本研究旨在探討單次衰竭運動後老鼠體內血液脂質過氧化、組織損傷、抗氧化調節能力等指標於0.5 h、1 h、2 h、24 h等不同恢復期之反應。40隻Sprague-Dawley雄鼠隨機分為控制組 (C = 8) 與衰竭運動組，其中衰竭運動組依犧牲時間均分為運動後0.5 h組 (E0.5h = 8) 、1 h組 ( E1h = 8) 、2 h組 (E2h = 8) 與24 h組 (E24h = 8) 共四組。讓衰竭運動組老鼠在跑步機上跑至衰竭。得到最後速度約30.4 ± 0.6 m/min，平均持續時間約64.5 ± 2.9 min。衰竭運動後依分組時間犧牲與收集血液，分析其血漿丙二醛 (malondialdehyde, MDA) 濃度與肌酸激酶 (creatine kinase, CK) 、乳酸脫氫酶 (lactate dehydrogenase, LDH) 活性等；以及紅血球麩胱甘肽 (glutathione, GSH) 、氧化態麩胱甘肽 (glutathione disulfide, GSSG) 濃度與超氧化物歧化酶 (superoxide dismutase, SOD) 活性等反應情形。經單因子變異數分析後，達顯著差異者再以杜凱氏法將各時間點與C組進行事後比較，結果如下。
一、MDA分別於E0.5h 與E1h增加10%與14.5% (p < .05) ，CK活性分別於E0.5h與E2h顯著增加99.3%與151.3%的峰值反應 (p < .05) ，LDH則僅在E2h顯著增加49.8%的峰值結果 (p < .05) 。
二、紅血球GSH與SOD於運動後各組與C組比較結果並無明顯改變 (p > .05) ；但GSSG直到E1h才明顯增加36.9% (p < .05) ，期間GSH/GSSG比值下降。
本研究老鼠於E0.5h至E1h 期間血漿MDA濃度與CK活性在E0.5h以及紅血球GSSG濃度在E1h明顯升高的結果，意味著老鼠因衰竭運動導致體內骨骼肌與心肌等組織細胞的脂質過氧化傷害將持續約1小時，期間氧化壓力亦干擾紅血球內GSH與GSSG的平衡狀態，並於運動後2 h恢復至安靜值；然而血漿CK與LDH活性在E2h的明顯升高反應，有可能受到了免疫分子誘發續發性發炎受損之影響所致。需要進一步擴大相關氧化、抗氧化分子的檢測，以清楚釐清老鼠歷經單次衰竭運動後恢復期，體內血液系統複雜的氧化調節機制。

The purpose of this study was to investigate the changes of blood biochemical marks include malondialdehyde (MDA) , creatine kinase (CK) , lactate dehydrogenase (LDH) , glutathione (GSH) , glutathione disulfide (GSSG) and superoxide dismutase (SOD) on different recovery following an exhaustive run in rats. 40 male Sprague-Dawley rats were randomly divided into five groups: a sedentary control (C = 8) and sacrificing at 0.5 h (E0.5h = 8) , 1 h (E1h = 8) , 2 h (E2h = 8) , 24 h (E24h = 8) following an exhaustive run on a motor treadmill with 10% grade at a final speed of 30.4 m/min and 64.5 min running time. The results showed a significant increase in plasma membrane lipid peroxidation endproduct (MDA) level at E0.5h (10%) and E1h (14.5%) and tissue-damage marks of CK activities significant increase at E0.5h (99.3%) and to peak at E2h (151.3%) and LDH activities only significant increase at E2h (49.8%) respectively of exercised rats compared with C rats. The antioxidative enzyme SOD activities and GSH concentrations in erythrocytes were no significant difference, whereas GSSG content increased at E1h (36.9%) and the GSH/GSSG ratio was depressed in exercised rats compared with C rats. These findings suggest that one single bout of exhaustive exercise may induce rats muscular and heart tissue-lipid peroxidation damage until E1h and reach to recovery at E2h, whereas the significant increase levels of CK and LDH at E2h may indicate that secondary inflammatory damage occurent with the immune molecules concentrated, and need research to confirm in rats blood circulation.

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