Muscle weakness

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Muscle weakness
Other namesMyasthenia
Specialty Neurology

Muscle weakness is a lack of muscle strength. Its causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle weakness can also be caused by low levels of potassium and other electrolytes within muscle cells. It can be temporary or long-lasting (from seconds or minutes to months or years). The term myasthenia is from my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness".

Contents

Types

Neuromuscular fatigue can be classified as either "central" or "peripheral" depending on its cause. Central muscle fatigue manifests as an overall sense of energy deprivation, while peripheral muscle fatigue manifests as a local, muscle-specific inability to do work. [1] [2]

Neuromuscular fatigue

Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.[ citation needed ]

For extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscle'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 muscle appears to simply ‘stop listening’ and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle 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 muscle 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 muscle 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.[ citation needed ]

Central fatigue

Central fatigue is a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output. [3] [4] [5] 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. [6] [7] 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. [8] [9] [10] During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction. [11] 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 muscle contraction are inhibited. [12]

Peripheral muscle fatigue

Peripheral muscle fatigue during physical work is an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national[ where? ] 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 muscle or local group of muscles 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 muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy. [13]

The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle 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.[ citation needed ]

Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, 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 muscle 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.[ citation needed ]

Lactic acid hypothesis

It was once believed that lactic acid build-up was the cause of muscle fatigue. [14] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.[ citation needed ]

Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. 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 muscles, reducing their inhibition of contraction and leaving K+ as the only restricting influence on muscle 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+.[ citation needed ]

Pathophysiology

Muscle cells work by detecting a flow of electrical impulses from the brain which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This causes there to be less calcium available for the muscle cell. In addition an enzyme is proposed to be activated by this released calcium which eats away at muscle fibers. [15]

Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so 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. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver which is known as the Cori cycle.[ citation needed ]

Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so.[ citation needed ]

Diagnosis

Grading

The severity of muscle weakness can be classified into different "grades" based on the following criteria: [16] [17]

Classification

Proximal and distal

Muscle weakness can also be classified as either "proximal" or "distal" based on the location of the muscles that it affects. Proximal muscle weakness affects muscles closest to the body's midline, while distal muscle weakness affects muscles further out on the limbs. Proximal muscle weakness can be seen in Cushing's syndrome [18] and hyperthyroidism.[ citation needed ]

True and perceived

Muscle weakness can be classified as either "true" or "perceived" based on its cause. [19]

  • True muscle weakness (or neuromuscular weakness) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy.
  • Perceived muscle weakness (or non-neuromuscular weakness) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example myalgic encephalomyelitis/chronic fatigue syndrome. [20]

In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but true weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions. [21] [22] [23] [24] [25] [26] [ excessive citations ]

Related Research Articles

<span class="mw-page-title-main">Lambert–Eaton myasthenic syndrome</span> Medical condition

Lambert–Eaton myasthenic syndrome (LEMS) is a rare autoimmune disorder characterized by muscle weakness of the limbs.

<span class="mw-page-title-main">Motor neuron</span> Nerve cell sending impulse to muscle

A motor neuron is a neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper motor neurons and lower motor neurons. Axons from upper motor neurons synapse onto interneurons in the spinal cord and occasionally directly onto lower motor neurons. The axons from the lower motor neurons are efferent nerve fibers that carry signals from the spinal cord to the effectors. Types of lower motor neurons are alpha motor neurons, beta motor neurons, and gamma motor neurons.

<span class="mw-page-title-main">Adenosine monophosphate deaminase deficiency type 1</span> Medical condition

Adenosine monophosphate deaminase deficiency type 1 or AMPD1, is a human metabolic disorder in which the body consistently lacks the enzyme AMP deaminase, in sufficient quantities. This may result in exercise intolerance, muscle pain and muscle cramping. The disease was formerly known as myoadenylate deaminase deficiency (MADD).

The muscular system is an organ system consisting of skeletal, smooth, and cardiac muscle. It permits movement of the body, maintains posture, and circulates blood throughout the body. The muscular systems in vertebrates are controlled through the nervous system although some muscles can be completely autonomous. Together with the skeletal system in the human, it forms the musculoskeletal system, which is responsible for the movement of the body.

<span class="mw-page-title-main">Skeletal muscle</span> One of three major skeletal system types that connect to bones

Skeletal muscles are organs of the vertebrate muscular system and typically are attached by tendons to bones of a skeleton. The muscle cells of skeletal muscles are much longer than in the other types of muscle tissue, and are often known as muscle fibers. The muscle tissue of a skeletal muscle is striated – having a striped appearance due to the arrangement of the sarcomeres.

<span class="mw-page-title-main">Post-polio syndrome</span> Human disease

Post-polio syndrome is a group of latent symptoms of poliomyelitis (polio), occurring at about a 25–40% rate. These symptoms are caused by the damaging effects of the viral infection on the nervous system. Symptoms typically occur 15 to 30 years after an initial acute paralytic attack. Symptoms include decreasing muscular function or acute weakness with pain and fatigue. The same symptoms may also occur years after a nonparalytic polio (NPP) infection.

