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Biochemical mechanisms for oxygen free radical formation during exercise

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Standard

Biochemical mechanisms for oxygen free radical formation during exercise. / Sjödin, B.; Hellsten Westing, Ylva; Hellsten, Ylva; Apple, F. S.

I: Sports Medicine, Bind 10, Nr. 4, 1990, s. 236-254.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Sjödin, B, Hellsten Westing, Y, Hellsten, Y & Apple, FS 1990, 'Biochemical mechanisms for oxygen free radical formation during exercise', Sports Medicine, bind 10, nr. 4, s. 236-254.

APA

Sjödin, B., Hellsten Westing, Y., Hellsten, Y., & Apple, F. S. (1990). Biochemical mechanisms for oxygen free radical formation during exercise. Sports Medicine, 10(4), 236-254.

Vancouver

Sjödin B, Hellsten Westing Y, Hellsten Y, Apple FS. Biochemical mechanisms for oxygen free radical formation during exercise. Sports Medicine. 1990;10(4):236-254.

Author

Sjödin, B. ; Hellsten Westing, Ylva ; Hellsten, Ylva ; Apple, F. S. / Biochemical mechanisms for oxygen free radical formation during exercise. I: Sports Medicine. 1990 ; Bind 10, Nr. 4. s. 236-254.

Bibtex

@article{5af0c81035bb11df8ed1000ea68e967b,
title = "Biochemical mechanisms for oxygen free radical formation during exercise",
abstract = "The biochemical mechanisms behind skeletal muscle soreness and damage with muscular overuse have remained unclear. Recently, however, a growing amount of evidence indicates that free radicals play an important role as mediators of skeletal muscle damage and inflammation. During exercise, two of the potentially harmful free radical generating sources are semiquinone in the mitochondria and xanthine oxidase in the capillary endothelial cells. During high intensity exercise the flow of oxygen through the skeletal muscle cells is greatly increased at the same time as the rate of ATP utilisation exceeds the rate of ATP generation. The metabolic stress in the cells causes several biochemical changes to occur, resulting in a markedly enhanced rate of production of oxygen free radicals from semiquinone and xanthine oxidase. During normal conditions free radicals are generated at a low rate and subsequently taken care of by the well developed scavenger and antioxidant systems. However, a greatly increased rate of free radical production may exceed the capacity of the cellular defence system. Consequently, a substantial attack of free radicals on the cell membranes may lead to a loss of cell viability and to cell necrosis and could initiate the skeletal muscle damage and inflammation caused by exhaustive exercise.",
author = "B. Sj{\"o}din and {Hellsten Westing}, Ylva and Ylva Hellsten and Apple, {F. S.}",
note = "Keywords: Adenosine Triphosphate; Animals; Energy Metabolism; Exercise; Free Radicals; Humans; Muscles; Oxygen; Xanthine Oxidase",
year = "1990",
language = "English",
volume = "10",
pages = "236--254",
journal = "Sports Medicine",
issn = "0112-1642",
publisher = "Springer",
number = "4",

}

RIS

TY - JOUR

T1 - Biochemical mechanisms for oxygen free radical formation during exercise

AU - Sjödin, B.

AU - Hellsten Westing, Ylva

AU - Hellsten, Ylva

AU - Apple, F. S.

N1 - Keywords: Adenosine Triphosphate; Animals; Energy Metabolism; Exercise; Free Radicals; Humans; Muscles; Oxygen; Xanthine Oxidase

PY - 1990

Y1 - 1990

N2 - The biochemical mechanisms behind skeletal muscle soreness and damage with muscular overuse have remained unclear. Recently, however, a growing amount of evidence indicates that free radicals play an important role as mediators of skeletal muscle damage and inflammation. During exercise, two of the potentially harmful free radical generating sources are semiquinone in the mitochondria and xanthine oxidase in the capillary endothelial cells. During high intensity exercise the flow of oxygen through the skeletal muscle cells is greatly increased at the same time as the rate of ATP utilisation exceeds the rate of ATP generation. The metabolic stress in the cells causes several biochemical changes to occur, resulting in a markedly enhanced rate of production of oxygen free radicals from semiquinone and xanthine oxidase. During normal conditions free radicals are generated at a low rate and subsequently taken care of by the well developed scavenger and antioxidant systems. However, a greatly increased rate of free radical production may exceed the capacity of the cellular defence system. Consequently, a substantial attack of free radicals on the cell membranes may lead to a loss of cell viability and to cell necrosis and could initiate the skeletal muscle damage and inflammation caused by exhaustive exercise.

AB - The biochemical mechanisms behind skeletal muscle soreness and damage with muscular overuse have remained unclear. Recently, however, a growing amount of evidence indicates that free radicals play an important role as mediators of skeletal muscle damage and inflammation. During exercise, two of the potentially harmful free radical generating sources are semiquinone in the mitochondria and xanthine oxidase in the capillary endothelial cells. During high intensity exercise the flow of oxygen through the skeletal muscle cells is greatly increased at the same time as the rate of ATP utilisation exceeds the rate of ATP generation. The metabolic stress in the cells causes several biochemical changes to occur, resulting in a markedly enhanced rate of production of oxygen free radicals from semiquinone and xanthine oxidase. During normal conditions free radicals are generated at a low rate and subsequently taken care of by the well developed scavenger and antioxidant systems. However, a greatly increased rate of free radical production may exceed the capacity of the cellular defence system. Consequently, a substantial attack of free radicals on the cell membranes may lead to a loss of cell viability and to cell necrosis and could initiate the skeletal muscle damage and inflammation caused by exhaustive exercise.

M3 - Journal article

C2 - 2247725

VL - 10

SP - 236

EP - 254

JO - Sports Medicine

JF - Sports Medicine

SN - 0112-1642

IS - 4

ER -

ID: 18765532