Use of Nonsteroidal Anti-Inflammatory Drugs Following Exercise-Induced Muscle Injury
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LEADING ARTICLE
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Use of Nonsteroidal Anti-Inflammatory Drugs Following Exercise-Induced Muscle Injury Angela Baldwin Lanier Department of Health, Physical Education and Sport Science, Kennesaw State University, Kennesaw, Georgia, USA
Abstract
The objective of this article is to examine the use of NSAIDs for attenuating exercise-induced muscle injuries (EIMI), with an emphasis on their safety and usefulness for improving muscle function and reducing soreness. NSAIDs are some of the most widely consumed medications in the world, and NSAID use as therapy for EIMI has increased dramatically over the last 20 years. However, there is a lack of agreement concerning NSAID effectiveness for this purpose. The lack of consensus about the efficacy of NSAID use in relation to EIMI has spawned a recent interest in sports medicine research regarding NSAIDs. The application of a variety of methods used to induce, assess and quantify muscle injury has contributed to the inconsistency among the findings regarding the efficacy of NSAIDs for EIMI. Therefore, future studies should focus on the evaluation of muscle injury and function, with the use of better functional measurement tools and more uniformity in the assessment tools used. However, from review of the current literature, it is concluded that NSAID use for brief periods of time is beneficial for short-term recovery of muscle function and is an important laboratory tool for the study of EIMI.
1. NSAIDs 1.1 NSAID Mechanism of Action
NSAIDs have been available for over 100 years, since aspirin became available in 1899.[1,2] However, their anti-inflammatory effect was not recognised until 70 years later when Vane[3] found that aspirin and similar agents inhibited the synthesis of prostaglandin E2 (PGE2), the primary mediator of acute
inflammation. PGE2 and prostacyclin are potent peripheral vasodilators that act synergistically with bradykinin and histamine in producing oedema and inflammatory pain.[4,5] Inhibition of prostaglandin synthesis is proposed as the main mechanism of action for the therapeutic effects of NSAIDs.[5] Most NSAIDs currently available reversibly inhibit cyclo-oxygenase (COX) by competing with the substrate arachidonic acid for the active site of the enzyme. Thus, the enzyme is
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prevented from converting arachidonic acid to prostaglandin. The exception is aspirin, which inhibits PGE2 synthesis by the irreversible acetylation of COX.[5] The effects of aspirin last longer because new COX must be synthesised to replace the altered ones. It is the general COX inhibition by NSAIDs that leads to the development of commonly reported adverse effects. In 1991, researchers discovered that the COX enzyme exists in another distinct isoform, COX-2.[6] Both isoforms of COX (COX-1 and COX-2) catalyse the conversion of arachidonic acid to prostaglandin. COX-1 is a constitutive enzyme found in most tissues and is responsible for the regulation of normal cell activity.[5] Inhibition of COX-1 is
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