Influence of low‐dose aspirin, resistance exercise, and sex on human skeletal muscle PGE(2)/COX pathway activity

Prostaglandin (PG) E(2) has been linked to increased inflammation and attenuated resistance exercise adaptations in skeletal muscle. Nonaspirin cyclooxygenase (COX) inhibitors have been shown to reduce these effects. This study examined the effect of low‐dose aspirin on skeletal muscle COX production of PGE(2) at rest and following resistance exercise. Skeletal muscle (vastus lateralis) biopsies were taken from six individuals (4 M/2 W) before and 3.5 hr after a single bout of resistance exercise for ex vivo PGE(2) production under control and low (10 μM)‐ or standard (100 μM)‐dose aspirin conditions. Sex‐specific effects of aspirin were also examined by combining the current findings with our previous similar ex vivo skeletal muscle investigations (n = 20, 10 M/10 W). Low‐dose aspirin inhibited skeletal muscle PGE(2) production (p < 0.05). This inhibition was similar to standard‐dose aspirin (p > 0.05) and was not influenced by resistance exercise (p > 0.05) (overall effect: −18 ± 5%). Men and women had similar uninhibited skeletal muscle PGE(2) production at rest (men: 1.97 ± 0.33, women: 1.96 ± 0.29 pg/mg wet weight/min; p > 0.05). However, skeletal muscle of men was 60% more sensitive to aspirin inhibition than women (p < 0.05). In summary, the current findings 1) confirm low‐dose aspirin inhibits the PGE(2)/COX pathway in human skeletal muscle, 2) show that resistance exercise does not alter aspirin inhibitory efficacy, and 3) suggest the skeletal muscle of men and women could respond differently to long‐term consumption of low‐dose aspirin, one of the most common chronically consumed drugs in the world.