Stiffness of active smooth muscle during forced elongation

1987 ◽  
Vol 253 (3) ◽  
pp. C484-C493 ◽  
Author(s):  
R. A. Meiss
Keyword(s):  
Smooth Muscle ◽  
Phase Angle ◽  
Muscle Length ◽  
Isometric Tension ◽  
Microcomputer System ◽  
Tension Development ◽  
Stretch Rate ◽  
Angle Data ◽  
Cross Bridges ◽  
System Phase

The stiffness of isometrically contracting mesotubarium superius and ovarian ligament smooth muscle from estrous female rabbits was measured continuously by using sinusoidal length perturbations (at 80 Hz, less than 15 microns peak to peak). Muscles were stimulated with alternating current fields, and all records were digitized using a microcomputer system. Phase-angle data were used to resolve computed stiffness into elastic and viscous components. Stiffness measurements were continued during long ramp-type stretches (up to 25% of muscle length) delivered as soon as force was maximal. To use the period of isometric tension development as a standard for comparison, the expected stiffness was computed during the long stretch. Stiffness was reduced in approximate proportion to the ramp stretch rate, and the reduction was confined largely to the elastic component. Cooling the muscle increased the stiffness deviation at a given stretch rate. It is proposed that the long stretch detaches cross bridges that can reattach to new sites as myofilaments shear past one another. At higher shearing speeds, less time is available for reattachment and stiffness is further reduced.

Force–velocity relationships in hypertensive arterial smooth muscle

1985 ◽  
Vol 63 (6) ◽  
pp. 669-674 ◽  
Author(s):  
C. S. Packer ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rat ◽  
Peripheral Resistance ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Isometric Tension ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Force Velocity ◽  
Wistar Kyoto

Increased total peripheral resistance is the cardinal haemodynamic disorder in essential hypertension. This could be secondary to alterations in the mechanical properties of vascular smooth muscle. Adequate study has not been made of the force–velocity (F–V) relationship in hypertensive arterial smooth muscle. Increased shortening in arterial smooth muscle would result in greater narrowing of arteries. The objectives of this investigation were to see if there is (i) increased shortening or increased maximum change in muscle length (ΔLmax where L stands for muscle length), (ii) an increased maximum velocity of shortening (Vmax) measured in lo per second where lo is the optimal muscle length for tension development, and (iii) a difference in maximum isometric tension (Po) developed in spontaneously hypertensive rat (SHR; N = 6) compared with normotensive Wistar Kyoto rat (WKY; N = 5) caudal artery strips. An electromagnetic muscle lever was employed in recording force–velocity data. Analysis of these data revealed the following: (a) the SHR mean Po of 6.21 ± 1.01 N/cm2 was not different from the mean WKY Po of 6.97 ± 1.64 N/cm2 (p > 0.05); (b) the SHR preparations showed greater shortening for all loads imposed; (c) the SHR Vmax of 0.016 lo/s was greater than the WKY Vmax of 0.013 lo/s (p < 0.05). This study provides evidence that while hypertensive arterial smooth muscle is not able to produce more force than normotensive arterial smooth muscle, it is capable of faster and greater shortening. The latter could result in increased narrowing of hypertensive arteries and increased blood pressure.

Changes of tracheal smooth muscle stiffness during an isotonic contraction

1989 ◽  
Vol 256 (2) ◽  
pp. C341-C350 ◽  
Author(s):  
C. Y. Seow ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Muscle Length ◽  
Fixed Time ◽  
Isometric Tension ◽  
Muscle Stiffness ◽  
Tracheal Smooth Muscle ◽  
Isotonic Contraction ◽  
Small Force ◽  
Cross Bridges ◽  
Contraction And Relaxation

Stiffness of the series elastic component (SEC) of canine tracheal smooth muscle in isotonic contraction and relaxation was measured by applying small force perturbations to the muscle and measuring the resulting length perturbations. The quick, elastic length transient was taken as the change in length of the SEC (delta L). The force perturbation was a train of 10-Hz rectangular force waves varying from 0 to 10% maximum isometric tension (Po) in magnitude (delta P = 10% Po). Stiffness of the SEC was estimated by the ratio delta P/delta L. The change in SEC stiffness with respect to the change in muscle length was further studied by obtaining the stress-strain curves of the SEC at different muscle lengths using the load-clamping method. The clamps were applied at a fixed time (10 s after stimulation). Length of the muscle 10 s after contraction was controlled by the magnitude of the isotonic afterload. It was found that the apparent SEC stiffness increased as muscle length decreased. This stiffness increase is not likely due to an increase in the number of attached cross bridges, but it is probably due to the gradual diminution of the SEC length itself during muscle shortening.

