Energy supply and muscle fatigue in humans.
Document identifier: oai:dalea.du.se:2329
Publication year: 1998Relevant Sustainable Development Goals (SDGs):
The SDG label(s) above have been assigned by OSDG.aiAbstract: Limitations in energy supply is a classical hypothesis of muscle fatigue. The present paper reviews the evidence available from human studies that energy deficiency is an important factor in fatigue. The maximal rate of energy expenditure determined in skinned fibres is close to the rate of adenosine triphosphate (ATP) utilisation observed in vivo and data suggest that performance during short bursts of exercise (<5 s duration) primarily is limited by other factors than energy supply (e.g. Vmax of myosine adenosine triphosphatase (ATPase), motor unit recruitment, engaged muscle mass). Within 10 s of exercise maximal power output decreases considerably and coincides with depletion of phosphocreatine. During recovery, maximal force and power output is restored with a similar time course as the resynthesis of phosphocreatine. Increases in muscle store of phosphocreatine through dietary supplementation with creatine increases performance during high-intensity exercise. These findings support the hypothesis that energy supply limits performance during high-intensity exercise. It is well documented that pre-exercise muscle glycogen content is related to performance during moderate intensity exercise. Recent data indicates that the interfibre variation in phosphocreatine is large after prolonged exercise to fatigue and that some fibres are depleted to the same extent as after high-intensity exercise. Despite relatively small decreases in ATP, the products of ATP hydrolysis (Pi and free ADP) may increase considerably. FreeADP calculated from the creatine kinase reaction increases 10-fold both after high-intensity exercise and after prolonged exercise to fatigue. It is suggested that local increases in ADP may reach inhibitory levels for the contraction process.
Authors
Kent Sahlin
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Michail Tonkonogi
Högskolan Dalarna; Medicinsk vetenskap
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Karin Söderlund
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identifier: oai:dalea.du.se:2329
datestamp: 2021-04-15T13:12:15Z
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titleInfo:
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lang: eng
title: Energy supply and muscle fatigue in humans.
abstract: Limitations in energy supply is a classical hypothesis of muscle fatigue. The present paper reviews the evidence available from human studies that energy deficiency is an important factor in fatigue. The maximal rate of energy expenditure determined in skinned fibres is close to the rate of adenosine triphosphate (ATP) utilisation observed in vivo and data suggest that performance during short bursts of exercise (<5 s duration) primarily is limited by other factors than energy supply (e.g. Vmax of myosine adenosine triphosphatase (ATPase) motor unit recruitment engaged muscle mass). Within 10 s of exercise maximal power output decreases considerably and coincides with depletion of phosphocreatine. During recovery maximal force and power output is restored with a similar time course as the resynthesis of phosphocreatine. Increases in muscle store of phosphocreatine through dietary supplementation with creatine increases performance during high-intensity exercise. These findings support the hypothesis that energy supply limits performance during high-intensity exercise. It is well documented that pre-exercise muscle glycogen content is related to performance during moderate intensity exercise. Recent data indicates that the interfibre variation in phosphocreatine is large after prolonged exercise to fatigue and that some fibres are depleted to the same extent as after high-intensity exercise. Despite relatively small decreases in ATP the products of ATP hydrolysis (Pi and free ADP) may increase considerably. FreeADP calculated from the creatine kinase reaction increases 10-fold both after high-intensity exercise and after prolonged exercise to fatigue. It is suggested that local increases in ADP may reach inhibitory levels for the contraction process.
language:
languageTerm: eng
genre:
publication/journal-article
ref
note:
Published
3
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Sahlin
Kent
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Tonkonogi
Michail
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Högskolan Dalarna
Medicinsk vetenskap
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0000-0003-1619-9758
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Söderlund
Karin
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originInfo:
dateIssued: 1998
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titleInfo:
title: Acta Physiologica Scandinavica
identifier:
0001-6772
1365-201X
part:
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@attributes:
type: volume
number: 162
extent:
start: 261
end: 266
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