title: Effect of a cyclooxygenase-2 inhibitor on postexercise muscle protein synthesis in humans.
abstract: Nonselective blockade of the cyclooxygenase (COX) enzymes in skeletal muscle eliminates the normal increase in muscle protein synthesis following resistance exercise. The current study tested the hypothesis that this COX-mediated increase in postexercise muscle protein synthesis is regulated specifically by the COX-2 isoform. Sixteen males (23 +/- 1 yr) were randomly assigned to one of two groups that received three doses of either a selective COX-2 inhibitor (celecoxib; 200 mg/dose, 600 mg total) or a placebo in double-blind fashion during the 24 h following a single bout of knee extensor resistance exercise. At rest and 24 h postexercise, skeletal muscle protein fractional synthesis rate (FSR) was measured using a primed constant infusion of [(2)H(5)]phenylalanine coupled with muscle biopsies of the vastus lateralis, and measurements were made of mRNA and protein expression of COX-1 and COX-2. Mixed muscle protein FSR in response to exercise (P < 0.05) was not suppressed by the COX-2 inhibitor (0.056 +/- 0.004 to 0.108 +/- 0.014%/h) compared with placebo (0.074 +/- 0.004 to 0.091 +/- 0.005%/h), nor was there any difference (P > 0.05) between the placebo and COX-2 inhibitor postexercise when controlling for resting FSR. The COX-2 inhibitor did not influence COX-1 mRNA, COX-1 protein, or COX-2 protein levels, whereas it did increase (P < 0.05) COX-2 mRNA (3.0 +/- 0.9-fold) compared with placebo (1.3 +/- 0.3-fold). It appears that the elimination of the postexercise muscle protein synthesis response by nonselective COX inhibitors is not solely due to COX-2 isoform blockade. Furthermore, the current data suggest that the COX-1 enzyme is likely the main isoform responsible for the COX-mediated increase in muscle protein synthesis following resistance exercise in humans.
authors.affiliation: Human Performance Laboratory, Ball State University, Muncie, IN 47306, USA.
authors.forename: Nicholas A
authors.initials: NA
authors.lastname: Burd
authors.forename: Jared M
authors.initials: JM
authors.lastname: Dickinson
authors.forename: Jennifer K
authors.initials: JK
authors.lastname: Lemoine
authors.forename: Chad C
authors.initials: CC
authors.lastname: Carroll
authors.forename: Bridget E
authors.initials: BE
authors.lastname: Sullivan
authors.forename: Jacob M
authors.initials: JM
authors.lastname: Haus
authors.forename: Bozena
authors.initials: B
authors.lastname: Jemiolo
authors.forename: Scott W
authors.initials: SW
authors.lastname: Trappe
authors.forename: Gordon M
authors.initials: GM
authors.lastname: Hughes
authors.forename: Charles E
authors.initials: CE
authors.lastname: Sanders
authors.forename: Todd A
authors.initials: TA
authors.lastname: Trappe
mesh_terms: D000068579:Celecoxib; D051545:Cyclooxygenase 1 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D004311:Double-Blind Method; D015444:Exercise / Q000502:physiology*; D006801:Humans; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000201:enzymology*; D014176:Protein Biosynthesis / Q000187:drug effects / Q000502:physiology; D011720:Pyrazoles / Q000494:pharmacology*; D012333:RNA, Messenger / Q000032:analysis; D012016:Reference Values; D055070:Resistance Training; D013449:Sulfonamides / Q000494:pharmacology*; D055815:Young Adult
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D012333:RNA, Messenger; D013449:Sulfonamides; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D000068579:Celecoxib