Sixteen weeks of high-speed treadmill running is insufficient to induce Achilles tendinopathy in a rat model.

Despite the high prevalence of Achilles tendinopathy, clinically relevant animal models of Achilles tendinopathy are lacking. Previous studies have demonstrated possible tendinopathic cell and matrix changes with high-speed treadmill running, but the consistency as well as functional and mechanical consequences of these changes were unclear. We sought to determine the applicability of this protocol as a tendinopathy model by defining changes in Achilles tendon structure, function, and mechanics associated with 16 wk of high-speed treadmill running (26.8 m/min, 60 min/day, and 5 days/wk). We expected that high-speed running would induce detrimental structural, functional, and mechanical changes that worsen over the course of the 16-wk protocol. Treadmill running did influence body weight, hindlimb gait, and tendon cross-sectional area. However, contrary to our hypothesis, treadmill running did not induce tendinopathic changes in matrix organization, cell morphology, or tendon mechanics. As such, alternative strategies for robust and reproducible induction of Achilles tendinopathy in preclinical animal models are needed. We demonstrated that 16 wk of high-speed treadmill running did not induce structural, functional, or mechanical changes consistent with Achilles tendinopathy in the rat. These findings underscore the importance of exploring alternative approaches to generating reliable and clinically relevant animal models of Achilles tendinopathy.