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Piroxicam fails to reduce myocellular enzyme leakage and delayed onset muscle soreness induced by isokinetic eccentric exercise

机译:吡罗昔康不能减少等速离心运动引起的肌细胞酶渗漏和延迟性肌肉酸痛

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摘要

To test the hypothesis that delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of prostaglandin E2 (PGE2), ten healthy male subjects were studied. Using a double-blind randomized crossover design, each subject performed two isokinetic tests separated by a period of at least 6 weeks: once with placebo, and once with piroxicam (Feldene®). They were given one capsule containing either placebo or piroxicam (20 mg) per day for 6 days with initial doses given starting 3 days prior to isokinetic testing. Exercise consisted of eight stages of five maximal contractions of the knee extensor and flexor muscle groups of both legs separated by 1 min rest phases, on a Kin Trex device at 60°/s angular velocity. The subjective presence and intensity of DOMS were evaluated using a visual analogue scale immediately after, and 24 and 48 h after each test. The mean plasma concentration of PGE2 measured at rest and after exercise was significantly lower in the group treated with piroxicam (p < 0.05). However, statistical analysis (two-way ANOVA test) revealed that exercise did not cause any significant change of mean plasma PGE2 over time in either of the two groups. Eccentric work was followed by severe muscle pain in extensor and flexor muscle groups. Maximal soreness was noted 48 h postexercise. Serum creatine kinase activity and the serum concentration of myoglobin increased significantly, and reached peak values 48 h after exercise in both experimental conditions (p < 0.001). By paired t-test, it appeared that there were no significant differences in the serum levels of these two markers of muscle damage between the two groups at any time point. We conclude that: (1) oral administration of piroxicam fails to reduce muscle damage and DOMS caused by strenuous eccentric exercise; and (2) the hypothetical role of increased PGE2 production in eccentric exercise-induced muscle damage, DOMS, and reduced isokinetic performance is not substantiated by the present results.
机译:为了检验假说,剧烈偏心肌收缩后迟发性肌肉酸痛(DOMS)可能是由于前列腺素E2(PGE2)产生增加所致,研究了十名健康男性受试者。使用双盲随机交叉设计,每个受试者进行两次等速试验,至少间隔6周:一次使用安慰剂,一次使用吡罗昔康(Feldene ®)。给他们一个含有安慰剂或吡罗昔康(20毫克)的胶囊,每天服用6天,在等速试验前3天开始给予初始剂量。锻炼包括在Kin Trex装置上以60 ° / s角速度在1分钟的休息阶段之间分开的两个腿的膝部伸肌和屈肌群的五个最大收缩的八个阶段。在每次测试后以及测试后24小时和48小时使用视觉模拟量表评估DOMS的主观存在和强度。在吡罗昔康治疗组中,静息和运动后测得的PGE2的平均血浆浓度显着降低(p <0.05)。但是,统计分析(双向ANOVA测试)显示,两组运动均未引起平均血浆PGE2随时间的显着变化。偏心工作后,伸肌和屈肌群出现严重的肌肉疼痛。运动后48小时观察到最大的酸痛。在两种实验条件下,运动后48小时血清肌酸激酶活性和肌红蛋白血清浓度均显着增加,并达到峰值(p <0.001)。通过配对t检验,两组在任何时间点的这两种肌肉损伤标志物的血清水平似乎都没有显着差异。我们得出以下结论:(1)口服吡罗昔康不能减轻剧烈离心运动引起的肌肉损伤和DOMS; (2)目前的结果并未证实PGE2产生增加在离心运动引起的肌肉损伤,DOMS和等速运动性能下降中的假设作用。

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