Inferior mechanical properties of spastic muscle bundles due to hypertrophic but compromised extracellular matrix material.
The passive mechanical properties of small muscle fiber bundles obtained from surgical patients with spasticity (n = 9) and patients without neuromuscular disorders (n = 21) were measured in order to determine the relative influence of intracellular and extracellular components. For both types of patient, tangent modulus was significantly greater in bundles compared to identical tests performed on isolated single cells (P < 0.05). However, the relative difference between bundles and single cells was much greater in normal tissue than spastic tissue. The tangent modulus of normal bundles (462.5 +/- 99.6 MPa) was 16 times greater than normal single cells (28.2 +/- 3.3 MPa), whereas the tangent modulus of spastic bundles (111.2 +/- 35.5 MPa) was only twice that of spastic muscle cells (55.0 +/- 6.6 MPa). This relatively small influence of the extracellular matrix (ECM) in spastic muscle was even more surprising because spastic muscle cells occupied a significantly smaller fraction of the total specimen area (38.5 +/- 13.6%) compared to normal muscle (95.0 +/- 8.8%). Based on these data, normal muscle ECM is calculated to have a modulus of 8.7 GPa, and the ECM from spastic muscle of only 0.20 GPa. These data indicate that spastic muscle, although composed of cells that are stiffer compared to normal muscle, contains an ECM of inferior mechanical strength. The present findings illustrate some of the profound changes that occur in skeletal muscle secondary to spasticity. The surgical implications of these results are discussed.
D000328:Adult; D001696:Biomechanical Phenomena; D016022:Case-Control Studies; D002648:Child; D004548:Elasticity; D005109:Extracellular Matrix / Q000378:metabolism*; D006801:Humans; D009128:Muscle Spasticity / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology*; D009469:Neuromuscular Junction / Q000503:physiopathology*