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.

A bladder contractility constant

1983 ◽  
Vol 245 (5) ◽  
pp. R673-R677
Author(s):  
J. C. Byrne ◽  
A. Tozeren
Keyword(s):  
Initial Velocity ◽  
Active Component ◽  
Isometric Force ◽  
Muscle Length ◽  
Rate Of Change ◽  
Contractile Element ◽  
Tetanic Contraction ◽  
Muscle Contractility ◽  
Maximum Isometric Force ◽  
The Moment

Muscle contractility can be characterized by two related properties: force and velocity. The initial velocity of a tetanic contraction is inversely related to preload. This was demonstrated experimentally by Hill and quantified in his well-known empiric equation. Subsequent investigators argued that a theoretical maximum contractile element velocity (V max) could be predicted from the rate of change of isometric force. V max has been applied clinically in heart studies, prompting others to use similar methods to evaluate bladder contractility. These attempts have so far been unsuccessful. The present study shows for whole canine bladders that the time to reach maximum isometric force from the moment of onset of active contraction is a constant independent of muscle length, preload, and maximum force. This can be expressed as a frequency constant (omega) whose calculation appears similar to that for V max. In contrast to V max, omega is obtained only from the active component of pressure.

Force-length relations in cardiac muscle segments

1983 ◽  
Vol 244 (5) ◽  
pp. H701-H707
Author(s):  
L. L. Huntsman ◽  
J. F. Rondinone ◽  
D. A. Martyn
Keyword(s):  
Cardiac Muscle ◽  
Central Region ◽  
Muscle Length ◽  
The Other ◽  
Segment Length ◽  
Isometric Contractions ◽  
Papillary Muscles ◽  
Passive Force ◽  
A New Technique ◽  
Length Dependent Activation

Using a new technique that measures the length of a segment in the central region of isolated papillaries, we have determined the force-segment length relation for ferret papillary muscles at 27 degrees C. The muscles contracted under muscle length isometric (auxotonic) and segment isometric conditions in physiological solutions containing 9.0, 4.5, 2.25, and 1.125 mM Ca2+. Force-segment length relations obtained from auxotonic and segment isometric contractions were identical in a given Ca2+ concentration. Calcium variations, however, changed the position, shape, and segment length intercept of the force-segment length relation. Force, at a given segment length, increased with increasing Ca2+ up to 9.0 mM Ca2+. The force-segment length relation changed shape from linear, in 4.5 mM Ca2+, to concave in 1.125 mM Ca2+. The segment length intercept was found by extrapolation to be 68, 69, and 74% SLmax in 4.5, 2.25, and 1.125 mM Ca2+, respectively. Two passive force corrections were used to calculate the developed force-segment length relations. Assuming passive force to be related primarily to segment length yields curves that change shape with Ca2+ concentration, suggesting length-dependent activation. On the other hand, assuming passive force to be related to muscle length results in curves for different Ca2+ concentrations that are nearly vertically shifted versions of each other, suggesting the influence of internal loads.

Aminophylline increases submaximum power but not intrinsic velocity of shortening of frog muscle

1992 ◽  
Vol 73 (1) ◽  
pp. 71-74 ◽  
Author(s):  
B. M. Block ◽  
S. R. Barry ◽  
J. A. Faulkner
Keyword(s):  
Skeletal Muscles ◽  
Isometric Force ◽  
Frog Muscle ◽  
Measured Parameter ◽  
Shortening Velocity ◽  
Force Development ◽  
Velocity Of Shortening ◽  
Force Velocity ◽  
Maximum Isometric Force ◽  
Frequency Of Stimulation

We hypothesized that methylxanthines, such as aminophylline, increase the power developed by submaximally activated frog skeletal muscles by increasing the force developed at any given velocity of shortening. Frog semitendinosus muscles were excised and tested at 20 degrees C in oxygenated control and aminophylline Ringer solutions. Force-velocity relationships were determined and power was calculated from muscles stimulated at frequencies of 80 and 300 Hz. The 300-Hz frequency of stimulation produced a maximum rate of force development. In 50 and 500 microM aminophylline, twitch force increased by 25 +/- 12 and 75 +/- 13%, respectively. Aminophylline did not affect maximum isometric force generation or the shortening velocity at any relative load. At 80-Hz stimulation and in the presence of 500 microM aminophylline, power increased by an average of 11% at 10 of 14 relative loads. At maximum frequencies of stimulation, aminophylline had no effect on any measured parameter. We conclude that aminophylline increases the power developed by submaximally activated frog muscles through an increase in the force generated particularly at the lower velocities of shortening.

