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1 Muscle Function Laboratory, Virginia Polytechnic Institute, Blacksburg, VA, USA
2 Brain Research Institute, University of California Los Angeles, Los Angeles, CA, USA
3 Physiological Science, University of California Los Angeles, Los Angeles, CA, USA; Brain Research Institute, University of California Los Angeles, Los Angeles, CA, USA
4 Biological Sciences, California State Polytechnic University, Pomona, CA, USA
* To whom correspondence should be addressed. E-mail: rjtalmadge{at}csupomona.edu.
To determine if long-term reductions in neuromuscular activity result in alterations in metabolic capacity, the activities of oxidative, i.e., succinate dehydrogenase (SDH) and citrate synthase (CS), and glycolytic, i.e.,
-glycerophosphate dehydrogenase (GPD), enzyme markers were quantified in rat soleus muscles 1, 3, and 6 months after a complete spinal cord transection (ST). In addition, the proportional content of lactate dehydrogenase (LDH) isozymes was used as a marker for oxidative and glycolytic capacities. The myosin heavy chain (MHC) isoform content of a fiber served as a marker of phenotype. In general, MHC isoforms shifted from MHC-I towards MHC-II, particularly MHC-IIx, after ST. Mean SDH and CS activities were higher in ST than control at all time points. The elevated SDH and CS activities were indicative of an enhanced oxidative capacity. GPD activities were higher in ST than control rats at all time points. The increase in activity of SDH was larger than GPD. Thus, the GPD/SDH ratio (glycolytic/oxidative) was decreased after ST. Compared to controls, total LDH activity increased transiently and the LDH isozymes profile shifted from LDH-1 towards LDH-5, indicative of an enhanced glycolytic capacity. Combined, these results indicate that 1) the metabolic capacities of soleus fibers were not compromised, but the inter-relationships among oxidative and glycolytic capacity and MHC content were apparently dissociated after ST; 2) enhancements in oxidative and glycolytic enzyme activities are not mutually exclusive; and 3) chronic reductions in skeletal muscle activity do not necessarily result in a reduced oxidative capacity.
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