Effect of Amino Acid Supplementation on Iron Regulation after Endurance Exercise.

The purpose of this study was to determine the effects of pre-exercise amino acid (AA) supplementation on post-exercise iron regulation. Ten healthy males participated under two different sets of conditions in a randomized, double-blind, crossover design with a washout period of at least 21 days. Participants received either an AA supplement or placebo (PLA) for five consecutive days (4 g/dose, 3 doses/day). On the sixth day, participants ran on a treadmill for 60 min at 70% of maximal oxygen consumption (V˙O2max). Venous blood samples were collected before (baseline), immediately after, and 1 and 3 h after exercise. The serum hepcidin levels increased significantly 3 h post-exercise in both trials when compared to the baseline (p < 0.001), but the levels were not different between trials. The plasma interleukin-6 (IL-6) level significantly increased immediately after exercise compared to the baseline (p < 0.001) and was significantly higher in the AA trial than in the PLA trial (p = 0.014). Moreover, the exercise-induced increase in serum glycerol level was significantly higher in the AA trial (21.20 ± 3.98 mg/L) than in the PLA trial (17.28 ± 4.47 mg/L, p = 0.017). No significant differences were observed between the AA and PLA trials for serum iron, ferritin, and total ketone body levels (p > 0.05). In conclusion, five days of AA supplementation augmented exercise-induced increases in IL-6 and glycerol in healthy males. However, it did not affect post-exercise iron status or regulation.

Sodium L-Aspartate Supplementation Improves Repeated-Sprint Performance.

Aspartate supplementation has been reported to improve endurance performance by facilitating the tricarboxylic acid cycle flux. The present study was performed to investigate the effects of aspartate supplementation on repeated-sprint performance and blood pH. Following an overnight fast, fourteen healthy males completed three sets of 10 × 6 s maximal sprints after consuming sodium L-aspartate (ASP) or placebo (PLA), in a double-blind manner. Both supplements were taken twice on each test day (2 × 4.5 g). Exercise performance (e.g., cadence and power output) and blood variables (e.g., pH and plasma amino acid levels) were measured. The ASP trial evidenced significantly higher plasma aspartate concentration during the first (ASP, 45.3 ± 9.2 µM; PLA, 6.1 ± 0.8 µM) and the second exercise sets (ASP, 24.2 ± 4.5 µM; PLA, 6.6 ± 0.9 µM) and peak cadence during the second set (ASP, 153 ± 3 rpm; PLA, 152 ± 3 rpm) compared with the PLA trial (all p < 0.05). The peak power output during the second exercise set (ASP, 743 ± 32 W; PLA, 734 ± 31 W; p = 0.060) and the blood pH immediately before (ASP, 7.280 ± 0.020; PLA, 7.248 ± 0.016; p = 0.087) and after the third exercise set (ASP, 7.274 ± 0.019; PLA, 7.242 ± 0.018; p = 0.093) tended to be higher in the ASP than in the PLA trial. In conclusion, ASP supplementation partially improved repeated-sprint performance (peak cadence during the second exercise set). However, it did not affect the mean power output.

Effect of long-term carnosine/anserine supplementation on iron regulation after a prolonged running session.

PURPOSE: 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. METHODS: Seventeen healthy male participants were allocated to two different groups: participants consuming 1,500 mg/day of carnosine/anserine supplements (n = 9, C+A group) and participants consuming placebo powder supplements (n = 8, PLA group). The participants consumed carnosine/anserine or placebo supplements daily for 30.7 ± 0.4 days. They performed an 80-running session at 70% VO2peak pre-and post-supplementation. Iron regulation and inflammation in response to exercise were evaluated. RESULTS: Serum iron concentrations significantly increased after exercise (p < 0.01) and serum haptoglobin concentrations decreased after exercise in both groups (p < 0.01). No significant differences in these variables were observed between pre-and post-supplementation. Serum hepcidin concentration significantly increased 180 min after exercise in both groups (p < 0.01). The integrated area under the curve of hepcidin significantly decreased after supplementation (p = 0.011) but did not vary between the C+A and PLA groups. CONCLUSION: Long-term carnosine/anserine supplementation does not affect iron metabolism after a single endurance exercise session.

Adding heat stress to repeated-sprint training in hypoxia does not enhance performance improvements in canoe/kayak athletes.

