Mechanisms of exertional fatigue in muscle glycogenoses

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Mechanisms of exertional fatigue in muscle glycogenoses. / Vissing, John; Haller, Ronald G.

I: Neuromuscular Disorders, Bind 22 Suppl 3, 2012, s. S168-71.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Vissing, J & Haller, RG 2012, 'Mechanisms of exertional fatigue in muscle glycogenoses', Neuromuscular Disorders, bind 22 Suppl 3, s. S168-71. https://doi.org/10.1016/j.nmd.2012.10.011

APA

Vissing, J., & Haller, R. G. (2012). Mechanisms of exertional fatigue in muscle glycogenoses. Neuromuscular Disorders, 22 Suppl 3, S168-71. https://doi.org/10.1016/j.nmd.2012.10.011

Vancouver

Vissing J, Haller RG. Mechanisms of exertional fatigue in muscle glycogenoses. Neuromuscular Disorders. 2012;22 Suppl 3:S168-71. https://doi.org/10.1016/j.nmd.2012.10.011

Author

Vissing, John ; Haller, Ronald G. / Mechanisms of exertional fatigue in muscle glycogenoses. I: Neuromuscular Disorders. 2012 ; Bind 22 Suppl 3. s. S168-71.

Bibtex

@article{23c3b3be5d7142a9bf02358f8ab9f00b,
title = "Mechanisms of exertional fatigue in muscle glycogenoses",
abstract = "Exertional fatigue early in exercise is a clinical hallmark of muscle glycogenoses, which is often coupled with painful muscle contractures and episodes of myoglobinuria. A fundamental biochemical problem in these conditions is the impaired generation of ATP to fuel muscle contractions, which relates directly to the metabolic defect, but also to substrate-limited energy deficiency, as exemplified by the {"}second wind{"} phenomenon in McArdle disease. A number of secondary events may also play a role in inducing premature fatigue in glycogenoses, including (1) absent or blunted muscle acidosis, which may be important for maintaining muscle membrane excitability by decreasing chloride permeability, (2) loss of the osmotic effect related to lactate accumulation, which may account for absence of the normal increase in water content of exercised muscle, and thus promote higher than normal concentrations of extracellular potassium in exercising muscle and (3) exaggerated accumulation of ADP during exercise that may inhibit sodium-potassium and calcium-ATPases. Disorders of muscle glycogenolysis and glycolysis reveal the crucial role of these metabolic processes for supplying both anaerobic and aerobic energy for muscle contraction; and the pathological fatigue that occurs when glycogenolysis and/or glycolysis is blocked imply an important role for theses metabolic pathways in normal muscle fatigue.",
author = "John Vissing and Haller, {Ronald G}",
note = "Copyright {\textcopyright} 2012 Elsevier B.V. All rights reserved.",
year = "2012",
doi = "10.1016/j.nmd.2012.10.011",
language = "English",
volume = "22 Suppl 3",
pages = "S168--71",
journal = "Journal of Neuromuscular Diseases",
issn = "0960-8966",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Mechanisms of exertional fatigue in muscle glycogenoses

AU - Vissing, John

AU - Haller, Ronald G

N1 - Copyright © 2012 Elsevier B.V. All rights reserved.

PY - 2012

Y1 - 2012

N2 - Exertional fatigue early in exercise is a clinical hallmark of muscle glycogenoses, which is often coupled with painful muscle contractures and episodes of myoglobinuria. A fundamental biochemical problem in these conditions is the impaired generation of ATP to fuel muscle contractions, which relates directly to the metabolic defect, but also to substrate-limited energy deficiency, as exemplified by the "second wind" phenomenon in McArdle disease. A number of secondary events may also play a role in inducing premature fatigue in glycogenoses, including (1) absent or blunted muscle acidosis, which may be important for maintaining muscle membrane excitability by decreasing chloride permeability, (2) loss of the osmotic effect related to lactate accumulation, which may account for absence of the normal increase in water content of exercised muscle, and thus promote higher than normal concentrations of extracellular potassium in exercising muscle and (3) exaggerated accumulation of ADP during exercise that may inhibit sodium-potassium and calcium-ATPases. Disorders of muscle glycogenolysis and glycolysis reveal the crucial role of these metabolic processes for supplying both anaerobic and aerobic energy for muscle contraction; and the pathological fatigue that occurs when glycogenolysis and/or glycolysis is blocked imply an important role for theses metabolic pathways in normal muscle fatigue.

AB - Exertional fatigue early in exercise is a clinical hallmark of muscle glycogenoses, which is often coupled with painful muscle contractures and episodes of myoglobinuria. A fundamental biochemical problem in these conditions is the impaired generation of ATP to fuel muscle contractions, which relates directly to the metabolic defect, but also to substrate-limited energy deficiency, as exemplified by the "second wind" phenomenon in McArdle disease. A number of secondary events may also play a role in inducing premature fatigue in glycogenoses, including (1) absent or blunted muscle acidosis, which may be important for maintaining muscle membrane excitability by decreasing chloride permeability, (2) loss of the osmotic effect related to lactate accumulation, which may account for absence of the normal increase in water content of exercised muscle, and thus promote higher than normal concentrations of extracellular potassium in exercising muscle and (3) exaggerated accumulation of ADP during exercise that may inhibit sodium-potassium and calcium-ATPases. Disorders of muscle glycogenolysis and glycolysis reveal the crucial role of these metabolic processes for supplying both anaerobic and aerobic energy for muscle contraction; and the pathological fatigue that occurs when glycogenolysis and/or glycolysis is blocked imply an important role for theses metabolic pathways in normal muscle fatigue.

U2 - 10.1016/j.nmd.2012.10.011

DO - 10.1016/j.nmd.2012.10.011

M3 - Journal article

C2 - 23182633

VL - 22 Suppl 3

SP - S168-71

JO - Journal of Neuromuscular Diseases

JF - Journal of Neuromuscular Diseases

SN - 0960-8966

ER -

ID: 48603512