• C Droste.
• Arzt für Innere Medizin und Kardiologie Benedikt Kreutz-Rehabilitationszentrum für Herz- und Kreislaufkranke, Südring 15, W-7812 Bad, Krozingen, Bundesrepublik Deutschland.
• Schmerz. 1991 Sep 1;5(3):138-47.

AbstractA series of studies with humans as well as experiments carried out on animals have shown that physical exercise leads to temporary hypoalgesia. Reduced sensitivity to pain is not only demonstrable after long-distance exercise (such as a marathon run) but also during and after intensive physical exercise on a laboratory ergometer. In a double blind study (20 mg naloxone versus placebo) experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy athletic men before, during, and after physical exercise on a cycle ergometer. A significant pain threshold elevation during exercise was found for finger (Anova,p<0.004) and dental pulp stimulation (p<0.01). Hypoalgesia remained present after exercise was stopped and the initial pain threshold level was returned to approximately 60 minutes after the exercise. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (p<0.001) after exercise. Naloxone failed to affect pain thresholds and plasma beta-endorphin did not correlate significantly with pain thresholds. The cause of the exercise-induced hypoalgesia is probably an activation of central pain inhibitory mechanisms by the "stimulus" of physical exercise (stimulation-induced analgesia). Central pain inhibitory systems are probably thereby activated by the stimulation of afferent nerves endings (group III and IV) in the skeletal muscle. The same trigger mechanism also plays a role as a release stimulus for hormones which are secreted in increased measure during physical exercise (catecholamines, pituitary hormones). Plasma beta-endorphin is probably not directly involved in the exercise-induced hypoalgesia but is rather a "marker" for the activating of central analgesia mechanisms.

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