Effects of load and tone on the mechanics of isolated human bronchial smooth muscle

1999 ◽  
Vol 86 (2) ◽  
pp. 488-495 ◽  
Author(s):  
François-Xavier Blanc ◽  
Sergio Salmeron ◽  
Catherine Coirault ◽  
Martin Bard ◽  
Elie Fadel ◽  
...  
Keyword(s):  
Smooth Muscles ◽  
Muscle Length ◽  
Isometric Tension ◽  
Shortening Velocity ◽  
Bronchial Smooth Muscle ◽  
Tension Development ◽  
Resting Tension ◽  
Muscle Shortening ◽  
Baseline Values ◽  
Cross Bridges

Isotonic and isometric properties of nine human bronchial smooth muscles were studied under various loading and tone conditions. Freshly dissected bronchial strips were electrically stimulated successively at baseline, after precontraction with 10−7 M methacholine (MCh), and after relaxation with 10−5 M albuterol (Alb). Resting tension, i.e., preload determining optimal initial length ( L o) at baseline, was held constant. Compared with baseline, MCh decreased muscle length to 93 ± 1% L o( P < 0.001) before any electrical stimulation, whereas Alb increased it to 111 ± 3% L o( P < 0.01). MCh significantly decreased maximum unloaded shortening velocity (0.045 ± 0.007 vs. 0.059 ± 0.007 L o/s), maximal extent of muscle shortening (8.4 ± 1.2 vs. 13.9 ± 2.4% L o), and peak isometric tension (6.1 ± 0.8 vs. 7.2 ± 1.0 mN/mm2). Alb restored all these contractile indexes to baseline values. These findings suggest that MCh reversibly increased the number of active actomyosin cross bridges under resting conditions, limiting further muscle shortening and active tension development. After the electrically induced contraction, muscles showed a transient phase of decrease in tension below preload. This decrease in tension was unaffected by afterload levels but was significantly increased by MCh and reduced by Alb. These findings suggest that the cross bridges activated before, but not during, the electrically elicited contraction may modulate the phase of decrease in tension below preload, reflecting the active part of resting tension.

Activation in frog atrial trabeculae: dependence on temperature and length

1990 ◽  
Vol 258 (4) ◽  
pp. H1087-H1096
Author(s):  
P. J. Reiser ◽  
B. D. Lindley
Keyword(s):  
Stimulus Frequency ◽  
Muscle Length ◽  
Initial Increase ◽  
Initial Tension ◽  
Tension Development ◽  
Temperature Jumps ◽  
Rapid Temperature ◽  
Tension Increase ◽  
Cross Bridges ◽  
Tension Transients

Isolated frog atrial trabeculae were activated using the method of Na+ withdrawal to induce contractures of relatively steady tension. External Na+ concentration [( Na+]o) during contractures was varied between 0.25 and 45 mM. Isometric contracture tension was measured at cold (4 degrees C) and warm (20 degrees C) temperatures. In addition, rapid temperature jumps (complete in approximately 400 ms) were imposed during cold contractures, resulting in tension transients that consisted of an initial increase in tension followed by a decrease, the latter phase being greater at small and moderate reductions in [Na+]o. Peak contracture tension varied with relative muscle length. The trabeculae became more sensitive with stretch to Na+ withdrawal at 20 degrees C and generated relatively greater tensions at a given [Na+]o. The initial tension increase after a temperature jump was directly proportional to the peak contracture tension immediately preceding the increase in temperature and was therefore interpreted as reflecting an effect of the higher temperature on the attached force-generating cross bridges. The effects of cold and warm steady temperatures and temperature jumps during isometric twitches were also studied. Peak twitch tension varied inversely with temperature (stimulus frequency = 0.2 Hz). In contrast, temperature jumps imposed during the rising phase of twitches at a steady cold temperature (approximately 4 degrees C) resulted in a large initial increase in tension followed by relaxation at a rate that was characteristic of the elevated temperature. The results suggest that, at the warmer temperature (approximately 20 degrees C), activation (i.e., number of attached cross bridges) of the myocardium is significantly less than maximal during the twitch response. The dependence of the tension vs. [Na+]o curves and the tension transients resulting from the temperature jumps on relative muscle length provide evidence for a length dependency of contractile activation in intact atrial trabeculae under conditions of steady-state tension development.

