External mechanical vibration applied during the relaxation phase accelerates relaxation in isolated rat papillary muscles, indicating an intrinsic myocyte property likely due to forced crossbridge detachment.
No immediate clinical implications; leaves open whether mechanical modulation of myocyte relaxation can be harnessed in human diastolic dysfunction.
OBJECTIVE: It has been demonstrated that the application of an external mechanical vibration during the ventricular relaxation phase of the heart (diastolic vibration) decreases the time needed for myocardial relaxation. The objective of this study is to see whether this vibration-induced decrease in relaxation time is an intrinsic property of the contractile proteins. We hypothesize that this decrease in duration of the late systolic phase by diastolic vibration is likely to be due to a forced detachment of crossbridges from the actin filament. This would then result in a decrease in the relaxation time of myocardial tissue. METHODS: A controlled vibration of variable amplitude and frequency was applied to isolated twitching rat papillary muscles. Vibration was initiated from directly after peak tension development and ended when tension had returned to baseline. Effects of applied vibration were expressed as changes in the time interval from 90% rising- to 50% falling-force level, which was termed the 'late systolic phase'. RESULTS: The data showed that in general diastolic vibration decreased the duration of this late systolic phase. A vibration of 1.0% of Lmax at 50 Hz in the late systolic phase shortened this period by 27 ms (20-30%) on average. At increasing amplitude of vibration the increase in the rate of relaxation was even more pronounced. Shortening of this duration was slightly less at frequencies of vibration below 40 Hz than at higher frequencies of vibration. Changes in the resting muscle length did not result in significant changes in shortening of the studied relaxation period. CONCLUSION: The results show that relaxation is accelerated during application of an external vibration during the period of tension fall of an isolated cardiac muscle preparation. Therefore, we can conclude that the acceleration of relaxation due to vibration is primarily due to properties of the myocytes themselves rather than to the complex geometric structure of the heart. Tension in the relaxation phase was reduced during diastolic vibration, which suggests that the number of crossbridges bound to the actin filament was reduced by the length perturbation.
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Paul M.L. Janssen (1996) studied this question.
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