Metabolic Factors in Fatigue1
Abstract
The supply of energy is of fundamental importance for the ability to sustain exercise. The maximal duration of exercise is negatively related to the relative intensity both during dynamic and static exercise. Since exercise intensity is linearly related to the rate of energy utilisation this suggests that energetic deficiency plays a major role in the aetiology of muscle fatigue. Characteristic metabolic changes in the muscle are generally observed at fatigue--the pattern being different after short term exercise (lactate accumulation and phosphocreatine depletion) from after prolonged exercise at moderate intensity (glycogen depletion). A common metabolic denominator at fatigue during these and many other conditions is a reduced capacity to generate ATP and is expressed by an increased catabolism of the adenine nucleotide pool in the muscle fibre. Transient increases in ADP are suggested to occur during energetic deficiency and may be the cause of fatigue. Experimental evidence from human studies demonstrate that near maximal power output can be attained during acidotic conditions. Decreases in muscle pH is therefore unlikely to affect the contractile machinery by a direct effect. However, acidosis may interfere with the energy supply possibly by reducing the glycolytic rate, and could by this mechanism be related to muscle fatigue.
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Exercise above lactate threshold incurs a nonlinear increase in metabolic, respiratory, and perceptual stress and more rapid fatigue due to metabolic acidosis or accelerated muscle glycogen depletion.
“Exercise above LT incurs a nonlinear increase in metabolic, respiratory, and perceptual stress and a more rapid fatigue development due to the effects of metabolic acidosis on contractile function or an accelerated depletion of muscle glycogen (Sahlin, 1992).”
From Contemporary Nutrition Strategies to Optimize Performance in Distance Runners and Race Walkers (2019) · cites this paper as Sahlin, 1992
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“Exercise-induced muscle fatigue, defined as the inability of the skeletal muscle to maintain a particular tension or a given exercise intensity [3], has been a focal point of research for many decades.”
Background
- Authors
- Sahlin, K.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Sahlin, Kent
- Venue
- Sports Medicine
- Published
- 1992-02
- Volume
- 13
- Issue
- 2
- Pages
- 99-107
- ISSN
- 0112-1642 (ISSN-L)
- OpenAlex
- W2061685389
- Cited by
- 201
- References
- 40
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 5 · 2022: 5 · 2021: 9 · 2020: 11 · 2019: 6 · 2018: 7 · 2017: 4 · 2016: 9 · 2015: 5 · 2014: 13 · 2013: 12 · 2012: 5
- FWCI
- 6.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Sports Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Sports Performance and Training
- Keywords
- muscle fatigue, ATP production, adenine nucleotide metabolism, phosphocreatine depletion, glycogen depletion, lactate accumulation, muscle acidosis, exercise intensity, exercise duration, glycolysis
- MeSH terms
- Adenosine Diphosphate, Adenosine Triphosphate, AMP Deaminase, Fatigue, Humans, Inosine Monophosphate, Maximal Voluntary Ventilation, Muscle Contraction, Exercise
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