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Increased muscle stiffness helps prevent excessive movement that can lead to ligament and soft-tissue damage. There is empirical evidence suggesting that muscles are important in preventing injuries caused by excessive translational movements. Very little is known, however, on how our muscles provide translational stiffness. This thesis uses complementary theoretical (Chapters 2 and 3) and experimental (Chapter 4) techniques to address how muscles provide translational joint stiffness. In Chapters 2 and 3, we used an elastic energy approach to successfully derive equations that quantify muscular contributions to joint stiffness. From the equations, we were able to determine how the geometric orientation and mechanical properties of an individual muscle allows it to provide translational stiffness. In Chapter 4, using the techniques developed in the previous chapters, we test the notion that the nervous system is responsive to translational loading. From these works, several important discoveries were found. We are the first to find that muscles with large squared projections (alignment) over a degree-of-freedom are well suited to provide translational stiffness. Further, by explicitly describing the interactions between the translational and rotational stiffnesses we found that ignoring these interactions resulted in an overestimation of principal stiffnesses. This has large implication for stability analyses, where such overestimations could suggest that an unsafe task is actually safe. Experimentally, we found that the nervous system is responsive to translational loading. This was accomplished through increased activity of muscle well suited to provide translational stiffness. Collectively, the works presented provide much needed knowledge on the role muscle play in stabilizing and protecting our joints. This thesis provides a strong foundation for continued joint stiffness, stability, and impedance research., Doctor of Science (PhD)