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
BackgroundHepcidin is an iron regulating hormone, and exercise-induced hepcidin elevation is suggested to increase the risk of iron deficiency among athletes.
ObjectiveWe compared serum hepcidin responses to resistance exercise and endurance (cycling) exercise.
MethodsTen 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 _ VO 2max 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).
ResultsBoth 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.
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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