Metabolic regulation of skeletal muscle energy metabolism during exercise

The metabolic and biochemical factors involved in the regulation of fuel and pathway selection, at appropriate rates and times, during elevated metabolic demands remains to be resolved. Therefore, the purpose of this investigation was to examine the metabolic interrelationships involved in energy pr...

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Bibliographic Details
Main Author: Parkhouse, Wade Stephen
Language:English
Published: University of British Columbia 2010
Online Access:http://hdl.handle.net/2429/27179
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Summary:The metabolic and biochemical factors involved in the regulation of fuel and pathway selection, at appropriate rates and times, during elevated metabolic demands remains to be resolved. Therefore, the purpose of this investigation was to examine the metabolic interrelationships involved in energy provision and its regulation during exercise at different intensities. Specifically, fuel selection and its control by adenine nucleotides and cytosolic redox and were investigated in red and white muscle of rainbow trout during various progressive intensities of exercise. The control of glycolysis was examined with respect to glycolytic enzyme disequilibrium. The effects of substrate limitations and end product accumulations were examined with regard to fatigue. Finally, the buffering capacity and various potential buffering constituents were investigated. It would appear that the energy turnovers required to perform the varied exercise intensities in this study were achieved by selecting the fiber type, fuel and pathway for optimizing ATP production rate versus substrate and proton accumulation. The purine nucleotide cycle was found to be operational within both fiber types. Fuel selection appeared to be intimately related to myofibrillar ATPase activation with free ADP acting as the metabolic signal to coordinate the phasing in of appropriate fuels/pathways at appropriate rates. HK, phos, PFK and PK were identified as regulatory enzymes in both fiber types. As well, the GPDH.PEK complex also appeared to exhibit regulation when glycogen was limiting and this regulation appeared to have been induced by a decreased ATP/ADP₊ ratio. The redox state of the NAD couple became more oxidized in both tissues when muscle glycogen was low. This finding was attributed to an induced shift in the equilibrium of LDH in the direction of NAD and lactate. The simultaneous ATP/ADP₊ induced disequilibrium of the PGK reaction would inhibit flux through the GPDH.PGK complex. Skeletal muscle buffering was found to be dominated by protein, inorganic phosphate and histidine related compounds. Thus, these metabolic and biochemical adjustments, allowed a coordinated integration of fiber type, fuel and pathway selection, to achieve the appropriate coupling of myofibrillar ATPase activity to ATP turnover, while minimizing substrate depletion and proton accumulations. === Science, Faculty of === Zoology, Department of === Graduate