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(Circulation Research. 2009;104:715.)
© 2009 American Heart Association, Inc.

Editorials

Pulling on the Heart Strings

A New Mechanism Within Starling’s Law of the Heart?

Mark B. Cannell

From the Department of Physiology, School of Medicine and Health Sciences, University of Auckland, New Zealand.

Correspondence to Prof M.B. Cannell, Department of Physiology, Faculty of Medicine and Health Sciences, University of Auckland, 85 Park Rd, PB 92019, Auckland, New Zealand. E-mail m.cannell@auckland.ac.nz

See related article, pages 787–795

Key Words: heart contraction • intracellular calcium • force • cytoskeleton

An extract of the first 250 words of the full text is provided, because this article has no abstract.

"Only...by way of experiment, can we hope to attain to a comprehension of ‘the wisdom of the body and the understanding of the heart,’ and thereby to the mastery of disease and pain."

—Ernest H. Starling, 1923¹

When heart muscle is stretched, it increases the force of contraction so that cardiac output matches venous return on a nearly beat-to-beat basis, and this was elegantly described by Ernest H. Starling (1866 to 1927), who formulated "Starling’s law of the heart" on the basis of earlier work (see historical review²). The physiological basis of this essential homeostatic mechanism has remained quite elusive however. Although the ascending limb of the length-tension relationship of the contractile machinery and its increasing calcium sensitivity provides a large part of the explanation,³ additional slow changes occur that augment the effect of changes in overlap between thin and thick filaments.^3,4 The latter "slow force response" (SFR) develops over several minutes following a stretch⁵ and is independent of excitation, because it develops during the resting period between contractions.⁶ Most of the SFR seems explainable on the basis of an increase in the amplitude of the intracellular Ca²⁺ transient,⁷ and many mechanisms have been implicated in the SFR of cardiac tissue (see reviews^8,9). Because a prominent SFR is also seen in isolated myocytes,¹⁰ we can conclude a large part of the ventricular SFR mechanism resides within the myocyte itself. One problem confounding study of the myocytes response is that mechanical experiments on isolated myocytes are extremely challenging and . . . [Full Text of this Article]