Mechanical stress is an important modulator of connective tissue repair. However, the effects on tendon healing are very poorly defined, preventing optimal use of mechanical stress. We hypothesized that early voluntary exercise initially retards tendon repair but results in a faster recovery rate at longer term. Male Wistar rats were injured by a collagenase injection in the Achilles tendon and exercise was voluntarily performed on a running wheel. We observed the persistent presence of neutrophils in injured tendons of rats that began exercise immediately after the trauma (injured+early exercise; INJ+EEX). Early exercise also increased the concentration of ED1⁺ macrophages in injured tendons after three and seven days compared to ambulatory injured rats (INJ). Similar results were obtained with the subset of ED2⁺ macrophages in the tendon core three days after the collagenase injection. Furthermore, collagen content returned to normal values more rapidly in the INJ+EEX tendons than in the INJ group but this was not associated with an increase in cell proliferation. Surprisingly, INJ+EEX tendons roughly displayed lower stiffness and force at rupture point relative to INJ tendons at day 28. Injured tendons of rats that began exercise only from day 7 had better mechanical properties than those of early-exercised rats 28 days post-injury. We speculate that the persistence of the inflammatory response and undue mechanical loading in the INJ+EEX tendons led to fibrosis and a loss of tendon function.