Muscle Length Adaptation Research Articles

Length adaptation of smooth muscle contractile filaments in response to sustained activation

Airway and bladder smooth muscles are known to undergo length adaptation under sustained contraction. This adaptation process entails a remodelling of the intracellular actin and myosin filaments which shifts the peak of the active force–length curve towards the current length. Smooth muscles are therefore able to generate the maximum force over a wide range of lengths. In contrast, length adaptation of vascular smooth muscle has attracted very little attention and only a handful of studies have been reported. Although their results are conflicting on the existence of a length adaptation process in vascular smooth muscle, it seems that, at least, peripheral arteries and arterioles undergo such adaptation. This is of interest since peripheral vessels are responsible for pressure regulation, and a length adaptation will affect the function of the cardiovascular system. It has, e.g., been suggested that the inward remodelling of resistance vessels associated with hypertension disorders may be related to smooth muscle adaptation. In this study we develop a continuum mechanical model for vascular smooth muscle length adaptation by assuming that the muscle cells remodel the actomyosin network such that the peak of the active stress–stretch curve is shifted towards the operating point. The model is specialised to hamster cheek pouch arterioles and the simulated response to stepwise length changes under contraction. The results show that the model is able to recover the salient features of length adaptation reported in the literature.

Responses of Medial Rectus Motoneurons in Monkeys with Strabismus

Monkeys reared under conditions of alternating monocular occlusion during their first few months of life show large horizontal strabismus, "A" patterns, and dissociated vertical deviation. "A" patterns manifest as an inappropriate horizontal component in the deviated eye during vertical eye movements (cross-axis movement). The objective of this study was to investigate response properties of medial rectus motoneurons (MRMNs) in relation to strabismus properties. Burst-tonic activity of 21 MRMNs in the oculomotor nucleus were recorded from two monkeys with exotropia as they performed horizontal and vertical smooth pursuit (0.2 Hz, ±10°) under monocular viewing conditions. Neuronal responses and horizontal component of eye movements were used to identify regression coefficients in a first-order model for each tracking condition. Comparison of position, velocity, and constant parameter coefficients, estimated from horizontal tracking data with either eye viewing, showed no significant differences (P > 0.07), indicating that neuronal activity could account for the horizontal misalignment. Comparison of the position, velocity, and constant parameter coefficients estimated from horizontal tracking and the cross-axis condition showed no significant differences (P > 0.07), suggesting that motoneuron activity could account for most of the inappropriate horizontal cross-axis movement observed in the covered eye during vertical smooth pursuit. These data suggest that, in animals with sensory-induced strabismus, central innervation to extraocular muscles is responsible for setting the state of strabismus. Mechanical factors such as muscle length adaptation (for horizontal misalignment) and pulley heterotopy or static torsion (for "A" patterns) likely do not play a major role in determining properties in a sensory-induced strabismus.

COX Inhibitors and Overactive Bladder: The Potential for Future Therapy

Studies spanning four decades suggest that prostaglandins (PGs) are synthesized at high levels within the bladder by cyclooxygenase (COX)-1 and COX-2 and that PG biosynthesis during bladder filling provides a non-neuronal vesicular volume signal. Evidence is presented that interstitial cells of Cajal within the bladder seem to play a key role in PG biosynthesis, that bladder PG concentration is a function of the degree of bladder wall stretch, and that PGs serve to 1) assist in detrusor smooth muscle length adaptation of tension during bladder storage by permitting synchronized spontaneous rhythmic contraction, 2) positively modulate sensory recognition of the bladder fill state, and 3) enhance voiding contraction. Provocative clinical and experimental data support a role for PGs in overactive bladder, but the data are of limited scope. Additional studies are needed to clarify the roles played by mechanical stretch, COX isotypes, PG species and receptor subtypes, and cell-to-cell communication in bladder biology.

Esotropia Associated With Early Presbyopia Caused by Inappropriate Muscle Length Adaptation

The purpose of this study is to investigate the occurrence of esotropia accompanying early presbyopia. The two primary long-term mechanisms for maintenance of ocular alignment are vergence adaptation (neurologic) and muscle length adaptation (anatomic). Both mechanisms depend upon disparity-driven motor fusion for proper operation. A possible cause for an esotropic shift in early presbyopic adults with insufficient or absent disparity-driven motor fusion is inappropriate muscle length adaptation (medial rectus muscle shortening) occurring in response to increased convergence tonus accompanying increased accommodative effort. Of 617 patients, age 10 and older who underwent surgery for esotropia during the period of 1980 to 1996, the age when the deviation occurred or worsened could be determined with confidence in 140. A plot was made of the number of these patients versus the age of onset of the deviation. This was compared with a similar plot of patients operated for exotropia. A statistically significant increase (P = 0.017) in the incidence of an esotropic shift in the age range from 30 to 50 years was found when compared with the incidence of an exotropic shift. If the postulated mechanism is correct, full correction of any hyperopia as well as prompt prescription of a reading add (or conversion to monovision correction) may help prevent further progression of small esodeviations accompanying early presbyopia.

