The Impact of Morning Versus Afternoon Exercise on Iron Absorption in Athletes

Rachel Mccormick; Diego Moretti; Alannah K. A. Mckay; Coby M. Laarakkers; Rachel Vanswelm; Debbie Trinder; Gregory R. Cox; Michael B. Zimmerman; Marc Sim; Carmel Goodman; Brian Dawson; Peter Peeling

Disclosures

Med Sci Sports Exerc. 2019;51(10):2147-2155. 

In This Article

Abstract and Introduction

Abstract

Purpose: This study examined postexercise inflammatory, hepcidin, and iron absorption responses to endurance exercise performed in the morning versus the afternoon.

Methods: Sixteen endurance-trained runners (10 male, 6 female) with serum ferritin (sFer) < 50 μg·L−1 completed a 90-min running protocol (65% vV̇O2max) in the morning (AM), or the afternoon (PM), in a crossover design. An iron-fortified fluid labeled with stable iron isotopes (57Fe or 58Fe) was administered with a standardized meal 30 min following the exercise and control conditions during each trial, serving as a breakfast and dinner meal. Venous blood samples were collected before, immediately after, and 3 h after the exercise and control conditions to measure sFer, serum interleukin-6 (IL-6), and serum hepcidin-25. A final venous blood sample was collected 14 d after each trial to determine the erythrocyte iron incorporation, which was used to calculate iron absorption. Linear mixed-modeling was used to analyze the data.

Results: Overall, exercise significantly increased the concentrations of IL-6 (4.938 pg·mL−1; P = 0.006), and hepcidin-25 concentrations significantly increased 3 h after exercise by 0.380 nM (P < 0.001). During the PM trial, hepcidin concentrations exhibited diurnal tendency, increasing 0.55 nM at rest (P = 0.007), before further increasing 0.68 nM (P < 0.001) from prerun to 3 h postrun. Fractional iron absorption was significantly greater at breakfast after the AM run, compared with both the rested condition (0.778%; P = 0.020) and dinner in the AM run trial (0.672%; P = 0.011).

Conclusions: Although exercise resulted in increased concentrations of IL-6 and hepcidin, iron was best absorbed in the morning after exercise, indicating there may be a transient mechanism during the acute postexercise window to promote iron absorption opposing the homeostatic regulation by serum hepcidin elevations.

Introduction

Iron deficiency (ID) is the most prevalent nutritional disorder worldwide and continues to be a prevailing health issue in athletes.[1] Existing literature reports the incidence of ID to be up to 17% in male and 50% in female endurance athletes across various cohort studies.[2–6] It has been established that ID impairs an individual's oxygen transport and energy metabolism, with severe cases (i.e., anemia) linked to decreases in work capacity and maximal oxygen consumption (V̇O2max).[7] The high prevalence of ID in athletes is likely due to a combination of insufficient iron intake and mechanisms of iron loss that are exacerbated by activity. These include sweating, hematuria, gastrointestinal (GI) bleeding, and hemolysis; and in female athletes, menstrual losses.[8] Moreover, the low bioavailability of dietary heme (15%–35%) and nonheme (2%–20%) iron[9] may substantiate the difficulty that the athletes experience in replenishing their daily iron losses from food. Recently, exercise-induced inflammation has also been implicated in the elevation of the primary iron regulatory hormone, hepcidin, which suppresses the absorption of dietary iron by duodenal enterocytes and iron recycling by macrophages.[10,11] To date, numerous research articles have explored the postexercise response of hepcidin and its impact on iron metabolism in athletes. This work has consistently shown twofold to fourfold increases in hepcidin levels at 3 h postexercise, with the magnitude of this response mediated by exercise duration, and by the athletes' preexercise serum ferritin (sFer) level.[11–13] Of note, both Peeling et al.[11] and Newlin et al.[12] observed a significant increase in interleukin-6 (IL-6) immediately after exercise, which preceded the peak in serum hepcidin concentrations by 3 to 6 h postexercise.

With the time course profile of hepcidin response (3–6 h postexercise) established,[11] it is likely that there is a period of impeded iron absorption in the GI tract after exercise, which may (negatively) affect an athlete's iron status. Since athletes are encouraged to eat immediately after exercise to enhance the rate of glycogen restoration and protein synthesis,[14] a possible disparity between mealtimes (i.e., breakfast or dinner) and optimal iron absorption may exist. Consequently, exercise-induced elevations in serum hepcidin concentration, and the prospect of subsequent postexercise reductions in iron absorption, are a likely mechanism of iron regulation that potentially contributes to ID in athletes; however, this hypothesis is yet to be confirmed. When considering iron absorption, Moretti and colleagues[15] recently explored the inflammatory and erythropoietic influences of exercise on plasma hepcidin concentration and iron absorption during a 3-wk training period using recreationally trained runners. In this study, the net effect of exercise was to decrease hepcidin concentrations and mildly increase iron absorption over time. These authors suggested a potential mechanism whereby, during the progression of training (additional 8 km run every second day), the impact of inflammation and hepcidin elevations are offset by the erythropoietic stimuli, to chronically increase iron mobilization and absorption for erythroid expansion, in an attempt to maintain iron balance in active individuals.[15] However, the effect of acute elevations in serum hepcidin concentration after exercise on measurements of iron absorption remains to be investigated. Therefore, the aim of this study was to examine the influence of an exercise bout on subsequent serum IL-6, hepcidin concentrations and iron absorption in endurance athletes, and to assess the impact of exercise timing (i.e., morning or afternoon exercise) on this relationship.

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