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.

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.

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.

Isometric and isovelocity contractile performance of red musle fibres from the dogfishScyliorhinus canicula

2002 ◽  
Vol 205 (11) ◽  
pp. 1585-1595 ◽  
Author(s):  
F. Lou ◽  
N. A. Curtin ◽  
R. C. Woledge
Keyword(s):  
Isometric Force ◽  
Maximum Velocity ◽  
Test Method ◽  
Muscle Fibres ◽  
Shortening Velocity ◽  
Fibre Bundles ◽  
Series Elasticity ◽  
In Series ◽  
Force Velocity ◽  
Maximum Isometric Force

SUMMARYMaximum isometric tetanic force produced by bundles of red muscle fibres from dogfish, Scyliorhinus canicula (L.), was 142.4±10.3 kN m-2 (N=35 fibre bundles); this was significantly less than that produced by white fibres 289.2±8.4 kN m-2(N=25 fibre bundles) (means ± S.E.M.). Part, but not all, of the difference is due to mitochondrial content. The maximum unloaded shortening velocity, 1.693±0.108 L0 s-1(N=6 fibre bundles), was measured by the slack-test method. L0 is the length giving maximum isometric force. The force/velocity relationship was investigated using a step-and-ramp protocol in seven red fibre bundles. The following equation was fitted to the data:[(P/P0)+(a/P0)](V+b)=[(P0*/P0)+(a/P0)]b,where P is force during shortening at velocity V,P0 is the isometric force before shortening, and a, band P0* are fitted constants. The fitted values were P0*/P0=1.228±0.053, Vmax=1.814±0.071 L0s-1, a/P0=0.269±0.024 and b=0.404±0.041 L0 s-1(N=7 for all values). The maximum power was 0.107±0.005P0Vmax and was produced during shortening at 0.297±0.012Vmax. Compared with white fibres from dogfish, the red fibres have a lower P0 (49%) and Vmax (48%), but the shapes of the force/velocity curves are similar. Thus, the white and red fibres have equal capacities to produce power within the limits set by the isometric force and maximum velocity of shortening of each fibre type. A step shortening of 0.050±0.003L0 (N=7) reduced the maximum isometric force in the red fibres' series elasticity to zero. The series elasticity includes all elastic structures acting in series with the attached cross-bridges. Three red fibre bundles were stretched at a constant velocity, and force (measured when length reached L0) was 1.519±0.032P0. In the range of velocities used here, -0.28 to -0.63Vmax, force varied little with the velocity.

Oxytocin-mediated recruitment of slowly cycling cross bridges and isometric force in rat myometrium

1996 ◽  
Vol 270 (2) ◽  
pp. E203-E208
Author(s):  
A. L. Ruzycky ◽  
B. T. Ameredes
Keyword(s):  
Isometric Force ◽  
Additional Stress ◽  
Shortening Velocity ◽  
Cycling Rate ◽  
Quick Release ◽  
Cross Bridge ◽  
Cross Bridges ◽  
Unit Stress ◽  
Release Method ◽  
The Relationship

The relationship between cross-bridge cycling rate and isometric stress was investigated in rat myometrium. Stress production by myometrial strips was measured under resting, K+ depolarization, and oxytocin-stimulated conditions. Cross-bridge cycling rates were determined from measurements of maximal unloaded shortening velocity, using the quick-release method. Force redevelopment after the quick release was used as an index of cross-bridge attachment. With maximal K+ stimulation, stress increased with increased cross-bridge cycling (+76%; P < 0.05) and attached cross bridges (+112%; P < 0.05). Addition of oxytocin during K+ stimulation further increased stress (+30%; P < 0.05). With this force component, the cross-bridge cycling rate decreased (-60%; P < 0.05) similar to that under resting conditions. Attached cross-bridges did not increase with this additional stress. The results suggest two distinct mechanisms mediating myometrial contractions. One requires elevated intracellular calcium and rapidly cycling cross bridges. The other mechanism may be independent of calcium and appears to be mediated by slowly cycling cross bridges, supporting greater unit stress.

scholarly journals Corticosteroid effects on isotonic contractile properties of rat diaphragm muscle

1997 ◽  
Vol 83 (4) ◽  
pp. 1062-1067 ◽  
Author(s):  
Roland H. H. Van Balkom ◽  
Wen-Zhi Zhan ◽  
Y. S. Prakash ◽  
P. N. Richard Dekhuijzen ◽  
Gary C. Sieck
Keyword(s):  
Isometric Force ◽  
Contractile Properties ◽  
Diaphragm Muscle ◽  
Peak Power Output ◽  
Rat Diaphragm ◽  
Fiber Morphology ◽  
Shortening Velocity ◽  
Maximum Isometric Force ◽  
Induced Changes ◽  
Isotonic Contractions

