NSAR in whiplash:: Is it reasonable?

Damage to skeletal muscle sets off a chemical cascade in which cyclooxygenases (COXs), a family of enzymes, catalyze the conversion of arachidonic acid to prostaglandins, which are physiologically active lipid compounds found in nearly every tissue in humans and other animals.

 

Various types of prostaglandin are present without injury. They play a wide range of roles throughout multiple systems, including platelet aggregation or disaggregation and gastrointestinal and kidney function. But the prostaglandins produced in response to muscle damage execute specific, more temporary functions: They sensitize neurons to pain, recruiting cells that first clean up debris in damaged muscles and then synthesizing the proteins to repair and reinforce the damaged areas.

NSAIDs block COX receptors, inhibiting the production of a wide spectrum of prostaglandins. Understanding this connection, researchers have tried feeding NSAIDs to rodents. A significant decrease in muscle hypertrophy was observed.

In one study, for example, researchers surgically removed the gastrocnemius and soleus muscles of rats, forcing them to rely more on their plantaris muscles. This normally causes rapid growth in the plantaris. But ibuprofen administration reduced plantaris muscle growth in rats by 50%-70%

It's a little harder to measure such effects on muscle repair and generation in people, and the trials so far have had mixed results. The mixed findings have made it challenging for sports medicine physicians to recommend for or against NSAIDs.

Most recent reviews have come down on the side of restricting the use of NSAIDs, pending more information. "Anti-inflammatory drugs seem to inhibit the healing process of connective tissue and the stimulating effect of exercise on connective tissue protein synthesis," concluded the authors of a 2014 review in the journal Connective Tissue Research.

 

One reason for caution is that NSAIDs can cause many side effects, including kidney disease, asthma exacerbation, gastrointestinal and renal side-effects, hypertension, and other cardiovascular diseases, in addition to whatever effects they have on muscle.

Some evidence shows that newer NSAIDs, such as celecoxib and rofecoxib, cause fewer of these systemic side effects by selectively targeting COX2, the type of COX most associated with inflammation. But it's too early to say whether they are any more beneficial when it comes to muscle repair and generation.

At least one study found that 400 mg of ibuprofen a day had no more effect on muscle soreness after exercise than a placebo.

In addition to hoping to feeling better, many people want to tamp down their inflammation, because recent reports suggested it could exacerbate systemic illnesses, including Alzheimer disease, heart disease, and obesity, says Dr Pizza. "Inflammation has got its hands in all kinds of different diseases," he says.

But NSAIDs don't offer much of a solution, Dr Pizza adds. "The problem is that you were injured. Maybe you did too much exercise. Maybe somebody hit you in the leg. You experienced trauma. The inflammation is a response to the damage. It's not the problem."

Laird Harrison. Is Long-Term NSAID Use Harmful to Athletes? Medscape. Oct 28, 2015.


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