Mechanical plasticity and contractile properties of airway smooth muscle

Smooth muscle has the unique ability to adapt easily and quickly to length changes without compromising its ability to generate force. This ability is referred to as mechanical plasticity and is now considered to be an important aspect of smooth muscle that affects both its contractile and relaxation behaviour. It is therefore important to incorporate knowledge of plasticity into further studies of smooth muscle behaviour. It is also important that future studies be focused on deciphering the mechanism of smooth muscle length adaptation and plasticity. This review outlines some of the proposed mechanisms determining plasticity. However, it should be said that there are other proposed mechanisms not touched upon here, which may be equally as important. This review also focuses on the relevance of smooth muscle plasticity in asthma, but it is important to remember that there are other places where smooth muscle plasticity may play an equally important role.

Smooth muscle length adaptation and actin filament length: a network model of the cytoskeletal dysregulation

Length adaptation of the airway smooth muscle cell is attributable to cytoskeletal remodeling. It has been proposed that dysregulated actin filaments may become longer in asthma, and that such elongation would prevent a parallel-to-series transition of contractile units, thus precluding the well-known beneficial effects of deep inspirations and tidal breathing. To test the potential effect that actin filament elongation could have in overall muscle mechanics, we present an extremely simple model. The cytoskeleton is represented as a 2-D network of links (contractile filaments) connecting nodes (adhesion plaques). Such a network evolves in discrete time steps by forming and dissolving links in a stochastic fashion. Links are formed by idealized contractile units whose properties are either those from normal or elongated actin filaments. Oscillations were then imposed on the network to evaluate both the effects of breathing and length adaptation. In response to length oscillation, a network with longer actin filaments showed smaller decreases of force, smaller increases in compliance, and higher shortening velocities. Taken together, these changes correspond to a network that is refractory to the effects of breathing and therefore approximates an asthmatic scenario. Thus, an extremely simple model seems to capture some relatively complex mechanics of airway smooth muscle, supporting the idea that dysregulation of actin filament length may contribute to excessive airway narrowing.

Length adaptation of airway smooth muscle: a stochastic model of cytoskeletal dynamics

To account for cytoskeleton remodeling as well as smooth muscle length adaptation, here we represent the cytoskeleton as a two-dimensional network of links (contractile filaments or stress fibers) that connect nodes (dense plaques or focal adhesions). The network evolves in continuous turnover with probabilities of link formation and dissolution. The probability of link formation increases with the available fraction of contractile units, increases with the degree of network activation, and decreases with increasing distance between nodes, d, as 1/d(s), where s controls the distribution of link lengths. The probability of link dissolution decays with time to mimic progressive cytoskeleton stabilization. We computed network force (F) as the vector summation of link forces exerted at all nodes, unloaded shortening velocity (V) as being proportional to the average link length, and network compliance (C) as the change in network length per change in elastic force. Imposed deformation caused F to decrease transiently and then recover dynamically; recovery ability decreased with increasing time after activation, mimicking observed biological behavior. Isometric contractions showed small sensitivity of F to network length, thus maintaining high force over a wide range of lengths; V and C increased with increasing length. In these behaviors, link length regulation, as described by the parameter s, was found to be crucial. Concerning length adaptation, all phenomena reported thus far in the literature were captured by this extremely simple network model.

A computational model for the adaptation of muscle and tendon length to average muscle length and minimum tendon strain

This paper hypothesizes that average muscle length and minimum tendon strain govern muscle and tendon length adaptation in all situations. A model has been implemented to test this hypothesis, and simulations have been performed for normal development, bone lengthening, immobilization, and retinacular release experiments in young and adult animals. The simulation results predict that both muscle and tendon lengthen during normal development, with the rate of tendon growth slowing faster than the rate of muscle growth. The results also predict that muscle length increases during bone lengthening in both young and adult animals, while tendon length increases only in young animals. For immobilization in adult animals, the results predict that muscle length increases when the muscle is immobilized in a lengthened position and decreases when the muscle is immobilized in a shortened position with no change in tendon length. For immobilization in young animals, the results predict reduced muscle growth and increased tendon growth regardless of immobilization position. Finally, the simulations predict that retinacular release which increases excursion of the musculotendinous unit leads to increased muscle length with decreased tendon length in young animals and decreased muscle length with no change in tendon length in adult animals. These simulation results are consistent with experimental findings reported in the literature by other investigators. This suggests that average muscle length and minimum tendon strain may represent general principles that govern muscle and tendon length adaptation.

Functional load abdominal training: part 1

This article reviews the principles of muscle imbalance relevant to abdominal training. Mobilisor and stabilisor muscle categories are described and muscle length adaptation is discussed. Examples of individual muscle tests to determine muscle lengthening and muscle shortening are given. Concepts of trunk stability are considered and integrated into abdominal training.

Functional load abdominal training: part 1

This article reviews the principles of muscle imbalance relevant to abdominal training. Mobilisor and stabilisor muscle categories are described and muscle length adaptation is discussed. Examples of individual muscle tests to determine muscle lengthening and muscle shortening are given. Concepts of trunk stability are considered and integrated into abdominal training.