Neuromuscular fatigue can be classified as either "central" or "peripheral" depending on its cause. Central<unk>  fatigue manifests as an overall sense of energy deprivation, while peripheral<unk>  fatigue manifests as a local,<unk> -specific inability to do work. Neuromuscular fatigue Nerves control the contraction of<unk> s by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the<unk>  that it innervates. Most movements require a force far below what a<unk>  could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue. For extremely powerful contractions that are close to the upper limit of a<unk> 's ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the<unk> 's ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal. After an extended period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the<unk>  appears to simply ‘stop listening’ and gradually cease to move, often lengthening. As there is insufficient stress on the<unk> s and tendons, there will often be no delayed onset<unk>  soreness following the workout. Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a<unk>  to contract with their greatest force. It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the<unk>  reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force. Central fatigue Central fatigue is a reduction in the neural drive or nerve-based motor command to working<unk> s that results in a decline in the force output. It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity. There has been a great deal of interest in the role of serotonergic pathways for several years because its concentration in the brain increases with motor activity. During motor activity, serotonin released in synapses that contact motoneurons promotes<unk>  contraction. During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motoneurons with the result that nerve impulse initiation and thereby<unk>  contraction are inhibited. Peripheral<unk>  fatigue Peripheral<unk>  fatigue' during physical work is an inability for the body to supply sufficient energy or other metabolites to the contracting<unk> s to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single<unk>  or local group of<unk> s to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the<unk> , causing the stereotypical burning sensation of local<unk>  fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy. The fundamental difference between the peripheral and central theories of<unk>  fatigue is that the peripheral model of<unk>  fatigue assumes failure at one or more sites in the chain that initiates<unk>  contraction. Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local<unk>  affected, whereas the central model of<unk>  fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating<unk>  fatigue through<unk>  derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore, the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed. Though not universally used, "metabolic fatigue" is a common alternative term for peripheral<unk> , because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the<unk>  fiber. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract. Lactic acid hypothesis It was once believed that lactic acid build-up was the cause of<unk>  fatigue. The assumption was lactic acid had a "pickling" effect on<unk> s, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder<unk>  fatigue. Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of<unk> s. This can lower the sensitivity of contractile apparatus to calcium ions (Ca2+) but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of potassium ions (K+) on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the<unk> s, reducing their inhibition of contraction and leaving K+ as the only restricting influence on<unk>  contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.
Muscle weakness
Muscle atrophy
Muscle imbalance
Paresis
Gastroparesis
Facial weakness
Peripheral edema
Dysuria