Muscle fatigue: mechanisms and regulation

Reid, Michael B.

doi:10.1016/b978-044482650-3/50022-5

Cited by 5 publications

(6 citation statements)

References 115 publications

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“…Also, it is possible that prolonged MV is associated with elevated diaphragmatic proteolysis and increased oxidative damage to muscle proteins. Each of these factors can promote intrinsic alter-ations in muscle proteins and could impair force production (9,12,(19)(20)(21).…”

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

“…A final potential mechanism to explain the MVinduced diaphragmatic force deficit is impairment in E-C coupling. For example, a reduction in calcium release from the sarcoplasmic reticulum is associated with reduced muscle force generation (21). Furthermore, a reduction in myofilament sensitivity to calcium is also associated with lowered force production (21).…”

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

“…For example, a reduction in calcium release from the sarcoplasmic reticulum is associated with reduced muscle force generation (21). Furthermore, a reduction in myofilament sensitivity to calcium is also associated with lowered force production (21). Hence, any factor that reduces the magnitude of calcium release from the sarcoplasmic reticulum and/or calcium sensitivity would negatively impact muscle force production.…”

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

“…These observations indicate that the pathways responsible for this contractile dysfunction are activated quickly after the induction of MV. In this regard, it seems possible that the activation of oxidant production and/or proteolytic pathways in the diaphragm during prolonged MV are candidate mechanisms that could negatively impact E-C coupling and muscle force production (7,19,21).…”

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

See 3 more Smart Citations

Mechanical ventilation results in progressive contractile dysfunction in the diaphragm

Powers

Shanely²,

Coombes³

et al. 2002

Journal of Applied Physiology

261

244

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These experiments tested the hypothesis that a relatively short duration of controlled mechanical ventilation (MV) will impair diaphragmatic maximal specific force generation (specific P(o)) and that this force deficit will be exacerbated with increased time on the ventilator. To test this postulate, adult Sprague-Dawley rats were randomly divided into one of six experimental groups: 1) control (n = 12); 2) 12 h of MV (n = 4); 3) 18 h of MV (n = 4); 4) 18 h of anesthesia and spontaneous breathing (n = 4); 5) 24 h of MV (n = 7); and 6) 24 h of anesthesia and spontaneous breathing (n = 4). MV animals were anesthetized, tracheostomized, and ventilated with room air. Animals in the control group were acutely anesthetized but were not exposed to MV. Animals in two spontaneous breathing groups were anesthetized and breathed spontaneously for either 18 or 24 h. No differences (P > 0.05) existed in diaphragmatic specific P(o) between control and the two spontaneous breathing groups. In contrast, compared with control, all durations of MV resulted in a reduction (P < 0.05) in diaphragmatic specific tension at stimulation frequencies ranging from 15 to 160 Hz. Furthermore, the MV-induced decrease in diaphragmatic specific P(o) was time dependent, with specific P(o) being approximately 18 and approximately 46% lower (P < 0.05) in animals mechanically ventilated for 12 and 24 h, respectively. These data support the hypothesis that relatively short-term MV impairs diaphragmatic contractile function and that the magnitude of MV-induced force deficit increases with time on the ventilator.

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Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

Section: Prolonged MV and Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

See 2 more Smart Citations

Mechanical ventilation results in progressive contractile dysfunction in the diaphragm

Powers

Shanely²,

Coombes³

et al. 2002

Journal of Applied Physiology

261

244

View full text Add to dashboard Cite

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“…Adicionalmente, os níveis elevados de Ca 2+ , conjuntamente com os períodos prolongados de exposição a períodos de isquemia/reperfusão decorrentes do exercício, activam a produção acrescida de espécies reactivas de oxigénio, que se apresentam associadas aos mecanismos indutores de lesão muscular esquelética, através da sua acção sobre algumas estruturas celulares (para refs. ver 96,110,121) . Essing e Nosek (31) referem ainda que o stress oxidativo decorrente do exercício se apresenta como uma das causas da diminuição da capacidade de gerar força pelas fibras musculares, particularmente a associada à FBF.…”

