Abstract: TH-PO519
Acute and Chronic Effects of Different Exercise Modalities on Hepcidin Levels in Non-Dialysis CKD
Session Information
- CKD: Clinical Trials and Tubulointerstitial Disorders
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Chronic Kidney Disease (Non-Dialysis)
- 305 CKD: Clinical Trials and Tubulointerstitial Disorders
Authors
- Xenophontos, Soteris, University of Leicester, Leicester, United Kingdom
- Gould, Douglas W., University of Leicester, Leicester, United Kingdom
- Wilkinson, Thomas James, University of Leicester, Leicester, United Kingdom
- Watson, Emma L., University of Leicester, Leicester, United Kingdom
- Viana, Joao L., University Institute of Maia, Maia, Portugal
- Smith, Alice C., University of Leicester, Leicester, United Kingdom
Background
Functional iron deficiency (FID) is common in chronic kidney disease (CKD). Iron is essential for many cellular processes including energy generation. FID has negative effects on skeletal and cardiac muscle as well as haemoglobin (Hb) production, and contributes to anaemia, functional deficits, fatigue and cardiovascular (CV) risk. Hepcidin, which is upregulated by inflammatory cytokines and inhibits release of iron stores, is implicated in CKD FID due to chronic inflammation and reduced renal clearance. We have previously shown that regular exercise exerts anti-inflammatory effects in CKD. In this study, we investigated the effects of different exercise modalities on hepcidin levels in non-dialysis CKD.
Methods
36 CKD patients (14 male, mean±SD age 61±12 years, eGFR 26±8 ml.min-1.1.73m-2, Hb 119±15 g/l) were randomised to 12 weeks thrice weekly aerobic exercise (AE, n=18) or combined aerobic and resistance exercise (CE, n=18). Plasma was collected to assess the chronic effects of exercise (resting samples at baseline and end of study) and the acute effects (collected 24h following the first and last exercise sessions). Hepcidin was measured by ELISA.
Results
Following 12 weeks training, resting hepcidin decreased by 21±35% (p=.037) in the CE group, but was unchanged in the AE group (1±50%, p=.976). Acutely, 24h after the first exercise session hepcidin decreased by 34±27% (p=.008) in the CE group and by 18±24% (p=.101) in the AE group. 24h after the final exercise session hepcidin decreased by 3±42% (p=.438) in the CE group and by 0±27% (p=.651) in the AE group, compared to resting levels.
Conclusion
CE training reduced resting plasma hepcidin, but there was no change with AE alone. An acute reduction in hepcidin was observed 24h after the first CE session, but not after the first AE session or in either group after the last session, indicating an adaptation effect of regular CE. Hepatic hepcidin release is stimulated by IL-6, which peaks after unaccustomed exertion but is reduced by regular exercise. Therefore, our results likely mirror the effects of exercise on circulating inflammatory cytokines. CE may ameliorate FID in CKD, thereby helping to reduce CV and anaemia risk, and improve muscle function and fatigue.
Funding
- Private Foundation Support