Chronic pain originating from the musculoskeletal system is a dominant cause of sick-leave in modern industry and often a very disabling and troublesome condition for the individual. Although the cause of this problem in skeletal muscle is unknown, one of the most frequent situations in which muscle pain is experienced is in industrial workers who have to move repeatedly and/or forcibly. The cumulative trauma disorder (CTD) which results from repetitive movements is of special interest because these repeat-motion injuries are one of the most difficult to anticipate and prevent. Our studies in humans have shown that exposure to a single bout of repeated strains at moderate intensity can lead to myofiber and fascial rupture without bleeding but accompanied by muscle pain, restricted motion, and loss of strength and power. Little is known about the effect of repeated strains on muscles or the dynamic components of repeated use such as velocity and acceleration which produce injury resulting in CTD or CTD risk. Since variations in human exposure and response, together with the necessity for repeated tissue sampling, make man unsuitable as a research subject, we have developed a rat model of repeated strain injury (CTD). The remarkable similarity of our injured rat muscles and the extensor carpi radialis brevis taken from humans with long standing lateral epicondylitis requiring surgery provides support for the rat as a good research model and muscles as important tissues in the development of pain and dysfunction. Since the extensor carpi radialis brevis is also very susceptible to strain injury (7), we believe that more studies using our chronic strain injury protocol in rats will reveal why repeated strain injury results in pain at the attachment sites of human muscles. Using our rat model of repeated strains, the present study was designed: 1) to determine the dynamic factors (velocity, acceleration and dose) which produce dysfunctional versus adaptive muscles, 2) to document changes in the extracellular matrix and myofibers which lead to a pathologic muscle, and 3) to study the functional outcome and reversibility of repeated injury at different speeds and accelerations commonly experienced by hand-intensive industrial jobs. This research consisted of experiments in which muscles were chronically injured by mechanical overloading in deeply anesthetized rats. The tissues were surveyed at various time intervals by biochemical, immunohistochemical and histological techniques for specific cellular markers, components and mediators involved in tissue injury and repair. The functional outcome of repeated injury was assessed by in vivo dynamometry of muscle performance. Insight into the dynamic factors producing muscle injury should provide a better understanding of the healing (adaptive) or failed-healing (pathologic) processes of muscle and aid in the design of preventative regimens for individuals in specific industrial settings. The long range goals are to determine: 1) if diminished muscle shock absorption due to increased stiffness from connective tissue proliferation is important in the development of clinical CTD; 2) if prevention of CTD can be implemented by behavioral alterations (work/rest intervals, etc.).
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