...
首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Mechanisms of fatigue-induced activation of group IV muscle afferents: the roles played by lactic acid and inflammatory mediators.
【24h】

Mechanisms of fatigue-induced activation of group IV muscle afferents: the roles played by lactic acid and inflammatory mediators.

机译:疲劳诱导IV组肌肉传入神经激活的机制:乳酸和炎性介质发挥的作用。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

We already showed that group IV muscle afferents are activated during electrically-induced fatigue. The purpose of this study is to identify the mechanisms of stimulation of these muscle afferents by electrically-induced fatigue at a high (100 Hz; high frequency fatigue, HFF) or a low rate (10 Hz; low frequency fatigue, LFF) of stimulation. In 23 paralyzed and anaesthetized rabbits, group IV afferent activity from the tibialis anterior muscle was recorded before and after 3-min HFF or 5-min LFF runs eliciting the same force failure. Plasma lactic acid concentration (LA) was also measured in leg venous blood. We tested the effects of dichloroacetate (DCA), which reduces lactic acid production, and of acetylsalicylic acid (ASA), a blocker of cyclooxygenase, on fatigue-induced activation of group IV muscle afferents after HFF and LFF trials. Pretreatment by ASA or DCA did not modify HFF-induced activation of muscle afferents. On the other hand, LFF-induced response was markedly depressed by each pharmacological agent (-44% after ASA and -75% after DCA). We verified that DCA markedly lowered LA production after LFF. The present results show that the activation of group IV muscle afferents by LFF or HFF results from different mechanisms and also demonstrate the major role played by lactic acid production and, to a lesser extent, the release of inflammatory mediators in LFF-induced activation of group IV muscle afferents.
机译:我们已经表明,IV组肌肉传入神经在电诱发的疲劳过程中被激活。这项研究的目的是确定在高(100 Hz;高频疲劳,HFF)或低(10 Hz;低频疲劳,LFF)刺激下通过电诱发的疲劳来刺激这些肌肉传入的机制。在23只瘫痪和麻醉的兔子中,在3分钟HFF或5分钟LFF引起相同的力衰竭之前和之后,记录了来自胫骨前肌的IV组传入活动。还测量了腿部静脉血中的血浆乳酸浓度(LA)。在HFF和LFF试验后,我们测试了二氯乙酸(DCA)和乙酸乙酰水杨酸(ASA)(环氧化酶的阻滞剂)对疲劳诱导的第IV组肌肉传入神经的激活的作用,DCA降低了乳酸的产生,乙酰水杨酸(ASA)对环氧化酶的阻滞作用。 ASA或DCA的预处理并未改变HFF诱导的肌肉传入神经的激活。另一方面,每种药理作用剂均明显抑制了LFF诱导的反应(ASA后为-44%,DCA后为-75%)。我们验证了LFF后DCA明显降低了LA产量。目前的结果表明,LFF或HFF对IV组肌肉传入神经的激活是由不同的机制引起的,并且还证明了乳酸产生的主要作用,以及在较小程度上,LFF诱导的组的激活中炎性介质的释放。静脉注射肌肉。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号