PURPOSE: The present study investigated the effects of adding heat stress to repeated-sprint training in hypoxia on performance and physiological adaptations in well-trained athletes. METHODS: Sixteen canoe/kayak sprinters conducted 2 weeks of repeated-sprint training consisting of three sets of 5 × 10 s sprints with 20 s active recovery periods under conditions of either normobaric hypoxia (RSH, FiO2: 14.5%, ambient temperature: 18 ℃, n = 8) or combined heat and normobaric hypoxia (RSHH, FiO2: 14.5%, ambient temperature: 38 ℃, n = 8). Before and after training, the 10 × 10 s repeated-sprint ability (RSA) test and 500 m time trial were performed on a canoe/kayak ergometer. RESULTS: Peak and average power outputs during the RSA test were significantly improved after training in both RSH (peak power: + 21.5 ± 4.6%, P < 0.001; average power: + 12.5 ± 1.9%, P < 0.001) and RSHH groups (peak power: + 18.8 ± 6.6%, P = 0.005; average power: + 10.9 ± 6.8%, P = 0.030). Indirect variables of skeletal muscle oxygen extraction (deoxygenated hemoglobin) and blood perfusion (total hemoglobin) during the RSA test were significantly increased after training in the RSH group (P = 0.041 and P = 0.034, respectively) but not in the RSHH group. In addition, finish time during the 500 m time trial was significantly shortened after the training only in the RSH group (RSH: - 3.9 ± 0.8%, P = 0.005; RSHH: - 3.1 ± 1.4%, P = 0.078). CONCLUSION: Adding heat stress to RSH does not enhance performance improvement and may partially mask muscle tissue adaptation.

Influence of an energy deficient and low carbohydrate acute dietary manipulation on iron regulation in young females.

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.

Muscle Oxygenation during Repeated Cycling Sprints in a Combined Hot and Hypoxic Condition.

The aim of the present study was to examine the effects of a combined hot and hypoxic environment on muscle oxygenation and performance during repeated cycling sprints. In a single-blind, counterbalanced, cross-over research design, 10 male athletes performed three sets of 3 × 10-s maximal pedaling interspersed with 40-s recovery between sprints under four different environments. Each condition consisted of a control (CON; 20°C, 20.9% FiO2), normobaric hypoxia (HYP; 20°C, 14.5% FiO2), hot (HOT; 35°C, 20.9% FiO2), and combined hot and normobaric hypoxia (HH; 35°C, 14.5% FiO2). Power output and vastus lateralis muscle oxygenation were measured. Peak power output was significantly higher in HOT (892±27 W) and HH (887±24 W) than in CON (866±25 W) and HYP (859±25 W) during the first set (p<0.05). The increase in total hemoglobin during recovery periods was larger in HH than in HYP (p<0.05), while change in tissue saturation index was smaller in HYP than in CON and HOT (p<0.05). The findings suggest that the combination of hot and hypoxia during repeated cycling sprints presented different characteristics for muscle metabolism and power output compared to temperature or altitude stressor alone.

Effects of combined hot and hypoxic conditions on muscle blood flow and muscle oxygenation during repeated cycling sprints.

PURPOSE: The purpose of the present study was to determine muscle blood flow and muscle oxygenation during repeated-sprint exercise under combined hot and hypoxic conditions. METHODS: In a single-blind, cross-over research design, 11 active males performed three sets of 5 × 6-s maximal sprints with 30-s active recovery on a cycling ergometer under control (CON; 23 °C, 50% rH, 20.9% FiO2), normobaric hypoxic (HYP; 23 °C, 50% rH, 14.5% FiO2), or hot + normobaric hypoxic (HH; 35 °C, 50% rH, 14.5% FiO2) conditions. The vastus lateralis muscle blood flow after each set and muscle oxygenation during each sprint were evaluated using near-infrared spectroscopy methods. RESULTS: Despite similar repeated-sprint performance among the three conditions (peak and mean power outputs, percent decrement score), HH was associated with significantly higher muscle blood flow compared with CON after the first set (CON: 0.61 ± 0.10 mL/min/100 g; HYP: 0.81 ± 0.13 mL/min/100 g; HH: 0.99 ± 0.16 mL/min/100 g; P < 0.05). The tissue saturation index was significantly lower in HYP than in CON during the latter phase of the exercise (P < 0.05), but it did not differ between HH and CON. CONCLUSION: These findings suggest that a combination of normobaric hypoxia and heat stress partially facilitated the exercise-induced increase in local blood flow, but it did not enhance tissue desaturation.

Hepcidin response to three consecutive days of endurance training in hypoxia.

