Insights into the velocity-dependent geometry and internal strain in accretionary wedges from analogue models

2017 ◽  
Vol 155 (5) ◽  
pp. 1089-1104 ◽  
Author(s):  
BIN DENG ◽  
LEI JIANG ◽  
GAOPING ZHAO ◽  
RUI HUANG ◽  
YUANBO WANG ◽  
...  
Keyword(s):  
Brittle Material ◽  
High Velocity ◽  
Frontal Zone ◽  
Volumetric Strain ◽  
Velocity Dependence ◽  
Shortening Velocity ◽  
Asymmetric Structures ◽  
Analogue Models ◽  
Velocity Of Shortening ◽  
Geometry And Kinematics

AbstractAlthough the brittle material in analogue models is characterized by a linear Navier-Coulomb behaviour and rate-independent deformation, the geometry and style of deformation in accretionary wedges is sensitive to shortening velocity. In this study we have constructed a series of analogue models with various shortening velocities in order to study the influence of shortening velocity on the geometry and kinematics of accretionary wedges. Model results illustrate how shortening velocity has an important influence on the geometry and kinematics of the resulting wedge. In general, for models having similar bulk shortening, the accretionary wedges with higher velocities of shortening are roughly steeper, higher and longer, as well as having larger critical wedge angles and height. It accommodates a number of foreland-vergent thrusts, larger fault spacing and displacement rates than those of low- to medium-velocity shortening, which indicates a weak velocity-dependence in geometry of the wedge. Moreover, models with a high velocity of shortening undergo larger amounts of volumetric strain and total layer-parallel shortening than models with low- to medium-velocity shortening. The former accommodate a greater development of back thrusts and asymmetric structures; a backwards-to-forwards style of wedge growth therefore occurs in the frontal zone under high-velocity shortening.

Unloaded shortening velocity of skinned rat myocardium: effects of volatile anesthetics

1990 ◽  
Vol 259 (4) ◽  
pp. H1118-H1125 ◽  
Author(s):  
J. S. Herland ◽  
F. J. Julian ◽  
D. G. Stephenson
Keyword(s):  
Isometric Force ◽  
Dose Dependence ◽  
Test Method ◽  
Dose Response Relationship ◽  
Shortening Velocity ◽  
Velocity Of Shortening ◽  
Cross Bridges ◽  
Dose Levels ◽  
Ventricular Trabeculae ◽  
Unloaded Velocity

The slack test method has been adapted for measurement of unloaded velocity of shortening in rat ventricular trabeculae that were skinned with saponin (50 micrograms/ml for 30 min). The method was sensitive enough to detect a 17% reversible change in the unloaded velocity of shortening produced by a 3 degrees C change in temperature. At pCa 5.30 (80-90% activation), halothane, enflurane, and isoflurane each slowed the shortening velocity by 25-30% at dose levels of 8 mM or greater but not at 4 mM or less. At pCa 5.48 (50-60% activation), halothane slowed the shortening velocity by 20-45% at dose levels of 4 mM or greater but not at 2 mM. The slowing effect of anesthetics on shortening velocity showed saturation at 8 mM for halothane, enflurane, and isoflurane when activation was at pCa 5.30. Saturation occurred at 4 mM for halothane when the pCa was 5.48. This result indicates that the dose-response relationship may be narrow, such that it can be demonstrated between 2 and 4 mM halothane for pCa 5.48 and between 4 and 8 mM halothane for pCa 5.30. The anesthetic dose dependence of isometric force and length axis intercept did not generally follow the same relationship as for the shortening velocity. Thus in several instances force did not significantly decrease when the velocity of shortening did. This may be interpreted as lack of simple inhibition by anesthetics on the number of interacting cross-bridges and as direct influence by anesthetics on the cross-bridge cycle.

