长期耐力运动对大鼠腓肠肌的损伤及一氧化氮的调节作用

Effect of long-term endurance exercise on rat gastrocnemius muscles and the regulatory effect of nitric oxide

背景:长期耐力运动常引起肌肉损伤,但其机制尚不清楚。目的:观察长期游泳运动对骨骼肌的损伤作用以及内源性一氧化氮的调节作用。设计、时间及地点:随机对照动物实验,于2006-12/2007-04在江苏大学基础医学与医学技术学院营养科学研究室完成。材料:健康雌性SD大鼠60只,体质量190～250g,用于制备大鼠游泳模型;L-NG-硝基精氨酸甲酯(L-NAME)用于抑制大鼠体内一氧化氮的生成。方法:60只大鼠随机数字表法分为静息组、运动组、静息联合L-NAME组和运动联合L-NAME组,每组15只。在静息联合L-NAME组和运动联合L-NAME组大鼠的饮水中添加一氧化氮合酶拮抗剂L-NAME,1g/L。运动组和运动联合L-NAME组大鼠游泳5d/周,2h/d。主要观察指标:3个月后取各组大鼠腓肠肌测定氮氧化物(NOx)的含量;苏木精-伊红染色观察腓肠肌的形态变化。结果:纳入大鼠60只,其中静息联合L-NAME组死亡5只、运动组死亡2只、运动联合L-NAME组死亡6只,死亡原因包括自然死亡、溺水或药物长期作用,进入结果分析47只。①运动组NOx含量高于静息组(P<0.01)。运动联合L-NAME组NOx含量低于运动组(P<0.05),但高于静息联合L-NAME组(P<0.05)。②腓肠肌的肌纤维较细,数量较多,染色较浅,肌纤维结构完整;运动组腓肠肌纤维明显粗大,深染,偶见肌纤维有断裂,少量巨噬细胞浸润;静息联合L-NAME组肌纤维有分支,结缔组织增生;运动联合L-NAME组也可见运动组中的变化,且肌纤维断裂和巨噬细胞浸润现象更明显,还表现为肌纤维坏死溶解,肌纤维有分支。结论:长期游泳运动造成了骨骼肌纤维的损伤;运动诱导产生的一氧化氮对运动性损伤可能有保护作用。

BACKGROUND： Long-term endurance exercise often induces muscle injury, but the mechanism is not clear. OBJECTIVE： To observe the effect of long-term endurance exercise on rat skeletal muscles and the role of endogenous nitric oxide. DESIGN, TIME AND SETTING： The randomized controlled animal experiment was performed at the Research Laboratory of Nutrient, School of Medical Science and Laboratory Medicine, Jiangsu University from December 2006 to April 2007. MATERIALS： A total of 60 healthy female Sprague Dawley rats weighing 190-250 g were used for establishing rat swimming models. L-NG-nitro-L-arginine methyl ester （L-NAME） was used to inhibit nitric oxide production in rats. METHODS： Sixty female Sprague-Dawley rats were randomly divided into a sedentary group （SED）, a sedentary plus L-NAME group （SED＋L-NAME）, an exercise group （EXE） and an exercise plus L-NAME group （EXE＋L-NAME）, 15 rats each. L-NAME （1 g/L） was administrated into the SED＋L-NAME group and the EXE＋L-NAME group by the drinking water. The rats in the EXE group and the EXE＋L-NAME group swam for 5 days in a week, 2 h/d. MAIN OUTCOME MEASURES： Three months later, Gastrocnemius was removed to analyze the nitric oxide contents; Morphological changes in gastrocnemius were obserVed by Hematoxylin and eosin staining. RESULTSt Of sixty included rats, 47 rats were included in the final analysis, and 13 died during the experiment （5 deaths in SED＋L-NAME group, 2 deaths in the EXE group, and 6 deaths in the EXE＋L-NAME group）. Death cause included natural death, drowning or long-term drug effects. Nitric oxide contents were higher in the EXE group compared with the SED group （P 〈 0.01）. Nitric oxide contents were lower in the EXE＋L-NAME group than in the EXE group （P 〈 0.05）, but higher than in the SED＋L-NAME group （P 〈 0.05）. Gastrocnemius fibers were thin, many, with shallow staining, with complete fibrous structure. In the EXE group, the muscle fiber was obviously hypertrophy with heavily hematoxylin and eosin staining, occasionally with disruption and macrophage infiltration. The muscle fiber of the gastrocnemius in the SED＋L-NAME group was obviously ruptured with desmoplasia. In the EXE＋L-NAME group, changes in the EXE group were presented, with more significantly disruption with the fiber necrosis, branching, and the obvious infiltration of macrophage. CONCLUSION： Long-term swimming exercise induced the damage of muscle fiber of the gastrocnemius. Nitric oxide induced by exercises can play an important protective role in injury due to exercises.