The concern with the use of NSAIDs involves the downstream effects of blocking the COX enzymes, as well as the consequences of chronic ingestion when individuals begin to use NSAIDs prophylactically. In response to injury, an injured muscle undergoes phases of healing that include degeneration, inflammation, regeneration, and fibrosis.
Each of these phases is important and tightly regulated by the body. Unfortunately, inflammation has gotten a bad rap over the years. Although there is usually some pain and discomfort associated with inflammation, inflammation is critical as it results in the release of various cytokines and cells that promote healing in most tissues.
Inflammation increases blood flow to the injured area and helps deliver nutrients necessary for repair. It also initiates a process that removes damaged cells from the area. Therefore, blocking COX and suppressing prostaglandin production may have a detrimental effect on the phases that occur after inflammation: tissue regeneration and adaptation.
Do They Work?
There's little scientific evidence to support that NSAIDs are an effective means to reduce muscle soreness following exercise-induced muscle damage (EIMD). A liberal review of the literature provides opposing views on the efficacy of NSAIDs in reducing post-exercise muscle soreness. Most investigators report no difference in pain perception or post-exercise muscle soreness when NSAIDs are taken for an acute injury, or for the duration of a resistance-training program.
Several reports have documented that the use of NSAIDs may result in a great deal of strength loss and creatine kinase (a circulating marker of muscle damage). Repeated use of NSAIDs may lead to severe skeletal muscle injury. Increased levels of creatine kinase following a bout of muscle-damaging activity, particularly when one takes NSAIDs, has the potential to contribute to rhabdomyolysis, a potentially fatal condition.
Many people use NSAIDs in an effort to reduce pain so they can continue to be active. But, that can harm the skeletal muscle protein synthesis. Inhibition of the COX enzyme has been shown to blunt increases in muscle mass and protein content in experimental investigations—with acute training and long term resistance training.
In animal models of endurance training, chronic ingestion of NSAIDs increased damage to the mitochondria (cellular respiration site), and it blunted typical adaptations seen with endurance training.
Since inhibition of the COX enzyme has been shown to contribute to gastrointestinal problems, particularly in older adults, there has been some speculation regarding the efficacy of a topical form of ibuprofen. The hypothetical advantage of this form of administration versus oral would be the lack of systemic effects on inhibiting COX. However, systemic absorption of topical ketoprofen has been reported and there have been no reported benefits of topical administration of ibuprofen in regards to muscle function and reduced soreness.