Graduation date: 2006 / We hypothesized that calpain activity is elevated in response to muscle damage. To test this hypothesis, we examined the degradation of α-fodrin into its 150 and 145 kDa fragments following either 20 eccentric or isometric contractions. In addition, experiments were performed in the presence or absence of E-64-d, a calpain inhibitor. Both EDL and SOL muscles displayed significant differences (p<0.003 and p<0.002 respectively) between the raw and normalized 150 and 145 kDa α-fodrin fragments of the DMSO + E-64-d compared to the other bath treatments. Based on our model of exercise-induced muscle damage, we expected to see greater levels of 150 and 145 kDa α-fodrin fragments in those muscles that performed the eccentric protocol. However, there was no evidence that eccentric muscle damage increased the levels of 150 and 145 kDa α-fodrin fragments over the levels observed in the isometric trials. These findings suggest that the magnitude of damage was insufficient to activate calpains.
Identifer | oai:union.ndltd.org:ORGSU/oai:ir.library.oregonstate.edu:1957/1940 |
Date | 23 May 2006 |
Creators | Boyd, Jeffrey |
Contributors | Widrick, Jeffrey J., Wilcox, Anthony, Bella, Deborah, Levenson, Rick |
Source Sets | Oregon State University |
Language | en_US |
Detected Language | English |
Type | Thesis |
Format | 464645 bytes, application/pdf |
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