Nitric oxide effects on shortening velocity and power production in the rat diaphragm

1996 ◽  
Vol 80 (3) ◽  
pp. 1065-1069 ◽  
Author(s):  
R. J. Morrison ◽  
C. C. Miller ◽  
M. B. Reid
Keyword(s):  
Nitric Oxide ◽  
Isometric Force ◽  
Maximum Velocity ◽  
Power Production ◽  
Ringer Solution ◽  
Fiber Bundles ◽  
Rat Diaphragm ◽  
Shortening Velocity ◽  
No Donor ◽  
Velocity Of Shortening

The present experiments tested nitric oxide (NO) effects on shortening velocity and power production in maximally activated rat diaphragm. Diaphragm fiber bundles (n = 10/group) were incubated at 37 degrees C in Krebs-Ringer solution containing no added drug (control), the NO synthase inhibitor N omega-nitro-L-arginine (L-NNA; 10 mM), the NO donor sodium nitroprusside (SNP; 1 mM), or a combination (L-NNA + SNP) Loaded shortening velocity was measured via the load-clamp technique over a range of afterloads. Force-velocity data were fitted to the Hill equation to determine maximum velocity of shortening (Vmax). Unloaded shortening velocity was measured in control and L-NNA-treated bundles (n = 12/group) by using the slack test. Maximal isometric force and unloaded shortening velocity were not altered by L-NNA. In contrast, L-NNA decreased maximum velocity of shortening (P < 0.05), loaded shortening velocity (P < 0.0001), and power production (P < 0.0001). All L-NNA effects were prevented by coincubating fiber bundles with L-NNA + SNP. SNP alone had no effect on any variable. These data indicate that endogenous NO is essential for optimal myofilament function during active shortening.

Effects of modulation of nitric oxide on rat diaphragm isotonic contractility during hypoxia

2003 ◽  
Vol 94 (2) ◽  
pp. 612-620 ◽  
Author(s):  
Xiaoping Zhu ◽  
Leo M. A. Heunks ◽  
Herwin A. Machiels ◽  
Leo Ennen ◽  
P. N. Richard Dekhuijzen
Keyword(s):  
Nitric Oxide ◽  
Power Generation ◽  
Muscle Contraction ◽  
Fatigue Properties ◽  
Rat Diaphragm ◽  
Shortening Velocity ◽  
No Donor ◽  
Diaphragm In Vitro ◽  
Spermine Nonoate

Nitric oxide (NO) is essential for optimal myofilament function of the rat diaphragm in vitro during active shortening. Little is known about the role of NO in muscle contraction under hypoxic conditions. Hypoxia might increase the NO synthase (NOS) activity within the rat diaphragm. We hypothesized that NO plays a protective role in isotonic contractile and fatigue properties during hypoxia in vitro. The effects of the NOS inhibitor N G-monomethyl-l-arginine (l-NMMA), the NO scavenger hemoglobin, and the NO donor spermine NONOate on shortening velocity, power generation, and isotonic fatigability during hypoxia were evaluated (Po 2 ∼ 7 kPa). l-NMMA and hemoglobin slowed the shortening velocity, depressed power generation, and increased isotonic fatigability during hypoxia. The effects ofl-NMMA were prevented by coadministration with the NOS substrate l-arginine. Spermine NONOate did not alter isotonic contractile and fatigue properties during hypoxia. These results indicate that endogenous NO is needed for optimal muscle contraction of the rat diaphragm in vitro during hypoxia.

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.

Skeletal muscle force and actomyosin ATPase activity reduced by nitric oxide donor

1997 ◽  
Vol 83 (4) ◽  
pp. 1326-1332 ◽  
Author(s):  
William J. Perkins ◽  
Young-Soo Han ◽  
Gary C. Sieck
Keyword(s):  
Nitric Oxide ◽  
Mechanical Properties ◽  
Atpase Activity ◽  
Muscle Force ◽  
Isometric Force ◽  
Nitric Oxide Donor ◽  
No Donor ◽  
Single Fibers ◽  
Actomyosin Atpase ◽  
Cross Bridge

