The purpose of this study was to evaluate pitching mechanics between female softball pitchers with upper extremity pain and those without upper extremity pain. Specifically, the trunk, shoulder and elbow kinematics and shoulder kinetics during the change-up softball pitch were examined. Fifty-five collegiate softball pitchers participated, divided into those with upper extremity pain (20.0±1.3 yrs.; 174.4±6.9 cm; 82.9±12.4 kg; 11.1±2.6 yrs. of experience; n=23) and those who were pain-free (19.9±1.4 yrs.; 173.8±6.9 cm; 81.4±12.5 kg; 10.0±2.5 yrs. of experience; n=32). Pitching mechanics were obtained via the trakSTAR electromagnetic tracking system (Ascension Technologies, Inc., Burlington, VT, USA). Mann-Whitney U tests revealed significant differences in shoulder horizontal abduction at foot contact (0.014, 153,2.450) and trunk lateral flexion at ball release (0.012, 150,-2.515); and between shoulder distraction force at ball release (0.034, 168,-2.124). The pain group illustrated greater shoulder horizontal abduction at foot contact, less trunk lateral flexion towards the throwing side at ball release, and greater shoulder distraction at ball release than the pain-free group. The differences in trunk and shoulder kinematics, and shoulder kinetics between groups allows for insight into further studies examining injury pervasiveness in softball pitching.

Extracellular matrix stiffening is a quintessential feature of cartilage aging, a leading cause of knee osteoarthritis. Yet, the downstream molecular and cellular consequences of age-related biophysical alterations are poorly understood. Here, we show that epigenetic regulation of α-Klotho represents a novel mechanosensitive mechanism by which the aged extracellular matrix influences chondrocyte physiology. Using mass spectrometry proteomics followed by a series of genetic and pharmacological manipulations, we discovered that increased matrix stiffness drove Klotho promoter methylation, downregulated Klotho gene expression, and accelerated chondrocyte senescence in vitro. In contrast, exposing aged chondrocytes to a soft matrix restored a more youthful phenotype in vitro and enhanced cartilage integrity in vivo. Our findings demonstrate that age-related alterations in extracellular matrix biophysical properties initiate pathogenic mechanotransductive signaling that promotes Klotho promoter methylation and compromises cellular health. These findings are likely to have broad implications even beyond cartilage for the field of aging research.