Staab Jeffery S, Sczuroski Cara E, Gwin Jess A, Geddis Alyssa V, Hughes Julie M, Roberts Brandon M
Military Performance Division, US Army Research Institute of Environmental Medicine, Natick, MA.
Military Nutrition Division, US Army Research Institute of Environmental Medicine, Natick, MA.
Med Sci Sports Exerc. 2025 Jan 1;57(1):201-209. doi: 10.1249/MSS.0000000000003553. Epub 2024 Sep 4.
Nonsteroidal anti-inflammatory drugs (NSAID) are associated with increased stress fracture risk, potentially due to inhibiting the adaptive bone formation responses to exercise. This study investigated if a single, maximal dose of three different NSAID alters bone formation biomarker response to strenuous exercise.
In a randomized, counterbalanced order, 12 participants (10 male, 2 female), performed four bouts of plyometric jumps, each separated by at least 1 wk. Two hours before exercise, participants consumed either placebo or NSAID: ibuprofen (800 mg), celecoxib (200 mg), flurbiprofen (100 mg). Blood was collected before (PRE), and at 0, 15, 60, 120, and 240 min postexercise. Parathyroid hormone, ionized calcium, procollagen type 1 N-terminal propeptide, bone alkaline phosphatase, osteocalcin, C-terminal telopeptide of type 1 collagen, tartrate-resistant acid phosphatase, and sclerostin were measured. Prostaglandin E2 metabolite and creatinine were measured in urine. Data were analyzed using repeated-measures ANOVA and area under the curve analysis. Data are mean ± SD.
There was an exercise effect for procollagen type 1 N-terminal propeptide, bone alkaline phosphatase, osteocalcin, C-terminal telopeptide of type 1 collagen, tartrate-resistant acid phosphatase, sclerostin, osteoprotegerin, parathyroid hormone, and ionized calcium (all P < 0.05), but no NSAID treatment effect for any biomarker (all P > 0.05). Area under the curve analyses were not different for any biomarker ( P > 0.05). Prostaglandin E2 metabolite was higher during the placebo trial (322 ± 153 pg·mg -1 creatinine, P < 0.05) compared with ibuprofen (135 ± 83 pg·mg -1 ), celecoxib (202 ± 107 pg·mg -1 ), and flurbiprofen (159 ± 74 pg·mg -1 ).
Plyometric exercise induced changes in bone metabolism, but the responses were unaltered by consuming NSAID 2 h before exercise.
非甾体抗炎药(NSAID)与应力性骨折风险增加有关,这可能是由于其抑制了骨骼对运动的适应性形成反应。本研究调查了单次最大剂量的三种不同NSAID是否会改变骨形成生物标志物对应激运动的反应。
12名参与者(10名男性,2名女性)按照随机、平衡的顺序进行了四组增强式跳跃练习,每组练习间隔至少1周。在运动前两小时,参与者服用安慰剂或NSAID:布洛芬(800毫克)、塞来昔布(200毫克)、氟比洛芬(100毫克)。在运动前(PRE)以及运动后0、15、60、120和240分钟采集血液。检测甲状旁腺激素、离子钙、1型前胶原N端前肽、骨碱性磷酸酶、骨钙素、1型胶原C端肽、抗酒石酸酸性磷酸酶和硬化蛋白。检测尿液中的前列腺素E2代谢物和肌酐。使用重复测量方差分析和曲线下面积分析对数据进行分析。数据以平均值±标准差表示。
1型前胶原N端前肽、骨碱性磷酸酶、骨钙素、1型胶原C端肽、抗酒石酸酸性磷酸酶、硬化蛋白、骨保护素、甲状旁腺激素和离子钙均有运动效应(所有P<0.05),但任何生物标志物均无NSAID治疗效应(所有P>0.05)。任何生物标志物的曲线下面积分析均无差异(P>0.05)。与布洛芬(135±83 pg·mg -1肌酐)、塞来昔布(202±107 pg·mg -1肌酐)和氟比洛芬(159±74 pg·mg -1肌酐)相比,安慰剂试验期间前列腺素E2代谢物水平更高(322±153 pg·mg -1肌酐,P<0.05)。
增强式运动引起了骨代谢变化,但在运动前2小时服用NSAID并不会改变这些反应。