Iron is essential for providing oxygen to working muscles during exercise, and iron deficiency leads to decreased exercise capacity during endurance events. However, the mechanism of iron deficiency among endurance athletes remains unclear. In this study, we compared iron status between two periods involving different training regimens. Sixteen female long-distance runners participated. Over a seven-month period, fasting blood samples were collected during their regular training period (LOW; middle of February) and during an intensified training period (INT; late of August) to determine blood hematological, iron, and inflammatory parameters. Three-day food diaries were also assessed. Body weight and lean body mass did not differ significantly between LOW and INT, while body fat and body fat percentage were significantly lower in INT (p < 0.05). Blood hemoglobin, serum ferritin, total protein, and iron levels, total iron-binding capacity, and transferrin saturation did not differ significantly between the two periods. Serum hepcidin levels were significantly higher during INT than LOW (p < 0.05). Carbohydrate and iron intakes from the daily diet were significantly higher during INT than LOW (p < 0.05). In conclusion, an elevated hepcidin level was observed during an intensified training period in long-distance runners, despite an apparently adequate daily intake of iron.

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.

This study determined the effects of high-intensity interval training on the exercise-induced growth hormone (GH) responses, whole body and regional fat content. Twenty-four sedentary males were randomized to either a high-intensity interval training (HIT) group or a low-intensity continuous training (LT) group. The HIT group performed intermittent exercises at 85% of [Formula: see text], whereas the LT group performed continuous exercise for 22 min at 45% of [Formula: see text]. Before and after 4 weeks of training, hormonal and metabolic responses to acute exercise were determined. Acute exercise significantly increased GH concentrations in both groups (p < 0.05). However, the responses did not change after training period in either group. Furthermore, the training did not significantly affect intramyocellular or intrahepatic lipid content in either group. The present study indicates that 4 weeks of high-intensity interval training does not alter the exercise-induced GH responses, whole body fat mass or intramyocellular and intrahepatic lipid content in sedentary males.

We investigated the effect of low energy availability (LEA) during three consecutive days of endurance training on muscle glycogen content and iron metabolism. Six male long distance runners completed three consecutive days of endurance training under LEA or neutral energy availability (NEA) conditions. Energy availability was set at 20 kcal/kg fat-free mass (FFM)/day for LEA and 45 kcal/kg FFM/day for NEA. The subjects ran for 75 min at 70% of maximal oxygen uptake ( V˙ O2max ) on days 1-3. Venous blood samples were collected following an overnight fast on days 1-4, immediately and 3 hr after exercise on day 3. The muscle glycogen content on days 1-4 was evaluated by carbon-magnetic resonance spectroscopy. In LEA condition, the body weight and muscle glycogen content on days 2-4, and the FFM on days 2 and 4 were significantly lower than those on day1 (p < .05 vs. day1), whereas no significant change was observed throughout the training period in NEA condition. On day 3, muscle glycogen content before exercise was negatively correlated with serum iron level (immediately after exercise, 3 hr after exercise), serum hepcidin level immediately after exercise, and plasma IL-6 level immediately after exercise (p < .05). Moreover, serum hepcidin level on day 4 was significantly higher in LEA condition than that in NEA condition (p < .05). In conclusion, three consecutive days of endurance training under LEA reduced the muscle glycogen content with concomitant increased serum hepcidin levels in male long distance runners.

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.