Training, Muscle Fatigue and Stress Fractures.
Abstract
The objective of this twenty month contract has been to identify the causative mechanical factors responsible for the stress fracture lesion. Over this period, the research has focussed exclusively on an animal model developed specifically for this work, the functionally isolated avian ulna. The stress fracture protocols have exploited this model's ability to withstand, in vivo, high cyclic loading, applied both axially and torsionally, with the aim of identifying that specific mechanical agent within the physical regimen which stimulates this debilitating condition. Previous work from our group suggests that the lesion is a product of tissue remodeling (intracortical porosis), not material microdamage. As importantly, the site of the lesion, when correlated to the mechanical environment to which the bone is subjected, emphasizes that the pathology predominates in areas of least normal strain, not those areas subject to greatest deformation. Finally, the pathology observed in this animal model is identical to that which occurs in humans, demonstrating the appropriateness of using these studies to better understand the etiology of the human condition. From these developments, we proposed that the stress fracture lesions, or rather elevated intracortical remodeling, was not intensity dependent, but instead was a product of redundant, cyclic activity.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 29, 1992
- Accession Number
- ADA255277
Entities
People
- Clinton T. Rubin
Organizations
- Stony Brook University