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Force-Repetition Interaction in a Rat Injury Model



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  • Personal Author:
  • Description:
    Using a voluntary rat model of work overuse, we examined rats performing low to high demand work tasks of reaching and grasping for 12 to 24 weeks for tissue injury and inflammation, systemic inflammatory responses, tissue degradation and fibrosis, and associated sensorimotor behaviors, including sickness behaviors occurring as a consequence of performing repetitive work tasks with or without high force. Our research shows that work-related overuse injuries, particularly those resulting from long-term performance of repetitive and forceful tasks, lead to local and systemic inflammation, which drives tissue degradation and even sickness behaviors. Our force-repetition interaction studies, in which rats perform different levels of tasks, indicate that even short-term performance of high repetition high force tasks leads to nerve damage, muscle and tendon injury, and eventually degeneration. High level tasks lead also to bone thinning, while moderate level tasks lead to bone growth. We found that even moderate demand tasks lead to chronic low grade-chronic tissue and systemic inflammation that contribute to tissue degradation and fibrosis. The inflammation also lead to reduced motor performance and strength and increased discomfort. The sensory and motor declines were linked to increased inflammatory cytokines in the muscles, tendons, nerves and bones of the arm and hand used to perform this upper extremity work task. Thus, our laboratory has found a clear link between musculoskeletal overuse disorders and increased inflammatory cytokines in musculoskeletal tissues that contribute to weakness and pain. We also observed sickness behaviors, specifically, decreased duration of social interaction and increased aggression in rats performing high demand tasks and in aged animals performing even moderate demand tasks. We assume the latter occurred since the systemic inflammatory response was greatly enhanced in aged animals compared to young adult animals performing the same work task. Several researchers have shown that increased inflammatory proteins in the blood, particularly pro-inflammatory cytokines can cause depression and other mood disorders, particularly in cancer patients treated with inflammatory cytokine drugs. And, several past studies have shown an increase in perceived job stress, depressed mood, increased absence from work due to sickness in patients with work-related musculoskeletal disorders. A link between perceived job stress and increased inflammatory proteins in blood has also been reported. However, we have demonstrated for the first time that there is a link between blood levels of pro-inflammatory cytokines, sickness behaviors, and work-related overuse injuries. We also found increased inflammatory cytokines in regions of the brain that form the blood brain barrier, and within the brain in regions that are responsible for sickness behaviors. In humans and animals, systemic infection causes many behavioral changes, including mood changes (such as anxiety and depression), fatigue, decreased motivation, reduced social interaction, and sleep disturbances. These symptoms are part of a coordinated brain response that changes the body's physiological and motivational state to preserve body integrity during illness. The possibility that patients with overuse musculoskeletal disorders may develop tissue degradation, fibrosis, and sickness behaviors as a consequence of work-induced tissue and systemic inflammation should be considered when treating these patients. [Description provided by NIOSH]
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  • Pages in Document:
    1-46
  • NIOSHTIC Number:
    nn:20056278
  • NTIS Accession Number:
    PB2019-101129
  • 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-003970, 2012 Oct; :1-46
  • Contact Point Address:
    Mary F Barbe, PHD, Dept of Anatomy & Cell Biology, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140
  • Email:
    mbarbe@temple.edu
  • Federal Fiscal Year:
    2013
  • NORA Priority Area:
  • Performing Organization:
    Temple University
  • Peer Reviewed:
    False
  • Start Date:
    20000601
  • Source Full Name:
    National Institute for Occupational Safety and Health
  • End Date:
    20120731
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  • Main Document Checksum:
    urn:sha-512:bc64091977f8c1c3623204dc2ed7a33f9947d0ec877413c97fd7304fd744005a3d37a45952e12824510452ca5e4adcee9484663509feb89b412adcca7c7e8ad4
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  • File Type:
    Filetype[PDF - 1.02 MB ]
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