Tendinopathy, degeneration of tendon that leads to pain and dysfunction, is common in both sports and occupational settings, but the mechanisms for tendinopathy are still unknown. Many studies attribute the initiation of tendinopathy to damage initiated by mechanical loading, leading to microstructural changes. Yet, the link between mechanical loading and microstructural changes, resulting in macroscopic changes, is not fully elucidated. Thus, the objective of the dissertation was to investigate the damage mechanisms and hierarchical structure of non-load- and load-bearing rat tendons, including the tail, plantaris, and Achilles tendons. Damage is defined as an irreversible change in micro-scale deformation that is observable in tissue-scale mechanical parameters. Multi-scale mechanical testing was conducted to investigate the damage mechanisms by simultaneously quantifying tissue-scale mechanical and microstructural changes. The hierarchical structures of these tendons were studied using multiple imaging methods including histology, scanning electron microscopy (SEM), and confocal microscopy.

At the tissue-scale, the transition strain, linear region modulus, and inflection point strain demonstrated strain-dependent changes in rat tail and plantaris tendons, suggesting that these metrics can be used to quantify the effect of damage. At the micro-scale, the micro-scale strain fully recovered following loading and unloading, yet the micro-scale sliding was only partially recoverable in all tendons. The non-recoverable sliding was strain-dependent in the tail and plantaris tendons, and the percentage of non-recoverable sliding was surprisingly similar between the tail and plantaris tendons. The nonrecoverable sliding was related to the altered tissue-scale transition strain in the tail and plantaris tendons. Collectively, the micro-scale sliding is responsible for both loading and damage mechanisms for both non-load and load-bearing tendons. Achilles tendon demonstrated some of the mechanical responses observed in plantaris and tail tendons, yet the results were inconclusive due to its complex structure. Studying the hierarchical structure of these tendons demonstrated that fascicles are absent in rat tendons, and thus the fiber is the largest tendon subunit in rats, with the exception of rat tail tendon. We provided a structurally-based definition of fiber as a bundle of collagen fibrils that is surrounded by elongated cells, and the fiber diameters were consistently 10-50 µm, which is conserved across larger species. Understanding the mechanisms responsible for the pathogenesis and progression of tendinopathy can improve prevention and rehabilitation strategies and guide therapies and design of engineered constructs.