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Journal ArticleDOI

A linear model of muscle respiration explains monoexponential phosphocreatine changes

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TLDR
Phosphocreatine content was measured by phosphorus nuclear magnetic resonance spectroscopy in the gastrocnemius muscles of pentobarbital-anesthetized rats during and after twitch stimulation to be consistent with a simple first-order electrical analog model of oxidative metabolism that is applicable at submaximal oxidative rates.
Abstract
Phosphocreatine (PCr) content was measured by phosphorus nuclear magnetic resonance spectroscopy in the gastrocnemius muscles of pentobarbital-anesthetized rats during and after twitch stimulation at rates up to 0.75 Hz. The monoexponential time constant for PCr changes was similar at the onset of vs. during recovery after stimulation and was not significantly different for different stimulation rates (mean time constant 1.44 min). Steady-state PCr level during stimulation was linearly related to the product of stimulation rate times peak twitch force. These results are shown to be consistent with a simple first-order electrical analog model of oxidative metabolism that is applicable at submaximal oxidative rates. The model assumes equilibrium of the creatine kinase reaction, which is modeled as a chemical capacitor, with capacitance proportional to the total creatine level, and PCr level proportional to the cytosolic free energy of ATP hydrolysis.

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Fractal Physiology

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Muscle O2 uptake kinetics in humans: implications for metabolic control

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Oxidative capacity and ageing in human muscle

TL;DR: It was shown that elderly subjects had nearly 50 % lower oxidative capacity per volume of muscle than adult subjects, and the cellular basis of this drop was a reduction in mitochondrial content, as well as a lower oxidativecapacity of the mitochondria with age.
References
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Journal ArticleDOI

Transport of energy in muscle: the phosphorylcreatine shuttle

TL;DR: It was proposed in 1951 that contracting muscle fibers liberate creatine, which acts to produce an acceptor effect--later called respiratory control--on the muscle mitochondria, which established a molecular basis for a phosphorylcreatine-creatine shuttle for energy transport in heart and skeletal muscle.
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A simple analysis of the "phosphocreatine shuttle"

TL;DR: Experimental results demonstrating the transport aspects of the CK reaction emphasize only one feature of a more general notion of facilitated diffusion by near-equilibrium metabolic reactions and do not per se establish the existence of any physical or functional compartmentation of ATP, ADP, PCr, or creatine.
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Control of oxidative metabolism and oxygen delivery in human skeletal muscle: a steady-state analysis of the work/energy cost transfer function

TL;DR: The concept of transfer function for organ performance (work output vs. biochemical input) is developed for skeletal and cardiac muscle under steady-state exercise conditions and appears to be useful in predicting the degree to which metabolic homeostasis is effective.
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First-order kinetics of muscle oxygen consumption, and an equivalent proportionality between QO2 and phosphorylcreatine level. Implications for the control of respiration.

TL;DR: The first-order kinetics of QO2 are consistent with the hypothesis that respiration is rate-limited by the mitochondrial CK reaction, and has as a corollary the "creatine shuttle" hypothesis.
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