Non-Steroidal Anti-Inflammatory Drugs Do Not Affect the Bone Metabolic Response to Exercise

Non-steroidal anti-inflammatory drugs (NSAID) are associated with increased stress fracture risk, potentially due to inhibiting the adaptive bone formation responses to exercise. This study investigated if a single, maximal dose of three different NSAIDs alters bone formation biomarker response to strenuous exercise. In a randomized, counter-balanced order, 12 participants (10 male, 2 female), performed four bouts of plyometric jumps, each separated by at least one week. Two hours before exercise, participants consumed either placebo (PLA) or NSAID: Ibuprofen (IBU, 800 mg), celecoxib (CEL, 200 mg), flurbiprofen (FLU, 100 mg). Blood was collected before (PRE), and at 0, 15, 60, 120, and 240 minutes post-exercise. Parathyroid hormone (PTH), ionized calcium (iCa), procollagen type 1 N-terminal propeptide (P1NP), bone alkaline phosphatase (BAP), osteocalcin (OCN), C-terminal telopeptide of type 1 collagen (CTX), tartrate resistant acid phosphatase (TRAP5b), and sclerostin (SCL) were measured. Prostaglandin E2 metabolite (PGE2M) and creatinine (Cr) were measured in urine. Data were analyzed using repeated measures ANOVA and area under the curve analysis (AUC). Data are mean ± SD. There was an exercise effect for P1NP, BAP, OCN, CTX, TRAP5b, SCL, OPG, PTH, and iCa (all p < 0.05), but no NSAID treatment effect for any biomarker (all p > 0.05). AUC analyses were not different for any biomarker (p > 0.05). PGE2M was higher during the PLA trial (322 ± 153 pg/mg Cr, p < 0.05) compared to IBU (135 ± 83 pg/mg), CEL (202 ± 107 pg/mg), and FLU (159 ± 74 pg/mg). Plyometric exercise induced changes in bone metabolism, but the responses were unaltered by consuming NSAIDs two hours before exercise.