Modified Fading Memory Model to Describe ASM Dynamics

2007 ◽  
Author(s):  
Y. Du ◽  
A. M. Al-Jumaily
Keyword(s):  
Muscle Length ◽  
Length Change ◽  
Step Change ◽  
Memory Model ◽  
Fading Memory ◽  
Frequency Range ◽  
Cross Bridge ◽  
Muscle Dynamics ◽  
Biophysical Processes ◽  
The Cross

A modified fading memory model is introduced in this work to describe the behavior of airway smooth muscle dynamics. The model is used to simulate two biophysical cases: a finite duration for the step change in length and a case for external longitudinal oscillations. For both cases, the model describes the cross-bridge behaviour well and indicates that the muscle length change is the most important factor to determine the degree of cross-bridge detachment. However, the frequency of oscillation represents the velocity of the length change, which affects the cross-bridge cycling rate as reflected in the lower frequency range. The model is intended to interpret certain biophysical processes and not to accurately model the biophysical events underlying muscle contraction.

Relaxant effect of superimposed length oscillation on sensitized airway smooth muscle

2015 ◽  
Vol 308 (5) ◽  
pp. L479-L484 ◽  
Author(s):  
Miguel Jo-Avila ◽  
Ahmed M. Al-Jumaily ◽  
Jun Lu
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Smooth Muscles ◽  
Airway Hyperreactivity ◽  
Frequency Range ◽  
Relaxant Effect ◽  
Airway Lumen ◽  
Cross Bridge ◽  
The Cross

Asthma is associated with reductions in the airway lumen and breathing difficulties that are attributed to airway smooth muscles (ASM) hyperconstriction. Pharmaceutical bronchodilators such as salbutamol and isoproterenol are normally used to alleviate this constriction. Deep inspirations and tidal oscillations (TO) have also been reported to relax ASM in healthy airways with less response in asthmatics. Little information is available on the effect of other forms of oscillation on asthmatic airways. This study investigates the effect of length oscillations (LO), with amplitude 1 and 1.5% in the frequency range 5–20 Hz superimposed on breathing equivalent LO, on contracted ASM dissected from sensitized mice. These mice are believed to show some symptoms such as airway hyperreactivity similar to those associated with asthma in humans. In the frequency range used in this work, this study shows an increase in ASM relaxation of an average of 10% for 1.5% amplitude when compared with TO, ISO, or the combination of both. No similar finding is observed with 1% amplitude. This suggests that superimposed length oscillation acting over the interaction of myosin and actin during contraction may lead to temporal rearrangement and disturbance of the cross-bridge process in asthmatic airways.

Simplified Model for ASM Dynamics

2011 ◽  
Author(s):  
A. M. Al-Jumaily ◽  
Y. Du
Keyword(s):  
Dynamic Response ◽  
Finite Length ◽  
Smooth Muscles ◽  
Low Frequency ◽  
Length Change ◽  
Simplified Model ◽  
Frequency Range ◽  
Cycling Rate ◽  
Cross Bridge ◽  
Length Changes

The dynamic response of contracted airway smooth muscles to a finite length change and longitudinal oscillations is described using a simplified model. The model is intended to interpret the biophysical events but not to accurately describe them. It shows that the value of tissue length changes have pronounced indications of cross-bridge detachment. However, the frequency of oscillations represents the velocity of the length change, which affects the cross-bridge cycling rate reflected in the low frequency range.

scholarly journals Current Understanding of Residual Force Enhancement: Cross-Bridge Component and Non-Cross-Bridge Component

2019 ◽  
Vol 20 (21) ◽  
pp. 5479 ◽  
Author(s):  
Atsuki Fukutani ◽  
Walter Herzog
Keyword(s):  
Isometric Force ◽  
Muscle Length ◽  
Eccentric Contraction ◽  
Force Enhancement ◽  
Mechanical Responses ◽  
Cross Bridge ◽  
Myosin Filaments ◽  
Residual Force ◽  
Residual Force Enhancement ◽  
The Cross

