Low-Frequency Fatigue

Keeton, R Benjamin; Binder‐Macleod, Stuart A.

doi:10.1093/ptj/86.8.1146

Cited by 52 publications

(32 citation statements)

References 47 publications

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“…Decreased force production and deleterious ROS effects on muscle function have been associated with numerous muscle disorders (Supinski et al 1999; Polkey & Moxham, 2001; Supinski & Callahan, 2005; Keeton & Binder‐Macleod, 2006; Smith & Reid, 2006). In this context, the present findings may have clinical implications.…”

Section: Discussionmentioning

confidence: 99%

“…the firing frequencies of human motor units during movements requiring low to moderate forces (Marsden et al 1971). This delayed force recovery was named low‐frequency fatigue and has been observed in numerous human muscles and also in various animal muscle preparations (Jones, 1996; Westerblad et al 2000; Keeton & Binder‐Macleod, 2006). Unfortunately, the meaning of the term low‐frequency fatigue has become uncertain because it is now also frequently used to describe fatigue induced by low frequency stimulation.…”

mentioning

confidence: 87%

“…PLFFD is implicated in various neuromuscular disorders, causing an increased sense of effort that can seriously limit the physical performance (Keeton & Binder‐Macleod, 2006). Moreover, PLFFD has been demonstrated after exhaustive respiratory work in the diaphragm of healthy subjects and hence it may cause respiratory failure (Polkey & Moxham, 2001).…”

mentioning

confidence: 99%

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Reactive oxygen species and fatigue‐induced prolonged low‐frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice

Bruton

Place

Yamada

et al. 2008

The Journal of Physiology

119

151

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Skeletal muscle often shows a delayed force recovery after fatiguing stimulation, especially at low stimulation frequencies. In this study we focus on the role of reactive oxygen species (ROS) in this fatigue-induced prolonged low-frequency force depression. Intact, single muscle fibres were dissected from flexor digitorum brevis (FDB) muscles of rats and wild-type and superoxide dismutase 2 (SOD2) overexpressing mice. ] i in wild-type mouse fibres, whereas rat fibres and mouse SOD2 overexpressing fibres instead displayed a decreased myofibrillar Ca 2+ sensitivity. The SOD activity was ∼50% lower in wild-type mouse than in rat FDB muscles. Myoplasmic ROS increased during repeated tetanic stimulation in rat fibres but not in wild-type mouse fibres. The decreased Ca 2+ sensitivity in rat fibres could be partially reversed by application of the reducing agent dithiothreitol, whereas the decrease in tetanic [Ca 2+ ] i in wild-type mouse fibres was not affected by dithiothreitol or the antioxidant N -acetylcysteine. In conclusion, we describe two different causes of fatigue-induced prolonged low-frequency force depression, which correlate to differences in SOD activity and ROS metabolism. These findings may have clinical implications since ROS-mediated impairments in myofibrillar function can be counteracted by reductants and antioxidants, whereas changes in SR Ca 2+ handling appear more resistant to interventions.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 87%

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Reactive oxygen species and fatigue‐induced prolonged low‐frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice

Bruton

Place

Yamada

et al. 2008

The Journal of Physiology

119

151

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“…Abbreviations: CT, contraction time; HRT, half-relaxation time; M-wave PPA, M-wave peak-to-peak area; MRFD, maximal rate of force development; MRR, maximal rate of relaxation; MVC, maximal voluntary contraction; Q pot , potentiated twitch force; PS10, lowfrequency (10 Hz) doublet force; PS100, high-frequency (100 Hz) doublet force; and VA, voluntary activation. Lowfrequency fatigue has been associated with a reduction of Ca 2+ release from the sarcoplasmic reticulum (Allen, Lamb, & Westerblad, 2008a;Balog, 2010;Keeton & Binder-Macleod, 2006;Rassier & MacIntosh, 2000). † P < 0.05 versus P-3 at POST.…”

