Active Voice: Ibuprofen Use Before Exercise: Good or Bad for Bone Health?

By Vanessa D. Sherk, Ph.D.

Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily reflect positions or policies of ACSM.

Vanessa D. Sherk, Ph.D., earned her doctoral degree in exercise physiology from the University of Oklahoma in Norman, Oklahoma. She completed postdoctoral training in gerontology and endocrinology at the University of Colorado Anschutz Medical Campus in Aurora, Colorado; there, she currently is an instructor of medicine in the Department of Medicine, Division of Endocrinology, Metabolism, & Diabetes. Dr. Sherk has been an ACSM member since 2006, and her main research focus is on the effect of nutrition and metabolic disease on bone health.

This commentary presents Dr. Sherk’s views on the topic of a research article that she and her colleagues authored together. Their article appeared in the May 2017 issue of
Medicine & Science in Sports & Exercise® (MSSE).

Bone-loading physical activity is recommended for improving and maintaining bone health (see ACSM Position Stand on Physical Activity and Bone Health). Factors that make a bone strong - and less likely to fracture - include bone mass, the distribution of the bone tissue around its center of mass and material characteristics such as the amount of mineral in bone. The skeleton adapts to small deformations (i.e., strain) that occur in response to loading, whereas larger, more rapid and novel deformations induce the greatest benefit. For adaptations to occur, the bone needs to be able to sense that the bone is being loaded. One factor that is important for bone tissue to be able to respond to mechanical stimuli is prostaglandin E2, which is converted from arachidonic acid via cyclooxygenase (COX) enzymes.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used medications. Many people take NSAIDs before or after exercise to prevent or reduce pain. NSAIDs work by blocking COX enzymes, which then can inhibit the conversion of arachidonic acid to prostaglandin E2. If prostaglandin E2 is sufficiently inhibited when the bone is being loaded, the adaptation to load may then be impaired. This was demonstrated in prior studies that measured bone formation after a single bout of mechanical loading. Therefore, if chronic use of NSAIDs reduces the skeletal benefit of exercise training, it could negatively impact bone health for many people across the world and across the lifespan.

As described in our paper published in the May 2017 issue of in MSSE, we used female rodents to determine whether taking the NSAID, ibuprofen, before treadmill running prevents the skeletal adaptations to 12 weeks of aerobic exercise training. Adult rats ran for an hour per day, 5 days per week, for 12 weeks, and were given an oral dose of ibuprofen or placebo one hour prior to every exercise bout. At the end of the study, we measured the size, resistance to bending, stiffness and strength of tibias and femurs. We also used a computational method called finite element modeling to simulate the behavior of bone in response to a standardized load.

Our running protocol was effective for improving bone size, stiffness, strength and resistance to bending compared to non-exercising controls. During the finite element modeling simulations, bones of exercised rats reacted more favorably to standardized loads. However, we did not detect any inhibitory effect of ibuprofen on the skeletal adaptation to exercise training. We may not have had the same result if we had used a long-acting NSAID (e.g., naproxen) or other means of inhibiting prostaglandin E2, but we chose ibuprofen because it is one of the more common NSAIDs. Additionally, we did not test what happens to the bone adaptation to exercise training if NSAIDs are taken after exercise, which is also a common practice. Published evidence thus far would lead us to hypothesize that taking an NSAID after exercise would not prevent the skeleton from responding to exercise.