Tendons exhibit greater resistance to tissue and molecular-level damage with increasing strain rate during cyclic fatigue

Musculoskeletal soft connective tissues are commonly injured due to repetitive use, but the evolution of mechanical damage to the tissue structure during repeated loading is poorly understood. We investigated the strain-rate dependence of mechanical denaturation of collagen as a form of structural microdamage accumulation during creep fatigue loading of rat tail tendon fascicles. We cycled tendons at three strain rates to the same maximum stress relative to their rate-dependent tensile strength. Collagen denaturation at distinct points during the fatigue process was measured by fluorescence quantification of collagen hybridizing peptide binding. The amount of collagen denaturation was significantly correlated with fascicle creep strain, independent of the cyclic strain rate, supporting our hypothesis that tissue level creep is caused by collagen triple-helix unfolding. Samples that were loaded faster experienced more creep strain and denaturation as a function of the number of loading cycles relative to failure. Although this increased damage capacity at faster rates may serve as a protective measure during high-rate loading events, it may also predispose these tissues to subsequent injury and indicate a mechanism of overuse injury development. These results build on evidence that molecular-level collagen denaturation is the fundamental mechanism of structural damage to tendons during tensile loading.

Automated summary

The study found that mechanical damage to tissue structure during repeated loading is mainly caused by collagen denaturation. Faster loading rates result in more creep strain and denaturation, which may serve as a protective measure during high-rate events but also predispose tissues to injury.