Hip fractures represent a significant cause of mortality and morbidity among the elderly. Profound weakness and atrophy of the hip musculature often follows fractures and can lead to functional decline. Physiologically, this weakness is thought to be mediated through increased expression of inflammatory and ceramide biosynthesis genes via the Toll-like receptor pathway (TLP). Rehabilitation programs post hip fracture have been shown to be effective in improving functionality and quality of life. however, there have been few studies that investigate the physiological effect of exercise programs on genetic expression of inflammatory markers in skeletal muscle post hip fracture.