Abstract

Menopause commonly presents the gradual accumulation of iron in the body over the years, which is a risk factor for diseases such as cancer, osteoporosis, or cardiovascular diseases. Running exercise is known to acutely increase hepcidin levels, which reduces iron absorption and recycling. As this fact has not been studied in postmenopausal women, this study investigated the hepcidin response to running exercise in this population. Thirteen endurance-trained postmenopausal women (age: 51.5 ± 3.89 years; height: 161.8 ± 4.9 cm; body mass: 55.9 ± 3.6 kg; body fat: 24.7 ± 4.2%; peak oxygen consumption: 42.4 ± 4.0 mL·min−1·kg−1) performed a high-intensity interval running protocol, which consisted of 8 × 3 min bouts at 85% of the maximal aerobic speed with 90-s recovery. Blood samples were collected pre-exercise, 0, 3, and 24 h post-exercise. As expected, hepcidin exhibited higher values at 3 h post-exercise (3.69 ± 3.38 nmol/L), but also at 24 h post-exercise (3.25 ± 3.61 nmol/L), in comparison with pre-exercise (1.77 ± 1.74 nmol/L; p = 0.023 and p = 0.020, respectively) and 0 h post-exercise (2.05 ± 2.00 nmol/L; p = 0.021 and p = 0.032, respectively) concentrations. These differences were preceded by a significant increment of interleukin-6 at 0 h post-exercise (3.41 ± 1.60 pg/mL) compared to pre-exercise (1.65 ± 0.48 pg/m, p = 0.003), 3 h (1.50 ± 0.00 pg/mL, p = 0.002) and 24 h post-exercise (1.52 ± 0.07 pg/mL, p = 0.001). Hepcidin peaked at 3 h post-exercise as the literature described for premenopausal women but does not seem to be fully recovered to pre-exercise levels within 24 h post-exercise, as it would be expected. This suggests a slower recovery of basal hepcidin levels in postmenopausal women, suggesting interesting applications in order to modify iron homeostasis as appropriate, such as the prevention of iron accumulation or proper timing of iron supplementation.

Highlights

  • Iron is an essential element for humans, being necessary for vital processes including oxygen transport and energy production, DNA synthesis, host defense, and cell signaling [1]

  • Figures show the individual response of participants with depleted ferritin stores (

  • The main finding is that hepcidin does not seem to fully regain pre-exercise concentrations within 24 h after exercise, suggesting a slower recovery of basal hepcidin levels compared to the recovery reported in men and premenopausal women [22,24,28,29]

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Summary

Introduction

Iron is an essential element for humans, being necessary for vital processes including oxygen transport and energy production, DNA synthesis, host defense, and cell signaling [1]. Its importance requires well-regulated iron levels in the body, since its lack or excess leads to health problems [2]. The main mechanism for maintaining body iron homeostasis is to balance iron supply with iron utilization and losses [3]. Since iron excretion cannot be controlled, the system is regulated according to the iron demands of the body. Iron supply into the plasma is primarily provided by iron recycling in the macrophages and duodenal absorption in the enterocytes, and if necessary, releasing iron from liver stores as ferritin [1]. The inlet flow of iron to plasma is controlled by hepcidin [4,5,6]

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