INFLUENCE OF NONSTEROIDAL ANTIINFLAMMATORY DRUGS ON EXERCISE-INDUCED MUSCLE DAMAGE IN RATS 374

In human, the delay observed between damaging eccentric exercise and the onset of muscle soreness suggests that, among other things, inflammation might contribute to exercise-induced muscle damage (EIMD). The objective of this study was to test whether nonsteroidal antiinflammatory drugs (NSAIDs) influence the time course of EIMD in rat. The extensor digitorum longus (EDL) was submitted to an in situ eccentric contraction protocol consisting of three 5 min periods separated by 5 min of recovery. During stimulation, a 0,6 s tetanic contraction was elicited every 2 s through anterior tibial nerve stimulation synchronized with ankle plantar flexion. Speed and extent of leightening were within physiological range. Nerve exposure alone (SHAM group) was performed on the opposite limb. Following contractions, rats received a NSAID (diclofenac, 1 mg/kg twice a day) in honey or vehicle alone (CTRL group) for 24, 48 or 72 hours prior to determination of isometric contraction properties in vitro. Contractile properties of SHAM-NSAID, SHAM-CTRL and NSAID without any surgery did not differ from values of control rats. At 24 hours, minimal variations in absolute and normalized values for force production were observed. A 35% decline in absolute maximum tetanic tension (Po) was observed 48 and 72 hours post-exercise in CTRL group; maximum specific tetanic tension (Po, N/cm2) was reduced by 46 and 17% in CTRL (p<0.001) and NSAID(p<0.05) groups at 48 hours compared to their respective SHAM groups. A similar situation was also observed at 72 hours. Overall, a significant protective effect of the NSAID could be seen for both absolute and specific Po values. These results clearly demonstrate the delayed nature of EIMD in rat muscle and indicate that NSAIDs have an important preventive effect on loss of muscle function following EIMD.