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, FiO 2 = 14.5%) or normoxia (NOR, FiO 2 = 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.

Team and racket sport athletes repeatedly produce brief bouts of maximal power output (~10 s) interspersed with insufficient recovery period (~60 s) during competition. This physical fitness component is known as "repeated-sprint ability" (RSA) (Bishop, Girard, & Mendez-Villanueva, 2011; Girard, Mendez-Villanueva, & Bishop, 2011). Recent studies have shown that several weeks of repeated-sprint training in hypoxia further improves RSA compared with the same

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 (F i O 2 ) = 20.9%, 10.6 ± 0.3 km/h], (b) exercise at the same relative exercise intensity with NOR in hypoxia (HYPR, F i O 2 = 14.5%, 9.4 ± 0.3 km/h), and (c) exercise at the same absolute exercise intensity with NOR in hypoxia (HYPA, F i O 2 = 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 CO 2 / 12 CO 2 ). 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.

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.

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