Suchergebnisse

OBJECTIVES: Military personnel are exposed to periods of energy deficit and stress, which is typically accompanied by reductions in testosterone concentrations and declines in iron status. Exogenous testosterone administration may increase erythropoiesis and iron availability. The objective of this study was to determine the effects of exogenous testosterone on iron homeostasis in healthy young males during energy deficit. METHODS: Fifty males (24.8 ± 5.0 y, 78.6 ± 12.2 kg) completed this randomized, double-blind, placebo-controlled trial. Participants were provided a eucaloric diet during a 2-week free-living phase (day 1–14). Following the free-living phase, participants completed a 4-week live-in phase (day 15–42). During the live-in phase participants were randomized to 200 mg testosterone enanthate/week (n = 24) or 1 mL sesame oil/week (placebo, n = 26) and were in an energy- and exercise-induced energy deficit equal to 53 ± 4%. Blood was collected on days 14 and 42 to determine concentrations of testosterone, hemoglobin, hematocrit, ferritin, hepcidin, and erythroferrone. Data are reported as change scores (mean ± SD). RESULTS: Total testosterone concentrations increased with testosterone and declined with placebo (569 ± 271 nmol/L and −83 ± 142 nmol/L, P < 0.0001). Testosterone attenuated the decline in hemoglobin (−0.04 ± 0.7 g/L and −0.6 ± 0.8 g/dL, P < 0.01) and hematocrit (0.6 ± 2.2% and −1.3 ± 2.1%, P < 0.01) that occurred with placebo. Hepcidin (−3.7 ± 5.0 ng/mL and 2.1 ± 5.0 ng/mL, P < 0.001) and ferritin (−32.5 ± 38.6 ng/mL and 15.4 ± 41.2 ng/mL, P < 0.0001 ) were reduced with testosterone as compared to placebo. Erythroferrone (−0.5 ± 2.1 ng/mL and 0.5 ± 2.0 ng/mL, P = 0.11) did not differ when comparing testosterone to placebo. CONCLUSIONS: Testosterone administration during energy deficit suppressed hepcidin concentrations and increased iron utilization in healthy young males. The reduction in hepcidin with testosterone administration appears to occur through an ...

OBJECTIVES: Tactical military personnel regularly undergo training and operations that place them under extreme physical and psychological stress. Severe negative energy balance is one stressor that occurs due to prolonged and strenuous physical exertion and limited access to food. During an energy deficit, the body predominately relies on fat stores, leading to greater fatty acid β-oxidation. Acylcarnitine species, intermediate products formed as acyl groups are moved into the mitochondria to undergo β-oxidation, have been shown to increase during periods of fasting and return to normal upon refeeding either a eucaloric or isocaloric diet in healthy individuals. Carnitine and acylcarnitine species have not been assessed during prolonged energy deficit in healthy men undergoing strenuous military training. OBJECTIVE: To determine longitudinal changes in carnitine and acyl derivatives during a severe energy deficit. METHODS: This secondary analysis examined carnitine and acylcarnitine concentrations before (PRE) and after (POST) 61-d U.S. Army Ranger training and following 2–6 wk of recovery (REC). During training, participants (n = 23; mean ± SD: 23.0 ± 2.8 y; 81.0 ± 9.6 kg; 16.8 ± 3.9% body fat) consumed ∼2200 kcal/d, but still averaged ∼1000–4000 kcal/d energy deficit. Carnitine and acylcarnitine (C2-C22) concentrations were measured by tandem mass spectrometry. RESULTS: At POST, male soldiers had increased concentrations of 18 of 58 acylcarnitine species (C2, C4-OH, C5, C6, C6:1, C8-DC, C12:1, C14:1, C16-OH, C16:1, C16:1-OH, C16:2, C18:1-OH, C18:1-DC, C18:2-OH, C20:2-OH, C20:3, C22:3; P ≤ 0.05) compared to PRE. Except for C20:3, all acylcarnitine species returned to PRE concentrations following REC (P > 0.05). Carnitine concentrations were no different from PRE to POST (40 ± 7 and 36 ± 7 µmol/L, respectively; P > 0.05), but concentrations were higher following REC (43 ± 5 µmol/L) compared to POST (P = 0.05). CONCLUSIONS: Severe energy deficit incurred during strenuous military training increased some, ...

BACKGROUND: Severe energy deficits during military operations, produced by significant increases in exercise and limited dietary intake, result in conditions that degrade lean body mass and lower-body muscle function, which may be mediated by concomitant reductions in circulating testosterone. METHODS: We conducted a three-phase, proof-of-concept, single centre, randomised, double-blind, placebo-controlled trial (CinicalTrials.gov, NCT02734238) of non-obese men: 14-d run-in, free-living, eucaloric diet phase; 28-d live-in, 55% exercise- and diet-induced energy deficit phase with (200 mg testosterone enanthate per week, Testosterone, n = 24) or without (Placebo, n = 26) exogenous testosterone; and 14-d recovery, free-living, ad libitum diet phase. Body composition was the primary end point; secondary endpoints included lower-body muscle function and health-related biomarkers. FINDINGS: Following energy deficit, lean body mass increased in Testosterone and remained stable in Placebo, such that lean body mass significantly differed between groups [mean difference between groups (95% CI), 2.5 kg (3.3, 1.6); P < .0001]. Fat mass decreased similarly in both treatment groups [0.2 (−0.4, 0.7), P = 1]. Change in lean body mass was associated with change in total testosterone (r = 0.71, P < .0001). Supplemental testosterone had no effect on lower-body muscle function or health-related biomarkers. INTERPRETATION: Findings suggest that supplemental testosterone may increase lean body mass during short-term severe energy deficit in non-obese, young men, but it does not appear to attenuate lower-body functional decline. FUNDING: Collaborative Research to Optimize Warfighter Nutrition projects I and II, Joint Program Committee-5, funded by the US Department of Defence.