Tuesday, June 12, 2012

For those who exercise and feel muscle pain afterwards, a new study finds that taking NSAIDS for muscle pain is ineffective and may interfere with the healing process. Maybe Vanilla Ice & Earthquake were right - "Ice, ice, Baby."

Sore Muscles May Not Benefit from Regular NSAIDs


Studies in healthy volunteers who exercised hard enough to cause muscle soreness indicated that the potent nonsteroidal anti-inflammatory drug (NSAID) ketoprofen inhibited the recovery process, according to Matthias Rother, MD, PhD, of International Medical Research in Graefelfing, Germany, and colleagues.

The total amount of pain, as quantified by the area under the curve (AUC) for pain severity over a one-week period after the exercise, was increased in participants who took ketoprofen at first onset of muscle soreness.

Celecoxib (Celebrex) treatment diminished total pain slightly, Rother and colleagues reported at the annual meeting of the European League Against Rheumatism.

But precisely because the reduction was small, and in light of the clear lack of benefit from ketoprofen, the researchers concluded that there is no value in NSAID treatment for muscle soreness.

Although NSAIDs are effective against a wide range of painful and inflammatory states, their benefit in exercise-induced muscle soreness has been controversial.

For example, a previous study found elevated cytokine levels in ultra-marathon runners who took ibuprofen relative to those who went untreated (Brain Behav Immun 2005; 9: 398-403). Another study by a different group indicated that ketoprofen extended the time with pain after tonsillectomy compared with celecoxib (Otolaryngol Head Neck Surg 2005; 132: 287-294).

In the current studies, Rother and colleagues had a total of 64 healthy volunteers walk down stairs for a total of 300 to 400 vertical meters, similar to walking all the way down from the top of a 100-story building.

Forty of the participants were randomized to take 200 mg of oral celecoxib or placebo twice daily for a week afterward, starting 12 to 26 hours after completing the stair test.

The other 24 completed an identical protocol except the NSAID was oral ketoprofen at 100 mg twice daily.

Participants in the latter study simply reported overall leg muscle pain, whereas those in the celecoxib study were asked to rate pain separately for the calf and thigh during contraction. All pain assessments were performed at pre-exercise baseline and at numerous intervals over the week after exercise.

At no point during the ketoprofen study did participants taking the active drug report less pain than those in the placebo group, Rother and colleagues found.

The AUC for pain scores was 462 (standard deviation 160) for ketoprofen versus 376 (SD 159) for placebo (P=0.02).

Most importantly, pain ended at hour 122 in the ketoprofen group versus hour 105 in the placebo group (P=0.005). Rother and colleagues said this was "the most negative effect" of ketoprofen.

In the celecoxib study, the drug was most effective in reducing calf pain on contraction. For thigh contraction, scores at each time point were virtually identical between participants taking the active drug versus placebo.

The sum of calf plus thigh pain was reduced 12% to 13% over the full study period, according to Rother and colleagues.

The peak reduction was measured 3 days after exercise (mean 2.7 for celecoxib compared with 2.0 for placebo, P-value not reported).

Overall, the findings imply "that the inflammatory reaction following muscle injury is essential for recovery," Rother and colleagues indicated in their poster presentation.

"Since the effect of celecoxib ... was only modest, usage of NSAIDs for the treatment of exercise induced muscle soreness cannot be supported," they concluded.

The trial had no commercial funding.
Rother is a shareholder and former employee of IDEA AG, which is developing a topical NSAID product. Other investigators declared they had no relevant financial interests.

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