Muscle shortening increases sensitivity of fatigue to severe hypoxia in canine diaphragm

1991 ◽  
Vol 71 (6) ◽  
pp. 2309-2316 ◽  
Author(s):  
B. T. Ameredes ◽  
M. W. Julian ◽  
T. L. Clanton
Keyword(s):  
Flow Characteristics ◽  
Muscle Length ◽  
Isometric Tension ◽  
Severe Hypoxia ◽  
Mean Power ◽  
Tension Development ◽  
Moderate Hypoxia ◽  
O2 Supply ◽  
Mean Power Output

The effects of inspired O2 on diaphragm tension development during fatigue were assessed using isovelocity (n = 6) and isometric (n = 6) muscle contractions performed during a series of exposures to moderate hypoxia [fraction of inspired O2 (FIO2) = 0.13], hyperoxia (FIO2 = 1), and severe hypoxia (FIO2 = 0.09). Muscle strips were created in situ from the canine diaphragm, attached to a linear ergometer, and electrically stimulated (30 Hz) to contract (contraction = 1.5 s/relaxation = 2 s) from optimal muscle length (Lo = 8.9 cm). Isovelocity contractions shortened to 0.70 Lo, resulting in a mean power output of 210 mW/cm2. Fatigue trials of 35 min duration were performed while inspired O2 was sequentially changed between the experimental mixtures and normoxia (FIO2 = 0.21) for 5-min periods. In this series, severe hypoxia consistently decreased isovelocity tension development by an average of 0.1 kg/cm2 (P less than 0.05), which was followed by a recovery of tension (P less than 0.05) on return to normoxia. These responses were not consistently observed in isometric trials. Neither isovelocity nor isometric tension development was influenced by moderate hypoxia or hyperoxia. These results demonstrate that the in situ diaphragm is relatively insensitive to rapid changes in O2 supply over a broad range and that the tension development of the shortening diaphragm appears to be more susceptible to severe hypoxia during fatigue. This may reflect a difference in either the metabolic or blood flow characteristics of shortening contractions of the diaphragm.

scholarly journals Series-to-parallel transition in the filament lattice of airway smooth muscle

2000 ◽  
Vol 89 (3) ◽  
pp. 869-876 ◽  
Author(s):  
Chun Y. Seow ◽  
Victor R. Pratusevich ◽  
Lincoln E. Ford
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Length ◽  
Thick Filament ◽  
Cycling Rate ◽  
Cross Bridge ◽  
Parallel Change ◽  
Force Velocity ◽  
Cross Bridges ◽  
Trachealis Muscle

Force-velocity curves measured at different times during tetani of sheep trachealis muscle were analyzed to assess whether velocity slowing could be explained by thick-filament lengthening. Such lengthening increases force by placing more cross bridges in parallel on longer filaments and decreases velocity by reducing the number of filaments spanning muscle length. From 2 s after the onset of stimulation, when force had achieved 42% of it final value, to 28 s, when force had been at its tetanic plateau for ∼15 s, velocity decreases were exactly matched by force increases when force was adjusted for changes in activation, as assessed from the maximum power value in the force-velocity curves. A twofold change in velocity could be quantitatively explained by a series-to-parallel change in the filament lattice without any need to postulate a change in cross-bridge cycling rate.

Yersinia enterocolitica enteritis affects rabbit intestinal longitudinal smooth muscle function

1992 ◽  
Vol 262 (2) ◽  
pp. G278-G284 ◽  
Author(s):  
R. B. Scott ◽  
D. T. Tan
Keyword(s):  
Smooth Muscle ◽  
Weight Gain ◽  
Food Intake ◽  
Yersinia Enterocolitica ◽  
Biomechanical Properties ◽  
Isometric Tension ◽  
Infected Group ◽  
Tension Development ◽  
Longitudinal Smooth Muscle ◽  
Tension Curves

To determine whether Yersinia enterocolitica (YE) enteritis has an effect on the biomechanical properties of intestinal smooth muscle, New Zealand White rabbits (600-900 g) were divided into an infected group (n = 9) and sham-infected animals fed ad libitum (n = 9), or pair fed with the infected group (n = 9). Animals were inoculated with 10(10) organisms of YE in 10 ml NaHCO3 (infected group) or 10 ml NaHCO3 (sham-infected control and pair-fed groups) at time 0. Daily food intake, weight gain, and YE excretion were noted. Six days later animals were killed and longitudinal smooth muscle strips prepared from proximal (P), medial (M), and distal (D) segments of intestine in each treatment group. Isometric tension was recorded in tissue baths perfused with oxygenated Krebs solution and 10(-6) M tetrodotoxin. Basal and active (the response to 10(-5) M carbachol) length-tension curves were generated. Then, with the muscle strips stretched to their optimum length for tension development, the dose response to carbachol and to graded depolarization with KCl was determined. Infected animals had a significantly reduced food intake and weight gain compared with controls. The development of basal tension with stretch was not significantly different in infected compared with control or pair-fed tissues from the same site.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium effects on contractility and heat production in mammalian myocardium

1986 ◽  
Vol 251 (1) ◽  
pp. H127-H132 ◽  
Author(s):  
J. E. Ponce-Hornos ◽  
A. C. Taquini
Keyword(s):  
Papillary Muscle ◽  
Heat Production ◽  
Muscle Length ◽  
Heat Rate ◽  
Isometric Tension ◽  
Tension Development ◽  
Contractile System ◽  
Dimensionless Ratio ◽  
Calcium Effects ◽  
Mammalian Myocardium

