Cycling cross-bridges increase myocardial stiffness at submaximal levels of Ca2+ activation.

Permeabilized multicellular preparations of canine myocardium were subjected to controlled length changes to investigate the extent to which cross-bridges augment passive stiffness components in myocardium at low levels of Ca(2+) activation. When the preparations were immersed in pCa 9.0 solution (negligible free [Ca(2+)]) they behaved as simple elastic systems (i.e., tension increased proportionately with length). In contrast, when the muscles were stretched in Ca(2+) activating solutions, tension rose much more rapidly during the initial phase of the movement than thereafter. Several lines of evidence suggest that the nonlinear response represents the displacement of populations of cycling cross-bridges that are perturbed by interfilamentary movement and take some time to recover. 1), The stiffness of the initial phase increased proportionately with the level of Ca(2+) activation. 2), The magnitude of the short-range response increased with stretch velocity. 3), The initial response was reversibly reduced by 5-mM 2,3-butanedione monoxime, a known cross-bridge inhibitor. The initial stiffness of the passive elastic (pCa 9.0) response was equivalent to the Ca(2+) dependent component at 2% (pCa approximately 6.2) of the maximal (pCa 4.5) level. These results suggest that cross-bridges may significantly affect diastolic chamber stiffness.