We investigated performance, energy metabolism, acid-base balance, and endocrine responses to repeated-sprint exercise in hot and/or hypoxic environment. In a single-blind, cross-over study, 10 male highly trained athletes completed a repeated cycle sprint exercise (3 sets of 3 × 10-s maximal sprints with 40-s passive recovery) under four conditions (control [CON; 20℃, 50% rH, FiO2 : 20.9%; sea level], hypoxia [HYP; 20℃, 50% rH, FiO2 : 14.5%; a simulated altitude of 3,000 m], hot [HOT; 35℃, 50% rH, FiO2 : 20.9%; sea level], and hot + hypoxia [HH; 35℃, 50% rH, FiO2 : 14.5%; a simulated altitude of 3,000 m]). Changes in power output, muscle and skin temperatures, and respiratory oxygen uptake were measured. Peak (CON: 912 ± 26 W, 95% confidence interval [CI]: 862-962 W, HYP: 915 ± 28 W [CI: 860-970 W], HOT: 937 ± 26 W [CI: 887-987 W], HH: 937 ± 26 W [CI: 886-987 W]) and mean (CON: 808 ± 22 W [CI: 765-851 W], HYP: 810 ± 23 W [CI: 765-855 W], HOT: 825 ± 22 W [CI: 781-868 W], HH: 824 ± 25 W [CI: 776-873 W]) power outputs were significantly greater when exercising in heat conditions (HOT and HH) during the first sprint (p < .05). Heat exposure (HOT and HH) elevated muscle and skin temperatures compared to other conditions (p < .05). Oxygen uptake and arterial oxygen saturation were significantly lower in hypoxic conditions (HYP and HH) versus the other conditions (p < .05). In summary, additional heat stress when sprinting repeatedly in hypoxia improved performance (early during exercise), while maintaining low arterial oxygen saturation.

Hepcidin is a liver-derived hormone that regulates iron metabolism. Recent studies suggest that an energy-deficient diet or low carbohydrate (CHO) availability may increase hepcidin in the absence of inflammation. The purpose of the present study was to examine the impact of either an energy-deficient diet or an ED diet with low CHO intake during three consecutive days on hepcidin responses, hematological variables, and energy metabolism in young Japanese women. Twenty-two young females were divided into two different groups, either an energy-deficient with low CHO intake group (ED + LCHO; 2.0 ± 0.3 g/kg/day CHO, 39%CHO, 1123 kcal/day) or an energy deficient with moderate CHO intake group (ED; 3.4 ± 0.3 g/kg/day CHO, 63%CHO, 1162 kcal/day). During the three consecutive days of the dietary intervention program, participants consumed only the prescribed diet and maintained their habitual physical activity levels. Body composition, substrate oxidation, iron metabolism, and inflammation were evaluated pre- and post-intervention. Serum iron and ferritin levels were significantly elevated following the intervention (p < 0.001, p = 0.003, respectively). Plasma interleukin-6 (IL-6) levels did not change following the intervention. Serum hepcidin levels significantly increased after the intervention (p = 0.002). Relative change in hepcidin levels was significantly higher in the ED + LCHO (264.3 ± 87.2%) than in the ED group (68.9 ± 22.1%, p = 0.048). Three consecutive days of an energy-deficient diet increased fasting hepcidin levels. Moreover, elevated hepcidin levels were further augmented when an energy-deficient diet was combined with a lower CHO intake.

Exercise-induced hemolysis, which is caused by metabolic and/or mechanical stress during exercise, is considered a potential factor for upregulating hepcidin. Intramuscular carnosine has multiple effects including antioxidant activity. Therefore, this study aimed to determine whether long-term carnosine/anserine supplementation modulates exercise-induced hemolysis and subsequent hepcidin elevation.