scholarly journals Relationship between isometric force and myofibrillar MgATPase at short sarcomere length in skeletal and cardiac muscle and its relevance to the concept of activation heat

2003 ◽  
Vol 30 (8) ◽  
pp. 570-575 ◽  
Author(s):  
D George Stephenson
Keyword(s):  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Isometric Force ◽  
Activation Heat

The Frank-Starling mechanism is not mediated by changes in rate of cross-bridge detachment

1997 ◽  
Vol 273 (5) ◽  
pp. H2428-H2435 ◽  
Author(s):  
Thomas Wannenburg ◽  
Paul M. L. Janssen ◽  
Dongsheng Fan ◽  
Pieter P. De Tombe
Keyword(s):  
Cardiac Muscle ◽  
Maximum Rate ◽  
Sarcomere Length ◽  
Myosin Head ◽  
Isometric Force ◽  
Force Development ◽  
Cross Bridge ◽  
Average Slope ◽  
The Cross ◽  
Kinetics Of

We tested the hypothesis that the Frank-Starling relationship is mediated by changes in the rate of cross-bridge detachment in cardiac muscle. We simultaneously measured isometric force development and the rate of ATP consumption at various levels of Ca2+ activation in skinned rat cardiac trabecular muscles at three sarcomere lengths (2.0, 2.1, and 2.2 μm). The maximum rate of ATP consumption was 1.5 nmol ⋅ s−1 ⋅ μl fiber vol−1, which represents an estimated adenosinetriphosphatase (ATPase) rate of ∼10 s−1 per myosin head at 24°C. The rate of ATP consumption was tightly and linearly coupled to the level of isometric force development, and changes in sarcomere length had no effect on the slope of the force-ATPase relationships. The average slope of the force-ATPase relationships was 15.5 pmol ⋅ mN−1 ⋅ mm−1. These results suggest that the mechanisms that underlie the Frank-Starling relationship in cardiac muscle do not involve changes in the kinetics of the apparent detachment step in the cross-bridge cycle.

Morphological Basis of the Disparity Between Muscle Length and Sarcomere Length in the Myocardium

1973 ◽  
Vol 31 ◽  
pp. 422-423
Author(s):  
G.E. Adomian ◽  
L. Chuck ◽  
W.W. Pannley
Keyword(s):  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Muscle Length ◽  
Contractile Force ◽  
Direct Function ◽  
Morphological Basis ◽  
Tension Curve

Sonnenblick, et al, have shown that sarcomeres change length as a function of cardiac muscle length along the ascending portion of the length-tension curve. This allows the contractile force to be expressed as a direct function of sarcomere length. Below L max, muscle length is directly related to sarcomere length at lengths greater than 85% of optimum. However, beyond the apex of the tension-length curve, i.e. L max, a disparity occurs between cardiac muscle length and sarcomere length. To account for this disproportionate increase in muscle length as sarcomere length remains relatively stable, the concept of fiber slippage was suggested as a plausible explanation. These observations have subsequently been extended to the intact ventricle.

scholarly journals Engineered Thin Filament Mutations to Study the Sarcomere Length Dependence of Cardiac Muscle Contractility

2018 ◽  
Vol 114 (3) ◽  
pp. 313a-314a
Author(s):  
Joseph D. Powers ◽  
Farid Moussavi-Harami ◽  
Jil C. Tardiff ◽  
Jennifer Davis ◽  
Michael Regnier
Keyword(s):  
Cardiac Muscle ◽  
Thin Filament ◽  
Sarcomere Length ◽  
Muscle Contractility ◽  
Length Dependence

scholarly journals Force enhancement after stretch of isolated myofibrils is increased by sarcomere length non-uniformities

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ricarda M. Haeger ◽  
Dilson E. Rassier
Keyword(s):  
Steady State ◽  
Sarcomere Length ◽  
Isometric Force ◽  
Force Production ◽  
Force Enhancement ◽  
Residual Force ◽  
Residual Force Enhancement ◽  
State Force ◽  
Isometric Forces

AbstractWhen a muscle is stretched during a contraction, the resulting steady-state force is higher than the isometric force produced at a comparable sarcomere length. This phenomenon, also referred to as residual force enhancement, cannot be readily explained by the force-sarcomere length relation. One of the most accepted mechanisms for the residual force enhancement is the development of sarcomere length non-uniformities after an active stretch. The aim of this study was to directly investigate the effect of non-uniformities on the force-producing capabilities of isolated myofibrils after they are actively stretched. We evaluated the effect of depleting a single A-band on sarcomere length non-uniformity and residual force enhancement. We observed that sarcomere length non-uniformity was effectively increased following A-band depletion. Furthermore, isometric forces decreased, while the percent residual force enhancement increased compared to intact myofibrils (5% vs. 20%). We conclude that sarcomere length non-uniformities are partially responsible for the enhanced force production after stretch.

