Effects Of Prolonged And Brisk Exercise On Apoptosis

Exercise is a well-known stress factor and is able to induce an inflammatory-like status and also activates immune system. Apoptosis or programmed cell death is an important mechanism for the regulation of the immune system. Apoptosis is the immune system‘s major mechanism to maintain immune‘s system homeostasis. PURPOSE: We sought investigate the effects of prolonged and brisk exercise on circulating proinflammatory cytokines and the soluble apoptosis mediators Fas (sFas) and Fas ligand (sFasL) in ultramarathon runners. METHODS: In 20 male athletes participating in the ultradistance foot race of the 246 Km "Spartathlon“ (continuous, prolonged, brisk exercise for up to 36 hours), we measured circulating concentrations of IL-6 using a validated Elisa kit (Quantikine; R&D Systems, Minneapolis, MN) and we determined sFas and sFasL using the multiplex assay kit Linco Human Sepsis/Apoptosis. Free plasma DNA was measured by quantitative real-time PCR using the LightCycle (Roche diagnostics, Manheim, Germany). All the measurements were performed in samples collected before the race, at the end of the race and 48h postrace. RESULTS: The mean values for IL-6 before the race (phase I) were 0.9±0.5 pg/ml, immediately after the race (phase II) were 7781.0±8317.3 pg/ml, and 48h after the race (phase III) were returned at pre-exercise levels (0.7±0.5 pg/ml). DNA damage was significantly increased at phase I from 14.8±13.9 genome equivalents/ml to 146.2±161.5 genome equivalents/ml at phase II and was significantly decreased to 51.5±73.2 genome equivalents/ml at phase III. Lastly, apoptosis was observed to remain steady as sFas and sFas ligand were 2.16±0.61 ng/ml and 0.13±0.02 ng/ml, respectively at phase I, 1.96±0.53 ng/ml and 0.12±0.02 ng/ml, respectively at phase II and 2.32±57 ng/ml and 0.13±0.02 ng/ml, respectively at phase III. CONCLUSION: Prolonged and strenuous exercise seems to induce a significant inflammatory response, which in turn induces DNA damage in cells, probably via oxidative stress‘s increase. However, it is observed that in well trained athletes apoptosis is not being altered because of the development of counterbalancing mechanisms.