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Muscle fatigue is a phenomenon where muscles that were initially generating a normal amount of force experience a declining ability to continue doing so. Muscle fatigue can be caused by vigorous exercise, but abnormal fatigue may be caused by barriers to or interference with the different stages of muscle contraction. There are two main causes of muscle fatigue: limitations of a nerve's ability to generate a sustained signal (neural fatigue) and the reduced ability of the muscle fiber to contract (metabolic fatigue). Metabolic fatigue can be caused by a shortage of, or inability to metabolize, fuel (substrates) within the muscle fiber, resulting in a low ATP reservoir. Muscle fatigue can also be caused by a lack of oxygen, known as oxygen debt, where the muscle's ability to generate force is limited by the nerve's ability to sustain a high-frequency signal.
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What You'll Learn
- Muscles require adenosine triphosphate (ATP) to function
- Muscle fatigue can be caused by barriers to or interference with the different stages of muscle contraction
- Neural fatigue is when a nerve signal weakens
- Metabolic fatigue is a shortage of, or inability to metabolize, fuel (substrates) within the muscle fibre
- Oxygen debt: the difference between the amount of oxygen needed by the muscles and the actual amount present
Muscles require adenosine triphosphate (ATP) to function
Muscle fatigue occurs when muscle use overwhelms the body's ability to deliver oxygen. This causes muscle fibres to switch to anaerobic metabolism and produce lactic acid, leading to muscle fatigue.
ATP is produced through three main processes: glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation. The latter two occur within the mitochondria of eukaryotic cells. During oxidative phosphorylation, mitochondria use oxygen to produce ATP. Slow-twitch (red) muscle fibres have high levels of mitochondria and rely on oxidative phosphorylation to make ATP, requiring high concentrations of oxygen.
Blood flow plays a crucial role in delivering oxygen for aerobic ATP production and removing by-products of metabolic processes in working muscles. This helps maintain force output and slows the development of muscle fatigue.
ATP is composed of three parts: a sugar, an amine base, and a phosphate group. The phosphate tail contains the available energy, which is released when the bonds between the phosphates are broken through hydrolysis. This process converts ATP to adenosine diphosphate (ADP), which has lower energy due to the loss of one phosphate molecule.
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Muscle fatigue can be caused by barriers to or interference with the different stages of muscle contraction
Muscle fatigue can be caused by a variety of factors, including a lack of oxygen. During exercise, the body's demand for oxygen increases, and if the muscles do not receive enough oxygen, they may become fatigued. However, muscle fatigue is a complex physiological phenomenon that involves various mechanisms and can be caused by barriers or interference at different stages of muscle contraction.
Muscle contraction involves the interaction of thick and thin filaments within the muscle fibres, known as the sliding filament model. The process begins with an electrical signal from the brain, which travels through the nervous system to the motor neurons. These motor neurons then transmit a signal to the muscle fibres, initiating muscle contraction. The release of calcium ions is essential for this process, as it triggers conformational changes in the sarcomere, leading to the interaction of thick and thin filaments and subsequent muscle contraction.
One critical factor contributing to muscle fatigue is the decrease in intracellular ATP (adenosine triphosphate) levels during sustained muscle contractions. ATP provides the energy required for muscle contraction. When ATP levels deplete, the muscle's ability to contract is impaired, leading to fatigue. Additionally, ATP is essential for the functioning of Ca++ pumps in the sarcoplasmic reticulum, which regulates calcium levels. A reduction in ATP can disrupt calcium homeostasis, impacting muscle contraction and potentially causing fatigue.
Moreover, muscle fatigue can be attributed to the accumulation of metabolic by-products, such as serum lactate, serum ammonia, and reactive oxygen species (ROS). During intense exercise, the production of these by-products increases, which may contribute to muscle fatigue. For example, the accumulation of H+ ions (from the conversion of pyruvate to lactic acid) can lower the pH, interfering with calcium release and cross-bridge cycling, ultimately impairing muscle force and leading to fatigue.
The repetitive activation of motor neurons during sustained contractions can also lead to a decrease in their excitability, resulting in reduced motor neuron firing rates. This decrease in neural activation contributes to muscle fatigue by impairing the initiation of muscle contractions. Additionally, muscle fatigue may be related to the decreased firing of muscle spindles (sensory receptors), which play a role in regulating muscle contraction and can influence the firing of motor neurons.
In summary, muscle fatigue is a multifaceted phenomenon that can be caused by various factors, including but not limited to, decreased ATP levels, accumulation of metabolic by-products, impaired neural activation, and reduced calcium release and sensitivity. These factors can interfere with the different stages of muscle contraction, from neural signalling to the mechanical sliding filament process, ultimately leading to muscle fatigue during sustained or intense physical activity.
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Neural fatigue is when a nerve signal weakens
Muscle fatigue can be caused by a lack of oxygen, among other factors. During exercise, the heart rate and respiratory rate increase to deliver more oxygen to the muscles. However, muscle use can sometimes overwhelm the body's ability to supply oxygen, leading to a switch to anaerobic metabolism and the production of lactic acid, resulting in muscle fatigue. This phenomenon is known as oxygen debt.
