Deficiencies in iron and vitamin D are frequently observed in athletes. Therefore, we examined whether different baseline vitamin D₃ levels have any impact on post-exercise serum hepcidin, IL-6 and iron responses in ultra-marathon runners. In this randomized control trial, the subjects (20 male, amateur runners, mean age 40.75 ± 7.15 years) were divided into two groups: experimental (VD) and control (CON). The VD group received vitamin D₃ (10,000 UI/day) and the CON group received a placebo for two weeks before the run. Venous blood samples were collected on three occasions—before the run, after the 100 km ultra-marathon and 12 h after the run—to measure iron metabolism indicators, hepcidin, and IL-6 concentration. After two weeks of supplementation, the intervention group demonstrated a higher level of serum 25(OH)D than the CON group (27.82 ± 5.8 ng/mL vs. 20.41 ± 4.67 ng/mL; p < 0.05). There were no differences between the groups before and after the run in the circulating hepcidin and IL-6 levels. The decrease in iron concentration immediately after the 100-km ultra-marathon was smaller in the VD group than CON (p < 0.05). These data show that various vitamin D₃ status can affect the post-exercise metabolism of serum iron.

Acute kidney injury (AKI) is described as a relatively common complication of exercise. In clinical practice the diagnosis of AKI is based on serum creatinine, the level of which is dependent not only on glomerular filtration rate but also on muscle mass and injury. Therefore, the diagnosis of AKI is overestimated after physical exercise. The aim of this study was to determine changes in uremic toxins: creatinine, urea, uric acid, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), trimethylamine N-oxide (TMAO) and urinary makers of AKI: albumin, neutrophil gelatinase-associated lipocalin (uNGAL), kidney injury molecule-1 and cystatin-C (uCyst-C) after long runs. Sixteen runners, mean age 36.7 ± 8.2 years, (2 women, 14 men) participating in 10- and 100-km races were studied. Blood and urine were taken before and after the races to assess markers of AKI. A statistically significant increase in creatinine, urea, uric acid, SDMA and all studied urinary AKI markers was observed. TMAO and ADMA levels did not change. The changes in studied markers seem to be a physiological reaction, because they were observed almost in every runner. The diagnosis of kidney failure after exercise is challenging. The most valuable novel markers which can help in post-exercise AKI diagnosis are uCyst-C and uNGAL.

Wołyniec, W, Ratkowski, W, Kasprowicz, K, Jastrzębski, Z, Małgorzewicz, S, Witek, K, Grzywacz, T, Żmijewski, P, and Renke, M. Glomerular filtration rate is unchanged by ultramarathon. J Strength Cond Res 32(11): 3207–3215, 2018—Acute kidney injury (AKI) is reported as a common complication of marathon and ultramarathon running. In previous studies, AKI was diagnosed on the basis of the creatinine level in serum and estimated glomerular filtration rate (eGFR). In this study, we calculated eGFR and also measured creatinine clearance after every 25 km of a 100-km run. Twenty healthy, amateur runners (males, mean age 40.75 ± 7.15 years, mean body mass 76.87 ± 8.39 kg) took part in a 100-km run on a track. Blood and urine were collected before the run, after every 25 km, and 12 hours after the run. Seventeen runners completed the study. There was increase in creatinine, urea, and uric acid observed after 100 km (p < 0.05). The mean increase in creatinine was 0.21 mg·dl⁻¹ (24.53%). Five runners fulfilled the AKI network criteria of AKI. The eGFR according to the modification of diet in renal disease, chronic kidney disease epidemiology collaboration, and Cockcroft-Gault formulas was significantly decreased after the run (p ≤ 0.05). Otherwise, creatinine clearance calculated from creatinine level in both serum and urine remained stable. In contrast to the majority of previous studies, we did not observe any decrease in the kidney function during an ultramarathon. In this study, the creatinine clearance, which is the best routine laboratory method to determine GFR was used. There is no evidence that long running is harmful for kidney.

Background and Aims: Urinary neutrophil gelatinase associated lipocalin (uNGAL) and urinary kidney injury molecule-1 (uKIM-1) are markers of acute kidney injury. The albuminuria is a well-known abnormality after physical exercise. The aim of this study was to investigate changes in uNGAL and uKIM-1 after intensive exercise causing albuminuria. Methods: The study population consisted of 19 participants (10 males and 9 females). The mean age of participants was 35.74 years. All were fit amateur runners; the mean body mass index was 21.99 in females and 24.71 in males. The subjects underwent a graded treadmill exercise test (GXT) according to the Bruce protocol. Maximal oxygen consumption (VO₂max) was measured. Immediately before and after the test urine was collected. Urinary creatinine, albumin, NGAL, and KIM-1 were measured. Albumin to creatinine (ACR), KIM-1 to creatinine (KCR), and NGAL to creatinine (NCR) ratios were calculated. Results: The mean VO₂max was 53.68 in females and 59.54 mL/min/kg in males. Albuminuria and ACR were significantly higher after exercise. An increase in the ACR from 8.82 to 114.35 mg/g (p < 0.01) was observed. uKIM-1 increased significantly after exercise from 849.02 to 1,243.26 pg/mL (p < 0.05). KCR increased from 1,239.1 to 1,725.9 ng/g but without statistical significance (p = 0.07). There were no statistical changes in pre- and post-run uNGAL levels. There was no correlation between post-GXT albuminuria and uKIM-1. Conclusions: uKIM-1 is a very sensitive marker of kidney dysfunction. In our study, uKIM-1 increased significantly after a very short period of exercise. It is not clear if the increase in KIM-1 is caused by post-exercise albuminuria.