Suppr超能文献

有氧运动改变慢性广泛性疼痛动物模型中的镇痛作用和神经营养因子-3 合成。

Aerobic exercise alters analgesia and neurotrophin-3 synthesis in an animal model of chronic widespread pain.

机构信息

Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Mail Stop 2002, 3901 Rainbow Blvd, Kansas City, KS 66160, USA.

出版信息

Phys Ther. 2010 May;90(5):714-25. doi: 10.2522/ptj.20090168. Epub 2010 Mar 25.

Abstract

BACKGROUND

Present literature and clinical practice provide strong support for the use of aerobic exercise in reducing pain and improving function for individuals with chronic musculoskeletal pain syndromes. However, the molecular basis for the positive actions of exercise remains poorly understood. Recent studies suggest that neurotrophin-3 (NT-3) may act in an analgesic fashion in various pain states.

OBJECTIVE

The purpose of the present study was to examine the effects of moderate-intensity aerobic exercise on pain-like behavior and NT-3 in an animal model of widespread pain.

DESIGN

This was a repeated-measures, observational cross-sectional study.

METHODS

Forty female mice were injected with either normal (pH 7.2; n=20) or acidic (pH 4.0; n=20) saline in the gastrocnemius muscle to induce widespread hyperalgesia and exercised for 3 weeks. Cutaneous (von Frey monofilament) and muscular (forceps compression) mechanical sensitivity were assessed. Neurotrophin-3 was quantified in 2 hind-limb skeletal muscles for both messenger RNA (mRNA) and protein levels after exercise training. Data were analyzed with 2-factor analysis of variance for repeated measures (group x time).

RESULTS

Moderate-intensity aerobic exercise reduced cutaneous and deep tissue hyperalgesia induced by acidic saline and stimulated NT-3 synthesis in skeletal muscle. The increase in NT-3 was more pronounced at the protein level compared with mRNA expression. In addition, the increase in NT-3 protein was significant in the gastrocnemius muscle but not in the soleus muscle, suggesting that exercise can preferentially target NT-3 synthesis in specific muscle types.

LIMITATIONS

Results are limited to animal models and cannot be generalized to chronic pain syndromes in humans.

CONCLUSIONS

This is the first study demonstrating the effect of exercise on deep tissue mechanical hyperalgesia in a rodent model of pain and providing a possible molecular basis for exercise training in reducing muscular pain.

摘要

背景

目前的文献和临床实践为使用有氧运动减轻慢性肌肉骨骼疼痛综合征患者的疼痛和改善功能提供了强有力的支持。然而,运动的积极作用的分子基础仍知之甚少。最近的研究表明,神经营养因子-3(NT-3)在各种疼痛状态下可能具有镇痛作用。

目的

本研究旨在检查中等强度有氧运动对广泛疼痛动物模型中疼痛样行为和 NT-3 的影响。

设计

这是一项重复测量、观察性的横断面研究。

方法

40 只雌性小鼠被注射正常(pH7.2;n=20)或酸性(pH4.0;n=20)生理盐水于腓肠肌,以诱导广泛的痛觉过敏,并进行 3 周的运动。评估皮肤(von Frey 单丝)和肌肉(镊子压缩)机械敏感性。运动训练后,在 2 条后肢骨骼肌中定量测定神经生长因子-3 的信使 RNA(mRNA)和蛋白水平。采用双因素重复测量方差分析对数据进行分析(组 x 时间)。

结果

中等强度有氧运动可减轻酸性生理盐水引起的皮肤和深部组织痛觉过敏,并刺激骨骼肌中 NT-3 的合成。与 mRNA 表达相比,NT-3 蛋白的增加更为明显。此外,NT-3 蛋白的增加在腓肠肌中很明显,但在比目鱼肌中不明显,这表明运动可以优先靶向特定肌肉类型的 NT-3 合成。

局限性

结果仅限于动物模型,不能推广到人类的慢性疼痛综合征。

结论

这是第一项研究表明运动对疼痛动物模型深部组织机械性痛觉过敏的影响,并为运动训练减轻肌肉疼痛提供了可能的分子基础。

相似文献

6
Fatiguing exercise enhances hyperalgesia to muscle inflammation.疲劳运动增强肌肉炎症的痛觉过敏。
Pain. 2010 Feb;148(2):188-197. doi: 10.1016/j.pain.2009.07.001. Epub 2009 Jul 25.

引用本文的文献

本文引用的文献

4
Intense exercise induces mitochondrial dysfunction in mice brain.高强度运动诱发小鼠大脑线粒体功能障碍。
Neurochem Res. 2008 Jan;33(1):51-8. doi: 10.1007/s11064-007-9406-x. Epub 2007 Jul 6.
6
Neurotrophins: mediators and modulators of pain.神经营养因子:疼痛的介质和调节因子
Annu Rev Neurosci. 2006;29:507-38. doi: 10.1146/annurev.neuro.29.051605.112929.
10
Exercise in fibromyalgia.纤维肌痛中的运动
Curr Opin Rheumatol. 2005 Mar;17(2):190-4. doi: 10.1097/01.bor.0000154202.56962.85.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验