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.

A Combined Hot and Hypoxic Environment during Maximal Cycling Sprints Reduced Muscle Oxygen Saturation: A Pilot Study.

The present study investigated the effects of a combined hot and hypoxic environment on muscle oxygenation during repeated 15-s maximal cycling sprints. In a single-blind, cross-over study, nine trained sprinters performed three 15-s maximal cycling sprints interspersed with 7-min passive recovery in normoxic (NOR; 23℃, 50%, FiO2 20.9%), normobaric hypoxic (HYP; 23℃, FiO2 14.5%), and hot normobaric hypoxic (HH; 35℃, FiO2 14.5%) environments. Relative humidity was set to 50% in all trials. The vastus lateralis muscle oxygenation was evaluated during exercise using near-infrared spectroscopy. The oxygen uptake (VO2) and arterial oxygen saturation (SpO2) were also monitored. There was no significant difference in peak or mean power output among the three conditions. The reduction in tissue saturation index was significantly greater in the HH (-17.0 ± 2.7%) than in the HYP (-10.4 ± 2.8%) condition during the second sprint (p < 0.05). The average VO2 and SpO2 were significantly lower in the HYP (VO2 = 980 ± 52 mL/min, SpO2 = 82.9 ± 0.8%) and HH (VO2 = 965 ± 42 mL/min, SpO2 = 83.2 ± 1.2%) than in the NOR (VO2 = 1149 ± 40 mL/min, SpO2 = 90.6 ± 1.4%; p < 0.05) condition. In conclusion, muscle oxygen saturation was reduced to a greater extent in the HH than in the HYP condition during the second bout of three 15-s maximal cycling sprints, despite the equivalent hypoxic stress between HH and HYP.

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.

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.

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".

Muscle Oxygenation During Repeated Double-Poling Sprint Exercise in Normobaric Hypoxia and Normoxia.

We compared upper limb muscle oxygenation responses during repeated double-poling sprint exercise in normobaric hypoxia and normoxia. Eight male kayakers completed a repeated double-poling sprint exercise (3 × 3 × 20-s maximal sprints, 40-s passive recovery, 5-min rest) in either hypoxia (HYP, FiO2 = 14.5%) or normoxia (NOR, FiO2 = 20.9%). Power output, muscle oxygenation of triceps brachii muscle (using near infrared spectroscopy), arterial oxygen saturation, and cardiorespiratory variables were monitored. Mean power output tended to be lower (-5.2%; P = 0.06) in HYP compared with NOR, while arterial oxygen saturation (82.9 ± 0.9% vs. 90.5 ± 0.8%) and systemic oxygen uptake (1936 ± 140 vs. 2408 ± 83 mL⋅min-1) values were lower (P < 0.05). Exercise-induced increases in deoxygenated hemoglobin (241.7 ± 46.9% vs. 175.8 ± 27.2%) and total hemoglobin (138.0 ± 18.1% vs. 112.1 ± 6.7%) were greater in HYP in reference to NOR (P < 0.05). Despite moderate hypoxia exacerbating exercise-induced elevation in blood perfusion of active upper limb musculature, power output during repeated double-poling exercise only tended to be lower.