Regular ArticleInteractions of Mitochondrial ATP Synthesis and the Creatine Kinase Equilibrium in Skeletal Muscle
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Muscle Energetics
2018, Muscle and Exercise PhysiologyDominant and sensitive control of oxidative flux by the ATP-ADP carrier in human skeletal muscle mitochondria: Effect of lysine acetylation
2018, Archives of Biochemistry and BiophysicsCitation Excerpt :ATP free energy based control models describe the near-linear relationship between oxidative flux and ΔGATP according to non-equilibrium thermodynamics (NET) [4,7,13–15]:v = (ΔΔGATP)(conductance)in which oxidative flux, v, rises linearly according to the product of the fall (“relaxation”) in ATP free energy and a phenomenological proportionality constant, the “conductance” of the oxidative pathway, which also includes the stoichiometry of the transduction [7]. Due to the near equilibrium maintained at CK, at constant pH these two feedback models are fundamentally related to each other [12]. Non-invasive measurement of intact skeletal muscle energy phosphates using 31P-MRS yields estimates of apparent KmADP in the range of 20–40 μM.
Mitochondria: Investigation of in vivo muscle mitochondrial function by <sup>31</sup>P magnetic resonance spectroscopy
2014, International Journal of Biochemistry and Cell BiologyCitation Excerpt :The second problem with the interpretation of ST data is that even if VATP did truly represent oxidative ATP synthesis flux, this still could not be taken as a measure of mitochondrial function (Balaban and Koretsky, 2011; Befroy et al., 2012; From and Ugurbil, 2011; Kemp, 2008; Kemp and Brindle, 2012). Mitochondrial ATP synthesis is a demand-driven process regulated by several feedback-loop error signals, such as the concentrations of ADP and Pi (Kemp, 1994; Wu et al., 2007; Jeneson et al., 2009). A decreased net ATP synthesis flux in combination with appropriately decreased error signals would simply represent a lower ATP demand.
Oscillations in energy metabolism
2010, Biochimica et Biophysica Acta - BioenergeticsCitation Excerpt :The independency between creatine phosphorylation and muscle mass [51] and exercise intensity [39,52] further evidences that mitochondrial ATP production can be reliably investigated from PCr kinetics. On a theoretical ground, the rate of mitochondrial ATP synthesis would be controlled through a feedback loop involving ADP [39,53,54] as it has been illustrated in isolated mitochondria, animals and humans [50,53,55–60]. Alternatively, it has been proposed that the rate of mitochondrial ATP synthesis could be controlled in a linear manner by the energy released through ATP hydrolysis, ΔGATP[39].
The mono-exponential pattern of phosphocreatine recovery after muscle exercise is a particular case of a more complex behaviour
2004, Biochimica et Biophysica Acta - BioenergeticsCitation Excerpt :There are more complex generalizations of this model, based on non-equilibrium thermodynamics [18,19] resulting in quasi-linear control of respiration rate by cytosolic free energy of ATP hydrolysis [19]. It has been proposed that the two classical models of the respiratory control, kinetic and thermodynamic, may be regarded as different expressions of the same metabolic mechanism [20], and that in skeletal muscle can be both conceivable at different metabolic conditions: equilibrium control being approached at low workloads while kinetic limitations at higher workloads [21]. The pattern of PCr recovery from exercise is reasonably well-described by mono-exponential functions [2–9].
Mitochondrial function and oxygen supply in normal and in chronically ischemic muscle: A combined <sup>31</sup>P magnetic resonance spectroscopy and near infrared spectroscopy study in vivo
2001, Journal of Vascular SurgeryCitation Excerpt :It will be seen (see “Results” section) that this is near unity and also that pH changes (and, therefore, lactate accumulation) are small, which independently suggest34 that the exercise is largely oxidative.7 Oxidative ATP synthesis is a function of three factors: mitochondrial volume and competence, oxygen supply, and the metabolic “driving force” (the change in, eg, ADP concentration33,35). The first two factors can be lumped as the “mitochondrial capacity,” the notional maximum oxidative ATP synthesis rate; in the absence of large pH changes in exercise,36,37 this is conveniently reflected by the postexercise PCr recovery rate constant (0.693/halftime).7,35,38