Objectives: The objective of the study was to reveal morphology, electrolyte and chosen biochemical parameters in terms of health risk in runners in reference to their age and running speed in the case of running a distance of 100 km, which occur after 12 h or 24 h of recovery. Material and Methods: Fourteen experienced, male, amateur, ultra-marathon runners, divided into two age and two speed groups took part in the 100-km run. Blood samples for analyses indexes were collected from the ulnar vein just before the run, after 25 km, 50 km, 75 km and 100 km, as well as 12 h and 24 h after termination of the run. Results: The sustained ultramarathon run along with the distance covered (p < 0.05) caused an increase in myoglobin (max 90-fold), bilirubin (max 2.8-fold) and total antioxidant status (max 1.15-fold), which also continued during the recovery. Significant changes in the number of white blood cells were observed with each sequential course and could be associated with muscle damage. The electrolyte showed changes towards slight hyperkalemia, but no changes in natrium and calcium concentrations. There were no significant differences between the age and speed groups for all the parameters after completing the 100-km run as well as after 12 h and 24 h of recovery. Conclusions: Considering changes in blood morphology and chosen biochemical parameters in ultra-marathon runners during a 100-km run it can be stated that such an exhausting effort may be dangerous for human health due to metabolic changes and large damage to the organs. Negative metabolic changes are independent of age of an ultramarathon runner and occur both in younger (32±5.33 years) and older participants (50.56±9.7 years). It can be concluded that organ damage and negative metabolic changes during a 100-km run occur similarly in participants less experienced as well as in well trained runners. Int J Occup Med Environ Health 2016;29(5):801-814
BackgroundThe aim of the present study was to investigate the effect of a single bout of mild exercise on autonomic nervous system activity in healthy subjects. Methods and ResultsThe study group comprised 18 healthy males, aged between 20 and 24 years, who had not been training regularly for the last 3 months. A supine recording of systolic arterial pressure (SAP) and RR interval and the administration of the phenylephrine test were performed at baseline and repeated after a 60-min recovery period following treadmill exercise training for 30 min at 65% of maximal heart rate. Mean SAP and RR interval, heart rate variability (HRV) indices (the standard deviation of normal-to-normal RR intervals (SDNN), the square root of the mean of squared differences between successive intervals and the percentage of adjacent RR intervals differing more than 50 ms), noninvasive spectral baroreflex sensitivity (Spe-BRS) and phenylephrine baroreflex sensitivity (Phe-BRS) were assessed before and after training. Mean SAP measured after exercise was lower than baseline (120±12 mmHg vs 128±12 mmHg, p=0.05). Spe-BRS and Phe-BRS increased significantly after exercise, from 11.8±6.1 ms/mmHg to 16.0±7.8 ms/mmHg (p=0.034), and from 16.0±8.8 ms/mmHg to 21.9±9.3 ms/mmHg (p=0.022), respectively. A parallel increase was also observed in SDNN (from 81±44 ms to 96±53 ms, p=0.02), but the other HRV indices showed no significant differences between pre-and post-exercise. Conclusions A single session of mild exercise performed by sedentary young men leads to significant autonomic nervous system improvement, which suggests that even mild physical activity is beneficial for neural cardiac regulation and should be recommended to sedentary healthy subjects. (Circ J 2005; 69: 976 -980)
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.
The aim of the present study was to analyse VEGFA rs699947, rs1570360, and rs2010963 polymorphisms with susceptibility to anterior cruciate ligament rupture (ACLR) in a Polish population. The study included 412 physically active Caucasian participants. The study group consisted of 222 individuals with surgically diagnosed primary ACLR qualified for ligament reconstruction (ACLR group). The control group consisted of 190 apparently healthy participants without any history of ACLR (CON group). Three polymorphisms within the VEGFA (rs699947, rs1570360, and rs2010963) gene were chosen for investigation due to their significance in the angiogenesis signalling pathway and previous associations with risk of ACLRs. Both single-locus and haplotype-based analyses were conducted. No significant differences in the allele and genotype frequency distributions were noted for the rs699947 and rs1570360 polymorphisms. In contrast, rs2010963 was associated with risk of ACLR in the codominant (p=0.047) and recessive model (p=0.017). In the latter, the CC genotype was overrepresented among individuals with ACL rupture (23.4% vs 14.2%, OR=1.85 [1.11-3.08]). Two VEGFA haplotypes were associated with ACLR under the additive (global score=11.39, p=0.022) and dominant model (global score=11.61, p=0.020). The [C;G;G] haplotype was underrepresented in the ACLR group (52.2% vs. 60.3%), whereas the [C;G;C] haplotype was overrepresented (2.9% vs 0.5%). The results obtained suggest a potential correlation between the VEGFA rs2010963 polymorphism and ACLR risk, suggesting that harbouring this specific C allele may be an unfavourable risk factor for a knee injury in Caucasian participants from Poland.
More than 100 substances have been identified as biomarkers of acute kidney injury. These markers can help to diagnose acute kidney injury (AKI) in its early phase, when the creatinine level is not increased. The two markers most frequently studied in plasma and serum are cystatin C and neutrophil gelatinase-associated lipocalin (NGAL). The former is a marker of kidney function and the latter is a marker of kidney damage. Some other promising serum markers, such as osteopontin and netrin-1, have also been proposed and studied. The list of promising urinary markers is much longer and includes cystatin C, NGAL, kidney injury molecule-1 (KIM-1), liver-type fatty-acid-binding protein (L-FABP), interleukin 18, insulin-like growth factor binding protein 7 (IGFBP-7), tissue inhibitor of metalloproteinases-2 (TIMP-2) and many others. Although these markers are increased in urine for no longer than a few hours after nephrotoxic agent action, they are not widely used in clinical practice. Only combined IGFBP-7/TIMP-2 measurement was approved in some countries as a marker of AKI. Several studies have shown that the levels of urinary AKI biomarkers are increased after physical exercise. This systematic review focuses on studies concerning changes in new AKI biomarkers in healthy adults after single exercise. Twenty-seven papers were identified and analyzed in this review. The interpretation of results from different studies was difficult because of the variety of study groups, designs and methodology. The most convincing data concern cystatin C. There is evidence that cystatin C is a better indicator of glomerular filtration rate (GFR) in athletes after exercise than creatinine and also at rest in athletes with a lean mass lower or higher than average. Serum and plasma NGAL are increased after prolonged exercise, but the level also depends on inflammation and hypoxia; therefore, it seems that in physical exercise, it is too sensitive for AKI diagnosis. It may, however, help to diagnose subclinical kidney injury, e.g., in rhabdomyolysis. Urinary biomarkers are increased after many types of exercise. Increases in NGAL, KIM-1, cystatin-C, L-FABP and interleukin 18 are common, but the levels of most urinary AKI biomarkers decrease rapidly after exercise. The importance of this short-term increase in AKI biomarkers after exercise is doubtful. It is not clear if it is a sign of mild kidney injury or physiological metabolic adaptation to exercise.
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.
Various forms of 2-month physical training led to a favourable shift in autonomic balance towards parasympathetic activity. Our findings suggest a clinically important effect of physical activity in patients after AMI.
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 glomerular filtration rate was used. There is no evidence that long running is harmful for kidney.
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