In vivo contractile properties of fatigued diaphragm

1987 ◽  
Vol 63 (2) ◽  
pp. 471-478 ◽  
Author(s):  
J. Road ◽  
R. Vahi ◽  
P. del Rio ◽  
A. Grassino
Keyword(s):  
Spontaneous Breathing ◽  
Central Fatigue ◽  
Contractile Properties ◽  
Peripheral Fatigue ◽  
Electromyographic Activity ◽  
Force Frequency ◽  
Shortening Velocity ◽  
Velocity Of Shortening ◽  
The Right

The effects of fatigue on diaphragmatic contractility in vivo are unknown. In this study we used sonomicrometry to examine the velocity of shortening and lengthening and the amount of shortening in the fresh and fatigued canine hemidiaphragm (8 dogs) including the force generated. Fatigue was produced by epiphrenic stimulation of the left phrenic nerve; the right hemidiaphragm acted as the control. We found that 1) hemidiaphragmatic fatigue caused an increase in frequency with reduced tidal volume; 2) fatigue resulted in a near complete cessation of tidal shortening during spontaneous breathing; 3) there was an initial decrease in central activation (electromyogram) to the fatigued hemidiaphragm, an indication of central fatigue; 4) force-frequency curves showed a considerable and prolonged loss of the amount of shortening, velocity, and force generated by the fatigued hemidiaphragm during supramaximal stimulation, an indication of peripheral fatigue; and 5) during spontaneous breathing in the fatigued hemidiaphragm, tidal shortening remained reduced for up to 3 h, whereas in the right right hemidiaphragm tidal shortening and electromyographic activity did not change. We conclude that fatigue of a hemidiaphragm alters the spontaneous breathing pattern and produces profound modifications in its contractile properties without altering contralateral hemidiaphragmatic performance.

Disuse inhibition of newly functional coronary collateral circulation in ponies

1992 ◽  
Vol 262 (2) ◽  
pp. H385-H390
Author(s):  
K. S. Rugh ◽  
C. R. Ross ◽  
R. D. Sarazan ◽  
R. B. Boatwright ◽  
D. O. Williams ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Shortening Velocity ◽  
Coronary Collateral ◽  
Work Index ◽  
Percent Recovery ◽  
Velocity Of Shortening ◽  
Stroke Work Index ◽  
Long Time

We evaluated the loss of coronary collateral function in the absence of stimulation (disuse inhibition) by doubling the interval between successive left anterior descending coronary artery (LAD) occlusions in ponies in which collateral function initially had been enhanced by 2-min occlusions at 30-min intervals. Before collateralization, occlusion caused segment systolic shortening, velocity of shortening, and stroke work index in the LAD-dependent left ventricular apex to decrease, whereas heart rate and left ventricular end-diastolic pressure increased. After 476 +/- 102 occlusions, segment function recovered to preocclusion levels and hemodynamics were unchanged during occlusion. Occlusion did not elicit sustained functional deterioration until the occlusion interval was greater than or equal to 32 h. During the occlusion after the 128-h interval, segment systolic shortening, velocity of shortening, and stroke work index were reduced 69 +/- 8, 38 +/- 9, and 46 +/- 13%, respectively. Percent recovery of systolic shortening during successive occlusions declined exponentially (T1/e = 102.0 +/- 17.3 h). Thus, in ponies collateral function progressively declines when the occlusion interval is greater than or equal to 32 h, but complete inhibition does not occur even after 128 h without occlusion. This indicates that collateral function in ponies can be maintained by occlusions that are far less frequent than those needed for initial collateral development. The long time constant of collateral disuse inhibition suggests that equine collaterals are quite resistant to the effects of occlusion cessation and differ from canine collaterals in that respect.

High-velocity expansion of a cavity within a brittle material

1999 ◽  
Vol 47 (3) ◽  
pp. 577-610 ◽  
Author(s):  
Sreten Mastilovic ◽  
Dusan Krajcinovic
Keyword(s):  
Brittle Material ◽  
High Velocity

Dynamic properties of denervated rat muscle treated with electrotherapy

1963 ◽  
Vol 205 (1) ◽  
pp. 173-176 ◽  
Author(s):  
D. R. Elliott ◽  
J. D. Thomson
Keyword(s):  
Dynamic Properties ◽  
Shortening Velocity ◽  
Rat Muscle ◽  
Extra Energy ◽  
Velocity Of Shortening ◽  
Normal Controls

Denervated rat gastrocnemii, compared with normal controls, showed slower shortening velocity and less shortening, performed less work, exhibited decreased values for Hill's constant a (shortening heat per centimeter shortening), a low P0 (maximum isometric tetanus tension) value and a higher a/P0 ratio, but showed no change in Hill's constant b (rate of extra energy released per gram tension decline from P0). Muscle not allowed to shorten during treatment ("isometric") showed greater shortening velocity than did denervated untreated muscle or muscle allowed to shorten freely during treatment ("isotonic"). Isotonically treated muscle showed a greater amount of shortening and a higher value for constant a than did denervated untreated or isometrically treated muscle, but no corresponding change in constant b. While isotonic treatment resulted in better maintenance of the amount of shortening and of the value for a than did isometric treatment, and isometric treatment resulted in better maintenance of velocity of shortening than did isotonic treatment, isometric treatment reduced constants a and b to values below those for denervated untreated muscle.

