許多研究證實，激烈運動會誘發體內氧化壓力增加而產生大量活性氧自由基，而這些自由基的形成會造成體內脂質過氧化物產生及組織的損傷，並引起體內抗氧化系統的受損。因此，運動所引起之氧化壓力被認為和降低運動表現、肌肉疲勞、組織損傷、發炎反應及訓練過度有密切的相關性。目前至少有三個主要生化機制：粒線體電子傳遞鏈、黃嘌呤氧化酶（XO）及嗜中性白血球是運動產生自由基的來源。本研究旨在以精胺酸補充對衰竭運動引起大鼠氧化壓力及發炎反應之影響。實驗共分為兩個部分，實驗一將32隻SD大鼠（8週齡）隨機分為控制組及運動組，再將兩大組細分為控制組（C）、精胺酸組（C+Arg）、衰竭運動組（E）及精胺酸衰竭運動組（E+Arg）。實驗組餵食添加佔總熱量2％精胺酸（25g/Day）共計30天。運動組大鼠在跑步機從事單次激烈運動至衰竭，運動最後速度為30m/min，陡度為10％，其最大攝氧量約為75-80％；運動組平均跑步時間E組為81±4min及E＋Arg為87±5min，兩組並未達到顯著差異。所有運動組織大鼠於衰竭運動後立刻予以犧牲，並對血液生化值及組織脂質過氧化物（MDA）、超氧化岐化酶（SOD）、過氧化氫酶（CAT）、麩胱甘肽過氧化酶（GPX）、麩胱肽過還原酶（GRD）及麩胱甘肽（GSH）之含量及活性加以分析。另外也針對XO及骨髓過氧化物酶（MPO）之活性來分析各組織承受氧化壓力及發炎之狀態。血漿中肌酸激酶（CK）、乳酸脫氫酶（LDH）、麩草酸轉胺基酶（GOT）、麩丙酮酸轉胺基酶（GPT）、乳酸、尿酸及一氧化氮之含量於衰竭運動組皆顯著高於控制組，而精胺酸衰竭運動組LDH之活性顯著低於衰竭運動組。此外，血漿中CK之活性及血乳酸的含量，精胺酸衰竭運動組與控制組間則未有顯著差異。衰竭運動組導致心臟、骨骼肌、肝臟、肺臟、腎臟及血漿中MDA的提昇並達顯著差異，然而精胺酸衰竭運動組可防止組織MDA的生成。衰竭運動組SOD之活性顯著提昇在心臟、骨骼肌、肝臟及肺臟，但在腎臟並未達顯著差異相較於控制組。精胺酸衰竭運動組SOD之活性並無顯著差異並略低於控制組。由此顯示精胺酸補充可降低因激烈運動誘發自由基的形成。而CAT及GPX之活性在衰竭運動組除了心臟與骨骼肌外，在肝臟、肺臟及腎臟並無顯著差異相較於控制組。衰竭運動組GRD之活性在骨骼肌及肺臟顯著提昇相較於控制組，然而在精胺酸衰竭運動組在心臟、肝臟及肺臟與控制組相較則無顯著差異。衰竭運動組會導致血漿及骨骼肌中GSH含量顯著下降，而精胺酸衰竭運動組在骨骼肌、肝臟、肺臟及腎臟中含量無顯著改變，僅在心臟之GSH含量顯著提昇相較於控制組。XO活性在血漿、心臟、骨骼肌、肝臟、肺臟及腎臟於衰竭運動組均達顯著提升。而針對運動誘發嗜中性白血球產生發炎現象之分析，其結果顯示衰竭運動組在心臟、骨骼肌、肝臟、肺臟及腎臟之MPO活性亦顯著提昇。然而精胺酸衰竭運動組可顯著下降XO及MPO活性在這些組織中相較於運動衰竭組。
實驗二動物之飼養、分組及運動處方同實驗一，於衰竭運動24小時後將老鼠犧牲，隨即收取老鼠腹腔沖洗液之巨噬細胞加以培養並以LPS刺激之，以測定促發炎細胞激素的分泌量。實驗二結果顯示衰竭運動組在24小時後腹腔沖洗液TNF-α及IL-6的含量顯著高於精胺酸衰竭運動組，而IL-1β兩組間則無顯著差異。然而，在以LPS刺激下，衰竭運動組TNF-α、IL-6及IL-1β濃度皆顯著高於精胺酸衰竭運動組。
綜合上述結果，精胺酸補充可降低因衰竭運動所產生之血乳酸含量堆積，並可減少在心臟、骨骼肌、肝臟、肺臟、腎臟及血漿中MDA的生成。而各組織大量激活的內生性抗氧化酵素對急性激烈運動所產生的氧化壓力有代償作用，以減緩激增之氧化壓力來防止可能對組織所產生的氧化損傷。由此推論精胺酸補充具有很好的抗氧化劑的功能，使這些酵素在衰竭運動後維持穩定狀態。精胺酸補充可以降低衰竭運動後各組織中XO及MPO活性之提昇。此外，精胺酸補充可降低相關促發炎激素的分泌，以減緩急性衰竭運動後初期產生的發炎現象。

Numerous studies have shown that strenuous exercise is to induce oxidative stress leading to reactive oxygen species (ROS). This increased generation of free radicals might cause to lipid peroxidation and tissue damage, more so under impaired antioxidant states. Thus, exercise-induce oxidative stress had been associated with decreased physical performance, muscular fatigue, tissue damage, inflammatory response and overtraining. At least three biochemical pathways, that is, mitochondrial electron transport chain, xanthine oxidase (XO), and polymorphoneutrophil have been identified as potential sources of intracellular free radical generation during exercise. The purpose of this study was to assess the effects o L-arginine (L-Arg) supplementation on the oxidative stress and inflammatory response induced by exhaustive exercise in rats. There were 2 experiments in this study. In exp1, thirty-two adult male Sprague-Dawley rats ( 8 weeks old ) , sedentary and exercise rats, were randomly divided into four subgroups: sedentary control (C), sedentary with L-Arg treatment (C+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L-Arg treatment (E+Arg). Rats in groups C+Arg and E+Arg were received a 2% L-Arg diet for 30 days (about 25g/day).Rats in groups E and E+Arg underwent a single bout of the strenuous exhaustion exercise on a motorized treadmill at a final speed of 30m/min, 10% grade, approximately 75-80% VO2max. Mean exercise duration was not significant difference between E and E+Arg rats (81±4min and 87±5min, respectively). All animals were anesthetized with ethyl ether and killed immediately after exhaustive exercise. Blood biochemistry parameters and malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) glutathione peroxidase (GPX), glutatione reductase(GRD) and glutathione (GSH) were investigated in this study. Also XO and myeloperoxidase (MPO) activity were assay in tissues for state