This proposal is designed to improve our understanding of the mechanical basis of injury that occurs after eccentric contraction as well as the adaptive mechanisms that protect muscle from further injury. Eccentric contraction-biased exercise (i.e., exercise that causes lengthening of an activated muscle) causes muscle injury and also provides a potent strengthening signal to muscle. Based on the potential application of eccentric contractions to athletics and rehabilitation, it is important to understand the mechanisms by which these contractions cause both injury and strengthening. In this way, rationale rehabilitative procedures can be developed based on sound scientific principles. In addition, since eccentric contraction represents a unique mechanical event, understanding the mechanism of eccentric contractions -induced injury can also provide insights into normal muscle structure-function relationships that exist within skeletal muscle.
The specific aims of this proposal are to: (1) to determine the relative role that mechanical properties play (primarily stress and strain) in causing muscle injury, (2) to understand mechanisms of stress transmission in muscle fibers by measuring the strain field across the costameric and myofibrillar structures during passive fiber elongation and, (3) to measure the relative strengthening ability of normal muscles compared to muscles devoid of the intermediate filament protein desmin. We hypothesize that the potent effects of eccentric contraction on muscle are due to the injury response initiated and are potentiated by the high muscle stresses that go along with eccentric contractions. These studies not only provide insights into the damage mechanism, but also shed light on important structure-function relationships in normal muscle.
| Meyer, Gretchen; Lieber, Richard L (2018) Muscle fibers bear a larger fraction of passive muscle tension in frogs compared with mice. J Exp Biol 221: |
| Lao, Dieu Hung; Esparza, Mary C; Bremner, Shannon N et al. (2015) Lmo7 is dispensable for skeletal muscle and cardiac function. Am J Physiol Cell Physiol 309:C470-9 |
| Palmisano, Michelle G; Bremner, Shannon N; Hornberger, Troy A et al. (2015) Skeletal muscle intermediate filaments form a stress-transmitting and stress-signaling network. J Cell Sci 128:219-24 |
| Chapman, Mark A; Zhang, Jianlin; Banerjee, Indroneal et al. (2014) Disruption of both nesprin 1 and desmin results in nuclear anchorage defects and fibrosis in skeletal muscle. Hum Mol Genet 23:5879-92 |
| Meyer, Gretchen A; Schenk, Simon; Lieber, Richard L (2013) Role of the cytoskeleton in muscle transcriptional responses to altered use. Physiol Genomics 45:321-31 |
| Meyer, Gretchen A; Lieber, Richard L (2012) Skeletal muscle fibrosis develops in response to desmin deletion. Am J Physiol Cell Physiol 302:C1609-20 |
| Derkacs, Amanda D Felder; Ward, Samuel R; Lieber, Richard L (2012) The use of neural networks and texture analysis for rapid objective selection of regions of interest in cytoskeletal images. Microsc Microanal 18:115-22 |
| Gillies, Allison R; Lieber, Richard L (2011) Structure and function of the skeletal muscle extracellular matrix. Muscle Nerve 44:318-31 |
| Meyer, G A; McCulloch, A D; Lieber, R L (2011) A nonlinear model of passive muscle viscosity. J Biomech Eng 133:091007 |
| Meyer, Gretchen A; Lieber, Richard L (2011) Elucidation of extracellular matrix mechanics from muscle fibers and fiber bundles. J Biomech 44:771-3 |
Showing the most recent 10 out of 71 publications