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.

scholarly journals Active shortening protects against stretch-induced force deficits in human skeletal muscle

2017 ◽  
Vol 122 (5) ◽  
pp. 1218-1226 ◽  
Author(s):  
Anjali L. Saripalli ◽  
Kristoffer B. Sugg ◽  
Christopher L. Mendias ◽  
Susan V. Brooks ◽  
Dennis R. Claflin
Keyword(s):  
Skeletal Muscle ◽  
High Velocity ◽  
Isometric Force ◽  
Human Subjects ◽  
Causative Factor ◽  
Negative Consequences ◽  
Shortening Velocity ◽  
Contracting Muscle ◽  
Working Hypothesis ◽  
Force Maintenance

Skeletal muscle contraction results from molecular interactions of myosin “crossbridges” with adjacent actin filament binding sites. The binding of myosin to actin can be “weak” or “strong,” and only strong binding states contribute to force production. During active shortening, the number of strongly bound crossbridges declines with increasing shortening velocity. Forcibly stretching a muscle that is actively shortening at high velocity results in no apparent negative consequences, whereas stretch of an isometrically (fixed-length) contracting muscle causes ultrastructural damage and a decline in force-generating capability. Our working hypothesis is that stretch-induced damage is uniquely attributable to the population of crossbridges that are strongly bound. We tested the hypothesis that stretch-induced force deficits decline as the prevailing shortening velocity is increased. Experiments were performed on permeabilized segments of individual skeletal muscle fibers obtained from human subjects. Fibers were maximally activated and allowed either to generate maximum isometric force (Fo), or to shorten at velocities that resulted in force maintenance of ≈50% Fo or ≈2% Fo. For each test condition, a rapid stretch equivalent to 0.1 × optimal fiber length was applied. Relative to prestretch Fo, force deficits resulting from stretches applied during force maintenance of 100, ≈50, and ≈2% Fo were 23.2 ± 8.6, 7.8 ± 4.2, and 0.3 ± 3.3%, respectively (means ± SD, n = 20). We conclude that stretch-induced damage declines with increasing shortening velocity, consistent with the working hypothesis that the fraction of strongly bound crossbridges is a causative factor in the susceptibility of skeletal muscle to stretch-induced damage. NEW & NOTEWORTHY Force deficits caused by stretch of contracting muscle are most severe when the stretch is applied during an isometric contraction, but prevented if the muscle is shortening at high velocity when the stretch occurs. This study indicates that velocity-controlled modulation of the number of strongly bound crossbridges is the basis for the observed relationship between stretch-induced muscle damage and prevailing shortening velocity.

scholarly journals cMyBP-C phosphorylation modulates the time-dependent slowing of unloaded shortening in murine skinned myocardium

2021 ◽  
Vol 153 (3) ◽  
Author(s):  
Jasmine Giles ◽  
Daniel P. Fitzsimons ◽  
Jitandrakumar R. Patel ◽  
Chloe Knudtsen ◽  
Zander Neuville ◽  
...  
Keyword(s):  
High Velocity ◽  
Thin Filament ◽  
Cardiac Myosin ◽  
Low Velocity ◽  
Shortening Velocity ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding ◽  
Low Levels ◽  
Cooperative Activation

