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Muscle molecular phenotype after stroke is associated with gait speed
Author(s) -
De Deyne Patrick G.,
HaferMacko Charlene E.,
Ivey Frederick M.,
Ryan Alice S.,
Macko Richard F.
Publication year - 2004
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20085
Subject(s) - stroke (engine) , medicine , physical medicine and rehabilitation , gait , phenotype , myosin , cardiology , biology , gene , genetics , mechanical engineering , engineering , biophysics
Abstract The disability of patients after stroke is generally attributed to upper motor neuron defects, but secondary changes in paretic muscle may enhance the disability. We analyzed the molecular phenotype and metabolic profile of the paretic and nonparetic vastus lateralis (VL) and we measured the severity of gait deficit in 13 patients at least 6 months after ischemic stroke. The results showed a significant increase in the proportion of fast myosin heavy chain (MHC, 68 ± 14%) in the paretic compared to the nonparetic VL (50 ± 13%). The specific activity of citrate synthase and glyceraldehyde phosphodehydrogenase was not significantly different between the two sides. The proportion of fast MHC was inversely associated with severity of gait deficit indexed by self‐selected walking speed in the paretic leg, but not the nonparetic leg. Our findings demonstrate significant and potentially modifiable secondary biologic changes in hemiparetic muscle phenotype that may contribute to the disability of stroke. Muscle Nerve 30: 209–215, 2004