Cumulative Trauma Disorder: Skeletal Muscle Dysfunction
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2005/07/18
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By Stauber WT
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Series: Grant Final Reports
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Description: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 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 why inflammation results from some but not all muscle strains. 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. The remarkable similarity of our injured rat muscles and the extensor carpi radialis brevis taken from humans with long standing lateral epicondylitis requiring surgery [22] 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 [21], we believe that more studies using our chronic strain injury protocol in rats will reveal why repeated strain injury results in pain and not adaptation. Using our rat model of repeated muscle strains, the present study was designed: 1) to determine if muscle fatigue, in addition to mechanical damage from repeated muscle strains, results in increased myofiber pathology and inflammation, 2) to understand the mechanisms of increased collagen deposition (fibrosis) and pathology in skeletal muscles resulting from chronic strain injury and 3) to develop blood biomarkers for the assessment of muscle inflammation and pathology. This research consisted of experiments in which muscles were acutely or chronically injured by mechanical overloading (stretching) in deeply anesthetized rats. After removal from the animals, skeletal muscles were surveyed at various time intervals following injury by biochemical, immunohistochemical and histological techniques for specific cellular markers, components and mediators involved in tissue injury, inflammation and repair. The functional outcome of repeated injury was assessed by in vivo dynamometry of muscle performance (e.g. muscle strength). From our studies, the mechanisms for muscle weakness (isometric force deficits) and histopathologic changes (inflammation) following repeated muscle strains can largely be dissociated from each other explaining why there is no correlation between weakness and inflammation. Apparently, injury leading to calcium accumulation that exceeds the buffering capacity of the cell is the most critical component in producing pathologic changes and inflammation in muscles. This calcium accumulation is a time-dependent process and long rest times attenuates the calcium accumulation. The individual variation in outcomes to repeated strains seen in humans probably results from differences in calcium buffering capacity or bioenergetics. Finally, functional testing in humans exposed to repeated muscle strains will not allow the assessment of the degree of muscle pathology or inflammation. [Description provided by NIOSH]
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Pages in Document:1-16
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NIOSHTIC Number:nn:20029563
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NTIS Accession Number:PB2006-105531
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Citation:Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, R01-OH-002918, 2005 Jul; :1-16
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Contact Point Address:William T Stauber PhD, Department of Physiology, Robert C Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506-9229
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Email:wstauber@hsc.wvu.edu
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Federal Fiscal Year:2005
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Performing Organization:West Virginia University, Morgantown, West Virginia
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Peer Reviewed:False
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Start Date:19920101
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Source Full Name:National Institute for Occupational Safety and Health
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End Date:20050531
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Main Document Checksum:urn:sha-512:9d6e51b75a6d6e3e6adf2f201f1efb5e18bc7479f7d36f023810b6db3d5ad9d72417666db9d3e72027869ecf2908b1ba2c82e74e3644dac878ba8698f6c2b346
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