Low-dose aspirin and COX inhibition in human skeletal muscle

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.