Human Performance Laboratory, Ball State University, Muncie, Indiana.
J Appl Physiol (1985). 2020 Dec 1;129(6):1477-1482. doi: 10.1152/japplphysiol.00512.2020. Epub 2020 Oct 1.
Skeletal muscle health has been shown to benefit from regular consumption of cyclooxygenase (COX)-inhibiting drugs. Aspirin, especially at low doses, is one of the most commonly consumed COX inhibitors, yet investigations of low-dose aspirin effects on skeletal muscle are nonexistent. The goal of this study was to examine the efficacy of low-dose aspirin on skeletal muscle COX production of the inflammatory regulator prostaglandin (PG)E at rest and after exercise. Skeletal muscle biopsies (vastus lateralis) were taken from eight individuals [4 men, 4 women; 25 ± 1 yr; 81.4 ± 3.4 kg; maximal oxygen consumption (V̇o): 3.33 ± 0.21 L/min] before and 3.5 h after 40 min of cycling at 70% of V̇o for the measurement of ex vivo PGE production. Muscle strips were incubated in Krebs-Henseleit buffer (control) or supplemented with one of two aspirin concentrations that reflected blood levels after a low (10 µM; typical oral dose: 75-325 mg) or standard (100 µM; typical oral dose: 975-1,000 mg) dose. Low (-22 ± 5%)- and standard (-28 ± 5%)-dose aspirin concentrations both reduced skeletal muscle PGE production, independent of exercise ( < 0.05). There was no difference in PGE suppression between the two doses ( > 0.05). In summary, low-dose aspirin levels are sufficient to inhibit the COX enzyme in skeletal muscle and significantly reduce production of PGE, a known regulator of skeletal muscle health. Aerobic exercise does not appear to alter the inhibitory efficacy of aspirin. These findings may have implications for the tens of millions of individuals who chronically consume low-dose aspirin. This study demonstrated that even low-dose aspirin concentrations can significantly reduce the prostaglandin (PG)E/cyclooxygenase (COX) pathway activity in human skeletal muscle and this effect is not altered during the recovery period following aerobic exercise. These findings are noteworthy since aspirin is one of the most commonly consumed drugs in the world and nonaspirin COX-inhibiting drugs have been shown to regulate skeletal muscle health in sedentary and exercise-training individuals.
已有研究表明，经常服用环氧化酶（COX）抑制剂有益于维持骨骼肌健康。阿司匹林是最常被使用的 COX 抑制剂之一，尤其在低剂量下，然而，目前尚无关于低剂量阿司匹林对骨骼肌影响的研究。本研究旨在探究低剂量阿司匹林对骨骼肌 COX 生成炎性调节因子前列腺素（PG）E 的作用，无论在休息时还是运动后，该作用都存在。研究人员从 8 名个体（4 男，4 女；25 ± 1 岁；81.4 ± 3.4kg；最大摄氧量（V̇o）：3.33 ± 0.21L/min）的股外侧肌获取骨骼肌活检样本，在以 70%V̇o 骑行 40 分钟后，于 3.5 小时再次获取样本，用于测量体外 PGE 的产生。肌肉条在 Krebs-Henseleit 缓冲液（对照组）或两种阿司匹林浓度（反映低剂量（10 μM；典型口服剂量：75-325mg）或标准剂量（100 μM；典型口服剂量：975-1000mg）后）下孵育。低（-22 ± 5%）和标准（-28 ± 5%）剂量的阿司匹林均可抑制运动前后的骨骼肌 PGE 产生（ < 0.05）。两种剂量的 PGE 抑制作用没有差异（ > 0.05）。综上所述，低剂量阿司匹林水平足以抑制骨骼肌中的 COX 酶，并显著降低 PGE 的产生，而 PGE 是一种已知的骨骼肌健康调节因子。有氧运动似乎不会改变阿司匹林的抑制作用。这些发现可能对数千万长期服用低剂量阿司匹林的个体具有重要意义。本研究表明，即使是低剂量阿司匹林浓度也能显著降低人类骨骼肌中的前列腺素（PG）E/环氧化酶（COX）通路活性，且该作用在有氧运动后的恢复期不会改变。这些发现值得注意，因为阿司匹林是世界上最常被使用的药物之一，而非阿司匹林 COX 抑制剂已被证明可以调节久坐不动和运动训练个体的骨骼肌健康。
