ArticleThe Journal of physiology2004
Effect of low cytoplasmic [ATP] on excitation-contraction coupling in fast-twitch muscle fibres of the rat.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 54 citations in OpenAlex.
- Pinewood Nematodes Manipulate Locomotion of the Vector Beetle Through ATP1-Driven Energy Metabolism.Integrative zoology · 2026Article
- Intermittent glucocorticoid treatment enhances skeletal muscle performance through sexually dimorphic mechanisms.The Journal of clinical investigation · 2022Article
- The Ryanodine Receptor as a Sensor for Intracellular Environments in Muscles.International journal of molecular sciences · 2021Review
- The effect of adenosine triphosphate on propofol-induced myopathy in rats: a biochemical and histopathological evaluation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Depletion of ATP Limits Membrane Excitability of Skeletal Muscle by Increasing Both ClC1-Open Probability and Membrane Conductance.Frontiers in neurology · 2020Article
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 2018Review
- CaTrends in biochemical sciences · 2017Review
- Role of physiological ClC-1 Cl- ion channel regulation for the excitability and function of working skeletal muscle.The Journal of general physiology · 2016Review
- Sarcoplasmic reticulum Ca2+ uptake and leak properties, and SERCA isoform expression, in type I and type II fibres of human skeletal muscle.The Journal of physiology · 2014Article
- Repeated-sprint ability - part I: factors contributing to fatigue.Sports medicine (Auckland, N.Z.) · 2011Review
- Altered Ca2+ homeostasis in the skeletal muscle of DJ-1 null mice.Neurobiology of aging · 2011Article
- Chloride conductance in the transverse tubular system of rat skeletal muscle fibres: importance in excitation-contraction coupling and fatigue.The Journal of physiology · 2008Article
- Store-operated Ca2+ entry during intracellular Ca2+ release in mammalian skeletal muscle.The Journal of physiology · 2007Article
- Effect of ADP on slow-twitch muscle fibres of the rat: implications for muscle fatigue.The Journal of physiology · 2006Article
- Tubular system excitability: an essential component of excitation-contraction coupling in fast-twitch fibres of vertebrate skeletal muscle.Journal of muscle research and cell motility · 2006Review
- Coupled calcium release channels and their regulation by luminal and cytosolic ions.European biophysics journal : EBJ · 2005Review
- Reactive oxygen species reduce myofibrillar Ca2+ sensitivity in fatiguing mouse skeletal muscle at 37 degrees C.The Journal of physiology · 2005Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we investigated the roles of cytoplasmic ATP as both an energy source and a regulatory molecule in various steps of the excitation-contraction (E-C) coupling process in fast-twitch skeletal muscle fibres of the rat. Using mechanically skinned fibres with functional E-C coupling, it was possible to independently alter cytoplasmic [ATP] and free [Mg2+]. Electrical field stimulation was used to elicit action potentials (APs) within the sealed transverse tubular (T-) system, producing either twitch or tetanic (50 Hz) force responses. Measurements were also made of the amount of Ca2+ released by an AP in different cytoplasmic conditions. The rate of force development and relaxation of the contractile apparatus was measured using rapid step changes in [Ca2+]. Twitch force decreased substantially (approximately 30%) at 2 mm ATP compared to the level at 8 mm ATP, whereas peak tetanic force only declined by approximately 10% at 0.5 mm ATP. The rate of force development of the twitch and tetanus was slowed only slightly at [ATP] > or = 0.5 mm, but was slowed greatly (> 6-fold) at 0.1 mm ATP, the latter being due primarily to slowing of force development by the contractile apparatus. AP-induced Ca2+ release was decreased by approximately 10 and 20% at 1 and 0.5 mm ATP, respectively, and by approximately 40% by raising the [Mg2+] to 3 mm. Adenosine inhibited Ca2+ release and twitch responses in a manner consistent with its action as a competitive weak agonist for the ATP regulatory site on the ryanodine receptor (RyR). These findings show that (a) ATP is a limiting factor for normal voltage-sensor activation of the RyRs, and (b) large reductions in cytoplasmic [ATP], and concomitant elevation of [Mg2+], substantially inhibit E-C coupling and possibly contribute to muscle fatigue in fast-twitch fibres in some circumstances.
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