Leukocyte chemotactic cytokine and leukocyte subset responses during ultra-marathon running

Cytokine ◽  
2013 ◽  
Vol 61 (2) ◽  
pp. 364-369 ◽  
Author(s):  
Young Oh Shin ◽  
Jeong Beom Lee
Keyword(s):  
Marathon Running ◽  
Leukocyte Subset ◽  
Chemotactic Cytokine

Thermoregulatory responses during competitive marathon running

1977 ◽  
Vol 42 (6) ◽  
pp. 909-914 ◽  
Author(s):  
M. B. Maron ◽  
J. A. Wagner ◽  
S. M. Horvath
Keyword(s):  
Skin Temperature ◽  
Marathon Running ◽  
Heat Illness ◽  
Mean Skin Temperature ◽  
Total Water ◽  
Water Losses ◽  
Thermoregulatory Responses ◽  
Marked Disparity ◽  
Skin Temperatures ◽  
Cool Conditions

To assess thermoregulatory responses occuring under actual marathon racing conditions, rectal (Tre) and five skin temperatures were measured in two runners approximately every 9 min of a competitive marathon run under cool conditions. Race times and total water losses were: runner 1 = 162.7 min, 3.02 kg; runner 2 = 164.6 min, 2.43 kg. Mean skin temperature was similar throughout the race in the two runners, although they exhibited a marked disparity in temperature at individual skin sites. Tre plateaued after 35--45 min (runner 1 = 40.0--40.1, runner 2 = 38.9--39.2 degrees C). While runner 2 maintained a relatively constant level for the remainder of the race, runner 1 exhibited a secondary increase in Tre. Between 113 and 119 min there was a precipitous rise in Tre from 40.9 to 41.9 degrees C. Partitional calorimetric calculations suggested that a decrease in sweating was responsible for this increment. However, runner 1's ability to maintain his high Tre and running pace for the remaining 44 min of the race and exhibit no signs of heat illness indicated thermoregulation was intact.

The Effects of Psychological Stress on Leukocyte Subset Distribution in Humans: Evidence of Immune Activation

1999 ◽  
Vol 39 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Michael Maes ◽  
Dirk R. van Bockstaele ◽  
Ann Van Gastel ◽  
Cai Song ◽  
Chris Schotte ◽  
...  
Keyword(s):  
Psychological Stress ◽  
Immune Activation ◽  
Leukocyte Subset ◽  
Subset Distribution

Abstract 3259: Leukocyte Subset Specific Gene Expression In Acute Stroke Patients

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Mateusz G Adamski ◽  
Yan Li ◽  
Hua Yu ◽  
Erin Wagner ◽  
Sareen Amarjeet ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Stroke ◽  
Whole Blood ◽  
Peripheral Blood ◽  
Fold Increase ◽  
Specific Gene ◽  
Related Gene ◽  
Stroke Patients ◽  
Leukocyte Subset ◽  
Control Subjects

Background: Alterations in gene expression in the peripheral blood of patients with acute stroke have been demonstrated using microarray technology. Whole blood and peripheral blood mononuclear cells (PBMCs) were used in prior studies in which panels of genes diagnostic for stroke were developed. We aimed to determine the cellular sources of alterations in gene expression by studying individual leukocyte subsets. Methods: The expression of four genes previously found to be upregulated in ischemic and hemorrhagic stroke (IL1R2, S100A9, ETS2 and F5) was measured in four leukocyte subsets: CD14+ monocytes, CD4+ T cell lymphocytes, CD20+ B cell lymphocytes and PBMCs. These four genes had been reported in at least two of the previously published stroke-related gene panels. Peripheral blood was obtained from six acute stroke patients (all <48 hours from symptom onset) and 6 age, race and sex matched control subjects. Leukocytes were separated from whole blood using density gradient centrifugation and column magnetic bead cell sorting. The purity of separated leukocyte subsets exceeded 90% and was verified with flow cytometry. Messenger RNA was isolated from each leukocyte subset and analyzed by two step RT PCR and qPCR. The expression of the four stroke-related genes was compared to the expression of a housekeeping gene (GAPDH). The relative expression of individual genes and of the 4 gene panel within cellular subsets was compared between stroke patients and control subjects. Results: Individually, IL1R2 and S100A9 were significantly over-expressed in stroke patients with a 10 fold increase for IL1R2 in PBMCs (p<0.05) and a 3 fold increase for S100A9 in the CD4+ T and CD20+ B lymphocyte subsets (p<0.05). When analyzed as a panel of four genes the expression of IL1R2, S100A9, ETS2 and F5 was significantly higher in both the CD4+ T lymphocytes (p<0.05) and CD20+ B lymphocytes (p<0.05) of stroke patients but not in the monocytes or the PBMCs. Conclusion: These results show the potential diagnostic value of selected genes from panels previously found in microarray studies in stroke patients. They also emphasize the value of panel analysis over that of single gene expression and the potential cellular specificity of alterations in gene expression. Analysis of whole blood and PBMCs alone may not reflect important dynamic changes in stroke-related gene expression.

