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抗炎药物对人类跑步引起的髌腱胶原合成增加的影响。

Effect of anti-inflammatory medication on the running-induced rise in patella tendon collagen synthesis in humans.

机构信息

Institute of Sports Medicine Copenhagen, Bispebjerg Hospital, and Center of Healthy Aging, University of Copenhagen, Copenhagen, Denmark.

出版信息

J Appl Physiol (1985). 2011 Jan;110(1):137-41. doi: 10.1152/japplphysiol.00942.2010. Epub 2010 Oct 28.

DOI:10.1152/japplphysiol.00942.2010
PMID:21030675
Abstract

NSAIDs are widely used in the treatment of inflammatory diseases as well as of tendon diseases associated with pain in sports and labor. However, the effect of NSAID intake, and thus blockade of PGE(2) production, on the tendon tissue adaptation is unknown. The purpose of the present study was to elucidate the possible effects of NSAID intake on healthy tendon collagen turnover in relation to a strenuous bout of endurance exercise. Fifteen healthy young men were randomly assigned into two experimental groups, with one group receiving indomethacin (oral 2 × 100 mg Confortid daily for 7 days; NSAID; n = 7) and a placebo group (n = 8). Both groups were exposed to a prolonged bout of running (36 km). The collagen synthesis NH₂-terminal propeptide of type I (PINP) and PGE₂ concentrations were measured before and 72 h following the run in the patella tendon by microdialysis. The peritendinous concentrations of PINP increased significantly in the placebo group as a result of the run, as shown previously. PGE₂ levels were significantly decreased 72 h after the run compared with basal levels in the subjects treated with NSAID and unchanged in the placebo group. The NSAID intake abolished the adaptive increase in collagen synthesis in the patella tendon found in the placebo group in response to the prolonged exercise (P < 0.05). The present study demonstrates that intake of NSAID decreased interstitial PGE₂ and abolished the exercise-induced adaptive increase in collagen synthesis in human tendons.

摘要

非甾体抗炎药(NSAIDs)广泛用于治疗炎症性疾病以及与运动和劳动相关的疼痛性肌腱疾病。然而,NSAID 摄入(即 PGE(2)产生的阻断)对肌腱组织适应性的影响尚不清楚。本研究的目的是阐明 NSAID 摄入对健康肌腱胶原周转的可能影响,以及与剧烈耐力运动有关的影响。15 名健康年轻男性被随机分为两组,一组接受吲哚美辛(口服 2×100mg Confortid,每天一次,持续 7 天;NSAID;n=7),另一组接受安慰剂(n=8)。两组均进行长时间的跑步(36 公里)。通过微透析在髌骨肌腱中测量 I 型胶原 NH₂-末端前肽(PINP)和 PGE₂浓度,在跑步前和跑步后 72 小时进行测量。与基线水平相比,安慰剂组的 PINP 浓度在跑步后显著升高,这与以前的研究结果一致。与安慰剂组相比,NSAID 治疗组的 PGE₂水平在跑步后 72 小时显著降低,而安慰剂组则保持不变。NSAID 摄入消除了安慰剂组在长时间运动后的适应性胶原合成增加(P<0.05)。本研究表明,NSAID 摄入降低了间质 PGE₂,并消除了人类肌腱中运动引起的适应性胶原合成增加。

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