Victor Forge
Muscle fatigue is a common phenomenon that limits athletic performance and other strenuous or prolonged activities. It is defined as an exercise-induced decrease in the ability to produce force. The mechanisms that cause fatigue are specific to the task being performed and can vary from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor command in the motor cortex. Fatigue can also be caused by molecular changes that occur with sustained exercise, such as the conformational change in the ryanodine receptor in skeletal muscle, resulting in “leaky” channels that are deficient in calcium release. Other factors that contribute to muscle fatigue include nervous fatigue, substrate shortage, and metabolic factors such as decreased pH and oxidative stress.
| Characteristics | Values |
|---|---|
| Definition | "Local muscle fatigue" is the reduction in force-generating capacity of skeletal muscle resulting from muscle activity under load that is reversible with rest. |
| Cause | Accumulation of metabolites within muscle fibres, inadequate motor command in the motor cortex, impaired calcium release, inadequate excitation due to changes in electrochemical gradients for K+, molecular changes, nervous fatigue, metabolic fatigue, etc. |
| Symptoms | Myalgia (muscle pain), shortness of breath, fasciculations (muscle twitching), myokymia (muscle trembling), muscle cramps, muscle soreness, inappropriate rapid heart rate response to exercise, etc. |
| Impact | Muscle weakness, muscle atrophy, reduced physical functioning, increased body pain, reduced sleep quality, psychological distress, limiting athletic performance, etc. |
| Diagnosis | Non-invasive techniques using electrical or magnetic stimulation of a muscle or other areas of the body that affect the muscle. |
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What You'll Learn
Metabolic changes
The accumulation of metabolites within muscle fibres can lead to muscle fatigue. For instance, the accumulation of inorganic phosphate (Pi) during intense skeletal muscle activity due to the breakdown of creatine phosphate (CrP) can hinder the transition to high-force states and decrease force production. Inorganic phosphate can also enter the SR and precipitate Ca2+, reducing the amount available for release.
Additionally, muscle fatigue can be caused by a decrease in intracellular ATP, which is essential for muscle contraction. ATP is consumed at a faster rate by fast isoforms of MHC isoforms, and fatigue occurs more slowly when cross-bridge ATP consumption is decreased. The major determinant of fatigue resistance is likely the muscle fibre's density of mitochondria and capacity for oxidative metabolism.
Intracellular acidosis, primarily due to lactic acid accumulation, has also been considered a significant cause of skeletal muscle fatigue. However, recent studies on mammalian muscle show little direct effect of acidosis on muscle function at physiological temperatures. Instead, the increased presence of hydrogen ions (H+) from the anaerobic breakdown of glycogen is the classic cause of skeletal muscle fatigue.
Furthermore, impaired calcium release from the SR has been identified as a contributor to fatigue in isolated skeletal muscle fibres. High-frequency stimulation may lead to extracellular K+ accumulation, decreasing voltage sensor activation and action potential amplitude, which in turn affects calcium release.
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Accumulation of metabolites
Muscle fatigue is a common phenomenon that can be defined as an exercise-induced decrease in the ability to produce force. It is important to note that the development of muscle fatigue is typically characterised by a decline in the maximal force or power capacity of a muscle.
The accumulation of substances (metabolites) within muscle fibres is one of the proposed causes of skeletal muscle fatigue. This accumulation can interfere with the release of calcium (Ca2+) and the ability of calcium to stimulate muscle contraction. Calcium plays a crucial role in muscle contraction, as it is released by the sarcoplasmic reticulum, leading to muscle fibres contracting upon detection of electrical impulses from the brain.
Metabolic fatigue, a common term for the reduction in contractile force, is influenced by two main factors: a shortage of, or inability to metabolise, fuel (substrates) within the muscle fibre, resulting in low ATP reserves. ATP (adenosine triphosphate) is a molecule that stores and delivers energy, and a decrease in ATP can lead to a decline in muscle performance.
Inorganic phosphate (Pi) is another metabolite that increases during muscle fatigue due to the breakdown of creatine phosphate. This increase in Pi may hinder the transition to high-force muscle contractions, resulting in a decrease in force production. Additionally, elevated Pi levels can inhibit or reverse the SR Ca2+ pump, further contributing to muscle fatigue.
Furthermore, muscle fatigue may be linked to molecular changes, such as the ryanodine receptor in skeletal muscle undergoing a conformational change during exercise, resulting in "leaky" channels deficient in calcium release. These "leaky" channels are believed to contribute to muscle fatigue and decreased exercise capacity.
Overall, the accumulation of metabolites within muscle fibres is a significant factor in skeletal muscle fatigue, impacting calcium release and muscle contraction, and influencing metabolic processes that reduce contractile force.
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Inadequate motor command
Muscle fatigue is a reduction in force-generating capacity, which is reversible with rest. It can be caused by many different mechanisms, one of which is inadequate motor command.
