目的:通过观察运动训练对老龄大鼠心肌多胺代谢、心肌抗炎及抗氧化能力的影响,探讨多胺代谢在运动训练延缓心肌衰老中的作用。方法:实验分为3组:老年运动组(Old+Ex),18月龄Wistar大鼠梯度跑台运动6周;老年组(Old),与Old+Ex组月龄相同的Wistar大鼠;青年组(Young),3月龄Wistar大鼠。高效液相色谱测定心肌组织中多胺(腐胺、精脒和精胺)含量;[14C]标记液闪计数方法测定心肌组织中多胺合成限速酶鸟氨酸脱羧酶(ODC)与多胺分解限速酶精脒/精胺乙酰转移酶(SSAT)活性;比色法检测心肌组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;酶联免疫吸附(ELISA)法检测心肌组织中肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)含量;超声心动图记录大鼠心脏功能;透射电镜观察心肌组织超微结构变化。结果:与Young组比,Old组大鼠心肌组织中ODC活性下降,SSAT活性升高,精脒、精胺及总多胺池水平显著降低;心肌SOD活性下降,MDA、TNF-α和IL-1β水平升高(P<0.05);超声心动图显示,Old组大鼠左心室收缩末期直径(LVESD)与舒张末期直径(LVEDD)均明显增大,左心室射血分数(LVEF)与缩短分数(LVFS)降低(与Young组比,P<0.01)。Old+Ex组大鼠心肌组织中ODC活性增加,SSAT活性下降,精脒及总多胺池水平明显增加;心肌SOD活性升高,MDA、TNF-α和IL-1β水平均显著降低(与Old组比,P<0.05);左室功能有明显改善。超微结构观察可见Old组心肌肌丝排列不整齐,可见大量脂褐素颗粒沉积,线粒体基质疏松;Old+Ex组心肌肌节结构清晰,线粒体基质致密,嵴排列整齐。结论:运动训练通过上调多胺合成代谢、抑制其分解代谢对抗衰老引起的心肌多胺水平降低;运动训练可提高老龄心肌抗炎、抗氧化能力。维持老龄心肌多胺池在适当水平可能是运动延缓心肌衰老的部分机制之一。 OBJECTIVE: To observe the effects of exercise training on myocardial polyamine metabolism, myocardial anti-inflammation and anti-oxidative capacity in aged rats and to explore the role of polyamine metabolism in delaying myocardial aging. Methods: The experiment was divided into three groups: Old + Ex, 18-month-old Wistar rats with treadmill exercise for 6 weeks, Old, Wistar rats with the same age as Old + Ex, Young, 3 month old Wistar rats. The contents of polyamine (putrescine, spermidine and spermine) in myocardial tissue were determined by high performance liquid chromatography (HPLC). The rate-limiting enzyme of ornithine decarboxylase (ODC) in myocardial tissue was measured by [14C] The enzyme-linked immunosorbent assay (ELISA) method was used to detect the activity of SOD and the content of malondialdehyde (MDA) in myocardium. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) were detected by enzyme-linked immunosorbent assay (ELISA). Cardiac function was recorded by echocardiography and the ultrastructure of myocardium was observed by transmission electron microscopy. Results: Compared with Young group, the ODC activity and the activity of SSAT in myocardial tissue of Old group were significantly decreased, and the levels of spermine, spermine and total polyamine pool were significantly decreased; the activities of SOD, MDA, TNF-α and IL- (P <0.05). Echocardiography showed that left ventricular end systolic diameter (LVESD) and left ventricular end diastolic diameter (LVEDD) in Old group were significantly increased, and left ventricular ejection fraction (LVEF) and shortening fraction (LVFS) decreased (P <0.01 compared with Young group). ODC activity and SSAT activity in myocardial tissue of old + Ex group were increased, and the levels of spermine and total polyamine pool were significantly increased; the activity of SOD in myocardium was increased, and the levels of MDA, TNF-α and IL-1β were significantly decreased Group than, P <0.05); left ventricular function was significantly improved. Ultrastructural observation showed that the myocardial filaments of the Old group were irregularly arranged, showing that a large number of lipofuscin granules were deposited and the mitochondrial matrix was loose. The structures of the myocardium in Old + Ex group were clear, the mitochondria matrix was dense, and the cristae were arranged neatly. Conclusion: Exercise training can reduce the level of myocardial polyamines induced by anti-aging by up-regulating the synthesis and metabolism of polyamines, and exercise training can improve anti-inflammatory and anti-oxidative ability of aged myocardium. Maintaining the aged myocardial polyamine pool may be one of the mechanisms by which exercise slows myocardial senescence at an appropriate level.