adenylate kinase/fatigue

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Fatigue resistance of rat extraocular muscles does not depend on creatine kinase activity.

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BACKGROUND Creatine kinase (CK) links phosphocreatine, an energy storage system, to cellular ATPases. CK activity serves as a temporal and spatial buffer for ATP content, particularly in fast-twitch skeletal muscles. The extraocular muscles are notoriously fast and active, suggesting the need for

Muscular fatigue: effects of hydrogen ions and inorganic phosphate.

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During muscular fatigue two metabolites, hydrogen ions (H+) and inorganic phosphate (Pi), increase in concentration. The effect of increase in [H+] has been modeled mathematically for a system containing creatine kinase (EC 2.7.3.2), adenylate kinase (EC 2.7.4.3), and the appropriate concentrations

Skeletal muscle contractile performance and ADP accumulation in adenylate kinase-deficient mice.

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The production of AMP by adenylate kinase (AK) and subsequent deamination by AMP deaminase limits ADP accumulation during conditions of high-energy demand in skeletal muscle. The goal of this study was to investigate the consequences of AK deficiency (-/-) on adenine nucleotide management and whole

Cerebral damage during open-heart surgery. Clinical, psychometric, biochemical and CT data.

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The incidence and extent of cerebral damage following open-heart surgery were prospectively investigated in 103 patients, using clinical assessment, psychometry, adenylate kinase analysis in cerebrospinal fluid (CSF-AK) and computed tomography (CT) of the brain. The surgical mortality was 1.9%.

Effect of physiological ADP concentrations on contraction of single skinned fibers from rabbit fast and slow muscles.

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To directly assess the possible role of ADP in muscle fatigue, we have studied the effect of physiological MgADP levels on maximum Ca(2+)-activated isometric force and unloaded shortening velocity (Vus) of single skinned fiber segments from rabbit fast-twitch (psoas) and slow-twitch (soleus)

AMP deamination delays muscle acidification during heavy exercise and hypoxia.

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In silico studies carried out by using a computer model of oxidative phosphorylation and anaerobic glycolysis in skeletal muscle demonstrated that deamination of AMP to IMP during heavy short term exercise and/or hypoxia lessens the acidification of myocytes. The concerted action of adenylate kinase

31P-NMR observation of free ADP during fatiguing, repetitive contractions of murine skeletal muscle lacking AK1.

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Metabolic control within skeletal muscle is designed to limit ADP accumulation even during conditions where ATP demand is out of balance with ATP synthesis. This is accomplished by the reactions of adenylate kinase (AK; ADP+ADP <--> AMP+ATP) and AMP deaminase (AMP+H(2)O --> NH(3)+IMP), which limit

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