[13] Although these studies have provided some insight into the

[13]. Although these studies have provided some insight into the benefits of using cycling as an alternate exercise modality, it remains unclear whether such differences may improve iron status

over an extended training period. Currently, limited studies have attempted to examine how exercise might affect AZD5363 solubility dmso post-exercise hepcidin production over an extended period, and what selleck kinase inhibitor the implications may be for iron status. Recently, Auersperger et al. [14] reported that serum hepcidin and ferritin decreased in athletes adopting an eight week interval running program. In addition, McClung et al. [15] showed that nine weeks of basic combat training (BCT) compromised numerous iron parameters in female soldiers. On the contrary, McClung et al. [16] reported that seven days of training (military specific exercise and ski marching) elevated hepcidin levels without affecting iron status in male soldiers. Of importance, the iron status of an athlete may also dictate both the pre-exercise Selleck Nutlin3 levels of hepcidin, and the magnitude of hepcidin response to an acute exercise stimulus (e.g. serum ferritin <30 μg.L−1, hepcidin suppressed) [17]. Considering that the aforementioned

investigations used mainly weight-bearing activity (that may have increased the degree of exercise-induced hemolysis), it remains to be investigated how accumulated bouts of weight-bearing (running) vs. MTMR9 non-weight-bearing (cycling) exercise may impact iron status over time. Additionally, previous investigations [14–16] have only measured basal hepcidin levels; however, the acute post-exercise hepcidin response over consecutive exercise bouts currently remains unknown. As such, this study set out to compare the effects of a seven day period of running vs. cycling exercise on hepcidin production and iron status in active individuals. Methods Ten active males participated in this study [age = 24 ± 1 y, body mass = 70.5 ± 3.2 kg, stature = 175.9 ± 2.6 cm, running peak oxygen

uptake (VO2peak) = 58.0 ± 2.0 ml.kg−1.min−1, cycling VO2peak = 49.7 ± 1.8 ml.kg−1.min−1]. At the time of recruitment, participants were performing a minimum of three exercise training sessions per week. The sample size was determined via customised computer software (GPOWER Version 2, Department of Psychology, Bonn University, Bonn, Germany) using effect sizes (ES) attained from similar research [3–7, 18]. A sample size of 10 was recommended to yield a power of 0.90 at a significance level of p ≤ 0.05. When recruited, all participants had a healthy iron status (serum ferritin = 79.3 ± 15.0 μg.L−1, transferrin saturation = 33 ± 3%), and were not taking any iron supplements. Prior to participation, written consent was obtained with approval granted by the Human Ethics Committee of The University of Western Australia (RA/4/1/5636).

Comments are closed.