scholarly journals Additional in-series compliance reduces muscle force summation and alters the time course of force relaxation during fixed-end contractions

2016 ◽  
Vol 219 (22) ◽  
pp. 3587-3596 ◽  
Author(s):  
Dean L. Mayfield ◽  
Bradley S. Launikonis ◽  
Andrew G. Cresswell ◽  
Glen A. Lichtwark
Keyword(s):  
Time Course ◽  
Muscle Force ◽  
Force Relaxation ◽  
In Series ◽  
Series Compliance ◽  
Fixed End

Cooperative attachment of cross bridges predicts regulation of smooth muscle force by myosin phosphorylation

2004 ◽  
Vol 287 (3) ◽  
pp. C594-C602 ◽  
Author(s):  
Christopher M. Rembold ◽  
Robert L. Wardle ◽  
Christopher J. Wingard ◽  
Timothy W. Batts ◽  
Elaine F. Etter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Time Course ◽  
Muscle Force ◽  
Regulatory System ◽  
Force Development ◽  
Cross Bridge ◽  
Cross Bridges ◽  
The Relationship ◽  
Cooperative Activation

Serine 19 phosphorylation of the myosin regulatory light chain (MRLC) appears to be the primary determinant of smooth muscle force development. The relationship between MRLC phosphorylation and force is nonlinear, showing that phosphorylation is not a simple switch regulating the number of cycling cross bridges. We reexamined the MRLC phosphorylation-force relationship in slow, tonic swine carotid media; fast, phasic rabbit urinary bladder detrusor; and very fast, tonic rat anococcygeus. We found a sigmoidal dependence of force on MRLC phosphorylation in all three tissues with a threshold for force development of ∼0.15 mol Pi/mol MRLC. This behavior suggests that force is regulated in a highly cooperative manner. We then determined whether a model that employs both the latch-bridge hypothesis and cooperative activation could reproduce the relationship between Ser19-MRLC phosphorylation and force without the need for a second regulatory system. We based this model on skeletal muscle in which attached cross bridges cooperatively activate thin filaments to facilitate cross-bridge attachment. We found that such a model describes both the steady-state and time-course relationship between Ser19-MRLC phosphorylation and force. The model required both cooperative activation and latch-bridge formation to predict force. The best fit of the model occurred when binding of a cross bridge cooperatively activated seven myosin binding sites on the thin filament. This result suggests cooperative mechanisms analogous to skeletal muscle that will require testing.

The Effect of Heating and Cooling on Time Course of Voluntary and Electrically Induced Muscle Force Variation

Medicina ◽  
2011 ◽  
Vol 47 (1) ◽  
pp. 6 ◽  
Author(s):  
◽  
◽  
◽  
◽  
Keyword(s):  
Muscle Fatigue ◽  
Time Course ◽  
Muscle Force ◽  
Peak Torque ◽  
Voluntary Contraction ◽  
Knee Extensors ◽  
Lower Body ◽  
Heating And Cooling ◽  
Force Variation ◽  
Voluntary Contractions

The aim of this study was to investigate the effect of heating and cooling on time course of voluntary and electrically induced muscle force variation. Material and Methods. Ten volunteers performed 50 maximal voluntary and electrically induced contractions of the knee extensors at an angle of 120 degrees under the control conditions and after passive lower body heating and cooling in the control, heating, and cooling experiments. Peak torque, torque variation, and half-relaxation time were assessed during the exercise. Results. Passive lower body heating increased muscle and core temperatures, while cooling lowered muscle temperature, but did not affect core temperature. We observed significantly lower muscle fatigue during voluntary contraction compared with electrically induced contractions. Body heating (opposite to cooling) increased involuntarily induced muscle force, but caused greater electrically induced muscle fatigue. In the middle of the exercise, the coefficient of correlation for electrically induced muscle torque decreased significantly as compared with the beginning of the exercise, while during maximal voluntary contractions, this relation for torque remained significant until the end of the exercise. Conclusion. It was shown that time course of voluntary contraction was more stable than in electrically induced contractions.