Muscle contraction is initiated by the interaction between actin and myosin filaments. The sliding of actin filaments relative to myosin filaments is produced by cross-bridge cycling, which is governed by the theoretical framework of the cross-bridge theory. The cross-bridge theory explains well a number of mechanical responses, such as isometric and concentric contractions. However, some experimental observations cannot be explained with the cross-bridge theory; for example, the increased isometric force after eccentric contractions. The steady-state, isometric force after an eccentric contraction is greater than that attained in a purely isometric contraction at the same muscle length and same activation level. This well-acknowledged and universally observed property is referred to as residual force enhancement (rFE). Since rFE cannot be explained by the cross-bridge theory, alternative mechanisms for explaining this force response have been proposed. In this review, we introduce the basic concepts of sarcomere length non-uniformity and titin elasticity, which are the primary candidates that have been used for explaining rFE, and discuss unresolved problems regarding these mechanisms, and how to proceed with future experiments in this exciting area of research.

The effects of pH on force and stiffness development in mouse muscles

1987 ◽  
Vol 65 (8) ◽  
pp. 1798-1801 ◽  
Author(s):  
J. M. Renaud ◽  
R. B. Stein ◽  
T. Gordon
Keyword(s):  
High Frequency ◽  
Small Amplitude ◽  
Force Production ◽  
Muscle Length ◽  
Low Ph ◽  
Muscle Stiffness ◽  
Average Force ◽  
Cross Bridge ◽  
Effects Of Ph ◽  
Cross Bridges

Changes in force and stiffness during contractions of mouse extensor digitorum longus and soleus muscles were measured over a range of extracellular pH from 6.4 to 7.4. Muscle stiffness was measured using small amplitude (<0.1% of muscle length), high frequency (1.5 kHz) oscillations in length. Twitch force was not significantly affected by changes in pH, but the peak force during repetitive stimulation (2, 3, and 20 pulses) was decreased significantly as the pH was reduced. Changes in muscle stiffness with pH were in the same direction, but smaller in extent. If the number of attached cross-bridges in the muscle can be determined from the measurement of small amplitude, high frequency muscle stiffness, then these findings suggest that (a) the number of cross-bridges between thick and thin filaments declines in low pH and (b) the average force per cross-bridge also declines in low pH. The decline in force per cross-bridge could arise from a reduction in the ability of cross-bridges to generate force during their state of active force production and (or) in an increased percentage of bonds in a low force, "rigor" state.

Selected Contribution: Effect of chronic passive length change on airway smooth muscle length-tension relationship

2001 ◽  
Vol 90 (2) ◽  
pp. 734-740 ◽  
Author(s):  
Lu Wang ◽  
Peter D. Paré ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Force Production ◽  
Muscle Length ◽  
Electrical Field Stimulation ◽  
Length Change ◽  
Electrical Field ◽  
Optimal Length ◽  
Active Length ◽  
Reference Length ◽  
Relationship Of

The ability of rabbit trachealis to undergo plastic adaptation to chronic shortening or lengthening was assessed by setting the muscle preparations at three lengths for 24 h in relaxed state: a reference length in which applied force was ∼1–2% of maximal active force (Po) and lengths considerably shorter and longer than the reference. Passive and active length-tension ( L-T) curves for the preparations were then obtained by electrical field stimulation at progressively increasing muscle length. Classically shaped L-T curves were obtained with a distinct optimal length ( L o) at which Podeveloped; however, both the active and passive L-T curves were shifted, whereas Po remained unchanged. L o was 72% and 148% that of the reference preparations for the passively shortened and lengthened muscles, respectively. The results suggest that chronic narrowing of the airways could induce a shift in the L-T relationship of smooth muscle, resulting in a maintained potential for maximal force production.

scholarly journals Muscle Length is a Determinant of Cross-Bridge Cycling Rate in Intact Cardiac Trabeculae: Studies from Rodents to Humans