PURPOSE: The purpose of this study was to determine the effects of 3 consecutive days of endurance training in hypoxia on hepcidin responses. METHOD: Nine active healthy males completed two trials, consisting of 3 consecutive days of endurance training in either hypoxia [fraction of inspired oxygen (FiO2): 14.5%) or normoxia (FiO2: 20.9%). On days 1-3, participants performed one 90 min session of endurance training per day, consisting of high-intensity endurance interval exercise [10 × 4 min of pedaling at 80% of maximal oxygen uptake ([Formula: see text]O2max) with 2 min of active rest at 30% of [Formula: see text]O2max] followed by 30 min of continuous exercise at 60% of [Formula: see text]O2max. Venous blood samples were collected prior to exercise each day during the experimental period (days 1-4) to determine serum hepcidin, iron, ferritin, haptoglobin, and ketone body concentrations. RESULT: Serum iron (p < 0.0001), ferritin (p = 0.005) and ketone body (p < 0.0001) concentrations increased significantly in both trials on days 2-4 compared with day 1, with no significant differences between trials. No significant changes in serum haptoglobin concentrations were observed throughout the experimental period in either trial. Serum hepcidin concentrations also increased significantly on days 2-4 compared with day 1 in both trials (p = 0.004), with no significant differences observed between trials. CONCLUSION: 3 consecutive days of endurance training in hypoxia did not affect hepcidin concentrations compared with endurance training in normoxia.

Endocrine and Metabolic Responses to Endurance Exercise Under Hot and Hypoxic Conditions.

PURPOSE: We explored the effect of heat stress during an acute endurance exercise session in hypoxia on endocrine and metabolic responses. METHODS: A total of 12 healthy males cycled at a constant workload (60% of the power output associated with their maximal oxygen uptake under each respective condition) for 60 min in three different environments: exercise under hot and hypoxia (H+H; fraction of inspiratory oxygen or FiO2: 14.5%, 32°C), exercise under hypoxia (HYP; FiO2: 14.5%, 23°C), and exercise under normoxia (NOR; FiO2: 20.9%, 23°C). After completing the exercise, participants remained in the chamber for 3 h to evaluate metabolic and endocrine responses under each environment. Changes in muscle oxygenation (only during exercise), blood variables, arterial oxygen saturation, and muscle temperature were determined up to 3 h after exercise. RESULTS: Serum erythropoietin (EPO) level was increased to similar levels in both H+H and HYP at 3 h after exercise compared with before exercise (P < 0.05), whereas no significant increase was found under NOR. No significant difference between H+H and HYP was observed in the serum EPO level, blood lactate level, or muscle oxygenation at any time (P > 0.05). Exercise-induced serum growth hormone (GH) elevation was significantly greater in H+H compared with HYP (P < 0.05) and HYP showed significantly lower value than NOR (P < 0.05). Arterial oxygen saturation during exercise was significantly lower in H+H and HYP compared with NOR (P < 0.05). Furthermore, H+H showed higher value compared with HYP (P < 0.05). CONCLUSION: The serum EPO level increased significantly with endurance exercise in hypoxia. However, the addition of heat stress during endurance exercise in hypoxia did not augment the EPO response up to 3 h after completion of exercise. Exercise-induced GH elevation was significantly augmented when the hot exposure was combined during endurance exercise in hypoxia. Muscle oxygenation levels during endurance exercise did not differ significantly among the conditions. These findings suggest that combined hot and hypoxic stresses during endurance exercise caused some modifications of metabolic and endocrine regulations compared with the same exercise in hypoxia.

Muscle oxygenation, endocrine and metabolic regulation during low-intensity endurance exercise with blood flow restriction.

PURPOSE: The present study investigated the effect of endurance exercise with blood flow restriction (BFR) performed at either 25% maximal oxygen uptake (V˙O2 max) or 40% V˙O2 max) on muscle oxygenation, energy metabolism, and endocrine responses. METHODS: Ten males were recruited in the present study. The subjects performed three trials: (1) endurance exercise at 40% V˙O2 max without BFR (NBFR40), (2) endurance exercise at 25% V˙O2 max with BFR (BFR25), and (3) endurance exercise at 40% V˙O2 max with BFR (BFR40). The exercises were performed for 15 min during which the pedaling frequency was set at 70 rpm. In BFR25 and BFR40, 2 min of pressure phase (equivalent to 160 mmHg) followed by 1 min of release phase were repeated five times (5 × 3 min) throughout 15 minutes of exercise. During exercise, muscle oxygenation and concentration of respiratory gases were measured. The blood samples were collected before exercise, immediately after 15 min of exercise, and at 15, 30, and 60 minutes after completion of exercise. RESULTS: Deoxygenated hemoglobin (deoxy-Hb) level during exercise was significantly higher with BFR25 and BFR40 than that with NBFR40. BFR40 showed significantly higher total-hemoglobin (total-Hb) than NBFR40 during 2 min of pressure phase. Moreover, exercise-induced lactate elevation and pH reduction were significantly augmented in BFR40, with concomitant increase in serum cortisol concentration after exercise. Carbohydrate (CHO) oxidation was significantly higher with BFR40 than that with NBFR40 and BFR25, whereas fat oxidation was lower with BFR40. CONCLUSION: Deoxy-Hb and total Hb levels were significantly increased during 15 min of pedaling exercise in BFR25 and BFR40, indicating augmented local hypoxia and blood volume (blood perfusion) in the muscle. Moreover, low-and moderate-intensity exercise with BFR facilitated CHO oxidation.