of oxidative stress and inflammatory response. The activities of creatinine kinase (CK) and lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), lactate, uric acid and NOx levels in the plasma significantly increased in exercised rats compared to sedentary control. The activities of plasma LDH were significantly decreased in E+Arg rats compared to exercised rats. In addition, plasma of CK activity and lactate concentration were not significant difference in E+Arg rats compared to controls. Exercised rats significantly enhanced MDA levels in heart, skeletal muscle, liver, lung, kidney and plasma compared to control. However, there were prevented in E+Arg rats. SOD activity was significantly elevated in exercised rats in heart, skeletal muscle, liver and lung but not in kidney compared to control. SOD activity in -fed -L-Arg animals at rest and after exercise remained well below the control levels, indicating the decreased generation of oxygen free radicals in them. CAT and GPX activities were unchanged either by E group or by E+Arg rats in liver, lung and kidney, but not in heart and skeletal muscle compared to those in the controls. GRD activity was significantly elevated in E group in skeletal muscle and lung compared to control. However, it remained unchanged in heart, liver, lung and skeletal muscle in E+Arg group compared to control. GSH levels in the plasma and skeletal muscle significantly decrease in exercised rats compared with sedentary control. E+Arg rats reversed the trend in various tissues and significantly increased in heart compared with control. The activity of XO in heart, skeletal muscle, liver, lung, kidney and plasma significantly increased in exercised rats compared to control. Also, exercise-induced tissue inflammation and significantly elevated MPO activity in heart, skeletal muscle, liver, lung and kidney compared to control. However, L-Arg supplementation significantly reduced exercise-induced elevations of XO and MPO activities in various tissues compared to exercised rats. In exp2, rats grouping, feeding and exercise protocol were the same in exp1. Rats were scarificed 24 hours after exhaustive exercise, then the peritoneal macrophages were harvested and stimulated by lipopolysaccharide (LPS) to investigate the secretion of proinflammatory cytokines. Results in Exp2 demonstrated that tumor necrosis factor-(TNF-α) and interleukin (IL)-6 concentration in peritoneal lavage fluid at 24 hours after exercise in the E group were significantly higher than the E+Arg group, but not in IL-1β. However, the concentration of TNF-α, IL-6 and IL-1β secreted by LPS
stimulated peritoneal macrophages of the E group were significantly
elevated than the E+Arg group. In summary, the present data would suggest the L-Arg administration reduce exercise-induced increased in plasma lactate and protected against oxidative lipid damage in the heart, skeletal muscle, liver, lung, kidney and plasma caused by exhaustive exercise in rats. The higher activity levels of antioxidant enzyme as result of exercise might be indicative of a compensatory measure to counteract the possible detrimental effects associated with oxidative stress. L-Arg supplementation was able to favorably influence tissue antioxidant defenses at rest and in response to exercise. L-Arg reduced elevation of XO and MPO activities in heart, skeletal muscle, liver, lung and kidney of rats induced by exhausting exercise. In addition, L-Arg treatment resulted in a low inflammatory related cytokines in early inflammatory stage after exhaustive exercise.

