Effect of High Intensity Exercise-Induced Oxidative Stress on Leukocytes Apoptosis

• Main Authors: Chiu Yi-Han, 邱亦涵
• Other Authors: Hsu Tai-Ger
• Format: Others
• Language: zh-TW
• Published: 2003
• Online Access: http://ndltd.ncl.edu.tw/handle/30007344058951343830

碩士 === 臺北巿立體育學院 === 運動科學研究所 === 91 === The intensity and duration of exercise will strongly influence the physical responses. After high intensity exercise (85% VO2max), the reactive oxygen species (ROS) are numerously generated, which makes an imbalance between the oxidatants and antioxidatants of organism to result in oxidative stress. Oxidative stress can potentially induce immune cell programmed cell death, or called apoptosis after high intensity exercise. However, the possible mechanisms have not been investigated. The purpose of this study was to investigate the effect of consecutive high intensity exercise induced-oxidative stress on leukocytes apoptosis. Twelve volunteers (22.8 ± 2.39 yrs) were recruited into this study. All subjects performed the session of aerobic exercise at an intensity of 85% VO2max for 30 min daily for 3 consecutive days. 20 mL of venous blood samples were collected before first day (D1) of exercise, immediately postexercise on the first day (D1’), preexercise on the third day (D3), immediately postexercise on the third day, the fifth day (D5) and the seventh day (D7). The oxidative stress and apoptosis in leukocytes were measured by flow cytometry, and the transcription and translation of the apoptosis associated genes also were determined by RT-PCR and western blotting. The results showed that exercise at 85% VO2max intensity leaded to a depletion of intracellular glutathione (GSH) (p＜.001) and quite often accompanied by a concomitant increase in ROS (p＜.001). This phenomenon could contribute to oxidative stress and apoptosis. In PBMC, it is extremely critical steps that both the loss of the mitochondrial transmembrane potential (MTP) (p＜.001) and the release of cytochrome c from the inner membrane of mitochondria can potentially trigger caspase cascade activation, then results in apoptosis. As for PMN, not only collapse of MTP and cytochrome c released to cytosol from mitochondria but also CD95 receptor activated particularly (p＜.001) could produced caspase cascade. In conclusion, it is proposed that the consecutive high intensity exercise will increase oxidative stress and induce PBMC apoptosis via mitochondria apoptotic pathway, whereas consecutive high intensity exercise induced PMN apoptosis were mediated via both mitochondria and Fas / FasL activated pathways.