The effects of changing external Ca concentration ([Ca]o) on contractile parameters and heat production were investigated in the interventricular rabbit septa and the dog papillary muscle. Double reciprocal plots of tension development as a function of [Ca]o yielded half-maximal activation values of 1.04 +/- 0.17 and 2.8 +/- 0.7 mM Ca for the septum and papillary muscle, respectively. Resting heat rate was similar in both preparations, 1.9 +/- 0.08 mW . g-1 for the septum and 1.7 +/- 0.07 mW . g-1 for the papillary muscle, and it was not altered by changes in [Ca]o. Active heat production (Ha) normalized per unit of force developed (19 +/- 1.3 microJ . mN-1 . g-1) for the septum and the dimensionless ratio Ha/(To . lo), (0.30 +/- 0.02) for the papillary muscle, where To is the isometric tension and lo, the muscle length, remained unaltered with changes in [Ca]o. Total heat production per beat normalized per unit of force developed (Ht/T) for the septum and the ratio Ht/(To . lo) for the papillary muscle decreased hyperbolically with [Ca]o. Therefore, as a result of the unaltered economy of the contractile system and the unchanged resting heat rate, muscle economy improves as [Ca]o approaches physiological levels. Further increase in [Ca]o, over the physiological levels, can only slightly improve muscle economy.

Dynamic stiffness of rabbit mesotubarium smooth muscle: effect of isometric length

1978 ◽  
Vol 234 (1) ◽  
pp. C14-C26 ◽  
Author(s):  
R. A. Meiss
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
Dynamic Stiffness ◽  
Muscle Tension ◽  
Muscle Length ◽  
Isometric Tension ◽  
Published Data ◽  
Tension Level ◽  
Tension Peak ◽  
Nonpregnant Adult

The dynamic stiffness of mesotubarium smooth muscle from nonpregnant adult rabbits was measured continuously during isometric contraction by applying small (0.5 percent of the muscle length) sinusoidal length perturbations and measuring the amplitude and phase of the resulting tension perturbations. Stiffness during contraction was directly proportional to muscle tension; during relaxation stiffness at all tensions was significantly increased as compared to the values encountered during the rise of tension. Peak isometric tension and dynamic stiffness (determined at a common tension level) both decreased at shorter muscle lengths; the relative falloff in stiffness was significantly less than the tension decrease. Varying levels of muscle activation (obtained by changing stimulus strength and by applying quick releases to active muscle) had little effect on the measured elastic modulus. Comparisons of these results with published data on single-cell contractile properties imply a cellular locus for a portion of the measured stiffness.

scholarly journals Could an increase in airway smooth muscle shortening velocity cause airway hyperresponsiveness?

2011 ◽  
Vol 300 (1) ◽  
pp. L121-L131 ◽  
Author(s):  
Sharon R. Bullimore ◽  
Sana Siddiqui ◽  
Graham M. Donovan ◽  
James G. Martin ◽  
James Sneyd ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Isometric Force ◽  
Muscle Length ◽  
Shortening Velocity ◽  
Bridge Model ◽  
Generating Capacity ◽  
Cross Bridges

Airway hyperresponsiveness (AHR) is a characteristic feature of asthma. It has been proposed that an increase in the shortening velocity of airway smooth muscle (ASM) could contribute to AHR. To address this possibility, we tested whether an increase in the isotonic shortening velocity of ASM is associated with an increase in the rate and total amount of shortening when ASM is subjected to an oscillating load, as occurs during breathing. Experiments were performed in vitro using 27 rat tracheal ASM strips supramaximally stimulated with methacholine. Isotonic velocity at 20% isometric force (Fiso) was measured, and then the load on the muscle was varied sinusoidally (0.33 ± 0.25 Fiso, 1.2 Hz) for 20 min, while muscle length was measured. A large amplitude oscillation was applied every 4 min to simulate a deep breath. We found that: 1) ASM strips with a higher isotonic velocity shortened more quickly during the force oscillations, both initially ( P < 0.001) and after the simulated deep breaths ( P = 0.002); 2) ASM strips with a higher isotonic velocity exhibited a greater total shortening during the force oscillation protocol ( P < 0.005); and 3) the effect of an increase in isotonic velocity was at least comparable in magnitude to the effect of a proportional increase in ASM force-generating capacity. A cross-bridge model showed that an increase in the total amount of shortening with increased isotonic velocity could be explained by a change in either the cycling rate of phosphorylated cross bridges or the rate of myosin light chain phosphorylation. We conclude that, if asthma involves an increase in ASM velocity, this could be an important factor in the associated AHR.

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