第一章 緒言‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥1
第一節 研究動機‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥1
第二節研究目的與假設‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥5
一、單次激烈衰竭性運動後氧化壓力之差異‥‥‥‥‥‥‥‥5
二、單次激烈衰竭性運動後發炎反應及細胞激素分泌之差異‥5
三、單次激烈衰竭性運動後疲勞現象與能量代謝之差異‥‥‥6
第三節 本研究之重要性‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥7
第二章 文獻探討‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥8
第一節 自由基與氧化壓力、氧化傷害及抗氧防禦機制‥‥‥‥8
一、自由基與氧化壓力 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥8
二、自由基氧化傷害與疾病‥‥‥‥‥‥‥‥‥‥‥‥‥‥11
三、抗氧防禦機制‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥11
（一）抗氧化營養素‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥11
1.維生素E ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥11
2.維生素C ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥12
3. β－胡蘿蔔素 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥13
（二）體內抗氧化物質‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥15
（三）抗氧化酵素系統‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥16
第二節 運動與自由基生成途徑及氧化壓力的相關研究 ‥‥22
一、運動所導致自由基產生之途徑‥‥‥‥‥‥‥‥‥‥‥22
（一）粒線體電子傳遞鏈‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥22
（二）黃嘌呤氧化酶（xanthine oxidase, XO） ‥‥‥‥‥‥23
（三）嗜中性白血球骨髓過氧化酶（myeloperoxidae, MPO）24
二、運動強度與氧化傷害‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥27
三、運動所導致的氧化傷害‥‥‥‥‥‥‥‥‥‥‥‥‥‥28
四、發炎反應‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥34
五、運動與疲勞之探討‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥37
（一）造成中樞疲勞的機制‥‥‥‥‥‥‥‥‥‥‥‥‥‥37
（二）週邊疲勞機轉‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥37
1.能量耗竭‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥37
2.乳酸與肌肉疲勞‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥38
3.自由基與離子代謝混亂機制‥‥‥‥‥‥‥‥‥‥‥‥38
第三節 精胺酸生成及生理代謝途徑‥‥‥‥‥‥‥‥‥‥‥40
一、精胺酸補充在生理醫學之抗氧化功能之研究 ‥‥‥‥40
（一）精胺酸與尿素代謝 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥40
（二）精胺酸與蛋白質合成 ‥‥‥‥‥‥‥‥‥‥‥‥‥40
（三）精胺酸與肌酸合成 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥40
（四）精胺酸與聚胺合成 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥41
（五）精胺酸與荷爾蒙分泌 ‥‥‥‥‥‥‥‥‥‥‥‥‥41
（六）精胺酸與免疫功能 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥41
（七）精胺酸與NO之生合成 ‥‥‥‥‥‥‥‥‥‥‥‥42
（八）精胺酸與抗氧化功能 ‥‥‥‥‥‥‥‥‥‥‥‥‥43
（九）服用精胺酸的安全性與副作用 ‥‥‥‥‥‥‥‥‥44
第四節 有關精胺酸補充在生理醫學上抗氧化功能之相關研究46
一、高血膽固醇症 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥46
二、吸煙 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥46
三、糖尿病 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥46
四、心血管疾病 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥47
五、肝病變 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥47
第五節 運動與一氧化氮之相關研究 ‥‥‥‥‥‥‥‥‥‥‥48
一、運動與NO之生成‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥48