During extremely powerful contractions that are close to the upper limit of a muscle's force-generating capacity, nervous fatigue (enervation) can occur. This is when the nerve signal weakens, and it is more likely to occur in untrained individuals. The nerve's ability to generate sustained, high-frequency signals is crucial for muscle contraction. Neural training, such as strength training, can improve the nerve's ability to sustain these signals, resulting in rapid strength gains.
However, once the nerve reaches its maximum contraction capacity, the focus shifts to increasing muscular strength through myofibrillar or sarcoplasmic hypertrophy. At this point, metabolic fatigue becomes the limiting factor for contractile force. Metabolic fatigue refers to the reduction in contractile force due to the direct or indirect effects of two main factors: the shortage of, or inability to metabolize, fuel (substrates) within the muscle fiber, resulting in low ATP levels; and the accumulation of metabolites within the muscle fiber, which interferes with calcium release or its ability to stimulate muscle contraction.
In summary, inadequate motor command resulting from nervous fatigue and metabolic fatigue can contribute to muscle fatigue by impairing the nerve's ability to generate and sustain the necessary signals for muscle contraction.
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Molecular changes
Muscle fatigue is a common issue, especially during and after exercise, and can be defined as an exercise-induced decrease in the ability to produce force. It is important to note that muscle fatigue is not the same as muscle weakness, although weakness may be an initial symptom. During muscle fatigue, an individual may experience a loss of hand grip or the inability to lift, push, or maintain an isometric position.
- Glycogen Depletion: Glycogen is the primary energy store in muscles and is rapidly depleted during intense exercise, leading to muscle fatigue. This relationship between glycogen levels and fatigue is well-established, but the exact mechanism is still not fully understood.
- Calcium (Ca2+) Handling: Impaired calcium release from the sarcoplasmic reticulum (SR) is a key factor in muscle fatigue. Calcium ions (Ca2+) are essential for muscle contraction, and any interference with their release or function can lead to fatigue. High-frequency stimulation, changes in intracellular ATP and magnesium (Mg2+) levels, and exposure to myoplasmic phosphate can all impact calcium release and contribute to fatigue.
- Inorganic Phosphate Accumulation: Inorganic phosphate levels increase during intense skeletal muscle activity, mainly due to the breakdown of creatine phosphate (CrP). This increased phosphate concentration hinders the transition to high-force muscle states, reducing force production.
- Lactic Acid Accumulation: Intracellular acidosis, primarily due to lactic acid accumulation, has been historically considered a major cause of muscle fatigue. However, recent studies on mammalian muscle suggest that acidosis may not directly impact muscle function at physiological temperatures.
- Metabolic Changes: Metabolic fatigue is caused by a shortage of fuel (substrates) within the muscle fiber, leading to low ATP levels. Accumulation of metabolites, such as chloride, potassium, lactic acid, and reactive oxygen species, can interfere with calcium release and muscle contraction, contributing to fatigue.
- Medications and Toxic Compounds: Chronic exposure to certain medications or toxic compounds can lead to persistent muscle fatigue. For example, peroxisome proliferator-activated receptor (PPAR) agonists, used to increase muscle fat oxidation, can negatively affect muscle function during sustained contraction.
- Muscle Fiber Types: There are two main types of skeletal muscle fibers: slow-twitch (Type I) and fast-twitch (Type II). Fast-twitch fibers generate more power but fatigue rapidly and are more susceptible to fatigue compared to slow-twitch fibers, which are more resilient and suitable for prolonged aerobic activities.
- Neural Fatigue: Nervous fatigue occurs when the nerve signal weakens during extremely powerful contractions. This can be a limiting factor in untrained individuals, as the nerve's ability to sustain a high-frequency signal determines the muscle's force generation.
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Nervous fatigue
Furthermore, muscle fatigue can be influenced by the endocrine system, which includes the hypothalamus-pituitary-adrenal axis (HPA axis). Fatigue reactants such as cortisol, catecholamine, IL-6, and HSPs may play a role in muscle function. HSP25 protein, a type of HSP, is abundantly expressed in skeletal muscle and increases with muscle contractile activity. While nervous fatigue is seldom an issue, it can be a limiting factor during extremely powerful contractions that approach the upper limit of a muscle's force-generating capacity.
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Frequently asked questions
Muscle fatigue is a reduction in force-generating capacity or a decrease in the ability to produce force, resulting from muscle activity under load that is reversible with rest.
Skeletal muscle fatigue has been linked to impaired calcium release from the SR, which is induced by muscle fatigue. Some other causes include:
- Molecular changes that occur with sustained exercise
- Intracellular acidosis due to lactic acid accumulation
- Inorganic phosphate, which increases during fatigue due to the breakdown of creatine phosphate
- Anaerobic metabolism
The simplest way to determine the onset of muscle fatigue is to measure the time during which an individual is able to perform certain work, such as keeping a defined level of static (isometric) contraction. This is known as the "mechanical manifestation of muscle fatigue".
