Short Communication - (2025) Volume 15, Issue 5
Received: 01-Sep-2025, Manuscript No. Jsmds-25-175825;
Editor assigned: 03-Sep-2025, Pre QC No. P-175825;
Reviewed: 17-Sep-2025, QC No. Q-175825;
Revised: 22-Sep-2025, Manuscript No. R-175825;
Published:
29-Sep-2025
, DOI: 10.37421/2161-0673.2025.15.454
Citation: Wei, Chen. "Muscle Fatigue: Complexity, Causes, and Solutions." J Sports Med Doping Stud 15 (2025):454.
Copyright: © 2025 Wei C. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution
and reproduction in any medium, provided the original author and source are credited
Muscle fatigue involves complex processes spanning central nervous system drive, neuromuscular transmission, and excitation-contraction coupling within the muscle itself [1].
This review highlights how both central and peripheral factors contribute, influencing everything from athletic performance to daily activities and overall health, emphasizing fatigue's role beyond just feeling tired [1].
Neuromuscular fatigue is a significant factor in athletic performance and injury risk, characterized by a decline in muscle force production capacity [2].
Understanding its mechanisms, whether central or peripheral, is crucial [2].
This article provides a framework for measuring and interpreting fatigue, emphasizing the need for comprehensive assessment methods in both research and applied settings [2].
This review delves into the cellular mechanisms underlying muscle fatigue, particularly whether it's more about the muscle's inability to meet energy demands or a failure in energy supply [3].
It highlights the complex interplay of ATP hydrolysis, metabolite accumulation, and ion homeostasis, suggesting that both supply and demand issues contribute depending on the type and intensity of exercise [3].
Central fatigue, originating from the central nervous system, plays a significant role in the overall perception of muscle fatigue and the reduction in motor drive [4].
This article emphasizes how changes in motor cortex excitability, spinal cord activity, and afferent feedback contribute to a diminished ability to voluntarily activate muscles, even when the muscle itself is not maximally fatigued [4].
Peripheral fatigue, occurring directly within the muscle, is primarily attributed to impairments in excitation-contraction coupling, energy metabolism, and ion homeostasis [5].
This article outlines how factors like calcium handling disruption, accumulation of inorganic phosphate, and depletion of ATP stores contribute to reduced force generation, directly impacting exercise performance and recovery [5].
This review explores significant sex differences in muscle fatigue, generally finding that females tend to be more resistant to fatigue during isometric and dynamic contractions compared to males, particularly at lower intensities [6].
The article discusses potential contributing factors including hormonal influences, muscle morphology, metabolism, and neural strategies, emphasizing the need for sex-specific considerations in research and training [6].
This systematic review synthesizes the current understanding of muscle fatigue and recovery during intermittent exercise, a common pattern in many sports [7].
It highlights how repeated bouts lead to progressive fatigue due to accumulating metabolic byproducts and impaired calcium handling, while recovery periods are crucial for restoring muscle function and energy substrates [7].
The balance between fatigue development and recovery determines sustained performance [7].
As we age, skeletal muscles become more susceptible to fatigue, impacting daily activities and quality of life [8].
This article reviews how age-related changes, such as sarcopenia, alterations in motor unit properties, and impaired mitochondrial function, contribute to increased fatigability [8].
Understanding these mechanisms is key to developing interventions that promote healthy aging and maintain functional independence [8].
This comprehensive review details the molecular events contributing to muscle fatigue, focusing on the interplay of calcium regulation, ATP hydrolysis, and the accumulation of various metabolites within muscle fibers [9].
It emphasizes how these changes disrupt excitation-contraction coupling at different levels, leading to a reduction in force generation and contractile speed, thereby providing a fundamental understanding of fatigue [9].
This review examines various nutritional strategies aimed at mitigating muscle fatigue and enhancing recovery [10].
It explores the roles of carbohydrates, proteins, amino acids, and other supplements in maintaining energy stores, reducing muscle damage, and modulating inflammatory responses [10].
The article suggests that targeted nutritional interventions can be effective tools for athletes and individuals engaging in strenuous physical activity [10].
