Abstract
Prostaglandins (PGs) are essential signaling factors in bone mechanotransduction. In animals, inhibition of the enzyme responsible for PG synthesis (cyclooxygenase) by nonsteroidal anti-inflammatory drugs (NSAIDs) blocks the bone-formation response to loading when administered before, but not immediately after, loading. The aim of this proof-of-concept study was to determine whether the timing of NSAID use influences bone mineral density (BMD) adaptations to exercise in humans. Healthy premenopausal women (n = 73) aged 21 to 40 years completed a supervised 9-month weight-bearing exercise training program. They were randomized to take (1) ibuprofen (400 mg) before exercise, placebo after (IBUP/PLAC), (2) placebo before, ibuprofen after (PLAC/IBUP), or (3) placebo before and after (PLAC/PLAC) exercise. Relative changes in hip and lumbar spine BMD from before to after exercise training were assessed using a Hologic Delphi-W dual-energy X-ray absorptiometry (DXA) instrument. Because this was the first study to evaluate whether ibuprofen use affects skeletal adaptations to exercise, only women who were compliant with exercise were included in the primary analyses (IBUP/PLAC, n = 17; PLAC/PLAC, n = 23; and PLAC/IBUP, n = 14). There was a significant effect of drug treatment, adjusted for baseline BMD, on the BMD response to exercise for regions of the hip (total, p < .001; neck, p = .026; trochanter, p = .040; shaft, p = .019) but not the spine (p = .242). The largest increases in BMD occurred in the group that took ibuprofen after exercise. Total-hip BMD changes averaged –0.2% ± 1.3%, 0.4% ± 1.8%, and 2.1% ± 1.7% in the IBUP/PLAC, PLAC/PLAC, and PLAC/IBUP groups, respectively. This preliminary study suggests that taking NSAIDs after exercise enhances the adaptive response of BMD to exercise, whereas taking NSAIDs before may impair the adaptive response. © 2010 American Society for Bone and Mineral Research.
Highlights
Prostaglandin E2 (PGE2) increases in bone in response to mechanical loading and appears to be an essential intermediate in the signaling pathway for bone formation.(6,34,36) The key enzyme involved in the production of PGE2 and other prostaglandins is cyclooxygenase (COX)
Based on the studies of the timing of nonsteroidal anti-inflammatory drugs (NSAIDs) administration on the bone-formation response to a single loading bout in animals,(7,20) we hypothesized that taking ibuprofen before exercise sessions would attenuate the increases in bone mineral density (BMD) in response to exercise training when compared with taking ibuprofen after exercise sessions or with placebo treatment
Other inclusion criteria were exercising less than 3 days per week at moderate to high intensity; body mass index (BMI) of less than 30 kg/m2; nonsmoker for more than 2 years; not pregnant or lactating; no NSAID intolerance or sensitivity; typical NSAID use less than 3 days per month; no use of drugs that affect bone metabolism; serum thyroid-stimulating hormone concentration of 0.5 to 5.0 mU/mL; hematocrit of 30% or greater; serum creatinine concentration of less than 1.4 mg/dL; no history of ulcers, gastrointestinal bleeding, gastroesophageal reflux disease, thrombocytopenia, or bleeding disorders; and no known liver disease, kidney disease, cardiovascular disease, diabetes, or hypertension
Summary
Prostaglandin E2 (PGE2) increases in bone in response to mechanical loading and appears to be an essential intermediate in the signaling pathway for bone formation (i.e., mechanotransduction).(6,34,36) The key enzyme involved in the production of PGE2 and other prostaglandins is cyclooxygenase (COX). Inhibition of COX with nonsteroidal anti-inflammatory drugs (NSAIDs) markedly diminishes the bone-formation response to mechanical stress in laboratory animals and cultured osteoblasts.[5,7,8,9,20] This effect has been observed in response to both nonselective[5,7,8,9] and COX-2 selective inhibitors,(9,20) which is consistent with the observation that mechanotransduction is mediated primarily through the activation of COX-2.(2) Importantly, the timing of NSAID administration appears to be a key determinant of the bone-formation response. An important limitation of these studies is that they evaluated the bone-formation response to acute mechanical loading only It is not clear whether the usual effects of repeated bouts of mechanical loading (i.e., exercise training) to increase bone mineral density (BMD) and strength are impaired by NSAID use. Based on the studies of the timing of NSAID administration on the bone-formation response to a single loading bout in animals,(7,20) we hypothesized that taking ibuprofen before exercise sessions would attenuate the increases in BMD in response to exercise training when compared with taking ibuprofen after exercise sessions or with placebo treatment
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