Possible in vivo tolerance of human polymorphonuclear neutrophil to low-grade exercise-induced endotoxaemia. Issue 6 (1998)

• Record Type: Journal Article
• Authors: Camus, G.; Nys, M.; Poortmans, J-R.; Venneman, I.; Monfils, T.; Deby-Dupont, G.; Juchmés-Ferir, A.; Deby, C.; Lamy, M.; Duchateau, J.
• Is Part Of: Mediators of inflammation. Volume 7:Issue 6(1998)
• Page Start: 413
• Page End: 415
• Publication Date: 1998
• Subjects: Exercise -- Endotoxin -- Myeloperoxidase -- Polymorphonuclear neutrophils; Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1080/09629359890794
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : To address the question of whether translocation of bacterial lipopolysaccharide (LPS) into the blood could be involved in the process of exercise-induced polymorphonuclear neutrophil (PMN) activation, 12 healthy male subjects who took part in a sprint triathlon (1.5 km river swim, 40 km bicycle race, 10 km road race) were studied. While there was no detectable amount of endotoxin in the blood samples drawn at rest, exercise was followed by the appearance of circulating endotoxin molecules at the end of competition in four subjects, and after one and 24 h recovery in three and seven athletes, respectively. The concentrations of plasma granulocyte myeloperoxidase ([MPO]), were significantly higher immediately after exercise and one hour later than baseline values( P < 0.001 ) . This variable returned to pre-race levels the day after exercise, despite the presence of detectable amounts of LPS, at that time, in seven athletes. The absence of significant correlation( r = 0.26 ; P = 0.383 ) and temporal association between [MPO]and plasma endotoxin levels led us to conclude that endotoxaemia was not involved in the process of exercise-induced PMN degranulation observed in our subjects.