Analysis Tools
homeostasis/metabolism
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• hearts display accelerated loss of contractile force on ischemia, however maintain postischemic contractile recovery at wild-type levels
• hearts show reduced adenine and guanine nucleotide salvage on reperfusion, resulting in lower ATP, GTP, ADP, and GDP levels and an altered metabolic steady state associated with diminished ATP-to-Pi and creatine phosphate-to-Pi ratios
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• muscle maintains contractile performance, however energy expenditure in muscle is increased to maintain contractile performance, as indicated by elevated ATP production and utilization and increased energy transduction rate
• aberrant redistribution of phosphotransfer flux and a 31% increase in energy expenditure in muscle during hypoxic stress
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• increase in intracellular concentration of glycolytic intermediates and increase in glucose-6-phosphate turnover in muscle, indicating elevated muscle glycolytic metabolism
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• dynamics of adenine nucleotide metabolism in skeletal muscle are altered even though adenine nucleotide levels are maintained
• production and utilization of guanine nucleotides are increased in muscle, with 50% higher intracellular GTP concentration in muscle
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muscle
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• although muscles maintain contractile performance, they show increased ATP consumption per contraction, indicating a reduction in energetic efficiency and an increase in muscle energy transduction rate
• increase in net creatine kinase-catalyzed phosphotransfer flux in skeletal muscle
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cellular
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• elevated aerobic Krebs cycle metabolism
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cardiovascular system
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• hearts display accelerated loss of contractile force on ischemia, however maintain postischemic contractile recovery at wild-type levels
• hearts show reduced adenine and guanine nucleotide salvage on reperfusion, resulting in lower ATP, GTP, ADP, and GDP levels and an altered metabolic steady state associated with diminished ATP-to-Pi and creatine phosphate-to-Pi ratios
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