ABSTRACT:
This a model from the article:
Common phenotype of resting mouse extensor digitorum longus and soleus muscles:
equal ATPase and glycolytic flux during transient anoxia.
Vinnakota KC, Rusk J, Palmer L, Shankland E, Kushmerick MJ. J Physiol
2010 Jun 1;588(Pt 11):1961-83 20308252
,
Abstract:
Rates of ATPase and glycolysis are several times faster in actively contracting
mouse extensor digitorum longus muscle (EDL) than soleus (SOL), but we find
these rates are not distinguishable at rest. We used a transient anoxic
perturbation of steady state energy balance to decrease phosphocreatine (PCr)
reversibly and to measure the rates of ATPase and of lactate production without
muscle activation or contraction. The rate of glycolytic ATP synthesis is less
than the ATPase rate, accounting for the continual PCr decrease during anoxia in
both muscles. We fitted a mathematical model validated with properties of
enzymes and solutes measured in vitro and appropriate for the transient
perturbation of these muscles to experimental data to test whether the model
accounts for the results. Simulations showed equal rates of ATPase and lactate
production in both muscles. ATPase controls glycolytic flux by feedback from its
products. Adenylate kinase function is critical because a rise in [AMP] is
necessary to activate glycogen phosphorylase. ATPase is the primary source of H+
production. The sum of contributions of the 13 reactions of the glycogenolytic
and glycolytic network to total proton load is negligible. The stoichiometry of
lactate and H+ production is near unity. These results identify a default state
of energy metabolism for resting muscle in which there is no difference in the
metabolic phenotype of EDL and SOL. Therefore, additional control mechanisms,
involving higher ATPase flux and [Ca2+], must exist to explain the well-known
difference in glycolytic rates in fast-twitch and slow-twitch muscles in
actively contracting muscle.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Vinnakota KC, Rusk J, Palmer L, Shankland E, Kushmerick MJ. (2010) - version=1.0
The original CellML model was created by:
Geoffrey Nunns
gnunns1@jhu.edu
The University of Auckland
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
Camille Laibe 
