Weakness is a symptom of many different medical conditions.[1] 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.[citation needed]
| Weakness | |
|---|---|
| Other names | Asthenia |
| Specialty | Neurology |
Pathophysiology
editMuscle 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 makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers.[2]
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 felt when people exhaust their 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]
Differential diagnosis
editTrue vs. perceived weakness
edit- True weakness (or neuromuscular) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy.
- Perceived weakness (or non-neuromuscular) 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.[3]
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 Myalgic encephalomyelitis/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.[4][5][6][7][8][9]
Asthenia vs. myasthenia
editAsthenia or asthaenia (Greek: ἀσθένεια, literally lack of strength but also disease) is a medical term referring to a condition in which the body lacks or has lost strength either as a whole or in any of its parts. It is a poorly defined condition that can include true or primary muscle weakness or perceived muscle weakness.[10] For perceived muscle weakness, asthenia has been described as the feeling of weak or tired muscles in the absence of muscle weakness, that is the muscle can generate a normal amount of force but it is perceived as requiring more effort.[11][12]
General asthenia occurs in many chronic wasting diseases (such as tuberculosis and cancer), sleep disorders or chronic disorders of the heart, lungs or kidneys, and is probably most marked in diseases of the adrenal gland. Asthenia may be limited to certain organs or systems of organs, as in asthenopia, characterized by ready fatiguability. Asthenia is also a side effect of some medications and treatments, such as Ritonavir (a protease inhibitor used in HIV treatment). [13]
Differentiating psychogenic (perceived) asthenia and true asthenia from myasthenia is often difficult, and in time apparent psychogenic asthenia accompanying many chronic disorders is seen to progress into a primary weakness.[citation needed]
Myasthenia or myasthaenia (my- from Greek: μυο meaning "muscle" + -asthenia [ἀσθένεια] meaning "weakness"), or simply muscle weakness, is a lack of muscle strength. The 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 diseases, such as myasthenia gravis. Perceived muscle weakness occurs in diseases such as sleep disorders, and depression.[11]
Types
editMuscle fatigue can be central, neuromuscular, or peripheral muscular. Central muscle fatigue manifests as an overall sense of energy deprivation, and peripheral muscle weakness manifests as a local, muscle-specific inability to do work.[14][15] Neuromuscular fatigue can be either central or peripheral.[citation needed]
Central fatigue
editThe central fatigue is generally described in terms of a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output.[16][17][18] 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.[19][20] The exact mechanisms of central fatigue are unknown, though there has been considerable interest in the role of serotonergic pathways.[21][22][23]
Neuromuscular fatigue
editNerves 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.
Peripheral muscle fatigue
editPeripheral muscle fatigue during physical work is considered[by whom?] 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.[24]
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 myocytes. 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.
Management
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References
edit- ^ 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.
- ^ Kolata, Gina (February 12, 2008). "Finding May Solve Riddle of Fatigue in Muscles". The New York Times.
- ^ Ropper, Allan H.; Samuels, Martin A. (2009). Adams and Victor's Principles of Neurology, Ninth Edition. McGraw-Hill. ISBN 978-0071499927.
- ^ 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.
- ^ McCully KK, Natelson BH (November 1999). "Impaired oxygen delivery to muscle in chronic fatigue syndrome". Clin. Sci. 97 (5): 603–8, discussion 611–3. doi:10.1042/CS19980372. PMID 10545311.
- ^ 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. Archived from the original on 2011-08-12. Retrieved 2011-03-12.
- ^ 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.
- ^ 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) - ^ 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.
- ^ Kauffman, Timothy L.; Kemmis, Karen (2014-01-01), Kauffman, Timothy L.; Scott, Ron; Barr, John O.; Moran, Michael L. (eds.), "Chapter 16 - Muscle weakness and therapeutic exercise", A Comprehensive Guide to Geriatric Rehabilitation (Third Edition), Oxford: Churchill Livingstone, pp. 112–119, ISBN 978-0-7020-4588-2, retrieved 2023-11-19
- ^ a b Saguil, Aaron (2005-04-01). "Evaluation of the Patient with Muscle Weakness". American Family Physician. 71 (7): 1327–1336. PMID 15832536.
Asthenia is a sense of weariness or exhaustion in the absence of muscle weakness.
- ^ "Muscle Weakness and Fatigue | Causes and Treatment". patient.info. 2021-06-28. Retrieved 2023-11-19.
Muscle tiredness: This is sometimes called asthenia. It is a sense of weariness or exhaustion that you feel when using the muscle. The muscle isn't genuinely weaker, it can still do its job but it takes you more effort to manage it.
- ^ "PubChem Compound Summary for CID 392622, Ritonavir". NCBI. 28 November 2022. Retrieved 28 November 2022.
- ^ Gandevia SC, Enoka RM, McComas AJ, Stuart DG, Thomas CK (1995). "Neurobiology of Muscle Fatigue". Fatigue. Advances in Experimental Medicine and Biology. Vol. 384. pp. 515–25. doi:10.1007/978-1-4899-1016-5_39. ISBN 978-1-4899-1018-9. PMID 8585476.
- ^ Kent-Braun JA (1999). "Central and peripheral contributions to muscle fatigue in humans during sustained maximal effort". European Journal of Applied Physiology and Occupational Physiology. 80 (1): 57–63. doi:10.1007/s004210050558. PMID 10367724. S2CID 22515865.
- ^ Gandevia SC (2001). "Spinal and supraspinal factors in human muscle fatigue". Physiol. Rev. 81 (4): 1725–89. doi:10.1152/physrev.2001.81.4.1725. PMID 11581501.
- ^ Kay D, Marino FE, Cannon J, St Clair Gibson A, Lambert MI, Noakes TD (2001). "Evidence for neuromuscular fatigue during high-intensity cycling in warm, humid conditions". Eur. J. Appl. Physiol. 84 (1–2): 115–21. doi:10.1007/s004210000340. PMID 11394239. S2CID 25906759.
- ^ Vandewalle H, Maton B, Le Bozec S, Guerenbourg G (1991). "An electromyographic study of an all-out exercise on a cycle ergometer". Archives Internationales de Physiologie, de Biochimie et de Biophysique. 99 (1): 89–93. doi:10.3109/13813459109145909. PMID 1713492.
- ^ Bigland-Ritchie B, Woods JJ (1984). "Changes in muscle contractile properties and neural control during human muscular fatigue". Muscle Nerve. 7 (9): 691–9. doi:10.1002/mus.880070902. PMID 6100456. S2CID 13606531.
- ^ Noakes TD (2000). "Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance". Scandinavian Journal of Medicine & Science in Sports. 10 (3): 123–45. doi:10.1034/j.1600-0838.2000.010003123.x. PMID 10843507. S2CID 23103331.
- ^ Davis JM (1995). "Carbohydrates, branched-chain amino acids, and endurance: the central fatigue hypothesis". International Journal of Sport Nutrition. 5 (Suppl): S29–38. doi:10.1123/ijsn.5.s1.s29. PMID 7550256.
- ^ Newsholme, E. A., Acworth, I. N., & Blomstrand, E. 1987, 'Amino acids, brain neurotransmitters and a functional link between muscle and brain that is important in sustained exercise', in G Benzi (ed.), Advances in Myochemistry, Libbey Eurotext, London, pp. 127-133.
- ^ 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.
- ^ 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.
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