ArticleThe Journal of physiology2004
External Ca(2+)-dependent excitation--contraction coupling in a population of ageing mouse skeletal muscle fibres.
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 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- Assessing the Potential of Nutraceuticals as Geroprotectors on Muscle Performance and Cognition in Aging Mice.Antioxidants (Basel, Switzerland) · 2021Article
- A chronic high-fat diet exacerbates contractile dysfunction with impaired intracellular CaJournal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Troponin T3 regulates nuclear localization of the calcium channel Cavβ1a subunit in skeletal muscle.Experimental cell research · 2015Article
- Mechanisms of skeletal muscle aging: insights from Drosophila and mammalian models.Disease models & mechanisms · 2013Review
- Troponin T nuclear localization and its role in aging skeletal muscle.Age (Dordrecht, Netherlands) · 2013Article
- Skeletal muscle neural progenitor cells exhibit properties of NG2-glia.Experimental cell research · 2013Article
- Parvalbumin gene transfer impairs skeletal muscle contractility in old mice.Human gene therapy · 2012Article
- Residual sarcoplasmic reticulum Ca2+ concentration after Ca2+ release in skeletal myofibers from young adult and old mice.Pflugers Archiv : European journal of physiology · 2012Article
- Molecular control of neuromuscular junction development.Journal of cachexia, sarcopenia and muscle · 2012Article
- Age-related changes in motor cortical properties and voluntary activation of skeletal muscle.Current aging science · 2011Review
- Expression and regulation of excitation-contraction coupling proteins in aging skeletal muscle.Current aging science · 2011Review
- Article
- Sarcoplasmic reticulum Ca2+ depletion in adult skeletal muscle fibres measured with the biosensor D1ER.Pflugers Archiv : European journal of physiology · 2010Article
- Article
- In vivo specific tension of the human quadriceps femoris muscle.European journal of applied physiology · 2009Article
- Role of Ca2+, membrane excitability, and Ca2+ stores in failing muscle contraction with aging.Experimental gerontology · 2009Article
- The presence of a functional t-tubule network increases the sensitivity of RyR1 to agonists in skinned rat skeletal muscle fibres.Cell calcium · 2008Article
- Compromised store-operated Ca2+ entry in aged skeletal muscle.Aging cell · 2008Article
- Skeletal myocyte plasticity: basis for improved therapeutic potential?Current opinion in pharmacology · 2008Review
- Sarcoplasmic reticulum Ca2+ release declines in muscle fibers from aging mice.Biophysical journal · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In the present work, we investigate whether changes in excitation-contraction (EC) coupling mode occur in skeletal muscles from ageing mammals by examining the dependence of EC coupling on extracellular Ca(2+). Single intact muscle fibres from flexor digitorum brevis muscles from young (2-6 months) and old (23-30 months) mice were subjected to tetanic contractile protocols in the presence and absence of external Ca(2+). Contractile experiments in the absence of external Ca(2+) show that about half of muscle fibres from old mice are dependent upon external Ca(2+) for maintaining maximal tetanic force output, while young fibres are not. Decreased force in the absence of external Ca(2+) was not due to changes in charge movement as revealed by whole-cell patch-clamp experiments. Ca(2+) transients, measured by fluo-4 fluorescence, declined in voltage-clamped fibres from old mice in the absence of external Ca(2+). Similarly, Ca(2+) transients declined in parallel with tetanic contractile force in single intact fibres. Examination of inward Ca(2+) current and of mRNA and protein assays suggest that these changes in EC coupling mode are not due to shifts in dihydropyridine receptor (DHPR) and/or ryanodine receptor (RyR) isoforms. These results indicate that a change in EC coupling mode occurs in a population of fibres in ageing skeletal muscle, and is responsible for the age-related dependence on extracellular Ca(2+).
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.