Fatigue (physical)

Name of Symptom/Sign:
**Fatigue (physical)**
[[Image:{{{Image}}}\|190px\|center\|]];
ICD-10	R53
ICD-O:
ICD-9	780.7
OMIM	[1]
MedlinePlus	[2]
eMedicine	/
DiseasesDB	30079

The word fatigue is used in everyday living to describe a range of afflictions, varying from a general state of lethargy to a specific work induced burning sensation within muscle. Physiologically, ‘fatigue’ describes the inability to continue functioning at a prescribed work rate (Gandevia et al., 1995; Hagberg, 1981; Hawley et al., 1997) in the presence of an increased perception of effort (Enoka & Stuart 1992). Fatigue is ubiquitous in everyday life, but becomes particularly marked during heavy exercise.

The development of fatigue is characterised by an initial, disproportionate increase in the perception of effort required to maintain or increase the work output before the inability to exert the required force is experienced (Cafarelli, 1988; Garner et al., 1990; Jones et al., 1983; Matthews, 1982). The seemingly dichotomous nature of fatigue has lead scientists to describe the aetiology of fatigue in terms of peripheral and central components (Gandevia, 1992; Kent-Braun, 1999).

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Enoka and Stuart (Enoka & Stuart 1992) propose that the origin of fatigue depends on the mode of work that is being undertaken; a concept that they called task dependency. St Clair Gibson et al (St Clair Gibson et al., 2001) used the task dependency model to examine neural control mechanisms during different types of activities. They concluded that the force output appears to be regulated through inhibitory efferent commands in order to maintain a reserve capacity within the muscle and other organs so that there is always reserve capacity during volitional exercise.

Fatigue can be dangerous when performing tasks that require constant concentration, such as driving a vehicle. When someone is sufficiently fatigued, they may experience microsleeps that can cause them to lose concentration; however, objective cognitive testing should be done to differentiate the neurocognitive deficits of brain disease from those attributable to tiredness.

The sense of fatigue is believed to originate in the reticular activating system of the lower brain. However, the brain did not evolve merely to register representations of the world; rather it evolved for adaptive action and behaviour. Musculoskeletal structures co-evolved with appropriate brain structures so that the complete unit functions together in an adaptive fashion (Edelman, 1989). The entire systems of muscles, joints, and proprioceptive and kinaesthetic functions plus parts of the brain evolve and function together in a unitary way (Kelso, 1995).

Types

There are seen to be two main types of fatigue; Central and Peripheral.

Central Fatigue The central component to fatigue is generally described in terms of a reduction in the neural drive or motor command to working muscles that results in a decline in the force output (Gandevia, 2001; Kay et al., 2001; Kent-Braun, 1999; Vandewalle et al., 1991). It has been suggested that the reduced central drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity (Bigland-Ritchie & Woods, 1984; Noakes, 2000). The exact mechanisms of central fatigue are unknown although there has been a great deal of interest in the role of serotonergic pathways (Davis, 1995; Newsholme et al., 1987; Newsholme et al., 1995).

Peripheral Fatigue Fatigue during physical work is usually modelled from the peripheral context of an inadequate capacity to supply metabolic substrate to the contracting muscles to meet the increased energy demand. This causes contractile dysfunction that is manifest in the inability to maintain or increase work output.

The fundamental difference between the peripheral and central theories of fatigue is that the peripheral model of fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation is therefore dependent on the localised accumulation or depletion of substrates within the active muscle. Whereas the central model of fatigue is an intregrated mechanism that works to preserve the integrity of the system by initiating fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore the feedback that is assimilated by the central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors is dependent on the nature of the work that is being performed.

Causes

It is typically the result of working, mental stress, jet lag or active recreation, but also from boredom or disease or simply lack of sleep. It may also have chemical causes, such as poisoning or mineral or vitamin deficiencies.

When chronic (meaning of six months or more duration) it is a symptom of nearly 30 different diseases. Post exertional fatigue, also known as exercise intolerance, is however far more rare, and is primarily found in organic brain diseases, mitochondrial disease, and neuromuscular disease.

Postprandial Repercussional Fatigue (PPRF)

Postprandial Repercussional Fatigue, as postulated by King's College London scholars Swaneet Singh and Derek Uittenbroek, refers to the fatigue and drowsiness that one experiences after eating a large meal. The biological justification for this is that the blood in the body is diverting to the digestive system in order to break down the meal and transport it through the body. A lower amount of blood, therefore, feeds through the brain and one may perceive themselves to be physically exhausted or drained. Meals rich in carbohydrates and starch (such as potatoes or pasta) may increase the intensity of the fatigue that the individual experiences. "Postprandial Repercussional Fatigue" as mentioned above, is also influenced by a condition referred to as "Acute Vegitative State" recognised by other King's College London scholars Jonathan Coshever and Robert Toscano. This condition concerns the activation of the 'parasympathetic and enteric' branches of the bodies autonomic nervous system'. The ingestion of food results in the release of many substances including 'Acetylcholine' (One of the bodies neurotransmitters), resulting in direct stimulation the parasympathetic neurones innervating the Gastro-Intestinal-Tract (GIT) and other numerous branches; this results in the dilation of the blood vessels carrying oxygenated blood to the GIT and the constriction of the many blood vessels supplying the extra GIT systems of the body (eg. skeletal muscle) - all of this contributing to the redirecting of blood flow as mentioned in the above theory of "Postprandial Repercussional Fatigue".

