A computational model of skeletal muscle metabolism linking cellular adaptations induced by altered loading states to metabolic responses during exercise |
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| Authors: | Ranjan K Dash II" target="_blank">John A DiBellaII " target="_blank">Marco E Cabrera |
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| Affiliation: | (1) Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH, USA;(2) Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA;(3) Department of Pediatrics, Case Western Reserve University, Cleveland, OH, USA;(4) Center for Modeling Integrated Metabolic Systems, Case Western Reserve University, Cleveland, OH, USA;(5) Biotechnology and Bioengineering Center, Department of Physiology, Medical College of Wisconsin, 53226 Milwaukee, WI, USA |
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| Abstract: | Background The alterations in skeletal muscle structure and function after prolonged periods of unloading are initiated by the chronic
lack of mechanical stimulus of sufficient intensity, which is the result of a series of biochemical and metabolic interactions
spanning from cellular to tissue/organ level. Reduced activation of skeletal muscle alters the gene expression of myosin heavy
chain isoforms to meet the functional demands of reduced mechanical load, which results in muscle atrophy and reduced capacity
to process fatty acids. In contrast, chronic loading results in the opposite pattern of adaptations. |
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