Effect of Marathon Running on Total and Free Serum Prostate-Specific Antigen Concentrations

2003 ◽  
Vol 127 (3) ◽  
pp. 345-348 ◽  
Author(s):  
Alexander Kratz ◽  
Kent B. Lewandrowski ◽  
Arthur J. Siegel ◽  
Patrick M. Sluss ◽  
Kelly Y. Chun ◽  
...  
Keyword(s):  
Prostate Specific Antigen ◽  
Specific Antigen ◽  
Physical Exertion ◽  
The United States ◽  
Marathon Running ◽  
Reliable Determination ◽  
Free Psa ◽  
Sporting Event ◽  
Exercise Induced ◽  
Total Psa

Abstract Context.—Prostate-specific antigen (PSA) is an important tumor marker for the most frequently diagnosed cancer in the United States. A major limitation of this marker is falsely elevated results in patients who are found not to have prostate cancer. The effects of vigorous physical exertion on PSA concentrations are controversial. Objective.—To determine the effects of marathon running on PSA levels. Design.—Measurement of total and free PSA levels in the sera of participants in a marathon before and within 4 and 24 hours after the race. Results.—None of the participants had elevated total PSA levels before the race. Although we found no statistically significant changes in average total or free PSA concentrations at either time point, after the marathon, 2 (11%) of 18 runners had total PSA concentrations outside the standard reference range. Changes in total PSA levels did not correlate with age or prerace PSA concentrations. Free PSA levels were not statistically significantly changed after the race and did not allow a reliable determination of exercise-induced PSA elevations. Conclusions.—Although it may not be necessary for men to abstain from exercise involving running before blood draws for PSA analysis, elevated PSA concentrations may be observed in some individuals after participation in a major sporting event. In these cases, repeat measurements should be considered at a time significantly removed from such exercise.

Cardiac Biomarkers Following Marathon Running: Is Running Time a Factor for Biomarker Change?

2020 ◽  
pp. 1-8
Author(s):  
Natthapon Traiperm ◽  
Rungchai Chaunchaiyakul ◽  
Martin Burtscher ◽  
Hannes Gatterer
Keyword(s):  
Cardiac Troponin ◽  
Troponin T ◽  
Transient Increase ◽  
Cardiac Biomarkers ◽  
Quadratic Model ◽  
Curvilinear Relationship ◽  
Marathon Running ◽  
Cardiac Troponin T ◽  
Running Time ◽  
Marathon Race

Purpose: Plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin T levels show a transient increase after marathon running. The aim of this study was to investigate whether running duration influences the patterns of changes in cardiac biomarkers. Methods: Twenty participants with fast and slow finishing times were included in the study. Blood samples were taken before the marathon race, immediately after, and 24 hours after the race. Samples were analyzed for NT-proBNP and cardiac troponin T concentration. Furthermore, a complete blood cell count was performed. Results: After the marathon race, the fast and slow runners showed similar changes of NT-proBNP and cardiac troponin T (ie, a transient increase). Curve estimation regression analysis showed a curvilinear relationship (quadratic model) between running times and NT-proBNP increments immediately after the race, with less of an increase in the very fast and the very slow runners (r2 = .359, P = .023). NT-proBNP increments immediately after the race were correlated to the decline 24 hours after the marathon (r = −.612, P = .004). Conclusions: This study indicates that NT-proBNP release immediately after marathon running varies in a curvilinear fashion with running time. It is speculated that low NT-proBNP release is associated with training adaptation in most elite runners and the relatively low cardiac stress in the slowest (but experienced) runners. The combination of less adaptation and relatively large cardiac wall and metabolic stress may explain the highest NT-proBNP values in runners with average running times. In addition, NT-proBNP decrements 24 hours after the race depend primarily on the values reached after the marathon and not on running time.

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