二、運動與補充精胺酸之研究‥‥‥‥‥‥‥‥‥‥‥‥‥48
第三章 研究方法 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥50
【實驗一】‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥50
（一）實驗材料 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥50
1.實驗實驗動物之飼養與分組‥‥‥‥‥‥‥‥‥‥‥‥50
2.動物飼料之組成與配製‥‥‥‥‥‥‥‥‥‥‥‥‥‥50
（二）實驗分組‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥52
（三）大白鼠適應與衰竭運動之操作處方（Protocol）‥‥‥53
1.適應處方‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥53
2.衰竭運動處方‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥53
（四）分析項目與方法‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥55
（五）血液常規值之分析‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥55
1.各種血球的計數（complete blood cell count, CBC）‥‥‥55
2.各種白血球分類所佔的比例（Differential count for WBC, DC）‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥56
（六）一般血液生化分析部分 ‥‥‥‥‥‥‥‥‥‥‥‥‥56
1.血液生化值之分析 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥56
（七）其他一般血液生化值之分析 ‥‥‥‥‥‥‥‥‥‥‥56
1.血漿中乳酸（lactate）濃度之分析‥‥‥‥‥‥‥‥‥‥56
2.血清中游離脂肪酸（non esterified fatty acid, NEFA）濃度
之分析‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥57
3.血清中D-3-羥基丁酸（D-3-hydroxybutyrate）濃度之分析58
4.血漿中一氧化氮（Nitric oxide, NO）之濃度‥‥‥‥‥‥58
（八）抗氧化相關分析部分 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥59
1.各組織中抗氧化酵素活性之分析 ‥‥‥‥‥‥‥‥‥‥59
(1)超氧化岐化酶（Superoxide dismutase, SOD）‥‥‥‥59
(2)過氧化氫酶（Catalase, CAT） ‥‥‥‥‥‥‥‥‥‥60
(3)麩胱甘肽過氧化酶（Glutathione peroxidase, GPX）‥61
(4)麩胱甘肽還原酶（Glutathione reductase, GRD） ‥‥61
2.各組織及血漿中抗氧化物質麩胱甘肽（Glutathione, GSH）
濃度之分析‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥62
3.脂質過氧化產物之分析 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥62
(1)血漿中脂質過氧化產物（Malondialdehyde，MDA）之
濃度‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥62
(2)各組織中脂質過氧化產物（Malondialdehyde, MDA）
之濃度‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥63
（九）血漿與各組織過氧化酵素XO活性‥‥‥‥‥‥‥‥63
（十）各組織中MPO活性 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥63
（十一）總蛋白質含量‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥64
【實驗二】‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥64
一、收集腹腔沖洗液細胞‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥64
二、腹腔灌洗液部分（細胞激素濃度之測定）‥‥‥‥‥‥65
三、統計分析方法‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥66
第四章 結果 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥67
一、體重與運動衰竭時間‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥67
二、血液常規值之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥67
（一）血液中各種血球的計算結果‥‥‥‥‥‥‥‥‥‥‥67
（二）血液中各種白血球分類所佔比例的計算結果‥‥‥‥67
三、血液生化值之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥67
（一）血漿中脂質代謝‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥67
