Force-velocity relations in mammalian heart muscle

Abstract

Force-velocity relations were studied in the cat papillary muscle. As with skeletal muscle, a characteristic relation has been demonstrated between the velocity of shortening (V) and the force developed (Po). Two generalities have been shown to pertain. First, increasing initial muscle length increases the maximal developed force (Po) without a change in the maximal velocity of shortening (Vmax). Secondly, at any one muscle length, changes in frequency of contraction and chemical environment (increased calcium and norepinephrine) increase Vmax with a variable change in Po. Changes in Vmax thus help to characterize an inotropic intervention (altered contractility). Work and power, at any one muscle length, are functions of afterload, with maxima when the load is approximately 40% of isometric tension. With increasing initial muscle length, the work and power at any one afterload as well as the maximal work and power of the muscle are both increased. At constant initial length, positive inotropic interventions (increased frequency, increased calcium, and norepinephrine) increase the work at any one afterload as well as shift the maximal work potential to a higher afterload. Work performance thus depends on muscle length, the prevailing force-velocity curve, and the afterload at which the muscle is operating.

Computational modeling of the electromechanical response of a ventricular fiber affected by eccentric hypertrophy

“…We use λ e and dλ e /dt instead of the total ones λ = λ e λ g = λ e θ f and dλ/dt because growth is carried out by adding new sarcomeres in cardiomyocytes rather than lengthening the preexistent ones (as observed in [7]). In particular, for a one-dimensional fiber, λ e is given by (14) λ e = C e 11 = F e 11 .…”

“…By considering all preloads from 0 to 4 kP a, tension-velocity relationships are derived from both afterloaded isotonic and quick-release tests (panels C). The afterloads on the abscissa correspond to the developed tensions during the isotonic phase, whereas the contraction velocities v contr on the ordinate (taken positive) are computed from the constant slopes of the length curves in time as soon as the two fibers start to contract isotonically [10,14]. In particular, when the afterload is zero, the initial reduction of the fiber length up to the rest value within the first ms in panel B of Figure 7 must be neglected for the measurement of the isotonic contraction velocity.…”

“…the isometric, afterloaded isotonic and quick-release ones [10,14], which are known to reproduce the different types of contraction and relaxation during the four phases of a cardiac cycle: the isovolumic systole, the blood efflux, the isovolumic diastole and the diastolic filling.…”

The step response of left ventricular pressure to ejection flow: A system oriented approach

“…However, such studies seldom attempt to quantitatively predict ventricular performance in terms of compressed data models as the present three-compartment model. Usually, a forcevelocity relation for heart muscle is built in (6,10,17), but then it is not explained how ventricular pressure-flow relations are linear (87,102), whereas force-velocity relations for cardiac muscle are hyperbolic (24,89). One reason for the difference might be that ventricular geometry, both with respect to muscle fiber orientation and complexity of shape, has not been accounted for in sufficient detail.…”

The greatest medical discovery of the millennium (Fundamental steps to the understanding of cardiac performance)

“…Within limits, a cardiac muscle that experiences several preloads (different stretch-outs) will not change its intrinsic shortening velocity (Vmax), since all curves converge at the same point (zero load) at the vertical axis. Calcium, digitalis, and norepinephrine not only increase the F that muscle is able to displace but also increase the velocity of shortening in the surcharged muscle 30 (fig. 5).…”