Resistance exercise and cyclooxygenase (COX) expression in human skeletal muscle: Implications for COX‐inhibiting drugs and protein synthesis

We have shown that ibuprofen (IBU) and acetaminophen (ACET) block COX synthesis of PGF 2α and the muscle protein synthesis increase following resistance exercise (RE). Confusingly, these two drugs are purported to work through different mechanisms, with ACET unable to block COX and IBU able to non‐specifically block COX‐1 and COX‐2. A recently discovered intron‐retaining COX, now known to have 3 variants, has been shown to be sensitive to both drugs. We measured the expression patterns and levels of the intron 1‐retaining COX‐1 variants (‐1b 1 , ‐1b 2 , and ‐1b 3 ), COX‐1, and COX‐2 at rest and following RE. Skeletal muscle biopsies were taken from 8M and 8F before, 4, and 24 h following a bout of RE and analyzed using real‐time RT‐PCR. Relatively few individuals expressed intron 1‐retaining COX‐1b variants (COX‐1b 1 , ‐1b 2 , and ‐1b 3 ) at any time point, and when expressed these variants were in very low abundance. COX‐1 was the most abundant COX mRNA before RE and remained unchanged ( P>0.05 ) following RE. COX‐2 was not expressed before RE, but increased ( P<0.05 ) at 4 and 24 h post RE. The inconsistent and low levels of expression of the intron 1‐retaining COX‐1 variants suggest that these variants are not likely responsible for the inhibition of PGF 2α production and skeletal muscle protein synthesis after RE by IBU and ACET. Skeletal muscle specific inhibition of COX‐1 or COX‐2 by these drugs should be considered. Support: R01 AG020532