Isotonic relaxation in cardiac muscle

1975 ◽  
Vol 229 (3) ◽  
pp. 646-651 ◽  
Author(s):  
JE Strobeck ◽  
AS Bahler ◽  
EH Sonnenblick
Keyword(s):  
Cardiac Muscle ◽  
Isometric Force ◽  
Muscle Length ◽  
Constant Load ◽  
Papillary Muscles ◽  
Initial Length ◽  
Total Load ◽  
Relaxation Velocity ◽  
Force Velocity ◽  
Maximum Isometric Force

The force-velocity-length determinants of isotonic relaxation were studied in 12 cat papillary muscles. Isotonic relaxation velocity (VL) was found to be a function of total load (preload + afterload), with peak VL increasing to a maximum at loads approximately .3 to .4 Po(L') (Po(L') defined as maximum isometric force developed during a twitch at the experimental length) and falling with increasing loads. Initial muscle length (ML) had no effect on the peak VL with constant load. Increasing the initial length at which isotonic relaxation occurred (LL) decreased peak VL but did not alter the unique length-velocity trajectory at constant load. This unique length-velocity trajectory occurred, despite a wide variation in time during the contraction when peak VL was measured. Increasing Ca++ from 2.5 to 7.5 mM increased peak VL (1.73 +/- .16 to 2.32 +/- .20 ML/s) and shifted the entire length-velocity trajectory toward higher velocities of lengthening. The addition of 10 mM caffeine increased peak VL also (1.67 +/- .18 to 2.54 +/- .20 ML/s) and had a similar effect on the length-velocity trajectory during lengthening as Ca++. Both increased Ca++ and caffeine (10 mM) augmented the maximum VL measured on addition of load.

Post-reextension force decay of relaxing cardiac muscle

1987 ◽  
Vol 253 (2) ◽  
pp. H256-H261 ◽  
Author(s):  
S. U. Sys ◽  
W. J. Paulus ◽  
V. A. Claes ◽  
D. L. Brutsaert
Keyword(s):  
Cardiac Muscle ◽  
Isometric Force ◽  
Muscle Length ◽  
Wall Stress ◽  
Left Ventricular ◽  
Segment Length ◽  
Force Decay ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
Ventricular Filling

Residual active cardiac muscle force during ventricular filling causes deviations of the pressure-volume and pressure-segment length relations from passive left ventricular compliance curves. A possible interaction at the myocardial level between muscle reextension and subsequent active force decay has not yet been investigated. We therefore studied the relation between isolated cat papillary muscle reextension, load during reextension, and isometric force decay after isotonic reextension. Both timing and extent of the isotonic muscle reextension phase were altered while load during reextension was lowered, subsequent residual isometric force was decreased. The extent of reextension or the final muscle length did not alter residual active isometric force after isotonic reextension at an identical load. Moreover, irrespective of the loading history of the shortening phase of the contraction, equal loads during reextension resulted in superimposable subsequent isometric force decay traces. From these results it therefore appears that residual isometric force after isotonic reextension is determined by the load during reextension. Extrapolation of these results to the filling ventricle implies the existence of a dynamic interaction between instantaneous extent of filling, wall stress, and residual force development.

Activation heat and latency relaxation in relation to calcium movement in skeletal and cardiac muscle

1982 ◽  
Vol 60 (4) ◽  
pp. 529-541 ◽  
Author(s):  
Louis A. Mulieri ◽  
Norman R. Alpert
Keyword(s):  
Skeletal Muscle ◽  
Refractory Period ◽  
Muscle Activation ◽  
Slow Component ◽  
Isometric Force ◽  
Fast Component ◽  
Bathing Solution ◽  
Latency Relaxation ◽  
In Series ◽  
Activation Heat

Measurements of activation heat, initial heat, twitch tension, and latency relaxation were made using thin-layer, vacuum-deposited thermopiles and isometric force transducers, respectively. Experiments were performed on frog skeletal muscle fiber bundles and on rabbit right ventricular papillary muscles at 0, 15, and 21 °C in normal and 1.75× to 2.5× mannitol hyperosmotic bathing solutions. In skeletal muscle, activation heat, obtained by stretching to zero overlap, was only slightly affected by 1.75× hyperosmotic solution and consisted of a fast and a slow component. Both components have a refractory period and a relatively refractory period which can be demonstrated by double pulse stimulation. The twitch potentiators Zn2+ and caffeine increase the total activation heat and the magnitude and rate of the fast component. The temporal relation between the latency relaxation and activation heat is demonstrated. The latency relaxation is independent of the number of sarcomeres in series in a muscle. Activation heat and latency relaxation records from heart muscle are obtained in 2.5× hyperosmotic bathing solution. A model of excitation–contraction coupling is presented which indicates that (1) the downstroke of the latency relaxation monitors the functioning of the Ca2+ -permeability or debinding mechanism in the terminal cisternae, (2) the fast component of activation heat monitors the amount of Ca2+ bound to troponin C, and (3) the total amplitude of activation heat is a measure of the total quantity of Ca2+ cycled in a twitch.

Force, velocity of shortening and sarcomere length in cardiac muscle

1985 ◽  
Vol 19 (9) ◽  
pp. 518-518
Author(s):  
H E D J T. KEURS ◽  
B WOHLFART ◽  
L RICCIARDI ◽  
B J M MULDER ◽  
J J J BUCX ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Velocity Of Shortening ◽  
Force Velocity
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