Articular cartilage is a soft biological tissue with impressive dissipation capacity and failure resistance. However, the dissipation mechanisms in the sub-failure mechanics and the failure mechanics of the tissue are incompletely understood. This dissertation attempts to address these gaps in knowledge through:​ (1) revealing fundamental mechanisms leading to broadband dissipation in cartilage (≥ about 5 degree phase shift), and (2) relating rate-dependent cartilage failure to dissipation mechanisms. The overall aim was accomplished via four sub-objectives. The first sub-objective was to examine the relative contribution of poroelasticity and viscoelasticity to cartilage dissipation across physiological loading rates (5-100 Hz). Poroelastic and viscoelastic dissipation mechanisms were uncoupled through dynamic testing at multiple length scales. The uncoupled mechanisms indicated that viscoelastic dissipation provided base broadband dissipation and poroelastic dissipation provided additional dissipation at relatively small length scales. The second sub-objective was to examine macroscopic cartilage dissipation as a function of matrix depletion under frequencies representative of traumatic loading (≥200 Hz). Microscopic intact and glycosaminoglycan (GAG) -depleted cartilage dissipation was measured up to 300 Hz. GAG depletion significantly increased cartilage dissipation due to altered poroelastic dissipation. The results provided the basis for understanding cartilage dissipation capacity at in vivo contact lengths under traumatic injury and high-rate physiological loading. The third sub-objective was to identify underlying mechanisms of rate-dependent cartilage failure. Localized cracks were induced by microindentation at two polarized loading rates. These results were analyzed via finite element modeling and nano/microscopic crack images. The results provided evidence of the link between rate-dependent cartilage failure and physical mechanisms, showing that large relaxation (collagen fibril realignment) around the tip delayed cartilage failure at the relatively slow loading rate. The fourth sub-objective was to establish the link between rate-dependent cartilage failure and poroviscoelastic relaxation as a function of matrix integrity. Rate-dependent crack nucleation in intact and GAG-depleted cartilage was generated from pre- to post-relaxation timescales. The correlation between rate-dependent crack nucleation and poroviscoelastic relaxation times was confirmed. These results indicated that rate-dependent cartilage failure was governed by the degree of relaxation prior to rupture at given matrix integrity and loading rates. These outcomes further our understanding of cartilage failure at different stages of degeneration. In conclusion, these findings in this dissertation widen our knowledge about the cartilage dissipation and failure.