ArticleThe Journal of physiology2001
Different Ca2+ releasing action of caffeine and depolarisation in skeletal muscle fibres of the rat.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Effect of Caffeine Ingestion on Indirect Markers of Exercise-Induced Muscle Damage: A Systematic Review of Human Trials.Nutrients · 2022Pooled it
- Review
- Caffeine as a tool to investigate sarcoplasmic reticulum and intracellular calcium dynamics in human skeletal muscles.Journal of muscle research and cell motility · 2021Review
- Neuromuscular junction instability and altered intracellular calcium handling as early determinants of force loss during unloading in humans.The Journal of physiology · 2021Article
- Skeletal muscle fibre swelling contributes to force depression in rats and humans: a mechanically-skinned fibre study.Journal of muscle research and cell motility · 2019Article
- The MyoRobot technology discloses a premature biomechanical decay of skeletal muscle fiber bundles derived from R349P desminopathy mice.Scientific reports · 2019Article
- Exciting perspectives for Translational Myology in the Abstracts of the 2018Spring PaduaMuscleDays: Giovanni Salviati Memorial - Chapter III - Abstracts of March 16, 2018.European journal of translational myology · 2018Article
- In vivo CaPhysiological reports · 2017Article
- Review of RyR1 pathway and associated pathomechanisms.Acta neuropathologica communications · 2016Review
- Inhibiting c-Jun N-terminal kinase partially attenuates caffeine-dependent cell death without alleviating the caffeine-induced reduction in mitochondrial respiration in C2C12 skeletal myotubes.Biochemical and biophysical research communications · 2016Article
- A quantitative description of tubular system Ca(2+) handling in fast- and slow-twitch muscle fibres.The Journal of physiology · 2016Article
- Ca(2+) leakage out of the sarcoplasmic reticulum is increased in type I skeletal muscle fibres in aged humans.The Journal of physiology · 2016Article
- The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.Physiological reviews · 2015Review
- Contribution of impaired myofibril and ryanodine receptor function to prolonged low-frequency force depression after in situ stimulation in rat skeletal muscle.Journal of muscle research and cell motility · 2015Article
- Caffeine promotes autophagy in skeletal muscle cells by increasing the calcium-dependent activation of AMP-activated protein kinase.Biochemical and biophysical research communications · 2014Article
- A mutation in the CASQ1 gene causes a vacuolar myopathy with accumulation of sarcoplasmic reticulum protein aggregates.Human mutation · 2014Article
- Eccentric contractions disrupt FKBP12 content in mouse skeletal muscle.Physiological reports · 2014Article
- IL-1α reversibly inhibits skeletal muscle ryanodine receptor. a novel mechanism for critical illness myopathy?American journal of respiratory cell and molecular biology · 2014Article
- 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
- Mild stress of caffeine increased mtDNA content in skeletal muscle cells: the interplay between Ca2+ transients and nitric oxide.Journal of muscle research and cell motility · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The relative abilities of caffeine and transverse tubular (T-) system depolarisation to induce Ca2+ release in mammalian skeletal muscle were compared in mechanically skinned fibres of the rat, in order to determine whether normal excitation-contraction (E-C) coupling is achieved by up-regulating the Ca2+-induced Ca2+ release process, as caffeine is known to do. 2. Caffeine triggered Ca2+ release in soleus (slow-twitch) fibres at much lower concentrations than in extensor digitorum longus (EDL) (fast-twitch) fibres when the sarcoplasmic reticulum (SR) of each type was loaded with Ca2+ at close to endogenous levels. The difference in caffeine sensitivity resulted at least in part from the SR being loaded endogenously at near maximal capacity in soleus fibres but at less than half of maximal capacity in EDL fibres. The caffeine sensitivity could be reversed by reversing the relative level of SR loading. 3. The ability of caffeine to induce Ca2+ release was markedly reduced by lowering the level of SR loading or by raising the free [Mg2+] from 1 to 3 mM. Caffeine, even at 30 mM, triggered little or no Ca2+ release in EDL fibres (a) at 1 mM (physiological) Mg2+ when the SR was loaded at two-thirds or less of the endogenous level, and (b) at 3 mM Mg2+ when the SR was loaded at close to the endogenous level. In contrast, depolarisation potently elicited Ca2+ release under these conditions in the same fibres. 4. The inability of 30 mM caffeine to induce Ca2+ release under certain conditions was not attributable to desensitisation or inactivation of the release channels, because there was no response even upon initial exposure to caffeine and depolarisation always remained able to trigger Ca2+ release. It instead appeared that caffeine was a relatively ineffectual stimulus in EDL fibres except under conditions where (a) the SR was heavily loaded, (b) the free [Mg2+] was low, or (c) a high [Cl-] was present. 5. These results show that the normal E-C coupling mechanism in mammalian skeletal muscle does not involve just enhancing Ca2+-induced Ca2+ release, and evidently requires the removal or bypassing of the inhibitory effect of Mg2+ on the Ca2+ release channels.
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