Search Results

You are looking at 1 - 10 of 24 items for :

  • Refine by Access: All Content x
Clear All
Restricted access

Nikita C. Fensham, Alannah K.A. McKay, Nicolin Tee, Bronwen Lundy, Bryce Anderson, Aimee Morabito, Megan L.R. Ross, and Louise M. Burke

gastrointestinal micro-ischemia, sweat, hemolysis, and hematuria ( Peeling et al., 2008 ). However, reduced bioavailability of dietary iron and iron recycling are also involved ( Sim et al., 2019 ) with the hormone hepcidin playing a major role in these processes. Hepcidin regulates iron flux by binding to the

Open access

Alannah K.A. McKay, Peter Peeling, David B. Pyne, Nicolin Tee, Marijke Welveart, Ida A. Heikura, Avish P. Sharma, Jamie Whitfield, Megan L. Ross, Rachel P.L. van Swelm, Coby M. Laarakkers, and Louise M. Burke

-regulatory hormone, hepcidin. This hormone regulates iron metabolism by internalizing ferroportin ( Nemeth et al., 2004b ), which impedes the absorption of iron from the gut and recycling of iron by macrophages. Hepcidin activity can be directly upregulated by the inflammatory cytokine interleukin-6 (IL-6; Nemeth

Restricted access

Alannah K. A. McKay, Ida A. Heikura, Louise M. Burke, Peter Peeling, David B. Pyne, Rachel P.L. van Swelm, Coby M. Laarakkers, and Gregory R. Cox

concentrations of the inflammatory cytokine interleukin-6 (IL-6) ( Hennigar et al., 2017 ), which may have downstream implications for the iron-regulatory hormone hepcidin ( Badenhorst et al., 2015 ). Adherence to a low-CHO diet (3 g/kg) for 24 hr can amplify the immediate postexercise IL-6 and the 3-hr

Restricted access

Claire E. Badenhorst, Katherine E. Black, and Wendy J. O’Brien

in isolation to diagnose LEA and that support from a biological marker may be beneficial in monitoring and detecting early changes to EA at an individual level ( Burke et al., 2018c ). One such potential marker is hepcidin, a 25 amino acid peptide hormone commonly recognized as the primary regulator

Restricted access

Alannah K.A. McKay, Rachel McCormick, Nicolin Tee, and Peter Peeling

, hemoglobin mass is positively associated with aerobic capacity (VO 2 max) ( Saunders et al., 2013 ), and therefore, the link between iron and red blood cell production becomes extremely important to support hematological adaptation in athletes. The primary regulator of systematic iron homeostasis is hepcidin

Restricted access

Alannah K.A. McKay, Marc Sim, Diego Moretti, Rebecca Hall, Trent Stellingwerff, Richard J. Burden, and Peter Peeling

, 1996 ), and from the hemolysis of RBCs from repetitive foot strike ( Miller et al., 1988 ), and/or compression of blood vessels by skeletal muscle during exercise ( Selby & Eichner, 1986 ). However, it was the discovery of hepcidin at the start of the 21st century ( Park et al., 2001 ), and its

Restricted access

Mia K. Newlin, Sara Williams, Tim McNamara, Harold Tjalsma, Dorine W. Swinkels, and Emily M. Haymes

Purpose:

To investigate the effects of acute exercise on serum hepcidin and iron (sFe) in active women. Changes in interleukin-6 (IL-6), hepcidin, ferritin, and sFe in response to 2 different exercise durations were compared.

Methods:

Twelve women age 19–32 yr performed 2 treadmill runs (60 and 120 min) at 65% of VO2max. Blood samples were obtained before, immediately after, and 3, 6, 9, and 24 hr after exercise. Two-way repeatedmeasures ANOVA was conducted to examine changes in measured variables. Significance was accepted at p < .05.

Results:

Significant effects for trial were observed for hepcidin (60 min: 1.15 ± 0.48 nmol/L; 120 min: 2.28 ± 1.44 nmol/L) and for time, with hepcidin significantly increased 3 hr postexercise in both trials (60 min: 3 hr – 1.99 ± 2.00 nmol/L; 120 min: 3 hr – 4.60 ± 4.61 nmol/L). Significant main effects for time occurred for sFe, ferritin, and IL-6. sFe was significantly decreased 9 hr postexercise compared with 3 and 24 hr postexercise. IL-6 was significantly increased immediately postexercise.

Conclusions:

Both runs resulted in significant increases in hepcidin 3 hr after exercise. Increases in hepcidin were preceded by significant increases in IL-6 immediately postexercise and followed by significant decreases in sFe 9 hr postexercise. It was concluded that endurance exercise increases the production of hepcidin, which affects sFe. The 2-hr exercise bout stimulated greater changes in serum hepcidin than the 1-hr bout.

