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Bone and muscle loss after spinal cord injury: organ interactions
Author(s) -
Qin Weiping,
Bauman William A.,
Cardozo Christopher
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05806.x
Subject(s) - spinal cord injury , skeletal muscle , endocrinology , muscle atrophy , medicine , atrophy , population , spasticity , sarcopenia , osteoporosis , spinal cord , physical medicine and rehabilitation , environmental health , psychiatry
Spinal cord injury (SCI) results in paralysis and marked loss of skeletal muscle and bone below the level of injury. Modest muscle activity prevents atrophy, whereas much larger—and as yet poorly defined—bone loading seems necessary to prevent bone loss. Once established, bone loss may be irreversible. SCI is associated with reductions in growth hormone, IGF‐1, and testosterone, deficiencies likely to exacerbate further loss of muscle and bone. Reduced muscle mass and inactivity are assumed to be contributors to the high prevalence of insulin resistance and diabetes in this population. Alterations in muscle gene expression after SCI share common features with other muscle loss states, but even so, show distinct profiles, possibly reflecting influences of neuromuscular activity due to spasticity. Changes in bone cells and markers after SCI have similarities with other conditions of unloading, although after SCI these changes are much more dramatic, perhaps reflecting the much greater magnitude of unloading. Adiposity and marrow fat are increased after SCI with intriguing, though poorly understood, implications for the function of skeletal muscle and bone cells.