2013 ◽  
Vol 104 (2) ◽  
pp. 315a-316a
Author(s):  
Nima Milani-Nejad ◽  
Ying Xu ◽  
Jonathan P. Davis ◽  
Kenneth S. Campbell ◽  
George S. Billman ◽  
...  
Keyword(s):  
Muscle Length ◽  
Cycling Rate ◽  
Cross Bridge

scholarly journals The cross-bridge cycle and skeletal muscle fatigue

2008 ◽  
Vol 104 (2) ◽  
pp. 551-558 ◽  
Author(s):  
Robert H. Fitts
Keyword(s):  
Peak Power ◽  
Molecular Mechanisms ◽  
Fiber Type ◽  
Low Ph ◽  
Forward Rate ◽  
Maximal Velocity ◽  
Functional Changes ◽  
Cross Bridge ◽  
The Cross

The functional correlates of fatigue observed in both animals and humans during exercise include a decline in peak force (P0), maximal velocity, and peak power. Establishing the extent to which these deleterious functional changes result from direct effects on the myofilaments is facilitated through understanding the molecular mechanisms of the cross-bridge cycle. With actin-myosin binding, the cross-bridge transitions from a weakly bound low-force state to a strongly bound high-force state. Low pH reduces the number of high-force cross bridges in fast fibers, and the force per cross bridge in both fast and slow fibers. The former is thought to involve a direct inhibition of the forward rate constant for transition to the strong cross-bridge state. In contrast, inorganic phosphate (Pi) is thought to reduce P0 by accelerating the reversal of this step. Both H+ and Pi decrease myofibrillar Ca2+ sensitivity. This effect is particularly important as the amplitude of the Ca2+ transient falls with fatigue. The inhibitory effects of low pH and high Pi on P0 are reduced as temperature increases from 10 to 30°C. However, the H+-induced depression of peak power in the slow fiber type, and Pi inhibition of myofibrillar Ca2+ sensitivity in slow and fast fibers, are greater at high compared with low temperature. Thus the depressive effects of H+ and Pi at in vivo temperatures cannot easily be predicted from data collected below 25° C. In vitro, reactive oxygen species reduce myofibrillar Ca2+ sensitivity; however, the importance of this mechanism during in vivo exercise is unknown.

scholarly journals The Frank-Starling mechanism involves deceleration of cross-bridge kinetics and is preserved in failing human right ventricular myocardium

2015 ◽  
Vol 309 (12) ◽  
pp. H2077-H2086 ◽  
Author(s):  
Nima Milani-Nejad ◽  
Benjamin D. Canan ◽  
Mohammad T. Elnakish ◽  
Jonathan P. Davis ◽  
Jae-Hoon Chung ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Muscle Length ◽  
Human Myocardium ◽  
Force Frequency ◽  
Heart Failure Patients ◽  
Cycling Rate ◽  
Physiological Conditions ◽  
Cross Bridge ◽  
The Right

Cross-bridge cycling rate is an important determinant of cardiac output, and its alteration can potentially contribute to reduced output in heart failure patients. Additionally, animal studies suggest that this rate can be regulated by muscle length. The purpose of this study was to investigate cross-bridge cycling rate and its regulation by muscle length under near-physiological conditions in intact right ventricular muscles of nonfailing and failing human hearts. We acquired freshly explanted nonfailing ( n = 9) and failing ( n = 10) human hearts. All experiments were performed on intact right ventricular cardiac trabeculae ( n = 40) at physiological temperature and near the normal heart rate range. The failing myocardium showed the typical heart failure phenotype: a negative force-frequency relationship and β-adrenergic desensitization ( P < 0.05), indicating the expected pathological myocardium in the right ventricles. We found that there exists a length-dependent regulation of cross-bridge cycling kinetics in human myocardium. Decreasing muscle length accelerated the rate of cross-bridge reattachment ( ktr) in both nonfailing and failing myocardium ( P < 0.05) equally; there were no major differences between nonfailing and failing myocardium at each respective length ( P > 0.05), indicating that this regulatory mechanism is preserved in heart failure. Length-dependent assessment of twitch kinetics mirrored these findings; normalized dF/d t slowed down with increasing length of the muscle and was virtually identical in diseased tissue. This study shows for the first time that muscle length regulates cross-bridge kinetics in human myocardium under near-physiological conditions and that those kinetics are preserved in the right ventricular tissues of heart failure patients.

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