In myocardium, phosphorylation of cardiac myosin-binding protein-C (cMyBP-C) is thought to modulate the cooperative activation of the thin filament by binding to myosin and/or actin, thereby regulating the probability of cross-bridge binding to actin. At low levels of Ca2+ activation, unloaded shortening velocity (Vo) in permeabilized cardiac muscle is comprised of an initial high-velocity phase and a subsequent low-velocity phase. The velocities in these phases scale with the level of activation, culminating in a single high-velocity phase (Vmax) at saturating Ca2+. To test the idea that cMyBP-C phosphorylation contributes to the activation dependence of Vo, we measured Vo before and following treatment with protein kinase A (PKA) in skinned trabecula isolated from mice expressing either wild-type cMyBP-C (tWT), nonphosphorylatable cMyBP-C (t3SA), or phosphomimetic cMyBP-C (t3SD). During maximal Ca2+ activation, Vmax was monophasic and not significantly different between the three groups. Although biphasic shortening was observed in all three groups at half-maximal activation under control conditions, the high- and low-velocity phases were faster in the t3SD myocardium compared with values obtained in either tWT or t3SA myocardium. Treatment with PKA significantly accelerated both the high- and low-velocity phases in tWT myocardium but had no effect on Vo in either the t3SD or t3SA myocardium. These results can be explained in terms of a model in which the level of cMyBP-C phosphorylation modulates the extent and rate of cooperative spread of myosin binding to actin.

Force-velocity relationship of myogenically active arterioles

2002 ◽  
Vol 282 (1) ◽  
pp. H165-H174 ◽  
Author(s):  
Michael J. Davis ◽  
Judy Davidson
Keyword(s):  
Smooth Muscle ◽  
Maximum Velocity ◽  
Cheek Pouch ◽  
Myogenic Tone ◽  
Internal Diameter ◽  
Wall Tension ◽  
Shortening Velocity ◽  
Hamster Cheek Pouch ◽  
Velocity Of Shortening

We compared the shortening velocity of smooth muscle in arterioles that had low or high levels of myogenic tone or norepinephrine (NE)-induced tone. We hypothesized that enhanced myogenic tone of arterioles reflects an enhanced maximum velocity of shortening of arteriolar smooth muscle in a way that is different from that produced by NE. These concepts are untested assumptions of arteriolar mechanics. Second-order arterioles from hamster cheek pouch (passive diameter at 40 mmHg = 42 μm) were isolated and cannulated for in vitro study. In the absence of flow, pressure was controlled by hydraulic pumps so that servo control of wall tension could be achieved from measurement of internal diameter and pressure. Isotonic quick-release protocols were used to measure the initial velocity of shortening following release from control wall tension (afterload) to a series of fractional afterloads. After release, the initial rates of shortening were fit to the Hill equation to obtain coefficients for a hyperbolic fit of the velocity-afterload relationship. The maximal unloaded shortening velocity for partially activated arterioles ( V′max) was determined from the y-intercept of each plot. Using this procedure, we compared V′max from two groups of arterioles equilibrated at low or high pressure, i.e., with low or high myogenic tone. Arterioles with higher myogenic tone had higher values of V′max than arterioles with lower myogenic tone. V′max for arterioles partially activated with NE at low pressure was comparable to V′max for arterioles with high myogenic tone, but NE produced high velocities at low force, whereas enhanced myogenic tone produced roughly parallel shifts in velocity and force. The results suggest that increased myogenic tone does indeed reflect enhanced activation of arteriolar smooth muscle, and this effect is mechanically different from that produced by NE.

Transient changes in isotonic shortening velocity of frog rectus abdominis muscles in potassium contracture

1965 ◽  
Vol 163 (991) ◽  
pp. 215-223 ◽  
Keyword(s):  
Muscle Length ◽  
Constant Load ◽  
Rectus Abdominis ◽  
Transient Condition ◽  
Shortening Velocity ◽  
Initial Tension ◽  
Constant Length ◽  
Potassium Contracture ◽  
Velocity Of Shortening ◽  
In Series

Shortening velocities of the frog rectus abdominis muscle during isotonic releases in potassium contracture have been determined under various conditions of initial length, initial tension and load. The velocity of shortening under constant load at any particular muscle length is dependent upon the length and tension of the muscle before release; there is no unique force-velocity relation at constant length. An empirical formulation of the relations between shortening velocity and length is given. These results cannot be explained in terms of a simple model of the muscle in which there is an undamped elastic element in series with a contractile component whose shortening velocity is instantaneously determined by tension. Some possible explanations of the phenomena are discussed, and it is tentatively suggested that the transient condition following an isotonic release is dependent upon the rates of formation and breakage of cross-linkages between the actin and myosin filaments in the muscle.

Sign in / Sign up

Export Citation Format

Share Document