Browsing by Author "Badenhorst C"

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    Influence of "live high-train low" on hemoglobin mass and post-exercise hepcidin response in female endurance athletes
    (Springer-Verlag GmbH, 2025-04-10) Kuorelahti T; Ihalainen JK; Linnamo V; Badenhorst C; Kettunen O; Mikkonen RS
    Purpose: The aim of this study was to investigate the effects of a 21-day ‘live high-train low’ (LHTL) intervention on hemoglobin mass (Hbmass) and post-exercise hepcidin response in female endurance athletes. Methods: 15 national to international level female endurance athletes completed either the LHTL intervention in normobaric hypoxia (2500 m, ~ 18 h·day−1, INT, n = 7) or lived and trained in normoxia for the same duration (CON, n = 8). Tests were conducted before (PRE) and within two days after (POST) the intervention including Hbmass measurements via a carbon monoxide rebreathing method and a roller skiing skate test. Venous blood samples were collected at rest, 0, and 3 h after the aerobic exercise to test for changes in serum hepcidin, ferritin, and interleukin-6 (IL-6). Results: Normobaric hypoxia increased Hbmass (3.3 ± 1.8%, p < 0.001) in INT, while no changes were observed in CON. There were no changes in performance parameters, resting levels of hepcidin, or IL-6 from PRE to POST, but ferritin decreased in both groups (p = 0.040). Hepcidin increased 0 h post-exercise in PRE for INT (p = 0.029) and both 0 and 3 h post-exercise for CON (p = 0.001, p = 0.019). In POST elevated post-exercise hepcidin was only observed in CON (0 h, p = 0.003; 3 h, p = 0.008). Conclusions: 21-day LHTL increased Hbmass and suppressed post-exercise hepcidin response after intensive aerobic exercise. This suggests that prolonged hypoxia may induce an acute physiological response that supports iron absorption within a few days following hypoxic exposure, which may assist in achieving the aerobic adaptations sought from prolonged hypoxic training camps.
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    Influence of an energy deficient and low carbohydrate acute dietary manipulation on iron regulation in young females
    (Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society, 2022-07) Hayashi N; Ishibashi A; Iwata A; Yatsutani H; Badenhorst C; Goto K
    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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    Menstrual blood loss as an initial trigger for adaptation of iron metabolism in eumenorrheic female athletes—An exploratory study
    (Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society, 2025-08-26) Nolte S; Maier C; Klügel S; Weyh C; Hacker S; Badenhorst C; Krüger K
    Iron deficiency is a risk factor for impaired performance and recovery. While exercise-related iron losses are well-documented, the role of menstrual blood loss (MBL) as a physiological trigger of iron regulation remains underexplored. This study examined whether MBL in eumenorrheic female athletes induces measurable hematological and iron-related responses, accounting for sex hormone fluctuations. Ten regional-level football players underwent menstrual cycle tracking and venous blood sampling in both the early follicular and mid-luteal phases. Hematological parameters, iron markers (ferritin and hepcidin), erythropoietic markers (erythropoietin and reticulocytes), and inflammatory markers (myeloperoxidase [MPO] and C-reactive protein [CRP]) were measured. MBL was assessed using the Pictorial Blood Loss Assessment Chart (PBAC). Analyses included descriptive statistics, correlation, and linear mixed modeling. MBL was significantly associated with ferritin (β = −0.289, p = 0.001), reticulocyte counts (β = 0.004, p = 0.019), and reticulocyte production index (β = 0.004, p = 0.027). MPO and CRP showed inverse correlations with MBL, suggesting potential immunomodulatory effects. No interaction between MBL and cycle phase was found. MBL appears to stimulate compensatory erythropoiesis in female athletes, largely independent of hormonal phase. Incorporating MBL assessment into athlete monitoring may support individualized strategies to maintain iron balance and optimize performance.