Neural fatigue, or nervous fatigue, is a specific type of muscle fatigue that occurs when the nerve signal weakens. It is often observed in novice strength trainers during extremely powerful contractions that approach the upper limit of a muscle's force-generating capacity. After a period of maximum contraction, the nerve's signal decreases in frequency, leading to a reduction in the force generated by the contraction. This can cause the muscle to appear to "stop listening" and gradually cease contracting.
The nerve's ability to generate sustained, high-frequency signals is crucial in allowing muscles to contract with maximum force. Strength training aims to improve this neural capacity, which can help delay the onset of muscle fatigue. Neural fatigue can also be influenced by neurotransmitters such as serotonin, dopamine, and noradrenaline, which play a key role in signal transmission between neurons. Changes in the concentrations of these neurotransmitters have been linked to central fatigue, which arises from alterations within the central nervous system.
Additionally, neural contributions to muscle fatigue can involve changes in the neuromuscular pathway during fatiguing contractions. This includes alterations in motor unit behaviour, motoneuron excitability, and motor cortical excitability. The intimate connection between the central nervous system and muscles is exemplified by the definition of the motor unit (MU), which consists of a spinal motoneuron and the muscle fibres it innervates. During fatiguing exercise, changes occur at each level of this neuromuscular pathway, impacting the force output of the muscles.
Furthermore, peripheral neuropathy, a condition affecting the peripheral nervous system, can also lead to muscle fatigue. It causes symptoms such as tingling, numbness, imbalance, and clumsiness due to problems with nerve signals. In severe cases, it can result in muscle weakness, paralysis, and atrophy. Understanding the intricate interplay between neural processes, neurotransmitters, and muscle function is essential for comprehending the complex nature of muscle fatigue.
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Metabolic fatigue is a shortage of, or inability to metabolize, fuel (substrates) within the muscle fibre
Muscle fatigue is when muscles that were initially generating a normal amount of force then experience a declining ability to generate force. It can be caused by vigorous exercise, but abnormal fatigue may be caused by barriers to or interference with the different stages of muscle contraction.
Metabolic fatigue is a common term for the reduction in contractile force due to the direct or indirect effects of two main factors. The first is a shortage of, or inability to metabolize, fuel (substrates) within the muscle fibre, causing a low ATP reservoir. Substrates within the muscle serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen, and creatine phosphate.
Creatine phosphate stores energy so that ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Muscle fatigue may be due to problems with the nerve supply, neuromuscular disease, inborn errors of metabolism, or problems with the muscle itself.
The accumulation of metabolites can directly or indirectly produce metabolic fatigue within muscle fibres through interference with the release of calcium (Ca2+) from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium. Intracellular chloride partially inhibits the contraction of muscles.
Muscle fatigue can also be caused by a lack of oxygen. Muscle use can quickly overwhelm the body's ability to deliver oxygen, at which point the muscle begins to fatigue. This is known as oxygen debt.
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Oxygen debt: the difference between the amount of oxygen needed by the muscles and the actual amount present
During exercise, the body's heart rate and respiratory rate increase to move more oxygen to actively respiring muscles. However, muscle use can quickly exceed the body's ability to deliver oxygen. This is when even red muscle fibres, which have high levels of mitochondria and use oxidative phosphorylation to make adenosine triphosphate (ATP), must switch to anaerobic metabolism and produce lactic acid. This is the point at which the muscle begins to fatigue.
The difference between the amount of oxygen needed by the muscles and the amount actually present is called the oxygen debt. Oxygen debt can last for up to 38 hours after a workout. The body must metabolise all the lactic acid it has produced during strenuous exercise. This process requires oxygen, and the amount of oxygen required to recover is equal to the oxygen debt.
Lactic acid is a by-product of exercising without using oxygen (anaerobically). It is recycled into other useful chemicals. For example, during an 800m race, half of the heart's energy may come from lactic acid, which is converted into pyruvic acid and used as energy by the heart and other muscles.
Excess post-exercise oxygen consumption (EPOC) is the scientific term for hyperventilating after a workout. Oxygen debt in the muscles is the reason for this. The body uses oxygen to return itself to stasis through various functions, including oxidising excess lactic acid so that it can be recycled throughout the body.
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Frequently asked questions
Muscle fatigue is when muscles that were initially generating a normal amount of force then experience a declining ability to generate force. It can be a result of vigorous exercise, but abnormal fatigue may be caused by barriers to or interference with the different stages of muscle contraction.
Muscle fatigue can be caused by a lack of oxygen. When a person exercises, heart rate and respiratory rate increase to move more oxygen to actively respiring muscles. However, muscle use can quickly overwhelm the body's ability to deliver oxygen. Muscles require adenosine triphosphate (ATP) to function, which requires high concentrations of oxygen to generate.
Symptoms of muscle fatigue include myalgia (muscle pain), shortness of breath, fasciculations (muscle twitching), myokymia (muscle trembling), and muscle cramps during exercise. Muscle soreness may also occur after exercising.
