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J Physiol. 2011 Nov 1;589(Pt 21):5021-31. doi: 10.1113/jphysiol.2011.212860. Epub 2011 Sep 12.

The role of in vivo Ca²⁺ signals acting on Ca²⁺-calmodulin-dependent proteins for skeletal muscle plasticity.

Author information

1
Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland. pasi.tavi@uef.fi

Abstract

Skeletal muscle fibres are highly heterogeneous regarding size, metabolism and contractile function. They also show a large capacity for adaptations in response to alterations in the activation pattern. A major part of this activity-dependent plasticity relies on transcriptional alterations controlled by intracellular Ca(2+) signals. In this review we discuss how intracellular Ca(2+) fluctuations induced by activation patterns likely to occur in vivo control muscle properties via effects on Ca(2+)-calmodulin-dependent proteins. We focus on two such Ca(2+) decoders: calcineurin and Ca(2+)-calmodulin-dependent protein kinase II. Inherent Ca(2+) transients during contractions differ rather little between slow- and fast-twitch muscle fibres and this difference is unlikely to have any significant impact on the activity of Ca(2+) decoders. The major exception to this is fatigue-induced changes in Ca(2+) transients that occur in fast-twitch fibres exposed to high-intensity activation typical of slow-twitch motor units. In conclusion, the cascade from neural stimulation pattern to Ca(2+)-dependent transcription is likely to be central in maintaining the fibre phenotypes in both fast- and slow-twitch fibres. Moreover, changes in Ca(2+) signalling (e.g. induced by endurance training) can result in altered muscle properties (e.g. increased mitochondrial biogenesis) and this plasticity involves other signalling pathways.

PMID:
21911615
PMCID:
PMC3225663
DOI:
10.1113/jphysiol.2011.212860
[Indexed for MEDLINE]
Free PMC Article

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