（二）白蛋白濃度變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥68
（三）血漿中葡萄糖、肌酸酐及尿素氮的濃度變化‥‥‥‥68
（四）血漿中乳酸的濃度變化‥‥‥‥‥‥‥‥‥‥‥‥‥68
（五）血漿中游離脂肪酸的濃度變化‥‥‥‥‥‥‥‥‥‥68
（六）D-3-羥基丁酸的濃度變化‥‥‥‥‥‥‥‥‥‥‥‥68
（七）尿酸的濃度變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥69
（八）血漿中各電解質離子的濃度變化‥‥‥‥‥‥‥‥‥69
（九）血漿中NO的濃度變化‥‥‥‥‥‥‥‥‥‥‥‥‥69
四、肝臟、心臟以及肌肉組織損傷指標‥‥‥‥‥‥‥‥‥69
五、體內抗氧化狀態之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥70
（一）血漿及各組織間脂質過氧化物之變化（MDA） ‥‥‥70
（二）血漿及各組織間抗氧化物質之變化（GSH）‥‥‥‥70
（三）各組織間抗氧化酵素之變化‥‥‥‥‥‥‥‥‥‥‥70
1.SOD活性之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥70
2.CAT活性之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥70
3.GPX活性之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥71
4.GRD活性之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥71
六、血漿與各組織中XO活性之變化‥‥‥‥‥‥‥‥‥‥71
七、體內發炎狀態之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥72
（一）CRP濃度之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥72
（二）MPO活性之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥72
（三）運動後24小時腹腔巨噬細胞培養液IL-6、TNF-α及
IL1-β之濃度 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥72
第五章 討論‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥119
一、衰竭運動對體內抗氧化狀態的影響 ‥‥‥‥‥‥‥‥119
（一）衰竭運動與血乳酸、XO及MDA之關係‥‥‥‥‥119
（二）衰竭運動與CK、LDH、GOT及GPT之關係 ‥‥‥120
（三）衰竭運動與NO形成之關係‥‥‥‥‥‥‥‥‥‥‥120
（四）衰竭運動與抗氧化酵素之關係‥‥‥‥‥‥‥‥‥‥121
（五）衰竭運動與GSH之關係 ‥‥‥‥‥‥‥‥‥‥‥‥122
二、衰竭運動與發炎反應‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥123
（一）衰竭運動與MPO之關係 ‥‥‥‥‥‥‥‥‥‥‥‥123
（二）衰竭運動與發炎細胞激素之分泌‥‥‥‥‥‥‥‥‥123
三、衰竭運動與能量代謝及抗疲勞狀態之關係‥‥‥‥‥‥124
（一）血糖‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥124
（二）乳酸‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥125
（三）D-3-hydroxybutyrate（酮體）‥‥‥‥‥‥‥‥‥‥‥125
（四）BUN與CRE ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥126
（五）自由基與離子代謝混亂機制‥‥‥‥‥‥‥‥‥‥‥126
第六章 結論與未來展望‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥128
參考文獻 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥129
附錄一 Effects of strenuous exercise on the immune system‥‥‥‥154

附錄二 衰竭運動組與精胺酸衰竭運動組各組織受損相關指標活性
之變化結果摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥155
附錄三 衰竭運動組與精胺酸衰竭運動組各組織MDA濃度之變化
結果摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥156
附錄四 衰竭運動組與精胺酸衰竭運動組各組織GSH濃度之變化
結果摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥157
附錄五 衰竭運動組與精胺酸衰竭運動組各組織抗氧化酵素之變化
結果摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥158
附錄六 衰竭運動組與精胺酸衰竭運動組各組織XO活性之變化結
果摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥159
附錄七 衰竭運動組與精胺酸衰竭運動組各組織MPO活性之變化
結果摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥160
附錄八 衰竭運動後24小時以LPS或無LPS刺激腹腔巨噬細胞培
養液IL-6、TNF-α和IL-1β濃度之變化結果摘要表‥‥‥161
附錄九 Postulated mechanism of action of arginine/nitric oxide on
