Plasticity in airway smooth muscle: an update

2005 ◽  
Vol 83 (10) ◽  
pp. 841-850 ◽  
Author(s):  
Lincoln E Ford
Keyword(s):  
Muscle Activation ◽  
Smooth Muscles ◽  
Muscle Length ◽  
Thick Filament ◽  
Myosin Filament ◽  
Shortening Velocity ◽  
Tetanic Force ◽  
Substantial Body ◽  
In Series ◽  
Mass Increase

At a similar meeting 10 years ago, we proposed (i) that the long functional range of some smooth muscles is accommodated by plastic alterations that place more myofilaments in series at longer lengths, (ii) that this plasticity is facilitated by myosin filament evanescence, with filaments dissociating partially during relaxation and reforming upon activation, and (iii) that filament lengthening during the rise of activation would cause velocity to fall. Since that meeting, we have accumulated a substantial body of evidence to support these proposals, as follows: (i) muscles develop nearly the same force when adapted to a range of lengths that can vary by 3-fold; (ii) other physiological parameters including shortening velocity, maximum power, compliance, ATPase rate, and thick-filament mass increase by about 2/3 for a doubling of muscle length; (iii) thick-filament density increases substantially during the rise of activation; and (iv) velocity falls as force rises during the rise of tetanic force, and when correction is made for differences in activation, velocity and force vary exactly in inverse proportion. This review explains the rationale for the different experimental measurements and their interpretation.Key words: muscle activation, series-to-parallel transition, myofilaments, myosin.

The EMG-force relationship of the cat soleus muscle and its association with contractile conditions during locomotion.

1995 ◽  
Vol 198 (4) ◽  
pp. 975-987 ◽  
Author(s):  
A C Guimaraes ◽  
W Herzog ◽  
T L Allinger ◽  
Y T Zhang
Keyword(s):  
Soleus Muscle ◽  
Adaptive Filtering ◽  
Muscle Activation ◽  
Stance Phase ◽  
Force Production ◽  
Muscle Length ◽  
Force Transducer ◽  
Shortening Velocity ◽  
Integrated Emg ◽  
Filtering Approach

The relationship between force and electromyographic (EMG) signals of the cat soleus muscle was obtained for three animals during locomotion at five different speeds (154 steps), using implanted EMG electrodes and a force transducer. Experimentally obtained force-IEMG (= integrated EMG) relationships were compared with theoretically predicted instantaneous activation levels calculated by dividing the measured force by the predicted maximal force that the muscle could possibly generate as a function of its instantaneous contractile conditions. In addition, muscular forces were estimated from the corresponding EMG records exclusively using an adaptive filtering approach. Mean force-IEMG relationships were highly non-linear but similar in shape for different cats and different speeds of locomotion. The theoretically predicted activation-time plots typically showed two peaks, as did the IEMG-time plots. The first IEMG peak tended to be higher than the second one and it appeared to be associated with the initial priming of the muscle for force production at paw contact and the peak force observed early during the stance phase. The second IEMG peak appeared to be a burst of high muscle activation, which might have compensated for the levels of muscle length and shortening velocity that were suboptimal during the latter part of the stance phase. Although it was difficult to explain the soleus forces on the basis of the theoretically predicted instantaneous activation levels, it was straightforward to approximate these forces accurately from EMG data using an adaptive filtering approach.

Models of contractile units and their assembly in smooth muscle

2005 ◽  
Vol 83 (10) ◽  
pp. 825-831 ◽  
Author(s):  
Farah Ali ◽  
Peter D Paré ◽  
Chun Y Seow
Keyword(s):  
Smooth Muscle ◽  
Striated Muscle ◽  
Dense Body ◽  
Unit Length ◽  
Muscle Length ◽  
Thick Filament ◽  
Contractile Apparatus ◽  
Thin Filaments ◽  
Dense Bodies ◽  
In Series

It is believed that the contractile filaments in smooth muscle are organized into arrays of contractile units (similar to the sarcomeric structure in striated muscle), and that such an organization is crucial for transforming the mechanical activities of actomyosin interaction into cell shortening and force generation. Details of the filament organization, however, are still poorly understood. Several models of contractile filament architecture are discussed here. To account for the linear relationship observed between the force generated by a smooth muscle and the muscle length at the plateau of an isotonic contraction, a model of contractile unit is proposed. The model consists of 2 dense bodies with actin (thin) filaments attached, and a myosin (thick) filament lying between the parallel thin filaments. In addition, the thick filament is assumed to span the whole contractile unit length, from dense body to dense body, so that when the contractile unit shortens, the amount of overlap between the thick and thin filaments (i.e., the distance between the dense bodies) decreases in exact proportion to the amount of shortening. Assembly of the contractile units into functional contractile apparatus is assumed to involve a group of cells that form a mechanical syncytium. The contractile apparatus is assumed malleable in that the number of contractile units in series and in parallel can be altered to accommodate strains on the muscle and to maintain the muscle's optimal mechanical function.Key words: contraction model, ultrastructure, length adaptation, plasticity.

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.