Section: Peripheral Fatigue After High-intensity Cycling Above Cpmentioning

confidence: 99%

“…These findings are in accordance with the reduction in PS10:100 (∼30%) reported by Temesi et al (2017) after 6 min cycling exercise within the severe-intensity domain (80% P peak ). Lowfrequency fatigue has been associated with a reduction of Ca 2+ release from the sarcoplasmic reticulum (Allen, Lamb, & Westerblad, 2008a;Balog, 2010;Keeton & Binder-Macleod, 2006;Rassier & MacIntosh, 2000). exercise, suggesting that sarcolemmal excitability is more affected after longer, low-intensity exercise.…”

Section: Peripheral Fatigue After High-intensity Cycling Above Cpmentioning

confidence: 99%

The magnitude of neuromuscular fatigue is not intensity dependent when cycling above critical power but relates to aerobic and anaerobic capacities

Schäfer

Hayes

Dekerle

2018

Experimental Physiology

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New Findings What is the central question of this study?Is the magnitude of neuromuscular fatigue dependent upon exercise intensity above critical power (CP) when W′ (the curvature constant of the power–duration relationship) is depleted? What is the main finding and its importance?The magnitude of neuromuscular fatigue is the same after two bouts of supra‐CP cycling (3 versus 12 min) when controlling for W′ depletion but is larger for individuals of greater anaerobic capacity after the shorter bout and smaller for individuals of greater aerobic capacity after the longer exercise bout. These findings provide new insight into the mechanisms underpinning exercise above CP. Abstract The aim of the present study was to test whether the development of neuromuscular fatigue within the severe‐intensity domain could be linked to the depletion of the curvature constant (W′) of the power–duration relationship. Twelve recreationally active men completed tests to determine peak oxygen consumption, critical power (CP) and W′, followed by two randomly assigned constant‐load supra‐CP trials set to deplete W′ fully in 3 (P‐3) and 12 min (P‐12). Pre‐ to postexercise changes in maximal voluntary contraction, potentiated quadriceps twitch force evoked by single (Qpot) and paired high‐ (PS100) and low‐frequency (PS10) stimulations and voluntary activation were determined. Cycling above CP reduced maximal voluntary contraction (P‐3, −20 ± 10% versus P‐12, −15 ± 7%), measures associated with peripheral fatigue (Qpot, −35 ± 13 versus −31 ± 14%; PS10, −38 ± 13 versus −37 ± 17%; PS100, −18 ± 9 versus −13 ± 8% for P‐3 and P‐12, respectively) and voluntary activation (P‐3, −12 ± 3% versus P‐12, −13 ± 3%; P < 0.05), with no significant difference between trials (P > 0.05). Changes in maximal voluntary contraction and evoked twitch forces were inversely correlated with CP and peak oxygen consumption after P‐12, whereas W′ was significantly correlated with changes in Qpot and PS10 after P‐3 (P < 0.05). Therefore, the magnitude of neuromuscular fatigue does not depend on exercise intensity when W′ is fully exhausted during severe‐intensity exercise; nonetheless, exploration of inter‐individual variations suggests that mechanisms underpinning exercise tolerance within this domain differ between short‐ and long‐duration exercise.

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Modulation of the actomyosin interaction during fatigue of skeletal muscle

Cooke

2007

Muscle and Nerve

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Fatigue of skeletal muscle involves many systems beginning with the central nervous system and ending with the contractile machinery. This review concentrates on those factors that directly affect the actomyosin interaction: the build-up of metabolites; myosin phosphorylation; and oxidation of the myofibrillar proteins by free radicals. The decrease in [ATP] and increase in [ADP] appear to play little role in modulating function. The increase in phosphate inhibits tension. The decrease in pH, long thought to be a major factor, is now known to play a more minor role. Myosin phosphorylation potentiates the force achieved in a twitch, and a further role in inhibiting velocity is proposed. Protein oxidation can both potentiate and inhibit the actomyosin interaction. It is concluded that these factors, taken together, do not fully explain the inhibition of the actomyosin interaction observed in living fibers, and thus additional modulators of this interaction remain to be discovered.

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Low-Frequency Fatigue

Cited by 52 publications

References 47 publications

Reactive oxygen species and fatigue‐induced prolonged low‐frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice

Reactive oxygen species and fatigue‐induced prolonged low‐frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice

The magnitude of neuromuscular fatigue is not intensity dependent when cycling above critical power but relates to aerobic and anaerobic capacities

Modulation of the actomyosin interaction during fatigue of skeletal muscle

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