Adding muscle where you need it: non-uniform hypertrophy patterns in elite sprinters.

Sprint runners achieve much higher gait velocities and accelerations than average humans, due in part to large forces generated by their lower limb muscles. Various factors have been explored in the past to understand sprint biomechanics, but the distribution of muscle volumes in the lower limb has not been investigated in elite sprinters. In this study, we used non-Cartesian MRI to determine muscle sizes in vivo in a group of 15 NCAA Division I sprinters. Normalizing muscle sizes by body size, we compared sprinter muscles to non-sprinter muscles, calculated Z-scores to determine non-uniformly large muscles in sprinters, assessed bilateral symmetry, and assessed gender differences in sprinters' muscles. While limb musculature per height-mass was 22% greater in sprinters than in non-sprinters, individual muscles were not all uniformly larger. Hip- and knee-crossing muscles were significantly larger among sprinters (mean difference: 30%, range: 19-54%) but only one ankle-crossing muscle was significantly larger (tibialis posterior, 28%). Population-wide asymmetry was not significant in the sprint population but individual muscle asymmetries exceeded 15%. Gender differences in normalized muscle sizes were not significant. The results of this study suggest that non-uniform hypertrophy patterns, particularly large hip and knee flexors and extensors, are advantageous for fast sprinting.

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model.

OBJECTIVE: This study was undertaken to test the hypothesis that abnormalities of the subchondral bone can result in osteoarthritis (OA). METHODS: We used a knockin model of human osteogenesis imperfecta, the Brittle IV (Brtl) mouse, in which defective type I collagen is expressed in bone. OA in individual mice was documented by micro-magnetic resonance imaging (micro-MRI) and micro-computed tomography (micro-CT). Alterations in the knee joints were confirmed by histopathologic and immunohistochemical analysis. In addition, atomic force microscopy (AFM) was used to assess the ultrastructure of the articular cartilage and subchondral bone matrix. RESULTS: Brtl mice had decreased integrity of bone but initially normal articular cartilage. However, by the second month of life, Brtl mice developed alterations of the cartilage that were characteristic of OA, as documented by micro-CT, micro-MRI, and histologic evaluation. In addition, chondrocyte loss and breakdown of the collagen matrix in the residual cartilage were demonstrated using AFM. CONCLUSION: The Brtl mouse model demonstrates that progressive destruction of articular cartilage characteristic of OA may be secondary to altered architecture of the underlying subchondral bone.