Consumption of a COX‐2 inhibitor stimulates muscle protein synthesis after resistance exercise in humans

Abstract

We have previously shown that non‐specific blockade of the cyclooxygenase (COX) enzymes in human skeletal muscle eliminates the normal increase in muscle protein synthesis following resistance exercise. We tested the hypothesis that this COX‐mediated increase in postexercise muscle protein synthesis is specifically regulated by the COX‐2 isoform. Sixteen males (23 ± 1 y, 177 ± 2 cm, 81.5 ± 3.4 kg) were randomly assigned to one of two groups that received three doses of either a specific COX‐2 inhibitor (celecoxib; 200 mg per dose, 600 mg total) or a placebo during the 24 h following a single bout of resistance exercise. Skeletal muscle fractional synthesis rate (FSR) was measured at rest and 24 hours postexercise. Mixed muscle FSR was increased following exercise to a greater extent (206%, p<0.05) in the COX‐2 group (0.052 ± 0.014 %/h) as compared with the placebo group (0.017 ± 0.007 %/h). These results suggest that specific inhibition of the COX‐2 isoform in human skeletal muscle causes a compensatory response in muscle protein synthesis. These data also highlight the involvement of the COX pathways in the regulation of muscle protein synthesis following resistance exercise.NIH R01 AG020532 (TT)