increases in both males and females following the P-2 HREP were significantly greater at all timepoints than corresponding P-1 values. Females exhibited significantly higher pre-exercise hGH levels compared to males. The P-1 exercise protocol did not result in any hGH increases in females. SM-C demonstrated random significant increases above rest in both males and females in response to both HREPs. These data suggest that the hormonal response patterns to HREPs are variable and in females differ from those in males due to significantly higher pre-exercise and exercise-induced serum T levels in males and higher pre-exercise serum hGH concentrations in females.

We tested the hypothesis that key endocrine responses to semistarvation would be attenuated by changing only the food intake in a multistressor environment that also included sustained workload, inadequate sleep, and thermal strain. Serum hormones were compared within and between two groups of healthy young male volunteers participating in the 8-wk US Army Ranger course, with four repeated cycles of restricted energy intakes and refeeding: group 1 ( n = 49) and group 2 ( n = 48); energy deficits averaged 1,200 and 1,000 kcal/day, respectively. After 8 wk, most of group 1 achieved a minimum body fat, serum 3,5,3′-triiodothyronine (T₃) was below normal (78 ± 20 ng/dl), testosterone (T) approached castrate levels (4.5 ± 3.9 nmol/l), insulin-like growth factor I (IGF-I) declined by one-half (75 ± 25 μg/l), and cholesterol rose from 158 ± 31 to 217 ± 39 mg/dl. Bioavailable T₃ and T were further reduced by increases in their specific binding proteins in response to declining insulin. Refeeding, even with continuation of the other stressors, produced prompt recovery of T₃, T, and IGF-I. Higher energy intakes in group 2 attenuated the subclinical hypothyroidism and hypercholesterolemia, whereas consistent luteinizing hormone suppression indicated centrally mediated threshold effects on gonadal hormone suppression. We conclude that low T, T₃, and IGF-I remained reliable markers of acute energy deficits in the presence of other stressors; elevated cholesterol and cortisol provided information about chronic status, corresponding to diminishing body fat stores.

Methods: In an intensive 8-wk military training course that included an average daily energy deficit of 1000 kcal·d−1, lower-body power output, maximal lifting strength, body composition, and serum concentrations of several somatotrophic hormones were measured in 50 male soldiers (24.6 ± 4.4 y; 176.1 ± 7.8 cm; 78.4 ± 8.7 kg; 14.7 ± 4.2% body fat) before and after the course. Results: Vertical jump height (−16%), explosive power output (−21%), maximal lifting strength. (−20%), body mass (−13%), fat-free mass (−6%), and fat mass (−50%) declined (P < 0.05) after the training course. Circulating total testosterone and insulin-like growth factor-I (IGF-I) experienced significant (P < 0.05) declines, and cortisol was significantly increased. Lower-body power output, but not maximal lifting strength, correlated with changes in fat-free mass. IGF-I and cortisol, but not total testosterone, were correlated with losses of tissue mass. Conclusion: Lower-body power output, estimated from vertical jump height and body mass, is a sensitive and field expedient measure that can be used to assess the influence of caloric deficit on physical performance after 8 wk of U.S. Army Ranger training. With severe weight loss (≥13% of body mass), IGF-I and cortisol correlate more closely with soft-tissue tissue adaptations than does testosterone....