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Articles in PresS, published online ahead of print March 15, 2002
J Appl Physiol, 10.1152/jap.01262.2001
Submitted on December 27, 2001
Accepted on March 11, 2002
1 Institute for Sports Medicine, University Clinic Muenster, Muenster, Germany
2 Department of Medicine B, University Clinic Muenster, Muenster, Germany
* To whom correspondence should be addressed. E-mail: mooren{at}uni-muenster.de.
Apoptosis or the programmed cell death is a process of fundamental importance for the regulation of the immune response. Several reasons suggest that apoptosis is involved in exercise-induced alterations of the immune system like post exercise lymphocytopenia. Healthy volunteers performed two treadmill exercise tests, the first was performed at 80% VO2max until exhaustion (exhaustive exercise) and the second two weeks later at 60% VO2max with the identical running time (moderate exercise). Blood samples were taken before, immediately after and 1 hour after the test. Lymphocytes were analyzed for apoptotic and necrotic cells using FITC labelled Annexin V-antibodies and nuclear propidium iodide uptake, respectively. In addition, apoptotic/necrotic cells were measured after a 24 hour incubation of lymphocytes in the presence of camptothecin or phytohemagglutinin (PHA). Finally, plasma membrane expression of CD95-receptor and CD95-receptor ligand was investigated. Immediately after the exhaustive exercise the percentage of apoptotic cells increased significantly whereas it remained unchanged after the moderate exercise. Similar results were obtained after 24 hour incubation of lymphocytes in medium alone or in the presence of camptothecine, but not with PHA. We found an upregulation of the CD95-receptor expression after both exercise tests. However, only after exhaustive exercise a characteristic shift in CD95 expression profile towards cells with a high receptor density was observed. Expression of the CD95-receptor ligand remained unchanged after both exhaustive and moderate exercise. These results suggest that apoptosis may contribute to the regulation of the immune response after exhaustive exercise. Whether this mechanism can be regarded either as beneficial, i.e. autoreactive cells are deleted, or harmful, i.e. suppression of the immune response, awaits further investigations.
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