Restricted access

Xiaoya Ma, Kaitlyn J. Patterson, Kayla M. Gieschen, and Peter F. Bodary

The prevalence of iron deficiency tends to be higher in athletic populations, especially among endurancetrained females. Recent studies have provided evidence that the iron-regulating hormone hepcidin is transiently increased with acute exercise and suggest that this may contribute to iron deficiency anemia in athletes. The purpose of this study was to determine whether resting serum hepcidin is significantly elevated in highly trained female distance runners compared with a low exercise control group. Due to the importance of the monocyte in the process of iron recycling, monocyte expression of hepcidin was also measured. A single fasted blood sample was collected midseason from twenty female distance runners averaging 81.9 ± 14.2 km of running per week. Ten age-, gender-, and BMI-matched low-exercise control subjects provided samples during the same period using identical collection procedures. There was no difference between the runners (RUN) and control subjects (CON) for serum hepcidin levels (p = .159). In addition, monocyte hepcidin gene expression was not different between the two groups (p = .635). Furthermore, no relationship between weekly training volume and serum hepcidin concentration was evident among the trained runners. The results suggest that hepcidin is not chronically elevated with sustained training in competitive collegiate runners. This is an important finding because the current clinical conditions that link hepcidin to anemia include a sustained elevation in serum hepcidin. Nevertheless, additional studies are needed to determine the clinical relevance of the well-documented, transient rise in hepcidin that follows acute sessions of exercise.

Restricted access

Peter Peeling, Brian Dawson, Carmel Goodman, Grant Landers, Erwin T. Wiegerinck, Dorine W. Swinkels, and Debbie Trinder

Urinary hepcidin, inflammation, and iron metabolism were examined during the 24 hr after exercise. Eight moderately trained athletes (6 men, 2 women) completed a 60-min running trial (15-min warm-up at 75–80% HRpeak + 45 min at 85–90% HRpeak) and a 60-min trial of seated rest in a randomized, crossover design. Venous blood and urine samples were collected pretrial, immediately posttrial, and at 3, 6, and 24 hr posttrial. Samples were analyzed for interleukin-6 (IL-6), C-reactive protein (CRP), serum iron, serum ferritin, and urinary hepcidin. The immediate postrun levels of IL-6 and 24-hr postrun levels of CRP were significantly increased from baseline (6.9 and 2.6 times greater, respectively) and when compared with the rest trial (p ≤ .05). Hepcidin levels in the run trial after 3, 6, and 24 hr of recovery were significantly greater (1.7–3.1 times) than the pre- and immediate postrun levels (p ≤ .05). This outcome was consistent in all participants, despite marked variation in the magnitude of rise. In addition, the 3-hr postrun levels of hepcidin were significantly greater than at 3 hr in the rest trial (3.0 times greater, p ≤ .05). Hepcidin levels continued to increase at 6 hr postrun but failed to significantly differ from the rest trial (p = .071), possibly because of diurnal influence. Finally, serum iron levels were significantly increased immediately postrun (1.3 times, p ≤ .05). The authors concluded that high-intensity exercise was responsible for a significant increase in hepcidin levels subsequent to a significant increase in IL-6 and serum iron.

Restricted access

Yu-Qian Liu, Yan-Zhong Chang, Bin Zhao, Hai-Tao Wang, and Xiang-Lin Duan

Some athletes are diagnosed as suffering from sports anemia because of iron deficiency, but the regulatory mechanism remains poorly understood. It is reported that hepcidin may provide a way to illuminate the regulatory mechanism of exercise-associated anemia. Here the authors investigate the hepcidin-involved iron absorption in exercise-associated anemia. Twelve male Wistar rats (300 ± 10 g) were randomly divided into 2 groups, 6 in a control group (CG) and 6 in an exercise group (EG, 5 wk treadmill exercise of different intensities with progressive loading). Serum samples were analyzed for circulating levels of IL-6 by means of enzyme-linked immunosorbent assay (ELISA). The expression of hepatic hepcidin mRNA was examined by real-time polymerase chain reaction analysis. The protein levels of divalent metal transporter 1 (DMT1), ferroportin1 (FPN1), and heme-carrier protein 1 (HCP1) of duodenum epithelium were examined by Western blot. The results showed that the amount of iron and ferritin in serum were lower in EG than in CG (p < .05). The levels of IL-6 and white blood cells were greater in EG than in CG (p < .01). The expression of DMT1, HCP1, and FPN1 was significantly lower in EG than in CG (p < .01). The mRNA expressions of hepatic hepcidin and hemojuvelin in skeletal muscle were remarkably higher in EG than in CG. The data indicated that inflammation was induced by strenuous exercise, and as a result, the transcriptional level of the hepatic hepcidin gene was increased, which further inhibited the expression of iron-absorption proteins and led to exercise-associated anemia.