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.

scholarly journals The maximum shortening velocity of muscle should be scaled with activation

1999 ◽  
Vol 86 (3) ◽  
pp. 1025-1031 ◽  
Author(s):  
John W. Chow ◽  
Warren G. Darling
Keyword(s):  
Isometric Force ◽  
Musculoskeletal Modeling ◽  
Type Model ◽  
Shortening Velocity ◽  
Activation Level ◽  
Maximum Activation ◽  
Force Velocity ◽  
Maximum Isometric Force ◽  
Release Method ◽  
Wrist Flexors

The purpose of this study was to determine whether the maximum shortening velocity ( V max) in Hill’s mechanical model (A. V. Hill. Proc. R. Soc. London Ser. B. 126: 136–195, 1938) should be scaled with activation, measured as a fraction of the maximum isometric force (Fmax). By using the quick-release method, force-velocity (F-V) relationships of the wrist flexors were gathered at five different activation levels (20–100% of maximum at intervals of 20%) from four subjects. The F-V data at different activation levels can be fitted remarkably well with Hill’s characteristic equation. In general, the shortening velocity decreases with activation. With the assumption of nonlinear relationships between Hill constants and activation level, a scaled V max model was developed. When the F-V curves for submaximal activation were forced to converge at the V max obtained with maximum activation (constant V max model), there were drastic changes in the shape of the curves. The differences in V max values generated by the scaled and constant V max models were statistically significant. These results suggest that, when a Hill-type model is used in musculoskeletal modeling, the V max should be scaled with activation.

scholarly journals Effect of Muscle Length on the Force-Velocity Relationship of Tetanized Cardiac Muscle

1972 ◽  
Vol 31 (2) ◽  
pp. 195-206 ◽  
Author(s):  
Robert Formon ◽  
Lincoln E. Ford ◽  
Edmund H. Sonnenblick
Keyword(s):  
Cardiac Muscle ◽  
Muscle Length ◽  
Velocity Relationship ◽  
Force Velocity ◽  
Relationship Of

Supraspinatus Muscle Architecture and Physiology in a Rabbit Model of Tenotomy and Repair

2021 ◽  
Author(s):  
Sydnee A. Hyman ◽  
Isabella T. Wu ◽  
Laura S. Vasquez-Bolanos ◽  
Mackenzie B. Norman ◽  
Mary C. Esparza ◽  
...  
Keyword(s):  
Rotator Cuff ◽  
Isometric Force ◽  
Rabbit Model ◽  
Muscle Length ◽  
Peak Stress ◽  
Structural Data ◽  
Rotator Cuff Tears ◽  
Time Data ◽  
Maximum Isometric Force ◽  
Over Time

Chronic rotator cuff tears can cause severe functional deficits. Addressing the chronic fatty and fibrotic muscle changes is of high clinical interest; however, the architectural and physiological consequences of chronic tear and repair are poorly characterized. We present a detailed architectural and physiological analysis of chronic tear and repair (both over 8 and 16 weeks) compared to age-matched control rabbit supraspinatus (SSP) muscles. Using female New Zealand White Rabbits (N=30, n=6/group) under 2% isofluorane anesthesia, the SSP was surgically isolated and maximum isometric force measured at 4-6 muscle lengths. Architectural analysis was performed, and maximum isometric stress was computed. Whole muscle length-tension curves were generated using architectural measurements to compare experimental physiology to theoretical predictions. Architectural measures are consistent with persistent radial and longitudinal atrophy over time in tenotomy that fail to recover after repair. Maximum isometric force was significantly decreased after 16 wks tenotomy and not significantly improved after repair. Peak isometric force reported here are greater than prior reports of rabbit SSP force after tenotomy. Peak stress was not significantly different between groups and consistent with prior literature of SSP stress. Muscle strain during contraction was significantly decreased after 8-wks of tenotomy and repair, indicating effects of tear and repair on muscle function. The experimental length-tension data was overlaid with predicted curves for each experimental group (generated from structural data), exposing the altered structure-function relationship for tenotomy and repair over time. Data presented here contribute to understanding the physiological implications of disease and repair in the rotator cuff

Force-Velocity Relationships of a Locust Flight Muscle at Different Times During a Twitch Contraction

1991 ◽  
Vol 159 (1) ◽  
pp. 65-87 ◽  
Author(s):  
JEAN G. MALAMUD ◽  
ROBERT K. JOSEPHSON
Keyword(s):  
Flight Muscle ◽  
Isometric Force ◽  
Velocity Curve ◽  
Shortening Velocity ◽  
Single Twitch ◽  
Emory University ◽  
Generating Capacity ◽  
Force Velocity ◽  
Maximum Isometric Force ◽  
Isometric Twitch

