Lengthening contraction-induced inflammation is linked to secondary damage but devoid of neutrophil invasion

Inflammation triggered by exercise-induced muscle damage (EIMD) has been postulated to influence the extent of tissue destruction. We tested the hypotheses that 1) repressing inflammation decreases secondary damage production and 2) EIMD leads to a sequential appearance of inflammatory cells in which neutrophil accumulation precedes macrophage invasion. Rat ankle dorsiflexor muscles were submitted to in situ lengthening contractions. Measurement of in vitro contractile properties, inflammatory cell concentrations, and histological staining were performed postprotocol. Rats were treated with diclofenac, a nonsteroidal anti-inflammatory drug (NSAID group) to repress inflammation or with the vehicle solution (EIMD group). Muscles from the NSAID group had smaller force deficits on days 2 and 3 postexercise. This effect was associated with significantly smaller increases in the concentration of muscle macrophage ED1(+) and ED2(+). Surprisingly, neutrophils did not accumulate post-EIMD. These results suggest that inflammation-induced ED1(+) macrophage accumulation is responsible for the secondary damage observed 2-3 days post-EIMD. We further conclude that an increase in ED1(+) macrophage concentration can occur in absence of previous neutrophil invasion.