Large sarcolemmal calcium fluxes in cardiac muscle are essential for facilitating rapid changes in contractility.
Should not change clinical practice; leaves open translation of calcium flux mechanisms to human cardiac disease.
In cardiac muscle, although most of the calcium that activates contraction comes from the sarcoplasmic reticulum (SR), a significant fraction (up to 30%, depending on the species) enters from outside the cell and is then pumped out at the end of systole. Although some of this calcium influx is required to trigger calcium release from the SR, the bulk serves to reload the cell (and thence the SR) with calcium to replace the calcium that is pumped out of the cell. An alternative strategy would be for the heart to have a much smaller calcium influx balancing a smaller efflux. We demonstrate that this would result in a slowing of inotropic responses due to changes of SR calcium content. We conclude that the large sarcolemmal calcium fluxes facilitate rapid changes of contractility.
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Eisner et al. (2009) studied this question.
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