ArticleBiomedical engineering online2007
A computational model of skeletal muscle metabolism linking cellular adaptations induced by altered loading states to metabolic responses during exercise.
Article in Biomedical engineering online, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 37 citations in OpenAlex.
- Phosphocreatine kinetics in the calf muscle of patients with bilateral symptomatic peripheral arterial disease during exhaustive incremental exercise.Molecular imaging and biologyTrial
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- Systems modelling of mitochondrial dynamics in different exercise regimes.The Journal of physiology · 2026Article
- Dynamic balance of myoplasmic energetics, redox state and protons in a fast-twitch oxidative glycolytic skeletal muscle fibre.The Journal of physiology · 2026Article
- Network model of skeletal muscle cell signalling predicts differential responses to endurance and resistance exercise training.Experimental physiology · 2024Article
- Kinetic Mathematical Modeling of Oxidative Phosphorylation in Cardiomyocyte Mitochondria.Cells · 2022Review
- Cardiopulmonary responses to maximal aerobic exercise in patients with cystic fibrosis.PloS one · 2019Article
- MITOsym®: A Mechanistic, Mathematical Model of Hepatocellular Respiration and Bioenergetics.Pharmaceutical research · 2015Article
- Use it or lose it: multiscale skeletal muscle adaptation to mechanical stimuli.Biomechanics and modeling in mechanobiology · 2015Review
- Computational modelling of the regulation of Insulin signalling by oxidative stress.BMC systems biology · 2013Article
- NAD(+)/NADH and skeletal muscle mitochondrial adaptations to exercise.American journal of physiology. Endocrinology and metabolism · 2012Review
- An integrated exercise response and muscle fatigue model for performance decrement estimates of workloads in oxygen-limiting environments.European journal of applied physiology · 2012Article
- Glycogenolysis in astrocytes supports blood-borne glucose channeling not glycogen-derived lactate shuttling to neurons: evidence from mathematical modeling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010Article
- Glucose sensing in the pancreatic beta cell: a computational systems analysis.Theoretical biology & medical modelling · 2010Article
- Numerical analysis of ischemia- and compression-induced injury in tissue-engineered skeletal muscle constructs.Annals of biomedical engineering · 2010Article
- Role of NADH/NAD+ transport activity and glycogen store on skeletal muscle energy metabolism during exercise: in silico studies.American journal of physiology. Cell physiology · 2009Article
- Article
- Models of muscle contraction and energetics.Drug discovery today. Disease models · 2008Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe 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.
methodsTo quantify interactions among cellular and skeletal muscle metabolic adaptations, and to predict metabolic responses to exercise after periods of altered loading states, we develop a computational model of skeletal muscle metabolism. The governing model equations - with parameters characterizing chronic loading/unloading states- were solved numerically to simulate metabolic responses to moderate intensity exercise (WR < or = 40% VO2 max).
resultsModel simulations showed that carbohydrate oxidation was 8.5% greater in chronically unloaded muscle compared with the loaded muscle (0.69 vs. 0.63 mmol/min), while fat oxidation was 7% higher in chronically loaded muscle (0.14 vs. 0.13 mmol/min), during exercise. Muscle oxygen uptake (VO2) and blood flow (Q) response times were 29% and 44% shorter in chronically loaded muscle (0.4 vs. 0.56 min for VO2 and 0.25 vs. 0.45 min for Q).
conclusionThe present model can be applied to test complex hypotheses during exercise involving the integration and control of metabolic processes at various organizational levels (cellular to tissue) in individuals who have undergone periods of chronic loading or unloading.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.