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

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.

1999 ◽  
Vol 86 (3) ◽  
pp. 1025-1031 ◽  
Author(s):  
John W. Chow ◽  
Warren G. Darling

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.


1991 ◽  
Vol 159 (1) ◽  
pp. 65-87 ◽  
Author(s):  
JEAN G. MALAMUD ◽  
ROBERT K. JOSEPHSON

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.


1992 ◽  
Vol 262 (3) ◽  
pp. L280-L285 ◽  
Author(s):  
K. Ikeda ◽  
R. W. Mitchell ◽  
K. A. Guest ◽  
C. Y. Seow ◽  
C. F. Kirchhoff ◽  
...  

We examined the effect of maturation on force-velocity (F-V) parameters in porcine tracheal smooth muscle (TSM) to determine the relationship between maximal isometric contractile force (Po) and maximal velocity of shortening (Vmax). Strips of TSM excised from 1-day-old neonatal swine (neo; n = 8), 2-wk-old swine (2ws; n = 7), and 10-wk-old swine (10ws; n = 7) were tethered to an electromagnetic lever system for F-V analysis of contractility. TSM strips were activated by electrical field stimulation at optimal resting tension, voltage, and length (Lo) so that maximal reproducible contractile force (Po) was elicited. Velocities were measured at the early phase of isometric contraction (3.1 +/- 0.1 s for neo, 2.9 +/- 0.1 s for 2ws, and 3.1 +/- 0.1 s for 10ws; P = NS). Shortening velocity increased progressively with maturation; Vmax was 0.164 +/- 0.011 Lo/s for neo, 0.194 +/- 0.013 Lo/s for 2ws (P less than 0.05 vs. neo), and 0.260 +/- 0.024 Lo/s for 10ws (P less than 0.01 vs. neo; P less than 0.05 vs. 2ws). Maximal isometric force generation increased substantially during the first 2 wk of postnatal life and thereafter returned to neonatal levels; Po was 71.5 +/- 2.1 mN/mm2 for neo, 95.4 +/- 7.0 mN/mm2 for 2ws, and 74.7 +/- 6.2 mN/mm2 for 10ws (P less than 0.05, 2ws vs. neo and 10ws). In separate studies, we also determined whether differences in Vmax occurred during the normal cycling phase of the cross bridge (3 s) or during the slowly cycling phase of the latch bridge (8 s) in tissue from 12 additional animals.(ABSTRACT TRUNCATED AT 250 WORDS)


2002 ◽  
Vol 205 (11) ◽  
pp. 1585-1595 ◽  
Author(s):  
F. Lou ◽  
N. A. Curtin ◽  
R. C. Woledge

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.


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

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.


1996 ◽  
Vol 271 (2) ◽  
pp. C676-C683 ◽  
Author(s):  
J. J. Widrick ◽  
S. W. Trappe ◽  
D. L. Costill ◽  
R. H. Fitts

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.


1990 ◽  
Vol 259 (4) ◽  
pp. H1118-H1125 ◽  
Author(s):  
J. S. Herland ◽  
F. J. Julian ◽  
D. G. Stephenson

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.


1975 ◽  
Vol 229 (3) ◽  
pp. 646-651 ◽  
Author(s):  
JE Strobeck ◽  
AS Bahler ◽  
EH Sonnenblick

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.


2000 ◽  
Vol 279 (5) ◽  
pp. H2493-H2501 ◽  
Author(s):  
Richard J. Paul ◽  
Peggy Sue Bowman ◽  
Michael S. Kolodney

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.


1993 ◽  
Vol 265 (6) ◽  
pp. L549-L554 ◽  
Author(s):  
R. W. Mitchell ◽  
I. M. Ndukwu ◽  
K. Arbetter ◽  
J. Solway ◽  
A. R. Leff

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.


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