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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.

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Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.


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.

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