Perkins, William J., Young-Soo Han, and Gary C. Sieck.Skeletal muscle force and actomyosin ATPase activity reduced by nitric oxide donor. J. Appl. Physiol.83(4): 1326–1332, 1997.—Nitric oxide (NO) may exert direct effects on actin-myosin cross-bridge cycling by modulating critical thiols on the myosin head. In the present study, the effects of the NO donor sodium nitroprusside (SNP; 100 μM to 10 mM) on mechanical properties and actomyosin adenosinetriphosphatase (ATPase) activity of single permeabilized muscle fibers from the rabbit psoas muscle were determined. The effects of N-ethylmaleimide (NEM; 5–250 μM), a thiol-specific alkylating reagent, on mechanical properties of single fibers were also evaluated. Both NEM (≥25 μM) and SNP (≥1 mM) significantly inhibited isometric force and actomyosin ATPase activity. The unloaded shortening velocity of SNP-treated single fibers was decreased, but to a lesser extent, suggesting that SNP effects on isometric force and actomyosin ATPase were largely due to decreased cross-bridge recruitment. The calcium sensitivity of SNP-treated single fibers was also decreased. The effects of SNP, but not NEM, on force and actomyosin ATPase activity were reversed by treatment with 10 mMdl-dithiothreitol, a thiol-reducing agent. We conclude that the NO donor SNP inhibits contractile function caused by reversible oxidation of contractile protein thiols.

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.

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 The influence of temperature on muscle function in the fast swimming scup. II. The mechanics of red muscle

1992 ◽  
Vol 163 (1) ◽  
pp. 281-295 ◽  
Author(s):  
L. C. Rome ◽  
A. Sosnicki ◽  
I. H. Choi
Keyword(s):  
Isometric Force ◽  
Maximum Velocity ◽  
Design Constraint ◽  
Velocity Of Shortening ◽  
Red Muscle ◽  
Different Temperatures ◽  
Influence Of Temperature On ◽  
The Mean ◽  
Important Design

To understand better how scup can swim twice as fast as carp with its red muscle, we measured the mechanical properties of red muscle bundles in scup. The values of the mean maximum velocity of shortening (Vmax) at 10 degrees C (3.32 muscle lengths s-1) and at 20 degrees C (5.55 muscle lengths s-1; Q10 = 1.69) were nearly the same as those in carp. Isometric force, however, was approximately 50% greater (183 kN m-2; Q10 = 1.08). The maximal power generation was correspondingly about 50% greater in scup than in carp (71 W kg-1 at 10 degrees C and 134 W kg-1 at 20 degrees C; Q10 = 1.88). The larger power output of its muscle may be important in the faster swimming of the scup. In addition, the fact that scup use a less undulatory style of swimming means that, when they are swimming twice as fast, their red muscle shortens at the same velocity (V) and with the same V/Vmax (0.37, i.e. where maximum power is generated) as that of carp. The importance of V/Vmax is further shown by the comparison of scup swimming at different temperatures. The 1.69-fold higher Vmax at 20 degrees C than at 10 degrees C enables scup to swim with a 1.67-fold faster V at 20 degrees C. Thus, at both 10 degrees C and 20 degrees C, red muscle is used only over the same narrow range of V/Vmax (0.17-0.37), where experiments on isolated muscle suggest that power and efficiency are maximal. Therefore, V/Vmax appears to be an important design constraint that limits the range of velocities over which muscle is used in vivo, both at different temperatures and in fast- and slow-locomoting species.

The energetics of the jump of the locust Schistocerca gregaria

1975 ◽  
Vol 63 (1) ◽  
pp. 53-83 ◽  
Author(s):  
H. C. Bennet-Clark
Keyword(s):  
Safety Factor ◽  
Power Output ◽  
Peak Power ◽  
Schistocerca Gregaria ◽  
Isometric Force ◽  
Maximum Velocity ◽  
Peak Power Output ◽  
Stored Energy ◽  
Distance Curve ◽  
Velocity Of Shortening

The anatomy of the metathoracic leg is redescribed with particular reference to storage of energy in cuticular elements and the way in which the stored energy is used in jumping. The jump of adult male locusts requires an energy of 9 mJ and that of the female requires 11 mJ. The semilunar processes of each metafemur store 4 mJ at a stress of 15 N, and the extensor tibiae apodeme stores a further 3 mJ at the same stress. The total stored energy in both metathoracic legs is 14 mJ. The extensor tibiae muscle produces a maximum isometric force of over 15 N at 30 degrees C and, when loaded with the extensor apodeme and semilunar processes, attains this force in 0.3 sec with a strain of 0.8 mm. The peak power output is 36 mW or 0.45 W.g-1. The peak isometric force is attained when the tibia is fully flexed and the force falls as the tibia extends. The extensor tibiae muscle A band is 5.5 mum long and the peak force is over 0.75 N.m-2. The peak velocity of shortening is 7 mm.sec-1 or about 1.75 lengths/sec at 30 degrees C. The tensile strength of the extensor apodeme is 0.6 kN.mm-2 and Young's modulus is 19 kN.mm-2. The safety factor does not exceed 1.2 and the safety factor of the semilunar processes and tibial cuticle is little higher. The jump impulse lasts 25–30 msec. A velocity of 3.2 m.sec-1 is reached after a peak acceleration of 180 m.sec-2. The peak power output is 0.75 W at close to maximum velocity. Energy losses in rotating the femur and tibia are small and it is shown that the leg is able to extend at 7 times the normal rate with losses of about 20%. Most of the stored energy is converted to kinetic energy as the animal jumps. A model is based on the relaxation of a spring that has the properties of the elastic elements of the locust leg into a lever with the same kinematics as the locust leg produces a force-distance curve similar to that measured for locust jumps. The major part of the jump energy is stored before the jump.