Exogenous glucose oxidation during endurance exercise in hypoxia.

PURPOSE: Endurance exercise in hypoxia promotes carbohydrate (CHO) metabolism. However, detailed CHO metabolism remains unclear. The purpose of this study was to evaluate the effects of endurance exercise in moderate hypoxia on exogenous glucose oxidation at the same energy expenditure or relative exercise intensity. METHODS: Nine active healthy males completed three trials on different days, consisting of 30 min of running at each exercise intensity: (a) exercise at 65% of normoxic maximal oxygen uptake in normoxia [NOR, fraction of inspired oxygen (Fi O2 ) = 20.9%, 10.6 ± 0.3 km/h], (b) exercise at the same relative exercise intensity with NOR in hypoxia (HYPR, Fi O2  = 14.5%, 9.4 ± 0.3 km/h), and (c) exercise at the same absolute exercise intensity with NOR in hypoxia (HYPA, Fi O2  = 14.5%, 10.6 ± 0.3 km/h). The subjects consumed 113 C-labeled glucose immediately before exercise, and expired gas samples were collected during exercise to determine 13 C-excretion (calculated by 13 CO2 /12 CO2 ). RESULTS: The exercise-induced increase in blood lactate was significantly augmented in the HYPA than in the NOR and HYPR (p = .001). HYPA involved a significantly higher respiratory exchange ratio (RER) during exercise compared with the other two trials (p < .0001). In contrast, exogenous glucose oxidation (13 C-excretion) during exercise was significantly lower in the HYPA than in the NOR (p = .03). No significant differences were observed in blood lactate elevation, RER, or exogenous glucose oxidation between NOR and HYPR. CONCLUSION: Endurance exercise in moderate hypoxia caused a greater exercise-induced blood lactate elevation and RER compared with the running exercise at same absolute exercise intensity in normoxia. However, exogenous glucose oxidation (13 C-excretion) during exercise was attenuated compared with the same exercise in normoxia.

Acute performance and physiological responses to repeated-sprint exercise in a combined hot and hypoxic environment.

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.

Partial sleep deprivation after an acute exercise session does not augment hepcidin levels the following day.

The purpose of the present study was to determine the effects of partial sleep deprivation (PSD) after an exercise session in the evening on the endurance exercise-induced hepcidin response the following morning. Ten recreationally trained males participated under two different conditions. Each condition consisted of 2 consecutive days of training (days 1 and 2). On day 1, participants ran for 60 min at 75% of maximal oxygen uptake ( V˙ O2max ) followed by 100 drop jumps. Sleep duration at night was manipulated, with a normal length of sleep (CON condition, 23:00-07:00 hr) or a shortened length of sleep (PSD condition). On the morning of day 2, the participants ran for 60 min at 65% of V˙ O2max . Sleep duration was significantly shorter under the PSD condition (141.2 ± 13.3 min) than under the CON condition (469.0 ± 2.3 min, p < .0001). Serum hepcidin, plasma interleukin (IL)-6, serum haptoglobin, iron, and myoglobin levels did not differ significantly between the conditions (p > .05) on the morning (before exercise) of day 2. Additionally, the 3-hr postexercise levels for the hematological variables were not significantly different between the two conditions (p > .05). In conclusion, the present study demonstrated that a single night of PSD after an exercise session in the evening did not affect baseline serum hepcidin level the following morning. Moreover, a 60 min run the following morning increased serum hepcidin and plasma IL-6 levels significantly, but the exercise-induced elevations were not affected by PSD.

No effect of supplemented heat stress during an acute endurance exercise session in hypoxia on hepcidin regulation.