Work-dependent deactivation of a crustacean muscle

1999 ◽  
Vol 202 (18) ◽  
pp. 2551-2565 ◽  
Author(s):  
R.K. Josephson ◽  
D.R. Stokes
Keyword(s):  
Muscle Activation ◽  
Isometric Force ◽  
Carcinus Maenas ◽  
Stimulus Frequency ◽  
Force Production ◽  
Muscle Length ◽  
Background Level ◽  
Shortening Velocity ◽  
Shortening Deactivation ◽  
Work Done

Active shortening of respiratory muscle L2B from the crab Carcinus maenas results in contractile deactivation, seen as (1) a decline of force during the course of isovelocity shortening, (2) a reduction in the rate of force redevelopment following shortening, (3) a depression of the level of isometric force reached following shortening, and (4) an accelerated relaxation at the end of stimulation. The degree of deactivation increases with increasing distance of shortening, decreases with increasing shortening velocity, and is approximately linearly related to the work done during shortening. Deactivation lasts many seconds if stimulation is maintained, but is largely although not completely removed if the stimulation is temporarily interrupted so that the force drops towards the resting level. Deactivation for a given distance and velocity of shortening increases with increasing muscle length above the optimum length for force production. Stimulating muscle L2B at suboptimal frequencies gives tetanic contractions that are fully fused but of less than maximal amplitude. The depression of force following shortening, relative to the force during an isometric contraction, is independent of the stimulus frequency used to activate the muscle, indicating that deactivation is not a function of the background level of stimulus-controlled muscle activation upon which it occurs. Deactivation reduces the work required to restretch a muscle after it has shortened, but it also lowers the force and therefore the work done during shortening. The net effect of deactivation on work output over a full shortening/lengthening cycle is unknown.

Plasticity in smooth muscle, a hypothesis

1994 ◽  
Vol 72 (11) ◽  
pp. 1320-1324 ◽  
Author(s):  
Lincoln E. Ford ◽  
Chun Y. Seow ◽  
Victor R. Pratusevich
Keyword(s):  
Smooth Muscle ◽  
Preliminary Finding ◽  
Muscle Length ◽  
Shortening Velocity ◽  
Thin Filaments ◽  
Thick Filaments ◽  
Initial Hypothesis ◽  
In Series ◽  
Cross Bridges ◽  
Muscle Myosin

The controversial finding that the thick filaments of smooth muscle can be evanescent leads to the hypothesis that the large functional range of this muscle is accommodated by plastic rearrangements that place more thick filaments in series at longer lengths. Our preliminary finding that the shortening velocity and compliance of dog tracheal muscle were strongly dependent on adapted muscle length, while force was much less length dependent, supports this hypothesis (V.R. Pratusevich, C.Y. Seow, and L.E. Ford. Biophys. J. 66: A139, 1994). The hypothesis leads to two further corollaries. The first is that the lengthening of the thick filaments that must accompany their reformation will cause a series to parallel transition: fewer long filaments span the muscle length, but the longer filaments have more cross bridges acting in parallel. The second is that there is more than one activating mechanism in smooth muscle. It is known that myosin light chain phosphorylation activates the actomyosin ATPase, but this same phosphorylation also causes a structural change that facilitates filament formation. The consideration that the unaggregated, phosphorylated myosin must be prevented from competing with myosin in thick filaments and hydrolyzing ATP suggests that there must be a second mechanism that must allow the thin filaments to interact selectively with filamentous myosin. This need for a second activating mechanism may explain the presence of tropomyosin, calponin, and caldesmon on thin filaments. Although the two corollaries follow from the initial hypothesis, it should be emphasized that the three are not mutually dependent, and that the proof or disproof of any one of them would not prove or disprove the others.Key words: smooth muscle, myosin, thick filaments, contraction.

Influence of calcium on myosin thick filament formation in intact airway smooth muscle

2002 ◽  
Vol 282 (2) ◽  
pp. C310-C316 ◽  
Author(s):  
Ana M. Herrera ◽  
Kuo-Hsing Kuo ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Calcium Level ◽  
Muscle Activation ◽  
Isometric Force ◽  
Smooth Muscles ◽  
Thick Filament ◽  
Filament Formation ◽  
Cross Sectional ◽  
Thick Filaments

Myosin thick filaments have been shown to be structurally labile in intact smooth muscles. Although the mechanism of thick filament assembly/disassembly for purified myosins in solution has been well described, regulation of thick filament formation in intact muscle is still poorly understood. The present study investigates the effect of resting calcium level on thick filament maintenance in intact airway smooth muscle and on thick filament formation during activation. Cross-sectional density of the thick filaments measured electron microscopically showed that the density increased substantially (144%) when the muscle was activated. The abundance of filamentous myosins in relaxed muscle was calcium sensitive; in the absence of calcium (with EGTA), the filament density deceased by 35%. Length oscillation imposed on the muscle under zero-calcium conditions produced no further reduction in the density. Isometric force and filament density recovered fully after reincubation of the muscle in normal physiological saline. The results suggest that in airway smooth muscle, filamentous myosins exist in equilibrium with monomeric myosins; muscle activation favors filament formation, and the resting calcium level is crucial for preservation of the filaments in the relaxed state.

