Impact of hydration with beverages containing free sugars or xylitol on metabolic and acute kidney injury markers after physical exercise.

The proper fluid and carbohydrates intake is essential before and during physical exercise, and for this reason most athletes drink beverages containing a high amount of free sugars. Sweetened soft drinks are also commonly consumed by those not doing any sport, and this habit seems to be both unhealthy and also the cause of metabolic problems. Recently, several sweeteners have been proposed to replace sugars in popular beverages. To examine the impact of free sugars and the popular sweetener xylitol on metabolic profile and the markers of kidney function and injury after exercise the present study was conducted with semi-professional football players. All participants were healthy, with a mean age of 21.91 years. Their sports skills were on the level of the 4th-5th division of the league. The subjects took part in four football training sessions. During each session they drank a 7% solution of sugar (sucrose, fructose, glucose) or xylitol. The tolerability of these beverages and well-being during exercise was monitored. Before and after each training session, blood and urine were collected. The markers of kidney function and injury, uric acid, electrolytes, complete blood count, CRP, serum albumin, serum glucose and the lipid profile were analyzed. The main finding of this study was that the xylitol beverage is the least tolerated during exercise and 38.89% of participants experienced diarrhea after training and xylitol intake. Xylitol also led to unfavorable metabolic changes and a large increase in uric acid and creatinine levels. A mean increase of 1.8 mg/dl in the uric acid level was observed after xylitol intake. Increases in acute kidney injury markers were observed after all experiments, but changes in urine albumin and cystatin C were highest after xylitol. The other three beverages (containing "free sugars" - glucose, fructose and sucrose) had a similar impact on the variables studied, although the glucose solution seems to have some advantages over other beverages. The conclusion is that sweeteners are not a good alternative to sugars, especially during exercise. Pure water without sweeteners should be drunk by those who need to limit their calorie consumption. Clinical Trial Registration: ClinicalTrials.gov, (NCT04310514).

The Effect of Vitamin D3 Supplementation on Hepcidin, Iron, and IL-6 Responses after a 100 km Ultra-Marathon.

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.

Factors influencing post-exercise proteinuria after marathon and ultramarathon races.

Post-exercise proteinuria is one of the most common findings observed after short and intensive physical activity, but is observed also after long runs with low intensity. The aim of this study was to analyze factors influencing proteinuria after marathon runs. Two groups of male amateur runners were studied. The results of 20 marathon finishers (42.195 m), with a mean age of 49.3 ± 6.85 years; and 17 finishers of a 100-km ultramarathon with a mean age of 40.18±4.57 years were studied. Urine albumin to creatinine ratio (ACR) was calculated before and after both races. The relationship between ACR and run pace, metabolites (lactate, beta hydroxybutyrate), markers of inflammation (CRP, IL-6) and insulin was studied. The significant increase in ACR was observed after both marathon races. ACR increased from 6.41 to 21.96 mg/g after the marathon and from 5.37 to 49.64 mg/g after the ultramarathon (p<0.05). The increase in ACR was higher after the ultramarathon that after the marathon. There was no correlation between run pace and proteinuria. There was no correlation between ACR and glucose, free fatty acids, lactate, beta-hydroxybutyrate and insulin levels. There was significant negative correlation between ACR and interleukin 6 (IL-6) (r =-0.59, p< 0.05) after ultramarathon. Proteinuria is a common finding after physical exercise. After very long exercises it is related to duration but not to intensity. There is no association between metabolic and hormonal changes and ACR after marathon runs. The role on inflammatory cytokines in albuminuria is unclear.

Changes in Water Soluble Uremic Toxins and Urinary Acute Kidney Injury Biomarkers After 10- and 100-km Runs.

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.

Biochemical Markers of Renal Hypoperfusion, Hemoconcentration, and Proteinuria after Extreme Physical Exercise.

