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Endurance exercise causes interaction among stress hormones, cytokines, neutrophil dynamics, and muscle damage
Ist Teil von
Journal of applied physiology (1985), 1999-10, Vol.87 (4), p.1360-1367
Ort / Verlag
Bethesda, MD: Am Physiological Soc
Erscheinungsjahr
1999
Quelle
MEDLINE
Beschreibungen/Notizen
1 Department of Hygiene,
Hirosaki University School of Medicine, Hirosaki, Aomori 036-8562;
2 Department of Health and
Physical Education, Faculty of Education, Hirosaki University,
Hirosaki, Aomori 036-8560; and
3 Oyokyo Kidney Research
Institute, Hirosaki, Aomori 036-8243, Japan
We analyzed adaptation mechanisms
regulating systemic inflammatory response of the stressed body by using
an experimental challenge of repeated exercise bouts and accompanying
muscle inflammation. Eight untrained men bicycled at 90 W for 90 min, 3 days in a row. Exercise induced peripheral neutrophilia with a leftward
shift of neutrophil nucleus and neutrophil priming for oxidative
activity determined by luminol-dependent chemiluminescence. Plasma
growth hormone and interleukin-6 rose significantly after exercise and were closely correlated with the neutrophil responses. Serum creatine kinase and myoglobin levels as muscle damage markers rose after exercise in "delayed onset" and were closely
correlated with the preceding neutrophil responses. These
exercise-induced responses were strongest on day
1 , but the magnitude gradually decreased with
progressive daily exercise. In contrast, the magnitude of catecholamine
responses to exercise sessions gradually rose, possibly suppressing
neutrophil oxidative responses. These results indicate that
stress-induced systemic release of bioactive substances may determine
neutrophil mobilization and functional status, which then may affect
local tissue damage of susceptible organs.
growth hormone; interleukin-6; catecholamine; reactive oxygen
species; systemic inflammatory response syndrome