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Serum Calprotectin, a Marker of Neutrophil Activation, and Other Mediators of Inflammation in Response to Various Types of Extreme Physical Exertion in Healthy Volunteers

Authors Niemelä M, Niemelä O, Bloigu R, Bloigu A, Kangastupa P, Juvonen T

Received 20 February 2020

Accepted for publication 1 May 2020

Published 22 May 2020 Volume 2020:13 Pages 223—231

DOI https://doi.org/10.2147/JIR.S250675

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Ning Quan


Markus Niemelä,1,2 Onni Niemelä,2 Risto Bloigu,3 Aini Bloigu,4 Päivikki Kangastupa,2 Tatu Juvonen1,5

1Department of Surgery, Oulu University Hospital, Oulu 90029, Finland; 2Department of Laboratory Medicine and Medical Research Unit, Seinäjoki Central Hospital and Tampere University, Seinäjoki 60220, Finland; 3Infrastructure for Population Studies, Faculty of Medicine, University of Oulu, Oulu 90014, Finland; 4Center for Life Course Health Research, University of Oulu, Oulu 90014, Finland; 5Department of Cardiac Surgery, Helsinki University Hospital, Helsinki 00029, Finland

Correspondence: Onni Niemelä Tel +358 50 474 4719
Email onni.niemela@epshp.fi

Purpose: While extreme physical exertion is known to induce changes in the status of inflammation comparisons of the responses for various mediators of inflammation after acute bouts of high-intensity exercise have been limited.
Subjects and Methods: We examined the responses in serum levels of novel inflammatory proteins, calprotectin, suPAR, CD163, and pro- and anti-inflammatory cytokines in 12 physically active volunteers (10 men, 2 women, mean age 37± 14 years) before and after completing various types of extreme physical exertion (marathon run, half-marathon run or 24-h cross-country skiing). For comparisons, the levels of the biomarkers were also measured at rest in 30 healthy controls (25 men, 5 women, mean age 42 ± 12 years) with low or sedentary activity.
Results: Extreme physical exertion induced significant increases in serum calprotectin (p < 0.0005), suPAR (p < 0.01), CD163 (p < 0.05), IL-6 (p < 0.0005), IL-8 (p < 0.01) and IL-10 (p < 0.0005) (pre- vs 3h-post-exercise). These responses were found to normalize within 48 hours. While the increases in blood leukocytes were of similar magnitude following the different types of exercise, markedly more pronounced responses occurred in serum TNF-α (p < 0.01), IL-8 (p < 0.01) and CD163 (p < 0.05) in those with more intense activity. In 3-h post-exercise samples significant correlations were observed between serum calprotectin and IL-6 (rs = 0.720, p < 0.01), IL-10 (rs = 0.615, p < 0.05), TNF-α (rs = 0.594, p < 0.05), suPAR (rs = 0.587, p < 0.05) and blood leukocytes (rs = 0.762, p < 0.01).
Conclusion: The present results suggest distinct exercise-intensity dependent changes in mediators of inflammation (including calprotectin, suPAR and CD163) following extreme physical exertion. Our findings indicate that there is a major reversible impact of high-intensity physical exertion on the status of inflammation.

Keywords: acute exercise, cytokine, immune status, leukocyte, oxidative stress
 

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