Background and Objectives: Physical exercise increases the blood perfusion of muscles, but decreases the renal blood flow. There are several markers of renal hypoperfusion which are used in the differential diagnosis of acute kidney failure. Albuminuria is observed after almost any exercise. The aim of this study was to assess changes in renal hypoperfusion and albuminuria after a 100-km race. Materials and Methods: A total of 27 males who finished a 100-km run were studied. The mean age of the runners was 38.04 ± 5.64 years. The exclusion criteria were a history of kidney disease, glomerular filtration rate (GFR) <60 ml/min, and proteinuria. Blood and urine were collected before and after the race. The urinary albumin/creatinine ratio (ACR), fractional excretion of urea (FeUrea) and sodium (FeNa), plasma urea/creatinine ratio (sUrea/Cr), urine/plasma creatinine ratio (u/pCr), urinary sodium to potassium ratio (uNa/K), and urinary potassium to urinary potassium plus sodium ratio (uK/(K+Na)) were calculated. Results: After the race, significant changes in albuminuria and markers of renal hypoperfusion (FeNa, FeUrea, sUrea/Cr, u/sCr, urinary Na, uNa/K, uK/(K+Na)) were found. Fifteen runners (55.56%) had severe renal hypoperfusion (FeUrea <35, uNa/K <1, and uK/(Na+K) >0.5) after the race. The mean ACR increased from 6.28 ± 3.84 mg/g to 48.43 ± 51.64 mg/g (p < 0.001). The ACR was higher in the group with severe renal hypoperfusion (59.42 ± 59.86 vs. 34.68 ± 37.04 mg/g), but without statistical significance. Conclusions: More than 50% of the runners had severe renal hypoperfusion after extreme exercise. Changes in renal hemodynamics are probably an important, but not the only, factor of post-exercise proteinuria.

Glomerular Filtration Rate Is Unchanged by Ultramarathon.

Wolyniec, W, Ratkowski, W, Kasprowicz, K, Jastrzebski, Z, Malgorzewicz, S, Witek, K, Grzywacz, T, Zmijewski, 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 (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.

Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise.

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.

Do high blood hepcidin concentrations contribute to low ferritin levels in young tennis players at the end of tournament season?

The purpose of the present study was to verify whether impaired iron metabolism in young athletes is a consequence of an excessive workload during the tournament season. Low levels of ferritin (under 25 µg·L(-1)) have been frequently observed in young tennis players. We considered this finding to be related to the high-intensity workload or to insufficient rest, which both trigger a strong immune response. Groups of male, well-trained young tennis players (16 ± 0.9 years old, average of 10-year training experience) and a control peer group participated in this study. The research consisted of two examination sessions (March and September 2010). Blood samples were collected to determine haematological and immunological parameters. Additionally, body composition and physical capacity were assessed. In both periods of the study, the trained groups were characterised by low levels of ferritin, but also elevated levels of pro- inflammatory cytokine IL-1ß. Moreover, an inverse correlation between IL-1ß and blood ferritin was observed. Additionally, an increased concentration of the iron homeostasis regulator hepcidin was found in blood samples (mean 71 ng·ml(-1); range from 48 to 100 ng·ml(-1)). We concluded that the pro- inflammatory cytokine IL-1ß, most likely induced by an extensive workload during the tournament season, was responsible for the low level of ferritin in young, professional athletes. Key PointsThe first research demonstrating low grade inflammation-induced iron deficiency to be associated with elevated blood hepcidin levels in young tennis athletes.Evaluation of immunological response after the complete tournament season in young male tennis players.Conclusion to introduce the assessment of hepcidin to monitor trainings as well as symptoms of overreaching more effectively.Research providing practical information for coaches that changes in diet and modifications in workloads applied in physical training could be more effective than iron supplementation in iron deficient athletes.

Repeated "all out" interval exercise causes an increase in serum hepcidin concentration in both trained and untrained men.

This investigation assessed effects of high-intensity interval exercise (HIE; triple Wingate anaerobic test) on inflammatory markers, iron metabolism and hepcidin concentrations. Group of highly trained judo athletes (TR) and non-trained control males (CG) completed a triple Wingate test separated by 4.5min rest. Venous blood samples were collected before, immediately after, 1h, 24h, and 5days following exercise and analysed for serum of IL-6, IL-10, iron, and ferritin. Physiological response to exercise was also determined. Concentration of IL-6 and hepcidin increased 1h after exercise in both groups (p<0.05). Hepcidin returned post testing 24h in TR, whereas in CG it remained elevated during 5days following exercise. Changes in hepcidin did not correlate with shifts in serum IL-6, iron and ferritin concentrations. Gathered data suggest that following HIE, hepcidin increased independently of IL-6 and neither blood nor storage iron affected this phenomena.