ArticleJournal of muscle research and cell motility2015
Contribution of impaired myofibril and ryanodine receptor function to prolonged low-frequency force depression after in situ stimulation in rat skeletal muscle.
Article in Journal of muscle research and cell motility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- Competing effects of activation history on force and cytosolic CaPflugers Archiv : European journal of physiology · 2025Article
- Myofiber structure, sarcoplasmic reticulum CaPhysiological reports · 2025Article
- Effects of S-glutathionylation on the passive force-length relationship in skeletal muscle fibres of rats and humans.Journal of muscle research and cell motility · 2020Article
- Intramuscular mechanisms of overtraining.Redox biology · 2020Review
- Alterations to neuromuscular properties of skeletal muscle are temporally dissociated from the oxygen uptake slow component.Scientific reports · 2020Article
- Effects of high-intensity intermittent exercise on the contractile properties of human type I and type II skeletal muscle fibers.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Effects of reduced muscle glycogen on excitation-contraction coupling in rat fast-twitch muscle: a glycogen removal study.Journal of muscle research and cell motility · 2019Article
- Thermal pretreatment facilitates recovery from prolonged low-frequency force depression in rat fast-twitch muscle.Physiological reports · 2018Article
- Physiological and biochemical characteristics of skeletal muscles in sedentary and active rats.Journal of muscle research and cell motility · 2018Article
- A mitochondrial-targeted antioxidant improves myofilament CaThe Journal of physiology · 2018Article
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 2018Review
- l-arginine ingestion inhibits eccentric contraction-induced proteolysis and force deficit via S-nitrosylation of calpain.Physiological reports · 2018Article
- Mechanisms of force depression caused by different types of physical exercise studied by direct electrical stimulation of human quadriceps muscle.European journal of applied physiology · 2016Article
- Reactive oxygen/nitrogen species and contractile function in skeletal muscle during fatigue and recovery.The Journal of physiology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to examine whether prolonged low-frequency force depression (PLFFD) that occurs in situ is the result of decreased myofibrillar Ca(2+) sensitivity and/or reduced sarcoplasmic reticulum (SR) Ca(2+) release. Intact rat gastrocnemius muscles were electrically stimulated via the sciatic nerve until force was reduced to ~50% of the initial and dissected 30 min following the cessation of stimulation. Skinned fibre and whole muscle analyses were performed in the superficial region composed exclusively of type IIB fibres. Fatiguing stimulation significantly reduced the ratio of force at low frequency to that at high frequency to 65% in skinned fibres (1 vs. 50 Hz) and 73% in whole muscles (20 vs. 100 Hz). In order to evaluate changes in myofibrillar Ca(2+) sensitivity and ryanodine receptor caffeine sensitivity, skinned fibres were activated in Ca(2+)- and caffeine-containing solutions, respectively. Skinned fibres from fatigued muscles displayed decreased caffeine sensitivity together with increased myofibrillar Ca(2+) sensitivity. Treatment with 2,2'-dithiodipyridine and reduced glutathione induced a smaller increase in myofibrillar Ca(2+)sensitivity in fatigued than in rested fibres. In fatigued muscles, S-glutathionylation of troponin I was increased and submaximal SR Ca(2+) release, induced by 4-chloro-m-cresol, was decreased. These findings suggest that in the early stage of PLFFD that occurs in fast-twitch muscles of exercising animals and humans, S-glutathionylation of troponin I may attenuate PLFFD by increasing myofibrillar Ca(2+) sensitivity and that under such a circumstance, PLFFD may be ascribable to failure of SR Ca(2+) release.
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