Structure-function correlation in airway smooth muscle adapted to different lengths

2003 ◽  
Vol 285 (2) ◽  
pp. C384-C390 ◽  
Author(s):  
Kuo-Hsing Kuo ◽  
Ana M. Herrera ◽  
Lu Wang ◽  
Peter D. Paré ◽  
Lincoln E. Ford ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Power ◽  
Isometric Force ◽  
Muscle Length ◽  
Length Change ◽  
Cell Length ◽  
Myosin Filament ◽  
Shortening Velocity ◽  
Cross Sectional

Airway smooth muscle is able to adapt and maintain a nearly constant maximal force generation over a large length range. This implies that a fixed filament lattice such as that found in striated muscle may not exist in this tissue and that plastic remodeling of its contractile and cytoskeletal filaments may be involved in the process of length adaptation that optimizes contractile filament overlap. Here, we show that isometric force produced by airway smooth muscle is independent of muscle length over a twofold length change; cell cross-sectional area was inversely proportional to cell length, implying that the cell volume was conserved at different lengths; shortening velocity and myosin filament density varied similarly to length change: increased by 69.4% ± 5.7 (SE) and 76.0% ± 9.8, respectively, for a 100% increase in cell length. Muscle power output, ATPase rate, and myosin filament density also have the same dependence on muscle cell length: increased by 35.4% ± 6.7, 34.6% ± 3.4, and 35.6% ± 10.6, respectively, for a 50% increase in cell length. The data can be explained by a model in which additional contractile units containing myosin filaments are formed and placed in series with existing contractile units when the muscle is adapted at a longer length.

Time course of isotonic shortening and the underlying contraction mechanism in airway smooth muscle

2011 ◽  
Vol 111 (3) ◽  
pp. 642-656 ◽  
Author(s):  
Harley T. Syyong ◽  
Abdul Raqeeb ◽  
Peter D. Paré ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Time Course ◽  
Muscle Activation ◽  
Striated Muscle ◽  
Myosin Filament ◽  
Disk Model ◽  
In Series ◽  
Force Velocity ◽  
Power Law Creep ◽  
Isotonic Shortening

Although the structure of the contractile unit in smooth muscle is poorly understood, some of the mechanical properties of the muscle suggest that a sliding-filament mechanism, similar to that in striated muscle, is also operative in smooth muscle. To test the applicability of this mechanism to smooth muscle function, we have constructed a mathematical model based on a hypothetical structure of the smooth muscle contractile unit: a side-polar myosin filament sandwiched by actin filaments, each attached to the equivalent of a Z disk. Model prediction of isotonic shortening as a function of time was compared with data from experiments using ovine tracheal smooth muscle. After equilibration and establishment of in situ length, the muscle was stimulated with ACh (100 μM) until force reached a plateau. The muscle was then allowed to shorten isotonically against various loads. From the experimental records, length-force and force-velocity relationships were obtained. Integration of the hyperbolic force-velocity relationship and the linear length-force relationship yielded an exponential function that approximated the time course of isotonic shortening generated by the modeled sliding-filament mechanism. However, to obtain an accurate fit, it was necessary to incorporate a viscoelastic element in series with the sliding-filament mechanism. The results suggest that a large portion of the shortening is due to filament sliding associated with muscle activation and that a small portion is due to continued deformation associated with an element that shows viscoelastic or power-law creep after a step change in force.

Filament lattice changes in smooth muscle assessed using birefringence

2005 ◽  
Vol 83 (10) ◽  
pp. 933-940 ◽  
Author(s):  
A V Smolensky ◽  
L E Ford
Keyword(s):  
Smooth Muscle ◽  
Time Course ◽  
Structural Changes ◽  
Thick Filament ◽  
Myosin Filament ◽  
Filament Formation ◽  
Tension Development ◽  
Thick Filaments ◽  
Contractile Parameters ◽  
In Series

The long functional range of some types of smooth muscle has been the subject of recent study. It has been proposed that the muscle filament lattice adapts to longer lengths by placing more filaments in series and that lattice plasticity is facilitated by myosin filament evanescence, with filaments dissociating during relaxation and reforming upon activation. Support for these dynamic changes in the filament lattice has been provided partly by changes in contractile parameters at different times in the contraction–relaxation cycle at different lengths. If the changes in contractile parameters result from filament formation and dissociation, these structural changes must occur on the time scale of tension development and relaxation. To assess whether thick-filament formation could account for the contractile changes, we measured birefringence continuously during activation and relaxation and compared these optical changes with the time course of force development and relaxation. Birefringence is a well-known property of muscle; striations in skeletal and cardiac muscle result from the A-bands being anisotropic, i.e., birefringent, and it is now known that this optical property is due to the presence of myosin thick filaments in the A-bands. Thus, the strength of birefringence is expected to represent the density of thick filaments. Here, we describe the principle of the method, the techniques for recording the optical signals, some initial results, and discuss the interpretation of results and some limitations of the method.Key words: airway smooth muscle, myosin filament, plasticity.

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.

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