The force-velocity relationships during isotonic shortening were determined for the metathoracic second tergocoxal muscle of the locust Schistocerca americana (Drury). This muscle is a synchronous flight muscle. During the plateau of a tetanic contraction, the maximum shortening velocity (Vmax) determined from the force-velocity curve was 5.2 muscle lengths s−1 (25°C) and the curvature (a/Po) was 0.62. The maximum isometric force (P0) was 36.3 N cm−2. Early in a twitch (at times shorter than the isometric twitch rise time) the values for Vmax and curvature were similar to those during the tetanic plateau, but the curves at different times during the twitch intercepted the force axis at values less than P0. Later in the twitch, Vmax declined. A variable termed degree of activation (DA) is developed as a measure of the force-generating capacity of a muscle when this may be time-varying, as throughout most of a twitch. DA is determined from the shortening velocity at an intermediate load and is the predicted intercept of the force-velocity curve with the force axis relative to the tetanic intercept. In the locust muscle, DA rose to a maximum in 2–3 ms after the end of the latent period. DA reached 80° of the tetanic value during a single twitch; during the second twitch of a pair, the peak DA reached approximately the tetanic value. After a brief plateau, DA declined approximately exponentially. The time constant of DA decay was about 14 ms. Note: Present address: Department of Physiology, Emory University, Atlanta, GA30322, USA.

Preload does not affect relaxation rate in normal, hypoxic, or hypertrophic myocardium

1990 ◽  
Vol 258 (1) ◽  
pp. H191-H197 ◽  
Author(s):  
M. R. Zile ◽  
C. H. Conrad ◽  
W. H. Gaasch ◽  
K. G. Robinson ◽  
O. H. Bing
Keyword(s):  
Relaxation Rate ◽  
Isometric Force ◽  
Muscle Length ◽  
Independent Effect ◽  
Shr Rats ◽  
Spontaneously Hypertensive ◽  
Maximum Isometric Force ◽  
Hypertrophic Myocardium ◽  
Wistar Kyoto ◽  
Tension Curves

To determine whether isolated changes in preload (end-diastolic force) can influence myocardial relaxation rate in normal or abnormal (hypoxic or hypertrophic) hearts, isolated LV papillary muscles from normal Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were studied using physiologically sequenced contractions. While total (systolic) load and late (lengthening) load were held constant, maximum isometric force decline (peak -dT/dt) and maximum isotonic lengthening rate (peak +dL/dt) were measured at seven levels of preload that varied from 115 to 55% of the resting tension at maximum length-tension curves (Lmax). Muscles from normal rats were studied in the oxygenated state (95% O2-5% CO2) and in the hypoxic state (95% N2-5% CO2). Preload did not effect peak -dT/dt or peak +dL/dt in either oxygenated or hypoxic muscles. During hypoxia, peak -dT/dt and peak +dL/dt were 9.5 +/- 1.0 g.mm-2.s-1 and 0.3 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 9.0 +/- 1.2 g.mm-2.s-1 and 0.2 +/- 0.1 at a preload of 55%. In separate experiments, the effect of preload on relaxation rate was studied in WKY and SHR rats. In neither group did preload have an independent effect on relaxation rate. In the SHRs, peak -dT/dt and peak +dL/dt were 24.3 +/- 5.3 g.mm-2.s-1 and 0.7 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 24.7 +/- 6.6 and 0.8 +/- 0.1 at a preload of 55%. Thus, in hypoxic and hypertrophic myocardium, as in normal muscle, an acute isolated change in preload did not influence the rate of force decline or muscle lengthening.

Onset of relaxation in cardiac muscle segments

1983 ◽  
Vol 245 (4) ◽  
pp. H610-H615
Author(s):  
J. F. Rondinone ◽  
D. A. Martyn ◽  
L. L. Huntsman
Keyword(s):  
Feedback Control ◽  
Cardiac Muscle ◽  
Time Course ◽  
Segment Length ◽  
Isometric Contractions ◽  
Papillary Muscles ◽  
Initial Length ◽  
Short Segment ◽  
Prolonged Time ◽  
Active Segment

The onset of relaxation has been studied in undamaged central segments of isolated ferret papillary muscles at 27 degrees C, 12 beats/min. A technique that provides a signal proportional to the length of a chosen segment was used to assess segment velocity and length. Feedback control was employed to obtain segment isometric contractions. At a variety of times during segment isometric twitches, rapid load clamps were imposed using a range of loads from resting force to greater than half peak developed force. For the purposes of this study, the onset of relaxation was defined as occurring when active segment shortening ceased and elongation began (i.e., Vseg = 0). Early load clamps to low loads resulted in V = 0 at comparatively short segment lengths and early times. Later load clamps caused zero velocity to occur at longer segment lengths and later times. The V = 0 points in fact formed a line in the segment length-time plane. Contractions clamped to higher loads exhibited reduced shortening and a prolonged time course so that the V = 0 points showed the same dependence on length and time. Remarkably, all the variations of load-clamp load, time, and initial length yielded V = 0 points that were intermixed along a single line. Increasing or decreasing extracellular Ca2+ caused the V equal to O points to shift to later times and shorter segment lengths or earlier times and longer segment lengths, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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