Weakness is a symptom of many different medical conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.

<span class="mw-page-title-main">Neuromuscular junction</span> Junction between the axon of a motor neuron and a muscle fiber

A neuromuscular junction is a chemical synapse between a motor neuron and a muscle fiber.

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. There are two main causes of muscle fatigue: the limitations of a nerve’s ability to generate a sustained signal ; and the reduced ability of the muscle fiber to contract.

<span class="mw-page-title-main">Muscle contraction</span> Activation of tension-generating sites in muscle

Muscle contraction is the activation of tension-generating sites within muscle cells. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length, such as when holding something heavy in the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.

In medicine, myopathy is a disease of the muscle in which the muscle fibers do not function properly. Myopathy means muscle disease. This meaning implies that the primary defect is within the muscle, as opposed to the nerves or elsewhere.

<span class="mw-page-title-main">Exercise intolerance</span> Medical condition

Exercise intolerance is a condition of inability or decreased ability to perform physical exercise at the normally expected level or duration for people of that age, size, sex, and muscle mass. It also includes experiences of unusually severe post-exercise pain, fatigue, nausea, vomiting or other negative effects. Exercise intolerance is not a disease or syndrome in and of itself, but can result from various disorders.

<span class="mw-page-title-main">Motor unit recruitment</span> Additional activation of motor units to increase contractile strength

Motor unit recruitment is the activation of additional motor units to accomplish an increase in contractile strength in a muscle. A motor unit consists of one motor neuron and all of the muscle fibers it stimulates. All muscles consist of a number of motor units and the fibers belonging to a motor unit are dispersed and intermingle amongst fibers of other units. The muscle fibers belonging to one motor unit can be spread throughout part, or most of the entire muscle, depending on the number of fibers and size of the muscle. When a motor neuron is activated, all of the muscle fibers innervated by the motor neuron are stimulated and contract. The activation of one motor neuron will result in a weak but distributed muscle contraction. The activation of more motor neurons will result in more muscle fibers being activated, and therefore a stronger muscle contraction. Motor unit recruitment is a measure of how many motor neurons are activated in a particular muscle, and therefore is a measure of how many muscle fibers of that muscle are activated. The higher the recruitment the stronger the muscle contraction will be. Motor units are generally recruited in order of smallest to largest as contraction increases. This is known as Henneman's size principle.

<span class="mw-page-title-main">Mitochondrial myopathy</span> Medical condition

Mitochondrial myopathies are types of myopathies associated with mitochondrial disease. Adenosine triphosphate (ATP), the chemical used to provide energy for the cell, cannot be produced sufficiently by oxidative phosphorylation when the mitochondrion is either damaged or missing necessary enzymes or transport proteins. With ATP production deficient in mitochondria, there is an over-reliance on anaerobic glycolysis which leads to lactic acidosis either at rest or exercise-induced.

<span class="mw-page-title-main">Neuromuscular disease</span> Medical condition

A neuromuscular disease is any disease affecting the peripheral nervous system (PNS), the neuromuscular junctions, or skeletal muscles, all of which are components of the motor unit. Damage to any of these structures can cause muscle atrophy and weakness. Issues with sensation can also occur.

Electrical muscle stimulation (EMS), also known as neuromuscular electrical stimulation (NMES) or electromyostimulation, is the elicitation of muscle contraction using electric impulses. EMS has received an increasing amount of attention in the last few years for many reasons: it can be utilized as a strength training tool for healthy subjects and athletes; it could be used as a rehabilitation and preventive tool for people who are partially or totally immobilized; it could be utilized as a testing tool for evaluating the neural and/or muscular function in vivo. EMS has been proven to be more beneficial before exercise and activity due to early muscle activation. Recent studies have found that electrostimulation has been proven to be ineffective during post exercise recovery and can even lead to an increase in Delayed onset muscle soreness (DOMS).

Acute muscle soreness (AMS) is the pain felt in muscles during and immediately, up to 24 hours, after strenuous physical exercise. The pain appears within a minute of contracting the muscle and it will disappear within two or three minutes or up to several hours after relaxing it.

<span class="mw-page-title-main">Metabolic myopathy</span> Type of myopathies

Metabolic myopathies are myopathies that result from defects in biochemical metabolism that primarily affect muscle. They are generally genetic defects that interfere with muscle's ability to create energy, causing a low ATP reservoir within the muscle cell.

<span class="mw-page-title-main">Central governor</span> Brain process

The central governor is a proposed process in the brain that regulates exercise in regard to a neurally calculated safe exertion by the body. In particular, physical activity is controlled so that its intensity cannot threaten the body’s homeostasis by causing anoxic damage to the heart muscle. The central governor limits exercise by reducing the neural recruitment of muscle fibers. This reduced recruitment causes the sensation of fatigue. The existence of a central governor was suggested to explain fatigue after prolonged strenuous exercise in long-distance running and other endurance sports, but its ideas could also apply to other causes of exertion-induced fatigue.

