A mathematical model successfully predicts the effects of external mechanical vibration on twitch contraction, suggesting direct modulation of crossbridge kinetics in cardiac muscle.
Extends crossbridge theory to vibration effects in isolated muscle; human studies needed before clinical consideration.
We previously reported that the application of an external mechanical vibration to the epicardial surface caused a vibration-induced-depression (VID) of left ventricular (LV) function. The magnitude of the VID of peak LV pressure increased as either the amplitude or the frequency of the vibration increased. When LV contractility was altered by the administration of propranolol or by continuous infusion of dobutamine, the magnitude of the VID of peak LV pressure was inversely correlated with LV contractility. These characteristics were observed in open-chest and isolated canine preparations. In the present study, we constructed a muscle model to obtain a theoretical explanation for these effects. This model was first proposed by Gray, Gonda and Cheung, and has been extended in this report to explain twitch tension. This new, improved model is able to explain twitch tension and the effects of external vibration on twitch contraction semi-quantitatively. The successful predictions of the this model support the idea that external vibration directly affects contractile protein and modulates crossbridge kinetics.
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Honda et al. (1994) studied this question.
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