macrophages and T-cell phenotypie expression and function‥162
表次
表一 運動與抗氧化劑補充抗氧化功能之相關研究摘要表‥‥‥‥14
表二 激烈運動與抗氧化酵素在各組織中之相關研究摘要表‥‥‥18
表三 激烈運動與脂質過氧化物在動物及人體各組織中之相關研究
摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥30
表四 激烈運動與蛋白質過氧化物在動物及人體各組織中之相關研
究摘要‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥32
表五 激烈運動與DNA氧化傷害在動物及人體各組織中之相關研
究摘要表‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥33
表六 激烈運動與嗜中性球呼吸爆發之反應‥‥‥‥‥‥‥‥‥‥36
表七 實驗飼料組成‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥51
表八 各組大白鼠體重之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥73
表九 各組大白鼠衰竭運動之時間‥‥‥‥‥‥‥‥‥‥‥‥‥‥74
表十 各組大白鼠各種血球血液常規值之結果‥‥‥‥‥‥‥‥‥75
表十一 各組大白鼠各種白血球之分類比‥‥‥‥‥‥‥‥‥‥‥76
表十二 各組大白鼠血漿中TC、TG、LDL-C及HDL-C濃度之變化‥77
表十三 各組大白鼠其他血漿中生化項目濃度之變化‥‥‥‥‥‥78
表十四 各組大白鼠組織中SOD活性之變化‥‥‥‥‥‥‥‥‥‥79
表十五 各組大白鼠組織中CAT活性之變化‥‥‥‥‥‥‥‥‥‥80
表十六 各組大白鼠組織中GPX活性之變化‥‥‥‥‥‥‥‥‥‥81
表十七 各組大白鼠組織中GRD活性之變化‥‥‥‥‥‥‥‥‥‥82




圖次
圖一 運動所產生的適應性反應及組織之氧化傷害‥‥‥‥‥‥‥10
圖二 動物體內抗氧化防禦系統‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥21
圖三 骨骼肌形成自由基的途徑‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥26
圖四 精胺酸生成及生理代謝途徑‥‥‥‥‥‥‥‥‥‥‥‥‥‥45
圖五 衰竭運動之操作處方‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥54
圖六 各組大白鼠血漿中乳酸濃度之變化‥‥‥‥‥‥‥‥‥‥‥83
圖七 各組大白鼠血漿中游離脂肪酸濃度之變化‥‥‥‥‥‥‥‥84
圖八 各組大白鼠血漿中D-3-羥基丁酸濃度之變化‥‥‥‥‥‥‥85
圖九 各組大白鼠血漿中尿酸濃度之變化‥‥‥‥‥‥‥‥‥‥‥86
圖十 各組大白鼠血漿中NOx濃度之變化‥‥‥‥‥‥‥‥‥‥‥87
圖十一 各組大白鼠血漿中GOT活性之變化‥‥‥‥‥‥‥‥‥‥88
圖十二 各組大白鼠血漿中GPT活性之變化‥‥‥‥‥‥‥‥‥‥89
圖十三 各組大白鼠血漿中LDH活性之變化‥‥‥‥‥‥‥‥‥‥90
圖十四 各組大白鼠血漿中CK活性之變化‥‥‥‥‥‥‥‥‥‥‥91
圖十五 各組大白鼠血漿中脂質過氧化物濃度之變化‥‥‥‥‥92
圖十六 各組大白鼠心臟中脂質過氧化物濃度之變化‥‥‥‥‥93
圖十七 各組大白鼠骨骼肌中脂質過氧化物濃度之變化‥‥‥‥94
圖十八 各組大白鼠肝臟中脂質過氧化物濃度之變化‥‥‥‥‥95
圖十九 各組大白鼠肺臟中脂質過氧化物濃度之變化‥‥‥‥‥96
圖二十 各組大白鼠腎臟中脂質過氧化物濃度之變化‥‥‥‥‥‥97
圖二十一 各組大白鼠血漿中麩胱甘肽濃度之變化‥‥‥‥‥‥‥98
圖二十二 各組大白鼠心臟中麩胱甘肽濃度之變化‥‥‥‥‥‥‥99
圖二十三 各組大白鼠骨骼肌中麩胱甘肽濃度之變化‥‥‥‥‥‥100

圖二十四 各組大白鼠肝臟中麩胱甘肽濃度之變化‥‥‥‥‥‥‥101
圖二十五 各組大白鼠肺臟中麩胱甘肽濃度之變化‥‥‥‥‥‥‥102
圖二十六 各組大白鼠腎臟中麩胱甘肽濃度之變化‥‥‥‥‥‥‥103
圖二十七 各組大白鼠血漿中黃嘌呤酶活性之變化‥‥‥‥‥‥‥104
圖二十八 各組大白鼠心臟中黃嘌呤酶活性之變化‥‥‥‥‥‥‥105
圖二十九 各組大白鼠骨骼肌中黃嘌呤酶活性之變化‥‥‥‥‥‥106
圖三十 各組大白鼠肝臟中黃嘌呤酶活性之變化‥‥‥‥‥‥‥‥107
圖三十一 各組大白鼠肺臟中黃嘌呤酶活性之變化‥‥‥‥‥‥‥108
圖三十二 各組大白鼠腎臟中黃嘌呤酶活性之變化‥‥‥‥‥‥‥109
圖三十三 各組大白鼠血漿中C－反應蛋白濃度之變化‥‥‥‥‥110
圖三十四 各組大白鼠心臟中骨髓過氧化酶活性之變化‥‥‥‥‥111
圖三十五 各組大白鼠骨骼肌中骨髓過氧化酶活性之變化‥‥‥‥112
圖三十六 各組大白鼠肝臟中骨髓過氧化酶活性之變化‥‥‥‥‥113
圖三十七 各組大白鼠肺臟中骨髓過氧化酶活性之變化‥‥‥‥‥114
圖三十八 各組大白鼠腎臟中骨髓過氧化酶活性之變化‥‥‥‥‥115
圖三十九 衰竭運動後24小時以LPS或無LPS刺激腹腔巨噬細胞
培養液IL-6濃度之變化 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥116
圖四十 衰竭運動後24小時以LPS或無LPS刺激腹腔巨噬細胞
培養液TNF-α濃度之變化 ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥117
圖四十一 衰竭運動後24小時以LPS或無LPS刺激腹腔巨噬細胞
培養液IL-1β濃度之變化‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥118

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