Expression levels of selected cytokines and microRNAs in response to vitamin D supplementation in ultra-marathon runners.

Ultra-marathon (UM) running is an extreme endurance exercise. However, the mechanisms triggered with its practice remain unclear. While it is documented that strenuous physical activity activates immune responses and vitamin D plays a role in immune system suppression, data on the relationship between vitamin D status and cytokine profile in athletic populations are limited. To analyse the relative mRNA expression levels of selected pro-inflammatory cytokines (IL-1ß, IL-6, IL-8, IL-17, TNF-α), COX-2, vitamin D receptor and abundance of selected inflammatory microRNAs (Hsa-miR-21, -miR-146a, -miR-150, -miR-155, -miR-222, -miR-223) before and after a 100 km race in amateur runners in the presence or absence of vitamin D supplementation. Twenty runners aged 36-40years were divided into two groups: with and without vitamin D3 supplementation (10,000units daily). Blood samples were collected before and 12 h after the UM. The mRNA expression levels of selected cytokines, COX-2 and VDR in peripheral blood and abundance of serum exosomal miRNAs were investigated using q-RT-PCR. After UM, the significant up-regulation of TNF-α and hsa-miR-155 and down-regulation of IL-1ß were observed in the group with vitamin D supplementation. In its absence, hsa-miR-155 and -miR-223 were significantly up-regulated. Additionally, a reverse correlation was observed between IL-6 expression level and abundance of hsa-miR-155 and -miR-223 in both groups. No statistical differences were noted when the other miRNAs and genes were examined in the groups and at the time points. The UM-induced mRNA expression pattern of pro-inflammatory cytokines could be influenced by vitamin D supplementation and/or miRNA.

Changes in electrolytes and uric acid excretion during and after a 100 km run.

Physical activity leads to changes in water and electrolyte homeostasis and to enhanced purine metabolism. The typical abnormalities observed after exercise are hyperkaliemia, hyper- or hyponatremia and hyperuricemia. The possible explanations of hyperuricemia are: increased metabolism and decreased elimination of uric acid. Changes in uric acid excretion are commonly observed in disturbances of sodium and water homeostasis. The aim of this study was to evaluate changes in electrolytes and uric acid excretion during a very long period of exercise. Twenty subjects with a mean age of 40.75±7.15 years took part in a 100 km run. The route of the run was based on the university stadium track. All subjects were experienced amateur runners, with a mean time of regular running of 6.11±7.19 years. Blood was collected before the start, after every 25 km and 12 hours after the run. The levels of electrolytes, creatinine, uric acid, cortisol, aldosterone, creatine kinase, C-reactive protein and interleukin-6 were measured. Creatinine clearance, urinary potassium-to-sodium ratio, fractional excretion of electrolytes and uric acid were calculated. Seventeen runners completed the study. Significant increases in sodium (from 141.65±1.90 to 144.29±3.65mmol/l), potassium (from 4.53±0.34 to 5.03±0.42mmol/l), creatinine (from 0.88±0.11 to 1.10±0.20mg/dl) and uric acid (from 5.15±0.87 to 5.94±1.50 mg/dl) were observed after 100 km (p less than 0.05). Other significant changes during the study were noted in fractional excretions of sodium (from 0.86±0.29 to 0.33±0.13%) and potassium (from 6.66±2.79 to 18.90±10.01%), probably reflecting the decrease in renal blood flow (RBF) and increase in renal tubule reabsorption. The fractional excretion of uric acid slightly increased but without statistical significance from 5.34±1.51 to 6.09±2.34%. The results of our study showed that during very long but not very intensive exercise there is no change in uric acid excretion, although at the same time profound changes in electrolyte excretion are found. Both hyperuricemia and hyperuricosuria may be harmful, therefore it seems logical that the best way to avoid those abnormalities is to maintain fractional uric acid excretion.

Changes in the acid-base balance and lactate concentration in the blood in amateur ultramarathon runners during a 100-km run.

The aim of this study was to analyse the acid-base balance and partial pressure of blood gases of participants during a 100-km run. Fourteen experienced amateur ultramarathon runners (age: 43.36±11.83 years; height: 175.29±6.98 cm; weight: 72.12±7.36 kg) completed the 100-km run. Blood samples were taken before the run; after 25, 50, 75, and 100 km; and 12 and 24 hours after the run. There were significant differences (p<0.05) between the mean values registered for acid-alkaline balance, buffering alkalies, and current bicarbonate in each segment of the run, especially during the third, fourth, and fifth segments of the run (i.e., between 50 and 100 km), and there were only significant differences associated with buffering alkalies and current bicarbonate during the recovery. However, all the changes were within the physiological norm. A significant decrease in the compressibility of oxygen was observed after 100 km (from 92.80±15.67 to 88.36±13.71 mmHg) and continued during the recovery to 75.06±8.60 mmHg 12 h after the run. Also there was a decrease in saturation to a mean value of 93.78±3.10 at 12 h after the run. Generally the amateurs runners are able to adjust their running speed so as not to provoke a significant acid-base imbalance or lactate acid accumulation.

Running a 100-km ultra-marathon induces an inflammatory response but does not raise the level of the plasma iron-regulatory protein hepcidin.

AIM: Exercise may induce an inflammatory response that may lead to changes in iron metabolism. The aim of this study was to examine the relationship between the inflammation induced by a 100 km run and the level of hepcidin, which is a hormone regulating iron metabolism. METHODS: Six males, age 44.5±13.5 years, running 100 km. SETTING: the CRP protein, IL-6 and leucocyte count were measured as an index of inflammation. RESULTS: A 100 km run caused a progressive increase in blood IL-6 concentration, which reached the highest values after 75 km. Furthermore, an increase in levels of CRP, a marker of inflammation, was observed after the 100 km run and continued to increase after a 14 h recovery period. Leucocyte number and markers of muscle damage were significantly elevated after the 100 km run. This was accompanied by a decrease in transferrin saturation and an increase in blood haemoglobin and ferritin. Despite all these changes, the 100 km race did not affect blood hepcidin concentration either during the run or after a 14 h recovery period. CONCLUSION: The study shows that a 100 km run induces an inflammatory response but does not trigger changes in the blood hepcidin level. Thus it can be concluded that changes in IL-6 are not sufficient to increase the blood hepcidin level in runners.