We tested the hypotheses that: (1) neutrophil accumulation after contraction‐induced muscle injury is dependent on the β₂ integrin CD18, (2) neutrophils contribute to muscle injury and oxidative damage after contraction‐induced muscle injury, and (3) neutrophils aid the resolution of contraction‐induced muscle injury. These hypotheses were tested by exposing extensor digitorum longus (EDL) muscles of mice deficient in CD18 (CD18^−/−; Itgb2^tm1Bay) and of wild type mice (C57BL/6) to in situ lengthening contractions and by quantifying markers of muscle inflammation, injury, oxidative damage and regeneration/repair. Neutrophil concentrations were significantly elevated in wild type mice at 6 h and 3 days post‐lengthening contractions; however, neutrophils remained at control levels at these time points in CD18−/− mice. These data indicate that CD18 is required for neutrophil accumulation after contraction‐induced muscle injury. Histological and functional (isometric force deficit) signs of muscle injury and total carbonyl content, a marker of oxidative damage, were significantly higher in wild type relative to CD18−/− mice 3 days after lengthening contractions. These data show that neutrophils exacerbate contraction‐induced muscle injury. After statistically controlling for differences in the force deficit at 3 days, wild type mice also demonstrated a higher force deficit at 7 days, a lower percentage of myofibres expressing embryonic myosin heavy chain at 3 and 7 days, and a smaller cross sectional area of central nucleated myofibres at 14 days relative to CD18−/− mice. These observations suggest that neutrophils impair the restoration of muscle structure and function after injury. In conclusion, neutrophil accumulation after contraction‐induced muscle injury is dependent on CD18. Furthermore, neutrophils appear to contribute to muscle injury and impair some of the events associated with the resolution of contraction‐induced muscle injury.