Section: Modelos De Estudounclassified

Fisiologia da fadiga muscular. Delimitação conceptual, modelos de estudo e mecanismos de fadiga de origem central e periférica

Ascensão¹,

Magalhães²,

Oliveira³

et al. 2003

RPCD

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RESUMOO tecido muscular esquelético dos mamíferos possui a capacidade de produzir níveis elevados de força quando activado. A incapacidade de produzir repetidamente no tempo um determinado nível de força ou potência muscular designa-se por fadiga neuromuscular, fenómeno que pode manifestar-se de forma aguda e que pode persistir durante dias ou mesmo semanas. A etiologia da fadiga muscular tem atraído o interesse dos investigadores desde há mais de um século. Contudo, os seus agentes e locais definitivos permanecem ainda por identificar. As causas da fadiga muscular durante o exercício residem nas regiões corticais e sub-corticais (fadiga de origem central) e ao nível do tecido muscular esquelético (fadiga de origem periféri-ca). Os objectivos desta revisão foram: (i) definir o conceito de fadiga, enumerando algumas áreas em que este fenómeno tem sido estudado; (ii) diferenciar os modelos experimentais em que a fadiga tem sido estudada, com particular destaque para os estudos in vivo recorrendo à electromiografia; (iii) analisar os principais factores descritos na literatura relacionados com a fadiga central, nomeadamente a relação desta com a variação de alguns neurotransmissores e alguns aminoácidos de cadeia ramificada; (iv) diferenciar e explicar os principais tipos de fadiga periférica descritos na literatura e (v) analisar os mecanismos indutores de fadiga com origem predominantemente periférica, com particular destaque para o papel da deplecção de alguns substratos energéticos necessários para a síntese de ATP e da variação das concentrações intracelulares de cálcio, H + , lactato, fosfato e ADP. Parece razoável associar, pelo menos em parte, a fadiga de origem predominantemente central com a variação das concentrações de glicose sanguínea, de aminoácidos de cadeia ramificada e da síntese de alguns neurotransmissores. Em relação à fadiga periférica, as evidências experimentais têm demonstrado que reduções nas concentrações mioplasmáticas de cálcio comprometem a tensão gerada pelas fibras durante contracções musculares induzidas por estimulações de frequência elevada. As alterações nas concentrações de H + , lactato, Pi, ADP ou ATP, embora influenciem a produção de força pelas fibras musculares, não parecem apresentar-se, per se, como factores determinantes da fadiga. Palavras

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Exercise Capacity in Chronic Obstructive Pulmonary Disease: Mechanisms of Limitation

Pepin

Saey

Laviolette

et al. 2007

COPD: Journal of Chronic Obstructive Pulmonary Disease

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Patients with chronic obstructive pulmonary disease (COPD) are often caught in a downward spiral that progresses from expiratory flow limitation to poor quality of life and invalidity. Within this downward spiral, exercise tolerance represents a key intermediate outcome. As recently stated by the GOLD initiative, improvement in exercise tolerance is now rec ognized as an important goal of COPD treatment. This objective will be achieved only by a comprehensive understanding of the mechanism of exercise limitation in this disease. The objective of this paper is to review the mechanisms of exercise limitation in COPD and discuss their relative contribution to exercise intolerance in patients suffering from this disease.

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Muscle fatigue: mechanisms and regulation

Cited by 5 publications

References 115 publications

Mechanical ventilation results in progressive contractile dysfunction in the diaphragm

Mechanical ventilation results in progressive contractile dysfunction in the diaphragm

Fisiologia da fadiga muscular. Delimitação conceptual, modelos de estudo e mecanismos de fadiga de origem central e periférica

Exercise Capacity in Chronic Obstructive Pulmonary Disease: Mechanisms of Limitation

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