Journal
JOURNAL OF REHABILITATION RESEARCH AND DEVELOPMENT
Volume 45, Issue 2, Pages 261-272Publisher
JOURNAL REHAB RES & DEV
DOI: 10.1682/JRRD.2007.02.0040
Keywords
body composition; exercise; inflammation; insulin-glucose metabolism; myosin heavy chain isoforms; rehabilitation; sarcopenia; skeletal muscle; stroke; walking
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Funding
- NATIONAL INSTITUTE ON AGING [R01AG019310, P60AG012583] Funding Source: NIH RePORTER
- NIA NIH HHS [R01 AG019310, P60 AG012583, P30-AG-12583, R01-AG-019310, R01 AG019310-05, P60 AG012583-10] Funding Source: Medline
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Stroke is the leading cause of disability in the United States. New evidence reveals significant structural and metabolic changes in skeletal muscle after stroke. Muscle alterations include gross atrophy and shift to fast myosin heavy chain in the hemiparetic (contralateral) leg muscle; both are related to gait deficit severity. The underlying molecular mechanisms of this atrophy and muscle phenotype shift are not known. Inflammatory markers are also present in contralateral leg muscle after stroke. Individuals with stroke have a high prevalence of insulin resistance and diabetes. Skeletal muscle is a major site for insulin-glucose metabolism. Increasing evidence suggests that inflammatory pathway activation and oxidative injury could lead to wasting, altered function, and impaired insulin action in skeletal muscle. The health benefits of exercise in disabled populations have now been recognized. Aerobic exercise improves fitness, strength, and ambulatory performance in subjects with chronic stroke. Therapeutic exercise may modify or reverse skeletal muscle abnormalities.
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