Van Balkom, Roland H. H., Wen-Zhi Zhan, Y. S. Prakash, P. N. Richard Dekhuijzen, and Gary C. Sieck. Corticosteroid effects on isotonic contractile properties of rat diaphragm muscle. J. Appl. Physiol. 83(4): 1062–1067, 1997.—The effects of corticosteroids (CS) on diaphragm muscle (Diam) fiber morphology and contractile properties were evaluated in three groups of rats: controls (Ctl), surgical sham and weight-matched controls (Sham), and CS-treated (6 mg ⋅ kg−1 ⋅ day−1prednisolone at 2.5 ml/h for 3 wk). In the CS-treated Diam, there was a selective atrophy of type IIx and IIb fibers, compared with a generalized atrophy of all fibers in the Sham group. Maximum isometric force was reduced by 20% in the CS group compared with both Ctl and Sham. Maximum shortening velocity in the CS Diamwas slowed by ∼20% compared with Ctl and Sham. Peak power output of the CS Diam was only 60% of Ctl and 70% of Sham. Endurance to repeated isotonic contractions improved in the CS-treated Diam compared with Ctl. We conclude that the atrophy of type IIx and IIb fibers in the Diam can only partially account for the CS-induced changes in isotonic contractile properties. Other factors such as reduced myofibrillar density or altered cross-bridge cycling kinetics are also likely to contribute to the effects of CS treatment.

Force-velocity and force-power properties of single muscle fibers from elite master runners and sedentary men

1996 ◽  
Vol 271 (2) ◽  
pp. C676-C683 ◽  
Author(s):  
J. J. Widrick ◽  
S. W. Trappe ◽  
D. L. Costill ◽  
R. H. Fitts
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Power Output ◽  
Peak Power ◽  
Isometric Force ◽  
Peak Force ◽  
Peak Power Output ◽  
Type I ◽  
Shortening Velocity ◽  
Force Velocity

Gastrocnemius muscle fiber bundles were obtained by needle biopsy from five middle-aged sedentary men (SED group) and six age-matched endurance-trained master runners (RUN group). A single chemically permeabilized fiber segment was mounted between a force transducer and a position motor, subjected to a series of isotonic contractions at maximal Ca2+ activation (15 degrees C), and subsequently run on a 5% polyacrylamide gel to determine myosin heavy chain composition. The Hill equation was fit to the data obtained for each individual fiber (r2 > or = 0.98). For the SED group, fiber force-velocity parameters varied (P < 0.05) with fiber myosin heavy chain expression as follows: peak force, no differences: peak tension (force/fiber cross-sectional area), type IIx > type IIa > type I; maximal shortening velocity (Vmax, defined as y-intercept of force-velocity relationship), type IIx = type IIa > type I; a/Pzero (where a is a constant with dimensions of force and Pzero is peak isometric force), type IIx > type IIa > type I. Consequently, type IIx fibers produced twice as much peak power as type IIa fibers, whereas type IIa fibers produced about five times more peak power than type I fibers. RUN type I and IIa fibers were smaller in diameter and produced less peak force than SED type I and IIa fibers. The absolute peak power output of RUN type I and IIa fibers was 13 and 27% less, respectively, than peak power of similarly typed SED fibers. However, type I and IIa Vmax and a/Pzero were not different between the SED and RUN groups, and RUN type I and IIa power deficits disappeared after power was normalized for differences in fiber diameter. Thus the reduced absolute peak power output of the type I and IIa fibers from the master runners was a result of the smaller diameter of these fibers and a corresponding reduction in their peak isometric force production. This impairment in absolute peak power production at the single fiber level may be in part responsible for the reduced in vivo power output previously observed for endurance-trained athletes.

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.

Effects of microtubule disruption on force, velocity, stiffness and [Ca2+]i in porcine coronary arteries

2000 ◽  
Vol 279 (5) ◽  
pp. H2493-H2501 ◽  
Author(s):  
Richard J. Paul ◽  
Peggy Sue Bowman ◽  
Michael S. Kolodney
Keyword(s):  
Smooth Muscle ◽  
Coronary Arteries ◽  
Isometric Force ◽  
Shortening Velocity ◽  
Cultured Fibroblasts ◽  
Microtubule Disruption ◽  
Highly Sensitive ◽  
Artery Stiffness ◽  
Force Velocity ◽  
Microtubule Stabilizer

Force generated by smooth muscle cells is believed to result from the interaction of actin and myosin filaments and is regulated through phosphorylation of the myosin regulatory light chain (LC20). The role of other cytoskeleton filaments, such as microtubules and intermediate filaments, in determining the mechanical output of smooth muscle is unclear. In cultured fibroblasts, microtubule disruption results in large increases in force similar to contractions associated with LC20 phosphorylation (15). One hypothesis, the “tensegrity” or “push-pull” model, attributes this increase in force to the disruption of microtubules functioning as rigid struts to resist force generated by actin-myosin interaction (9). In porcine coronary arteries, the disruption of microtubules by nocodazole (11 μM) also elicited moderate but significant increases in isometric force (10–40% of a KCl contracture), which could be blocked or reversed by taxol (a microtubule stabilizer). We tested whether this nocodazole-induced force was accompanied by changes in coronary artery stiffness or unloaded shortening velocity, parameters likely to be highly sensitive to microtubule resistance elements. Few changes were seen, ruling out push-pull mechanisms for the increase in force by nocodazole. In contrast, the intracellular calcium concentration, measured by fura 2 in the intact artery, was increased by nocodazole in parallel with force, and this was inhibited and/or reversed by taxol. Our results indicate that microtubules do not significantly contribute to vascular smooth muscle mechanical characteristics but, importantly, may play a role in modulation of Ca2+ signal transduction.