The motor unit consists of a voluntary alpha motoneuron and all of the collective muscle fibers that it controls, known as the effector muscle. The alpha motoneuron communicates with acetylcholine receptors on the motor end plate of the effector muscle. Reception of acetylcholine neurotransmitters on the motor end plate causes contraction of that effector muscle.

References

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  10. ↑ Newsholme EA, Blomstrand E (1995). "Tryptophan, 5-Hydroxytryptamine and a Possible Explanation for Central Fatigue". Fatigue. Advances in Experimental Medicine and Biology. Vol. 384. pp. 315–20. doi:10.1007/978-1-4899-1016-5_25. ISBN   978-1-4899-1018-9. PMID   8585461.
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  12. ↑ Cotel F, Exley R, Cragg SJ, Perrier JF; Exley; Cragg; Perrier (2013). "Serotonin spillover onto the axon initial segment of motoneurons induces central fatigue by inhibiting action potential initiation". Proc Natl Acad Sci U S A. 110 (12): 4774–9. Bibcode:2013PNAS..110.4774C. doi: 10.1073/pnas.1216150110 . PMC   3607056 . PMID   23487756.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ↑ R. Robergs; F. Ghiasvand; D. Parker (2004). "Biochemistry of exercise-induced metabolic acidosis". Am J Physiol Regul Integr Comp Physiol. 287 (3): R502–16. doi:10.1152/ajpregu.00114.2004. PMID   15308499. S2CID   2745168.
  14. ↑ Sahlin K (1986). "Muscle fatigue and lactic acid accumulation". Acta Physiol Scand Suppl. 556: 83–91. PMID   3471061.
  15. ↑ Kolata, Gina (February 12, 2008). "Finding May Solve Riddle of Fatigue in Muscles". The New York Times.
  16. ↑ Page 59 in: Hugue Ouellette (2008). Orthopedics Made Ridiculously Simple (Medmaster Ridiculously Simple) (Medmaster Ridiculously Simple). MedMaster Inc. ISBN   978-0-940780-86-6.
  17. ↑ Neurologic Examination Archived 2009-05-11 at the Wayback Machine at First Year Medical Curriculum at University of Florida College of Medicine. By Richard Rathe. Created: January 15, 1996. Modified: December 19, 2000
  18. ↑ White, Bruce A (2019). Endocrine and Reproductive Physiology (5th ed.). Mosby/Elsevier. p. 166. ISBN   978-0-323-59573-5.
  19. ↑ Marx, John (2010). Rosen's Emergency Medicine: Concepts and Clinical Practice (7th ed.). Philadelphia, PA: Mosby/Elsevier. p. Chapter 11. ISBN   978-0-323-05472-0.
  20. ↑ Enoka RM, Stuart DG (1992). "Neurobiology of muscle fatigue". J. Appl. Physiol. 72 (5): 1631–48. doi:10.1152/jappl.1992.72.5.1631. PMID   1601767. S2CID   1572573.
  21. ↑ Paul L, Wood L, Behan WM, Maclaren WM (January 1999). "Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome". Eur. J. Neurol. 6 (1): 63–9. doi:10.1046/j.1468-1331.1999.610063.x. PMID   10209352. S2CID   33480143.
  22. ↑ McCully KK, Natelson BH (November 1999). "Impaired oxygen delivery to muscle in chronic fatigue syndrome". Clin. Sci. 97 (5): 603–8, discussion 611–3. CiteSeerX   10.1.1.585.905 . doi:10.1042/CS19980372. PMID   10545311.
  23. ↑ De Becker P, Roeykens J, Reynders M, McGregor N, De Meirleir K (November 2000). "Exercise capacity in chronic fatigue syndrome". Arch. Intern. Med. 160 (21): 3270–7. doi:10.1001/archinte.160.21.3270. PMID   11088089.
  24. ↑ De Becker P, McGregor N, De Meirleir K (September 2001). "A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome". J. Intern. Med. 250 (3): 234–40. doi: 10.1046/j.1365-2796.2001.00890.x . PMID   11555128.
  25. ↑ Carruthers, Bruce M.; Jain, Anil Kumar; De Meirleir, Kenny L.; Peterson, Daniel L.; Klimas, Nancy G.; et al. (2003). Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols. Vol. 11. pp. 7–115. doi:10.1300/J092v11n01_02. ISBN   978-0-7890-2207-3. ISSN   1057-3321.{{cite book}}: |journal= ignored (help)
  26. ↑ Jammes Y, Steinberg JG, Mambrini O, Brégeon F, Delliaux S (March 2005). "Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise". J. Intern. Med. 257 (3): 299–310. doi: 10.1111/j.1365-2796.2005.01452.x . PMID   15715687.

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