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  • Articles: DFG German National Licenses  (3)
  • Myeloperoxidase  (3)
  • Tumour necrosis factor α  (1)
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  • Articles: DFG German National Licenses  (3)
Material
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Are similar inflammatory factors involved in strenuous exercise and sepsis? (1994)
    Springer
    Intensive care medicine 20 (1994), S. 602-610 
    Details
    ISSN: 1432-1238
    Keywords: Exercise ; Leukocyte ; Inflammatory response ; Cytokine ; Endotoxin ; Myeloperoxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An increasing body of data suggest that strenuous exercise triggers an inflammatory response having some similarity with those occurring in sepsis. Indices of this inflammatory response to exercise (IRE) especially include leukocytosis, release of inflammatory mediators and acute phase reactants, tissue damage, priming of various white blood cell lines, production of free radicals; activation of complement, coagulation and fibrinolytic cascades. Inflammatory responses to strenuous exercise and sepsis could in part be due to the release of endotoxin in blood as common triggering factor, but it seems that tissue damage and/or contact system activation are more important triggering mechanisms in exercising subjects. While the magnitude and duration of cellular and humoral changes associated with IRE are quite different from those observed in sepsis, recent human studies suggested that chronic and/or excessive IRE could have adverse effects. Among the possible consequences of acute and chronic IRE are delayed onset muscular soreness and loss of force, cardiovascular complications, intravascular hemolysis, hypoferraemia and increased susceptibility to infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01705731
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Endotoxaemia, production of tumour necrosis factor α and polymorphonuclear neutrophil activation following strenuous exercise in humans (1998)
    Springer
    European journal of applied physiology 79 (1998), S. 62-68 
    Details
    ISSN: 1439-6327
    Keywords: Key words Exercise ; Endotoxin ; Anti-lipopolysaccharide antibodies ; Tumour necrosis factor α ; Myeloperoxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine whether endotoxaemia accompanying long-term, strenuous physical exercise is involved in exercise-induced increase in plasma tumour necrosis factor alpha (TNF-α) concentration and polymorphonuclear neutrophil (PMN) activation, 14 male recreational athletes [mean age 28 (SEM 1) years] were studied. Exercise consisted of a 1.5-km river swim, a 40-km bicycle race, and a 10-km road race. Mean time to complete the race was 149.8 (SEM 4.8) min. The plasma concentrations of granulocyte myeloperoxidase (MPO) and TNF-α were significantly higher than baseline values immediately and 1 h after exercise (P 〈 0.001). Both variables returned to pre-race levels the day after exercise. Marked, transient decreases in plasma concentrations of anti-lipopolysaccharide (LPS) immunoglobulin G (IgG) and immunoglobulin M (IgM) antibodies directed against a panel of selected smooth gram-negative LPS were observed after the race, reaching in most cases minimal values in the blood sample drawn immediately following the completion of the triathlon. There was no significant correlation between the magnitude of PMN activation, as assessed by the increase in plasma concentrations of MPO, and the humoral markers of endotoxaemia and TNF-α. An inverse, highly significant relationship between the increase in plasma TNF-α concentrations and the changes in circulating anti-LPS IgM antibodies concentrations was observed (r = −0.7; P 〈 0.01). These findings suggest that exercise-induced endotoxaemia was involved in the release of TNF-α, that the magnitude of the TNF-α response to exercise was down-regulated by anti-LPS antibodies of the IgM class, and that the production of TNF-α and endotoxaemia did not seem to play a role in the activation of circulating PMN in the exercising subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004210050474
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Exercise induces pentane production and neutrophil activation in humans. Effect of propranolol (1990)
    Springer
    European journal of applied physiology 61 (1990), S. 319-322 
    Details
    ISSN: 1439-6327
    Keywords: Exercise ; Pentane ; β-Adrenergic blockade ; Myeloperoxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of β-adrenergic receptor blockade on exercise-induced lipid peroxidation in man has been examined by measuring the production of pentane in expired air. For this purpose, five healthy male subjects were subjected to dynamic exercise of graded intensity on a cycle ergometer (10 min at 45%, 5 min at 60% and 75% maximal oxygen uptake 1 h after ingestion of either a placebo or 40-mg propranolol. At rest, mean pentane concentration ([pent]) with placebo was 4.13 pmol · l−1, SD 2.14. After exercise, this value significantly increased by 310% (17.1 pmol · l−1, SD 7.73, P 〈 0.01). Oral administration of 40-mg propranolol significantly lowered the mean resting [pent] to 1.75 pmol · l−1, SD 0.77, P 〈 0.05. After exercise, the increase of [pent] was much smaller (240%) and was less significant (P 〈 0.2) than with the placebo. The mechanism of this inhibitory effect of propranolol remains to be elucidated. However, as indicated by the measurement of plasma myeloperoxidase concentration, it can be concluded that the antioxidant property of propranolol cannot be attributed to the inhibition of neutrophil activation, a possible source of free radicals during exercise.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00357620
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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