Specht Jonathan W, Bailly Alyssa R, Garcia Serena, Klepacz Steven, Andrade DE Oliveira Suzana, Lucero David, McKenna Zachary J, Schlader Zachary J, Amorim Fabiano T
Department of Health, Exercise, and Sports Sciences, University of New Mexico, Albuquerque, NM.
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, and University of Texas Southwestern Medical Center, Dallas, TX.
Med Sci Sports Exerc. 2025 Jun 1;57(6):1092-1102. doi: 10.1249/MSS.0000000000003659. Epub 2025 Jan 29.
To test the hypothesis that ibuprofen ingestion exacerbates markers of acute kidney injury (AKI), gastrointestinal (GI) injury, and endotoxemia after running in the heat.
Using a randomized double-blind crossover design, 11 physically active individuals (six women) ingested 600 mg of ibuprofen or placebo 12- and 1-h before running 1 h in a heated chamber (35°C, 20%-60% R.H.) at an intensity of 60% V̇O 2peak . Blood and urine samples were collected preexercise, postexercise, and 1-h postexercise to assess cytokines and markers of AKI, GI injury, and endotoxemia.
One hour of running in the heat increased markers of AKI (urinary product of IGFBP7•TIMP2 [Placebo: ∆ 1.8 ± 0.8 log 10 (ng·mL 2 )/1000, Ibuprofen: ∆ 1.8 ± 0.9 log 10 (ng·mL 2 )/1000], urinary NGAL, and serum cystatin C), GI damage (I-FABP [Placebo: ∆ 631 ± 446 pg·mL -1 , Ibuprofen: ∆ 576 ± 455 pg·mL -1 ]), and inflammatory cytokines (TNFα [Placebo: ∆ 5.2 ± 3.5 pg·mL -1 , Ibuprofen: ∆ 6.2 ± 4.9 pg·mL -1 ], IL-6, IL-10, and MCP-1), but these changes were not exacerbated by ibuprofen ingestion. There were effects of time ( P < 0.001) and condition ( P = 0.03) for serum IL-8, with greater concentrations in the ibuprofen (pre: 11.4 ± 5.1 pg·mL -1 , post: 15.5 ± 7.3 pg·mL -1 ) trials than placebo (pre: 9.7 ± 4.2 pg·mL -1 , post: 11.7 ± 5.4 pg·mL -1 ). There were no effects of time or condition on markers of endotoxemia (LBP [Placebo: ∆ -1.2 ± 3.2 μg·mL -1 , Ibuprofen: ∆ 1.0 ± 1.6 μg·mL -1 ], sCD14).
These findings indicate that ibuprofen ingestion does not worsen intestinal or renal injury experienced during 1 h of exercise in the heat, but increases pro-inflammatory IL-8.
验证布洛芬摄入会加剧热环境下跑步后急性肾损伤(AKI)、胃肠道(GI)损伤和内毒素血症标志物的这一假设。
采用随机双盲交叉设计,11名身体活跃的个体(6名女性)在35°C、相对湿度20%-60%的热室中以60%最大摄氧量强度跑步1小时前12小时和1小时分别摄入600毫克布洛芬或安慰剂。在运动前、运动后和运动后1小时采集血液和尿液样本,以评估细胞因子以及AKI、GI损伤和内毒素血症的标志物。
在热环境下跑步1小时会增加AKI标志物(胰岛素样生长因子结合蛋白7•金属蛋白酶组织抑制因子2的尿产物[安慰剂组:∆1.8±0.8 log₁₀(ng·mL²)/1000,布洛芬组:∆1.8±0.9 log₁₀(ng·mL²)/1000]、尿中性粒细胞明胶酶相关脂质运载蛋白和血清胱抑素C)、GI损伤标志物(肠脂肪酸结合蛋白[安慰剂组:∆631±446 pg·mL⁻¹,布洛芬组:∆576±455 pg·mL⁻¹])以及炎性细胞因子(肿瘤坏死因子α[安慰剂组:∆5.2±3.5 pg·mL⁻¹,布洛芬组:∆6.2±4.9 pg·mL⁻¹]、白细胞介素-6、白细胞介素-10和单核细胞趋化蛋白-1),但布洛芬摄入并未加剧这些变化。血清白细胞介素-8存在时间效应(P<0.001)和条件效应(P = 0.03),布洛芬试验中的浓度(运动前:11.4±5.1 pg·mL⁻¹,运动后:15.5±7.3 pg·mL⁻¹)高于安慰剂试验(运动前:9.7±4.2 pg·mL⁻¹,运动后:11.7±5.4 pg·mL⁻¹)。内毒素血症标志物(脂多糖结合蛋白[安慰剂组:∆ -1.2±3.2 μg·mL⁻¹,布洛芬组:∆1.0±1.6 μg·mL⁻¹]、可溶性CD14)不存在时间或条件效应。
这些发现表明,布洛芬摄入不会加重热环境下1小时运动期间所经历的肠道或肾脏损伤,但会增加促炎性白细胞介素-8。