Enhanced contractility during relaxation of cat papillary muscle

1975 ◽  
Vol 228 (6) ◽  
pp. 1708-1716 ◽  
Author(s):  
BG Bass
Keyword(s):  
Papillary Muscle ◽  
Time Course ◽  
Isometric Tension ◽  
Contractile Element ◽  
Cat Papillary Muscle ◽  
Postextrasystolic Potentiation ◽  
Peak Tension ◽  
Time To Peak ◽  
In Series ◽  
Antecedent Control

Contractility during relaxation of isometric tension was studied in isolated, electrically driven cat papillary muscle by interpolation of test extrasystoles, all of whichpartially fused with their antecedent (control) contractions, were separated by computer from the fused contractions and then analyzed. The time course of the restitutionof contractility during relaxation was defined by plotting maximal positive dT/dt andtime-to-peak tension of the computer-separated extrasystole versus delay preceding the extrasystole. The dT/dt and time-to-peak tension, which steadily decline with progressive prematurity between contractions, both increase again during late relaxation, become progressively greater still earlier in relaxation, peak shortly after peak isometric tension, and then again decline. This phase of an apparently enhanced contractilityduring relaxation is depressed in low Ca'++ and is transmitted into the postextrasystolic period (in which it is superimposed on the usual postextrasystolic potentiation). The possible contributions of variations in series-elastic component and contractile-element lengths, actionpotential characteristics, and other factors on contractility during relaxation are discussed. It is suggested that enhanced contractility during relaxation may also be related in part to the decay of the intracellular free Ca'++ transient.

A metabolic basis for impaired muscle force production and neuromuscular compensation during sprint cycling

2006 ◽  
Vol 291 (5) ◽  
pp. R1457-R1464 ◽  
Author(s):  
Matthew W. Bundle ◽  
Carrie L. Ernst ◽  
Matthew J. Bellizzi ◽  
Seth Wright ◽  
Peter G. Weyand
Keyword(s):  
External Force ◽  
Time Course ◽  
Muscle Force ◽  
Anaerobic Metabolism ◽  
Maximum Voluntary Contraction ◽  
Force Production ◽  
Neuromuscular Activity ◽  
Sprint Cycling ◽  
Metabolic Basis ◽  
Muscle Force Production

For both different individuals and modes of locomotion, the external forces determining all-out sprinting performances fall predictably with effort duration from the burst maximums attained for 3 s to those that can be supported aerobically as trial durations extend to roughly 300 s. The common time course of this relationship suggests a metabolic basis for the decrements in the force applied to the environment. However, the mechanical and neuromuscular responses to impaired force production (i.e., muscle fatigue) are generally considered in relation to fractions of the maximum force available, or the maximum voluntary contraction (MVC). We hypothesized that these duration-dependent decrements in external force application result from a reliance on anaerobic metabolism for force production rather than the absolute force produced. We tested this idea by examining neuromuscular activity during two modes of sprint cycling with similar external force requirements but differing aerobic and anaerobic contributions to force production: one- and two-legged cycling. In agreement with previous studies, we found greater peak per leg aerobic metabolic rates [59% (±6 SD)] and pedal forces at V̇o2 peak [30% (±9)] during one- vs. two-legged cycling. We also determined downstroke pedal forces and neuromuscular activity by surface electromyography during 15 to 19 all-out constant load sprints lasting from 12 to 400 s for both modes of cycling. In support of our hypothesis, we found that the greater reliance on anaerobic metabolism for force production induced compensatory muscle recruitment at lower pedal forces during two- vs. one-legged sprint cycling. We conclude that impaired muscle force production and compensatory neuromuscular activity during sprinting are triggered by a reliance on anaerobic metabolism for force production.

Predictions of the time course of force and power output by dogfish white muscle fibres during brief tetani.

1998 ◽  
Vol 201 (1) ◽  
pp. 103-114 ◽  
Author(s):  
N A Curtin ◽  
A R Gardner-Medwin ◽  
R C Woledge
Keyword(s):  
Power Output ◽  
Constant Velocity ◽  
Time Course ◽  
White Muscle ◽  
Muscle Fibres ◽  
After Effects ◽  
In Series ◽  
Principal Factors ◽  
Strain Relationship ◽  
Relationship Of

The aim of this study was to identify the principal factors that determine the time course of force and power output by muscle during patterns of stimulation and movement similar to those during fish swimming. Fully activated, white muscle fibres isolated from dogfish Scyliorhinus canicula were used to characterize the force-velocity relationship of the contractile component (CC) and the stress-strain relationship of the passive, elastic component (SEC) in series with the CC. A simple model of the time course of crossbridge activation during brief contractions was devised. Using the mechanical properties of the CC and SEC and the activation time course, force and power were predicted for brief contractions with constant-velocity movement and also for brief contractions starting at various times during sinusoidal movement. The predicted force and power were compared with observations for these patterns of stimulation and movement. The predictions matched the observations well for the period during stimulation. Matching of force was much less good for some specific conditions during relaxation, the period during which force persists after the end of stimulation. If either the slow rise of activation or the SEC was omitted from the calculation, the predictions were poor, even during stimulation. Additional factors which may influence force are discussed. These include the after-effects of shortening and stretch, the variation of force during constant-velocity stretch and non-uniform behaviour within the muscle.

