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Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms

BACKGROUND: During infections, polymorphonuclear neutrophilic granulocytes (PMN) are mobilized from their bone marrow stores, travel with blood to the affected tissue, and kill invading microbes there. The signal(s) from the inflammatory site to the marrow are unknown, even though a number of humora...

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Autores principales: Risøy, Bjørn Audun, Raastad, Truls, Hallén, Jostein, Lappegård, Knut T, Bæverfjord, Kjersti, Kravdal, Astrid, Siebke, Else Marie, Benestad, Haakon B
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC317276/
https://www.ncbi.nlm.nih.gov/pubmed/14667246
http://dx.doi.org/10.1186/1472-6793-3-14
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author Risøy, Bjørn Audun
Raastad, Truls
Hallén, Jostein
Lappegård, Knut T
Bæverfjord, Kjersti
Kravdal, Astrid
Siebke, Else Marie
Benestad, Haakon B
author_facet Risøy, Bjørn Audun
Raastad, Truls
Hallén, Jostein
Lappegård, Knut T
Bæverfjord, Kjersti
Kravdal, Astrid
Siebke, Else Marie
Benestad, Haakon B
author_sort Risøy, Bjørn Audun
collection PubMed
description BACKGROUND: During infections, polymorphonuclear neutrophilic granulocytes (PMN) are mobilized from their bone marrow stores, travel with blood to the affected tissue, and kill invading microbes there. The signal(s) from the inflammatory site to the marrow are unknown, even though a number of humoral factors that can mobilize PMN, are well known. We have employed a standardized, non-infectious human model to elucidate relevant PMN mobilizers. Well-trained athletes performed a 60-min strenuous strength workout of leg muscles. Blood samples were drawn before, during and just after exercise, and then repeatedly during the following day. Cortisol, GH, ACTH, complement factors, high-sensitive CRP (muCRP), IL-6, G-CSF, IL-8 (CXCL8) and MIP-1β (CCL4) were measured in blood samples. PMN chemotaxins in test plasma was assessed with a micropore membrane technique. RESULTS: About 5 hr after the workout, blood granulocytosis peaked to about 150% of baseline. Plasma levels of GH increased significantly 30 min into and 5 min after the exercise, but no increase was recorded for the other hormones. No significant correlation was found between concentrations of stress hormones and the subjects' later occurring PMN increases above their individual baselines. Plasma G-CSF increased significantly – but within the normal range – 65 min after the workout. IL-6 increased very slightly within the normal range, and the chemokines IL-8 and MIP-1β did not increase consistently. However, we found a significant increase of hitherto non-identified PMN-chemotactic activity in plasma 35, 50, and 60 min after the exercise. No systemic complement activation was detected, and (mu)CRP was within the reference range at rest, 5 h and 23 h after the exercise. After endurance exercise, similar findings were made, except for a cortisol response, especially from non-elite runners. CONCLUSION: Apparently, a multitude of humoral factors can – directly or indirectly – mobilize PMN from marrow to blood; some of the factors are, others are not known to be, chemotactic. Under different conditions, different selections of these mobilizers may be used. In the late granulocytosis after heavy, long-lasting exercise a number of factors thought capable of mimicking the granulocytosis of infectious diseases were apparently irrelevant.
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spelling pubmed-3172762004-01-23 Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms Risøy, Bjørn Audun Raastad, Truls Hallén, Jostein Lappegård, Knut T Bæverfjord, Kjersti Kravdal, Astrid Siebke, Else Marie Benestad, Haakon B BMC Physiol Research Article BACKGROUND: During infections, polymorphonuclear neutrophilic granulocytes (PMN) are mobilized from their bone marrow stores, travel with blood to the affected tissue, and kill invading microbes there. The signal(s) from the inflammatory site to the marrow are unknown, even though a number of humoral factors that can mobilize PMN, are well known. We have employed a standardized, non-infectious human model to elucidate relevant PMN mobilizers. Well-trained athletes performed a 60-min strenuous strength workout of leg muscles. Blood samples were drawn before, during and just after exercise, and then repeatedly during the following day. Cortisol, GH, ACTH, complement factors, high-sensitive CRP (muCRP), IL-6, G-CSF, IL-8 (CXCL8) and MIP-1β (CCL4) were measured in blood samples. PMN chemotaxins in test plasma was assessed with a micropore membrane technique. RESULTS: About 5 hr after the workout, blood granulocytosis peaked to about 150% of baseline. Plasma levels of GH increased significantly 30 min into and 5 min after the exercise, but no increase was recorded for the other hormones. No significant correlation was found between concentrations of stress hormones and the subjects' later occurring PMN increases above their individual baselines. Plasma G-CSF increased significantly – but within the normal range – 65 min after the workout. IL-6 increased very slightly within the normal range, and the chemokines IL-8 and MIP-1β did not increase consistently. However, we found a significant increase of hitherto non-identified PMN-chemotactic activity in plasma 35, 50, and 60 min after the exercise. No systemic complement activation was detected, and (mu)CRP was within the reference range at rest, 5 h and 23 h after the exercise. After endurance exercise, similar findings were made, except for a cortisol response, especially from non-elite runners. CONCLUSION: Apparently, a multitude of humoral factors can – directly or indirectly – mobilize PMN from marrow to blood; some of the factors are, others are not known to be, chemotactic. Under different conditions, different selections of these mobilizers may be used. In the late granulocytosis after heavy, long-lasting exercise a number of factors thought capable of mimicking the granulocytosis of infectious diseases were apparently irrelevant. BioMed Central 2003-12-11 /pmc/articles/PMC317276/ /pubmed/14667246 http://dx.doi.org/10.1186/1472-6793-3-14 Text en Copyright © 2003 Risøy et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
spellingShingle Research Article
Risøy, Bjørn Audun
Raastad, Truls
Hallén, Jostein
Lappegård, Knut T
Bæverfjord, Kjersti
Kravdal, Astrid
Siebke, Else Marie
Benestad, Haakon B
Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms
title Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms
title_full Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms
title_fullStr Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms
title_full_unstemmed Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms
title_short Delayed leukocytosis after hard strength and endurance exercise: Aspects of regulatory mechanisms
title_sort delayed leukocytosis after hard strength and endurance exercise: aspects of regulatory mechanisms
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC317276/
https://www.ncbi.nlm.nih.gov/pubmed/14667246
http://dx.doi.org/10.1186/1472-6793-3-14
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