TP9.2 Neuromuscular Strategies in Hip Dysplasia: Evidence from Maximal Isometric Tasks

Abstract Hip dysplasia alters the shape of the acetabulum and reduces the inherent stability of the hip joint. Although its influence on surrounding musculature has been increasingly recognized, little is known about how individuals with dysplasia coordinate muscle activity to manage this instability. One mechanism that may play a role is muscle co-contraction, the concurrent activation of opposing muscle groups that can increase joint stiffness when stability is challenged. Individuals with structurally unstable hips could plausibly rely on this strategy even during controlled, non dynamic tasks. However, increased reliance on co-contraction may also have consequences, as greater joint stiffening could elevate internal joint forces and potentially contribute to accelerated wear. The objective of this study was to characterize muscle activation patterns during maximal isometric contraction in people with hip dysplasia, with the expectation that they would demonstrate elevated co-contraction. Maximal isometric contractions were completed on a Biodex dynamometer by sixteen patients with hip dysplasia and sixteen matched controls. These contractions were performed in four positions and directions: hip abduction at 30°, hip abduction at 15°, hip adduction at 15° of abduction, and hip extension at 10°. Surface EMG recorded activation of the gluteus maximus (GMax), gluteus medius (GMed), tensor fasciae latae (TFL), and adductor longus (ADD). A co contraction index (CCI) was calculated for four muscle pairs (GMed–ADD, TFL–ADD, ADD–GMed, GMax–TFL). Maximal torque and CCI values were averaged across groups, and comparisons between the affected limb and controls were performed using independent t-tests. Preliminary results show no group differences in torque across tasks. Co-contraction did not differ between groups during hip abduction or adduction. However, during hip extension, patients with dysplasia exhibited lower co-contraction (controls: 0.20 ± 0.18; dysplasia: 0.13 ± 0.14; p = 0.028), primarily driven by lower TFL activity. These findings highlight task-specific differences in neuromuscular strategies between patients with hip dysplasia and healthy controls. Contrary to the stated hypothesis, patients with dysplasia displayed lower CCI values compared to control in the extension task. Characterizing the activation patterns in this population may deepen understanding of hip instability and support the development of targeted rehabilitation approaches.