Cartilage fissures, surface fibrillation, and delamination represent early signs of hip osteoarthritis (OA). This damage may be caused by elevated first principal (most tensile) strain and maximum shear stress. The objectives of this study were to use a population of validated finite element (FE) models of normal human hips to evaluate the required mesh for converged predictions of cartilage tensile strain and shear stress, to assess the sensitivity to cartilage constitutive assumptions, and to determine the patterns of transchondral stress and strain that occur during activities of daily living. Five specimen-specific FE models were evaluated using three constitutive models for articular cartilage: quasilinear neo-Hookean, nonlinear Veronda Westmann, and tension-compression nonlinear ellipsoidal fiber distribution (EFD). Transchondral predictions of maximum shear stress and first principal strain were determined. Mesh convergence analysis demonstrated that five trilinear elements were adequate through the depth of the cartilage for precise predictions. The EFD model had the stiffest response with increasing strains, predicting the largest peak stresses and smallest peak strains. Conversely, the neo-Hookean model predicted the smallest peak stresses and largest peak strains. Models with neo-Hookean cartilage predicted smaller transchondral gradients of maximum shear stress than those with Veronda Westmann and EFD models. For FE models with EFD cartilage, the anterolateral region of the acetabulum had larger peak maximum shear stress and first principal strain than all other anatomical regions, consistent with observations of cartilage damage in disease. Results demonstrate that tension-compression nonlinearity of a continuous fiber distribution exhibiting strain induced anisotropy incorporates important features that have large effects on predictions of transchondral stress and strain. This population of normal hips provides baseline data for future comparisons to pathomorphologic hips. This approach can be used to evaluate these and other mechanical variables in the human hip and their potential role in the pathogenesis of osteoarthritis (OA).