Effect of airway inflammation on smooth muscle shortening and contractility in guinea pig trachealis

1993 ◽  
Vol 265 (6) ◽  
pp. L549-L554 ◽  
Author(s):  
R. W. Mitchell ◽  
I. M. Ndukwu ◽  
K. Arbetter ◽  
J. Solway ◽  
A. R. Leff
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Neurogenic Inflammation ◽  
Isometric Force ◽  
Electrical Field Stimulation ◽  
Shortening Velocity ◽  
Lever System ◽  
Force Velocity

We studied the effect of either 1) immunogenic inflammation caused by aerosolized ovalbumin or 2) neurogenic inflammation caused by aerosolized capsaicin in vivo on guinea pig tracheal smooth muscle (TSM) contractility in vitro. Force-velocity relationships were determined for nine epithelium-intact TSM strips from ovalbumin-sensitized (OAS) vs. seven sham-sensitized controls and TSM strips for seven animals treated with capsaicin aerosol (Cap-Aer) vs. eight sham controls. Muscle strips were tethered to an electromagnetic lever system, which allowed isotonic shortening when load clamps [from 0 to maximal isometric force (Po)] were applied at specific times after onset of contraction. Contractions were elicited by supramaximal electrical field stimulation (60 Hz, 10-s duration, 18 V). Optimal length for each muscle was determined during equilibration. Maximal shortening velocity (Vmax) was increased in TSM from OAS (1.72 +/- 0.46 mm/s) compared with sham-sensitized animals (0.90 +/- 0.15 mm/s, P < 0.05); Vmax for TSM from Cap-Aer (0.88 +/- 0.11 mm/s) was not different from control TSM (1.13 +/- 0.08 mm/s, P = NS). Similarly, maximal shortening (delta max) was augmented in TSM from OAS (1.01 +/- 0.15 mm) compared with sham-sensitized animals (0.72 +/- 0.14 mm, P < 0.05); delta max for TSM from Cap-Aer animals (0.65 +/- 0.11 mm) was not different from saline aerosol controls (0.71 +/- 0.15 mm, P = NS). We demonstrate Vmax and delta max are augmented in TSM after ovalbumin sensitization; in contrast, neurogenic inflammation caused by capsaicin has no effect on isolated TSM contractility in vitro. These data suggest that airway hyperresponsiveness in vivo that occurs in association with immunogenic or neurogenic inflammation may result from different effects of these types of inflammation on airway smooth muscle.

scholarly journals The effects of inorganic phosphate on muscle force development and energetics: challenges in modelling related to experimental uncertainties

2019 ◽  
Author(s):  
Alf Månsson
Keyword(s):  
Inorganic Phosphate ◽  
Muscle Force ◽  
Isometric Force ◽  
Shortening Velocity ◽  
Apparent Contradiction ◽  
Sequence Of Events ◽  
Velocity Relationship ◽  
Force Velocity ◽  
Cross Bridges ◽  
Experimental Findings

Abstract Muscle force and power are developed by myosin cross-bridges, which cyclically attach to actin, undergo a force-generating transition and detach under turnover of ATP. The force-generating transition is intimately associated with release of inorganic phosphate (Pi) but the exact sequence of events in relation to the actual Pi release step is controversial. Details of this process are reflected in the relationships between [Pi] and the developed force and shortening velocity. In order to account for these relationships, models have proposed branched kinetic pathways or loose coupling between biochemical and force-generating transitions. A key hypothesis underlying the present study is that such complexities are not required to explain changes in the force–velocity relationship and ATP turnover rate with altered [Pi]. We therefore set out to test if models without branched kinetic paths and Pi-release occurring before the main force-generating transition can account for effects of varied [Pi] (0.1–25 mM). The models tested, one assuming either linear or non-linear cross-bridge elasticity, account well for critical aspects of muscle contraction at 0.5 mM Pi but their capacity to account for the maximum power output vary. We find that the models, within experimental uncertainties, account for the relationship between [Pi] and isometric force as well as between [Pi] and the velocity of shortening at low loads. However, in apparent contradiction with available experimental findings, the tested models produce an anomalous force–velocity relationship at elevated [Pi] and high loads with more than one possible velocity for a given load. Nevertheless, considering experimental uncertainties and effects of sarcomere non-uniformities, these discrepancies are insufficient to refute the tested models in favour of more complex alternatives.

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