This list is incomplete; you can help by expanding it.

Relaxation
Lack of sleep
Chronic fatigue syndrome (CFS)
Depression
Diabetes
Hyperparathyroidism
Hypothyroidism
Myasthenia gravis
Addison's disease
Pregnancy
Parkinson's disease
Anemia
Multiple sclerosis
Arthritis
Mononucleosis
Mitral valve prolapse/Mitral regurgitation
Certain medications, e.g. lithium salts, ciprofloxacin

External links

References

Bigland-Ritchie, B & Woods, JJ. 1984, 'Changes in muscle contractile properties and neural control during human muscular fatigue'. Muscle Nerve, vol. 7, pp. 691-699.
Cafarelli, E. 1988, 'Force sensation in fresh and fatigued human skeletal muscle'. Exercise and Sport Science Review, vol. 16, pp. 139-168.
Davis, JM. 1995, 'Carbohydrates, branched-chain amino acids, and endurance: the central fatigue hypothesis'. International Journal of Sport Nutrition, vol. 5 Suppl, pp. S29-S38.
Edelman, GM 1989, The remembered present : a biological theory of consciousness. Basic Books, New York.
Enoka, RM & Stuart, DG. 1992, 'Neurobiology of muscle fatigue'. Journal of Applied Physiology, vol. 72, pp. 1631-1648.
Gandevia, SC. 1992, 'Some central and peripheral factors affecting human motoneuronal output in neuromuscular fatigue'. Sports Medicine, vol. 13, pp. 93-98.
Gandevia, SC. 2001, 'Spinal and supraspinal factors in human muscle fatigue'. Physiological Review, vol. 81, pp. 1725-1789.
Gandevia, S. C., Enoka, R. M., McComas, A. J., Stuart, D. G., & Thomas, C. K. 1995, 'Neurobiology of muscle fatigue - Advances and issues'. Advances in Experimental Medicine and Biology, vol. 384. pp. 515-25.
Garner, SH, Sutton, JR, Burse, RL, McComas, AJ, Cymerman, A, & Houston, CS. 1990, 'Operation Everest II: neuromuscular performance under conditions of extreme simulated altitude'. Journal of Applied Physiology, vol. 68, pp. 1167-1172.
Hagberg, M. 1981, 'Muscular endurance and surface electromyogram in isometric and dynamic exercise'. Journal of Applied Physiology, vol. 51, pp. 1-7.
Hawley, JA & Reilly, T. 1997, 'Fatigue revisited'. Journal of Sport Science, vol. 15, pp. 245-246.
Jones, LA & Hunter, IW. 1983, 'Effect of fatigue on force sensation'. Experimental Neurology, vol. 81, pp. 640-650.
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'. European Journal of Applied Physiology, vol. 84, pp. 115-121.
Kelso, JAS 1995, Dynamic patterns : the self-organization of brain and behavior. MIT Press, Cambridge, MA.
Kent-Braun, JA. 1999, 'Central and peripheral contributions to muscle fatigue in humans during sustained maximal effort'. European Journal of Applied Physiology, vol. 80, pp. 57-63.
Matthews, PB. 1982, 'Where does Sherrington's "muscular sense" originate? Muscles, joints, corollary discharges?'. Annu.Rev.Neurosci, vol. 5, pp. 189-218.
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, E. A. & Blomstrand, E. 1995, 'Tryptophan, 5-hydroxytryptamine and a possible explanation for central fatigue', in SC Gandevia (ed.), Fatigue, Plenum Press, New York, pp. 315-320.
Noakes, TD. 2000, 'Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance'. Scandinavian Journal of Medicine and Science in Sports, vol. 10, pp. 123-145.
St Clair Gibson, A, Lambert, MI, & Noakes, TD. 2001, 'Neural control of force output during maximal and submaximal exercise'. Sports Medicine, vol. 31, pp. 637-650.
Vandewalle, H, Maton, B, Le Bozec, S, & Guerenbourg, G. 1991, 'An electromyographic study of an all-out exercise on a cycle ergometer'. Arch.Int.Physiol.Biochem.Biophys, vol. 99, pp. 89-93.

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