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Books on the topic 'Neuromuscular fatigue'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 April 2024

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1

J, Sargeant A., and Kernell D, eds. Neuromuscular fatigue. Amsterdam: North-Holland, 1993.

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2

Advanced neuromuscular exercise physiology. Champaign, IL: Human Kinetics, 2011.

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3

C, Gandevia Simon, ed. Fatigue: Neural and muscular mechanisms. New York: Plenum Press, 1995.

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4

1949-, Enoka Roger M., and Society for Neuroscience Meeting, eds. Neural and neuromuscular aspects of muscle fatigue: Miami, Florida, November 10-13, 1994. New York: Wiley, 1996.

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5

Brooks, Barbara. CFIDS, an "owner's manual". 2nd ed. Silver Spring, MD: BBNS Publishers, 1990.

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6

Ratel, Sébastien, and Craig A. Williams. Neuromuscular fatigue. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0009.

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Scientific evidence supports the proposition that prepubertal children fatigue less than adults when performing whole-body dynamic activities like maximal cycling, running bouts, and maximal voluntary isometric/isokinetic muscle contractions. Although the mechanisms underpinning differences in fatigue between children and adults are not all fully understood, there is a consensus that children experience less peripheral fatigue (i.e. muscular fatigue) than their older counterparts. Central factors may also account for the lower fatigability in children. Some studies report a higher reduction of muscle voluntary activation during fatiguing exercise in prepubertal children compared to adults. This could reflect a strategy of the central nervous system aimed at limiting the recruitment of motor units, in order to prevent any extensive peripheral fatigue. Further studies are required to clarify this proposition.
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7

Stuart, Douglas G., Christine K. Thomas, Alan J. McComas, Simon C. Gandevia, Roger M. Enoka, and Patricia A. Pierce. Fatigue: Neural and Muscular Mechanisms. Springer, 2013.

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8

Quinlivan, Ros, and Pascal Laforêt. Chronic Fatigue and Acute Rhabdomyolysis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0068.

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Chronic fatigue syndrome is usually idiopathic, management involves a multi-disciplinary approach, advice on pacing activities and cognitive behavioral therapy. Metabolic myopathies that cause exercise intolerance may lead to a fatigue syndrome due to deconditioning, other neuromuscular disorders presenting with paroxysmal fatigue and weakness such as the myasthenic syndromes and channelopathies can occasionally be mistaken for a metabolic disorder. Acute rhabdomyolysis, a potentially life-threatening complication, has many causes both acquired and genetic. Urgent treatment is required and prevention of future episodes requires a careful search for an underlying genetic cause.
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9

Shaibani, Aziz. Fatigability. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0025.

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Undue fatigability is common in neuromuscular clinics but non-neuromuscular causes are much more common than neuromuscular causes. Generalized fatigue is commonly caused by anemia, hypothyroidism, obstructive sleep apnea, depression, chronic fatigue syndrome, uremia, COPD, etc. Physiological fatigue is accentuated by neuromuscular disorders. Most strikingly, myasthenia gravis causes undue fatigue of the ocular, chewing, swallowing, and breathing muscles. However, ALS, myopathies, and motor neuropathies are also associated with abnormal fatigue. Myasthenia rarely causes isolated fatigue. Examination for fatigability should be part of neuromuscular evaluation and is conducted by inducing repetitive or sustained contraction of the suspected muscles (typically extraocular muscles) for a minute and reevaluation after 2 minutes of rest of the tested muscles.
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10

Shaibani, Aziz. Fatigability. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0025.

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Undue fatigability is common in neuromuscular clinics, but nonneuromuscular causes are much more common than neuromuscular causes. Generalized fatigue is commonly caused by anemia, hypothyroidism, obstructive sleep apnea, depression, chronic fatigue syndrome (CFS), uremia, chronic obstructive pulmonary disease (COPD), and other diseases. Physiological fatigue is accentuated by neuromuscular disorders. Most strikingly, myasthenia gravis (MG) causes undue fatigue of the ocular, chewing, swallowing, and breathing muscles. However, amyotrophic lateral sclerosis (ALS), myopathies, and motor neuropathies are also associated with abnormal fatigue. Central causes like multiple sclerosis are notorious for fatigue. It is hard to measure fatigue because it is subjective and varies with the psychological status. Myasthenia hardly causes isolated fatigue.
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11

Burke, David, and James Howells. The motor unit. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0002.

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The motor unit represent the final output of the motor system. Each consists of a motoneuron, its axon, neuromuscular junctions, and muscle fibres innervated by that axon. The discharge of a motor unit can be followed by recording its electromyographic signature, the motor unit action potential. Motoneurons are not passive responders to the excitatory and inhibitory influences on them from descending and segmental sources. Their properties can change, e.g. due to descending monoaminergic pathways, which can alter their responses to other inputs (changing ‘reflex gain’). Contraction strength depends on the number of active motor units, their discharge rate, and whether the innervated muscle fibres are slow-twitch producing low force, but resistant to fatigue, fast-twitch producing more force, but susceptible to fatigue, or intermediate fast-twitch fatigue-resistant. These properties are imposed by the parent motoneurons, and the innervated muscle fibres have different histochemical profiles (oxidative, glycolytic, or oxidative-glycolytic, respectively).
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12

Dinser, Robert, and Ulf Müller-Ladner. Skeletal muscle physiology and damage. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0055.

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This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.
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13

Dinser, Robert, and Ulf Müller-Ladner. Skeletal muscle physiology and damage. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0055_update_001.

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This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.
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14

Seabra, Victor F., and Bertrand L. Jaber. Haemodialysis. Edited by Jonathan Himmelfarb. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0259_update_001.

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Since its first successful performance in 1945, haemodialysis has become a widely performed routine and safe procedure. However, despite significant improvements in the dialysis equipment, staff training, and patient monitoring, acute complications can occur during the therapy, ranging from mild to life-threatening. This chapter reviews selected acute complications that are encountered during or are directly related to the haemodialysis procedure, including cardiovascular, neuromuscular, haematological, and pulmonary complications, technical malfunctions, dialysis reactions (including anaphylactic and anaphylactoid reactions), and other complications such as post-dialysis fatigue, pruritus, priapism, and hearing and visual loss.
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15

Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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16

Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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17

Vassilakopoulos, Theodoros, and Charis Roussos. Respiratory muscle function in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0077.

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The inspiratory muscles are the diaphragm, external intercostals and parasternal internal intercostal muscles. The internal intercostals and abdominal muscles are expiratory. The ability of a subject to take one breath depends on the balance between the load faced by the inspiratory muscles and their neuromuscular competence. The ability of a subject to sustain the respiratory load over time (endurance) depends on the balance between energy supplied to the inspiratory muscles and their energy demands. Hyperinflation puts the diaphragm at a great mechanical disadvantage, decreasing its force-generating capacity. In response to acute increases in load the inspiratory muscles become fatigued and inflammed. In response to reduction in load by the use of mechanical ventilation they develop atrophy and dysfunction. Global respiratory muscle function can be tested using maximum static inspiratory and expiratory mouth pressures, and sniff pressure. Diaphragm function can be tested by measuring the transdiaphragmatic and twitch pressures developed upon electrical or magnetic stimulation of the phrenic nerve.
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