Contraction dynamics and power production of pink muscle of the scup (Stenotomus chrysops).

1996 ◽  
Vol 199 (12) ◽  
pp. 2703-2712 ◽  
Author(s):  
D J Coughlin ◽  
G Zhang ◽  
L C Rome
Keyword(s):  
Fibre Orientation ◽  
Maximum Velocity ◽  
Power Production ◽  
Velocity Of Shortening ◽  
Red Muscle ◽  
Oscillatory Power ◽  
Myotomal Muscle ◽  
Longitudinal Fibre ◽  
Stenotomus Chrysops

Although the contribution of red muscle to sustained swimming in fish has been studied in detail in recent years, the role of pink myotomal muscle has not received attention. Pink myotomal muscle in the scup (Stenotomus chrysops) lies just medial to red muscle, has the same longitudinal fibre orientation and is recruited along with the red muscle during steady sustainable swimming. However, pink muscle has significantly faster rates of relaxation, and the maximum velocity of shortening of pink muscle (7.26 +/- 0.18 muscle lengths s-1, N = 9, at 20 degrees C, and 4.46 +/- 0.15 muscle lengths s-1, N = 6, at 10 degrees C; mean +/- S.E.M.) is significantly faster than that of red muscle. These properties facilitate higher mass-specific maximum oscillatory power production relative to that of red muscle at frequencies similar to the tailbeat frequency at maximum sustained swimming speeds in scup. Additionally, pink muscle is found in anatomical positions in which red muscle is produces very little power during swimming: the anterior region of the fish, which undergoes the lowest strain during swimming. Pink muscle produces more oscillatory power than red muscle under low-strain conditions (+/- 2-3%) and this may allow pink muscle to supplement the relatively low power generated by red muscle in the anterior regions of swimming scup.

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.

scholarly journals High ionic strength and low pH detain activated skinned rabbit skeletal muscle crossbridges in a low force state.

1993 ◽  
Vol 101 (4) ◽  
pp. 487-511 ◽  
Author(s):  
C Y Seow ◽  
L E Ford
Keyword(s):  
Skeletal Muscle ◽  
Ionic Strength ◽  
Isometric Force ◽  
Maximum Velocity ◽  
Low Ph ◽  
High Ionic Strength ◽  
Rabbit Skeletal Muscle ◽  
Shortening Velocity ◽  
Force Ratio ◽  
Force Difference

The effects of varying pH and ionic strength on the force-velocity relations and tension transients of skinned rabbit skeletal muscle were studied at 1-2 degrees C. Both decreasing pH from 7.35 to 6.35 and raising ionic strength from 125 to 360 mM reduced isometric force by about half and decreased sarcomere stiffness by about one-fourth, so that the stiffness/force ratio was increased by half. Lowering pH also decreased maximum shortening velocity by approximately 29%, while increasing ionic strength had little effect on velocity. These effects on velocity were correlated with asymmetrical effects on stiffness. The increase in the stiffness/force ratio with both interventions was manifest as a greater relative force change associated with a sarcomere length step. This force difference persisted for a variable time after the step. At the high ionic strength the force difference was long-lasting after stretches but relaxed quickly after releases, suggesting that the structures responsible would not impose much resistance to steady-state shortening. The opposite was found in the low pH experiments. The force difference relaxed quickly after stretches but persisted for a long time after releases. Furthermore, this force difference reached a constant value of approximately 8% of isometric force with intermediate sizes of release, and was not increased with larger releases. This value was almost identical to the value of an internal load that would be sufficient to account for the reduction in maximum velocity seen at the low pH. The results are interpreted as showing that both low pH and high ionic strength inhibit the movement of crossbridges into the force-generating parts of their cycle after they have attached to the actin filaments, with very few other effects on the cycle. The two interventions are different, however, in that detained bridges can be detached readily by shortening when the detention is caused by high ionic strength but not when it is caused by low pH.

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