Dissecting muscle power output

1999 ◽  
Vol 202 (23) ◽  
pp. 3369-3375 ◽  
Author(s):  
R.K. Josephson
Keyword(s):  
Time Course ◽  
Muscle Activation ◽  
Muscle Force ◽  
Muscle Power ◽  
Muscle Length ◽  
Velocity Relationship ◽  
Shortening Deactivation ◽  
Force Velocity ◽  
Work Done ◽  
Kinetics Of

The primary determinants of muscle force throughout a shortening-lengthening cycle, and therefore of the net work done during the cycle, are (1) the shortening or lengthening velocity of the muscle and the force-velocity relationship for the muscle, (2) muscle length and the length-tension relationship for the muscle, and (3) the pattern of stimulation and the time course of muscle activation following stimulation. In addition to these primary factors, there are what are termed secondary determinants of force and work output, which arise from interactions between the primary determinants. The secondary determinants are length-dependent changes in the kinetics of muscle activation, and shortening deactivation, the extent of which depends on the work that has been done during the preceding shortening. The primary and secondary determinants of muscle force and work are illustrated with examples drawn from studies of crustacean muscles.

scholarly journals Department of Physiology, Box 642, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, U.S.A

1990 ◽  
Vol 266 (3) ◽  
pp. 719-726 ◽  
Author(s):  
T J Shuttleworth
Keyword(s):  
Plasma Membrane ◽  
Time Course ◽  
Receptor Activation ◽  
Transient Increase ◽  
Exocrine Cells ◽  
School Of Medicine ◽  
In Series ◽  
Rochester School

Currently, most models describing receptor-activated Ca2+ entry in exocrine cells invoke a pathway for the entry of extracellular Ca2+ directly linking the agonist-sensitive intracellular Ca2+ pools with the plasma membrane. In the avian nasal gland, a model exocrine ion-secreting tissue, we have found that Ca2+ entry during refilling of the intracellular pools following termination of receptor activation (by atropine) occurs via the cytoplasm and not directly into the empty pools. Under appropriate conditions this can be demonstrated as a transient increase in [Ca2+]i (intracellular Ca2+ concn.) seen on restoration of normal extracellular Ca2+ concentrations after atropine to stimulated cells whose intracellular stores have been prevented from refilling by incubation in a low-extracellular-Ca2+ medium. The magnitude of these [Ca2+]i transients decays with time, but with a time course markedly slower than for the corresponding decrease in intracellular Ins(1,4,5)P3. Further experiments have revealed that Ca2+ entry into the cytoplasm during the initial stimulation phase is also direct and not via the intracellular pools. Thus the initial rates of increase in [Ca2+]i during stimulation are always faster in conditions where both Ca2+ entry and Ca2+ release occur (i.e. they are additive). These differences could not be explained by any effects of extracellular Ca2+ on the initial increases in intracellular Ins(1,4,5)P3 after addition of carbachol. These data are therefore inconsistent with the current models in which the rate of Ca2+ entry through the agonist-sensitive pools cannot exceed the rate of Ca2+ release. It appears therefore that Ca2+ entry and Ca2+ release must occur via separate pathways operating in parallel, and not in series as previously predicted.

scholarly journals Transverse tubule remodeling enhances Orai1-dependent Ca2+ entry in skeletal muscle

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Antonio Michelucci ◽  
Simona Boncompagni ◽  
Laura Pietrangelo ◽  
Maricela García-Castañeda ◽  
Takahiro Takano ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Acute Exercise ◽  
Muscle Force ◽  
Contractile Function ◽  
Force Production ◽  
High Frequency Stimulation ◽  
Frequency Stimulation ◽  
Muscle Force Production ◽  
Muscle Contractile

Exercise promotes the formation of intracellular junctions in skeletal muscle between stacks of sarcoplasmic reticulum (SR) cisternae and extensions of transverse-tubules (TT) that increase co-localization of proteins required for store-operated Ca2+ entry (SOCE). Here, we report that SOCE, peak Ca2+ transient amplitude and muscle force production during repetitive stimulation are increased after exercise in parallel with the time course of TT association with SR-stacks. Unexpectedly, exercise also activated constitutive Ca2+ entry coincident with a modest decrease in total releasable Ca2+ store content. Importantly, this decrease in releasable Ca2+ store content observed after exercise was reversed by repetitive high-frequency stimulation, consistent with enhanced SOCE. The functional benefits of exercise on SOCE, constitutive Ca2+ entry and muscle force production were lost in mice with muscle-specific loss of Orai1 function. These results indicate that TT association with SR-stacks enhances Orai1-dependent SOCE to optimize Ca2+ dynamics and muscle contractile function during acute exercise.

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