Hepcidin is a novel factor for iron deficiency in athletes, which is suggested to be regulated by interleukin-6 (IL-6) or erythropoietin (EPO). PURPOSE: The purpose of the present study was to compare endurance exercise-induced hepcidin elevation among "normoxia", "hypoxia" and "combined heat and hypoxia". METHODS: Twelve males (21.5 ± 0.3 years, 168.1 ± 1.2 cm, 63.6 ± 2.0 kg) participated in the present study. They performed 60 min of cycling at 60% of [Formula: see text] in either "heat and hypoxia" (HHYP; FiO2 14.5%, 32 °C), "hypoxia" (HYP; FiO2 14.5%, 23 °C) or "normoxia" (NOR; FiO2 20.9%, 23 °C). After completing the exercise, participants remained in the prescribed conditions for 3 h post-exercise. Blood samples were collected before, immediately and 3 h after exercise. RESULTS: Plasma IL-6 level significantly increased immediately after exercise (P < 0.05), with no significant difference among the trials. A significant elevation in serum EPO was observed 3 h after exercise in hypoxic trials (HHYP and HYP, P < 0.05), with no significant difference between HHYP and HYP. Serum hepcidin level increased 3 h after exercise in all trials (NOR, before 18.3 ± 3.9 and post180 31.2 ± 6.3 ng/mL; HYP, before 13.5 ± 2.5 and post180 23.3 ± 3.6 ng/mL, HHYP; before 15.8 ± 3.3 and post180 31.4 ± 5.3 ng/mL, P < 0.05). However, there was no significant difference among the trials during post-exercise. CONCLUSION: Endurance exercise in "combined heat and hypoxia" did not exacerbate exercise-induced hepcidin elevation compared with the same exercise in "hypoxia" or "normoxia".

Resistance exercise causes greater serum hepcidin elevation than endurance (cycling) exercise.

BACKGROUND: Hepcidin is an iron regulating hormone, and exercise-induced hepcidin elevation is suggested to increase the risk of iron deficiency among athletes. OBJECTIVE: We compared serum hepcidin responses to resistance exercise and endurance (cycling) exercise. METHODS: Ten males [mean ± standard error: 172 ± 2 cm, body weight: 70 ± 2 kg] performed three trials: a resistance exercise trial (RE), an endurance exercise trial (END), and a rest trial (REST). The RE consisted of 60 min of resistance exercise (3-5 sets × 12 repetitions, 8 exercises) at 65% of one repetition maximum, while 60 min of cycling exercise at 65% of [Formula: see text] was performed in the END. Blood samples were collected before exercise and during a 6-h post-exercise (0h, 1h, 2h, 3h, 6h after exercise). RESULTS: Both RE and END significantly increased blood lactate levels, with significantly higher in the RE (P < 0.001). Serum iron levels were significantly elevated immediately after exercise (P < 0.001), with no significant difference between RE and END. Both the RE and END significantly increased serum growth hormone (GH), cortisol, and myoglobin levels (P < 0.01). However, exercise-induced elevations of GH and cortisol were significantly greater in the RE (trial × time: P < 0.001). Plasma interleukin-6 (IL-6) levels were significantly elevated after exercise (P = 0.003), with no significant difference between the trials. Plasma hepcidin levels were elevated after exercise (P < 0.001), with significantly greater in the RE (463 ± 125%) than in the END (137 ± 27%, P = 0.03). During the REST, serum hepcidin and plasma IL-6 levels did not change significantly. CONCLUSION: Resistance exercise caused a greater exercise-induced elevation in hepcidin than did endurance (cycling) exercise. The present findings indicate that caution will be required to avoid iron deficiency even among athletes in strength (power) types of events who are regularly involved in resistance exercise.

Effects of diet before endurance exercise on hepcidin response in young untrained females.

PURPOSE: We examined the effects of diet before endurance exercise on hepcidin response in young untrained females. METHODS: Ten young untrained females [age: 20.6 ± 0.8 y, height: 157.5 ± 1.0 cm, weight: 54.4 ± 1.5 kg, and maximal oxygen uptake (VO2max): 35.9 ± 1.1 mL/kg/min] were involved in two experimental conditions with a crossover design. The two conditions were separated by approximately 1 month, and each condition was performed during the follicular phase. Subjects completed 60 min of pedaling at 65% of VO2max after consuming a meal (FED) or not consuming a meal (CON). Blood samples were collected before, immediately after, and 3 h after exercise. RESULTS: Serum ferritin levels before exercise did not differ between the two conditions (P > 0.05). Blood glucose and lactate levels were significantly elevated immediately after exercise only under the FED condition (P < 0.05). Serum iron levels were significantly elevated after exercise under both conditions. However, the plasma interleukin-6 and serum hepcidin levels were not significantly different 3 h after exercise under either condition (P > 0.05). CONCLUSION: Consuming a meal before endurance exercise at moderate intensity did not affect exercise-induced hepcidin elevation in young untrained females.