Muscle fatigue involves complex processes spanning central nervous system drive, neuromuscular transmission, and excitation-contraction coupling within the muscle itself [1]. This phenomenon influences athletic performance, daily activities, and overall health, emphasizing fatigue's role beyond just feeling tired [1]. Neuromuscular fatigue is a significant factor in athletic performance and injury risk, characterized by a decline in muscle force production capacity. Understanding its mechanisms, whether central or peripheral, is crucial. This article provides a framework for measuring and interpreting fatigue, emphasizing the need for comprehensive assessment methods in both research and applied settings [2].
Central fatigue, originating from the central nervous system, plays a significant role in the overall perception of muscle fatigue and the reduction in motor drive. Changes in motor cortex excitability, spinal cord activity, and afferent feedback contribute to a diminished ability to voluntarily activate muscles, even when the muscle itself is not maximally fatigued [4]. Peripheral fatigue, occurring directly within the muscle, is primarily attributed to impairments in excitation-contraction coupling, energy metabolism, and ion homeostasis. Factors like calcium handling disruption, accumulation of inorganic phosphate, and depletion of ATP stores contribute to reduced force generation, directly impacting exercise performance and recovery [5].
The cellular mechanisms underlying muscle fatigue often involve whether it's more about the muscle's inability to meet energy demands or a failure in energy supply. The complex interplay of ATP hydrolysis, metabolite accumulation, and ion homeostasis suggests that both supply and demand issues contribute depending on the type and intensity of exercise [3]. Detailed molecular events contributing to muscle fatigue focus on calcium regulation, ATP hydrolysis, and the accumulation of various metabolites within muscle fibers. These changes disrupt excitation-contraction coupling at different levels, leading to a reduction in force generation and contractile speed, thereby providing a fundamental understanding of fatigue [9].
Significant sex differences in muscle fatigue have been observed, generally finding that females tend to be more resistant to fatigue during isometric and dynamic contractions compared to males, particularly at lower intensities. Potential contributing factors include hormonal influences, muscle morphology, metabolism, and neural strategies, emphasizing the need for sex-specific considerations in research and training [6]. As we age, skeletal muscles become more susceptible to fatigue, impacting daily activities and quality of life. Age-related changes such as sarcopenia, alterations in motor unit properties, and impaired mitochondrial function contribute to increased fatigability. Understanding these mechanisms is key to developing interventions that promote healthy aging and maintain functional independence [8].
During intermittent exercise, a common pattern in many sports, muscle fatigue and recovery involve unique mechanisms. Repeated bouts lead to progressive fatigue due to accumulating metabolic byproducts and impaired calcium handling, while recovery periods are crucial for restoring muscle function and energy substrates. The balance between fatigue development and recovery determines sustained performance [7]. Various nutritional strategies can mitigate muscle fatigue and enhance recovery. These include exploring the roles of carbohydrates, proteins, amino acids, and other supplements in maintaining energy stores, reducing muscle damage, and modulating inflammatory responses. Targeted nutritional interventions are effective tools for athletes and individuals engaging in strenuous physical activity [10].
Muscle fatigue is a complex, multifaceted phenomenon significantly impacting athletic performance and daily activities. It involves intricate processes across the central nervous system, neuromuscular transmission, and excitation-contraction coupling within the muscle itself [1]. This decline in muscle force production capacity is crucial for understanding injury risk and optimizing performance [2]. Fatigue can be broadly categorized into central fatigue, which originates from the brain's reduced motor drive and perception [4], and peripheral fatigue, caused by disruptions within the muscle, such as impaired calcium handling, energy metabolism, and ion homeostasis [5]. At a cellular level, both energy supply and demand issues contribute, involving ATP hydrolysis and metabolite accumulation [3, 9]. Moreover, physiological differences like sex, where females often exhibit greater fatigue resistance [6], and age, with increased fatigability in older adults due to sarcopenia and mitochondrial dysfunction [8], play significant roles. The dynamics of fatigue and recovery during intermittent exercise are also critical, influenced by metabolic byproducts [7]. Finally, nutritional strategies, including appropriate intake of carbohydrates, proteins, and supplements, are explored as effective tools to mitigate fatigue and enhance recovery in strenuous physical activity [10].
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Journal of Sports Medicine & Doping Studies received 1022 citations as per Google Scholar report