Considerations on the history dependence of muscle contraction

2004 ◽  
Vol 96 (2) ◽  
pp. 419-427 ◽  
Author(s):  
Dilson E. Rassier ◽  
Walter Herzog
Keyword(s):  
Muscle Contraction ◽  
Isometric Force ◽  
Force Production ◽  
Passive Component ◽  
Force Enhancement ◽  
History Dependence ◽  
Cross Bridge ◽  
Force Depression ◽  
Length Relationship ◽  
Length Changes

When a skeletal muscle that is actively producing force is shortened or stretched, the resulting steady-state isometric force after the dynamic phase is smaller or greater, respectively, than the purely isometric force obtained at the corresponding final length. The cross-bridge model of muscle contraction does not readily explain this history dependence of force production. The most accepted proposal to explain both, force depression after shortening and force enhancement after stretch, is a nonuniform behavior of sarcomeres that develops during and after length changes. This hypothesis is based on the idea of instability of sarcomere lengths on the descending limb of the force-length relationship. However, recent evidence suggests that skeletal muscles may be stable over the entire range of active force production, including the descending limb of the force-length relationship. The purpose of this review was to critically evaluate hypotheses aimed at explaining the history dependence of force production and to provide some novel insight into the possible mechanisms underlying these phenomena. It is concluded that the sarcomere nonuniformity hypothesis cannot always explain the total force enhancement observed after stretch and likely does not cause all of the force depression after shortening. There is evidence that force depression after shortening is associated with a reduction in the proportion of attached cross bridges, which, in turn, might be related to a stress-induced inhibition of cross-bridge attachment in the myofilament overlap zone. Furthermore, we suggest that force enhancement is not associated with instability of sarcomeres on the descending limb of the force-length relationship and that force enhancement has an active and a passive component. Force depression after shortening and force enhancement after stretch are likely to have different origins.

HISTORY DEPENDENCE OF SKELETAL MUSCLE FORCE PRODUCTION: A FORGOTTEN PROPERTY

2002 ◽  
Vol 02 (03n04) ◽  
pp. 347-358 ◽  
Author(s):  
W. HERZOG ◽  
D. E. RASSIER
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Sarcomere Length ◽  
Force Production ◽  
Passive Component ◽  
Total Force ◽  
Force Enhancement ◽  
Length Relationship ◽  
History Of ◽  
Muscle Force Production

Steady-state force enhancement following active muscle stretching has been observed for well over fifty years, and is a widely accepted property of skeletal muscle contraction. Force enhancement has typically been associated with instability of sarcomere length on the descending limb of the force-length relationship. Here, we demonstrate that the sarcomere length non-uniformity paradigm, based on instability, cannot explain much of the newly discovered results. We provide evidence that force enhancement can occur on the stable ascending limb of the force-length relationship, that force enhancement can exceed the isometric tetanic plateau forces, that it is associated with an increased passive force, and that it occurs for perfectly stable sarcomere lengths on the descending limb of the force-length relationship. Combining all the results, we conclude that force enhancement has at least two components, an active and a passive component, that contribute towards the total force enhancement to varying degrees, depending on the contractile history of muscle contraction.

scholarly journals Modifiability of the history dependence of force through chronic eccentric and concentric biased resistance training

2019 ◽  
Vol 126 (3) ◽  
pp. 647-657 ◽  
Author(s):  
Jackey Chen ◽  
Geoffrey A. Power
Keyword(s):  
Steady State ◽  
Resistance Training ◽  
Isometric Force ◽  
Eccentric Training ◽  
Force Enhancement ◽  
History Dependence ◽  
Force Depression ◽  
Residual Force ◽  
Residual Force Enhancement ◽  
Concentric Training

The increase and decrease in steady-state isometric force following active muscle lengthening and shortening are referred to as residual force enhancement (RFE) and force depression (FD), respectively. The RFE and FD states are associated with decreased (activation reduction; AR) and increased (activation increase; AI) neuromuscular activity, respectively. Although the mechanisms have been discussed over the last 60 years, no studies have systematically investigated the modifiability of RFE and FD with training. The purpose of the present study was to determine whether RFE and FD could be modulated through eccentric and concentric biased resistance training. Fifteen healthy young adult men (age: 24 ± 2 yr, weight: 77 ± 8 kg, height: 178 ± 5 cm) underwent 4 wk of isokinetic dorsiflexion training, in which one leg was trained eccentrically (−25°/s) and the other concentrically (+25°/s) over a 50° ankle excursion. Maximal and submaximal (40% maximum voluntary contraction) steady-state isometric torque and EMG values following active lengthening and shortening were compared to purely isometric values at the same joint angles and torque levels. Residual torque enhancement (rTE) decreased by ~36% after eccentric training ( P < 0.05) and increased by ~89% after concentric training ( P < 0.05), whereas residual torque depression (rTD), AR, AI, and optimal angles for torque production were not significantly altered by resistance training ( P ≥ 0.05). It appears that rTE, but not rTD, for the human ankle dorsiflexors is differentially modifiable through contraction type-dependent resistance training. NEW & NOTEWORTHY The history dependence of force production is a property of muscle unexplained by current cross bridge and sliding filament theories. Whether a muscle is actively lengthened (residual force enhancement; RFE) or shortened (force depression) to a given length, the isometric force should be equal to a purely isometric contraction—but it is not! In this study we show that eccentric training decreased RFE, whereas concentric training increased RFE and converted all nonresponders (i.e., not exhibiting RFE) into responders.

scholarly journals Residual force enhancement exceeds the isometric force at optimal sarcomere length for optimized stretch conditions

2008 ◽  
Vol 105 (2) ◽  
pp. 457-462 ◽  
Author(s):  
Eun-Jeong Lee ◽  
Walter Herzog
Keyword(s):  
Steady State ◽  
Sarcomere Length ◽  
Isometric Force ◽  
Passive Component ◽  
Force Enhancement ◽  
Single Fibers ◽  
Length Relationship ◽  
Residual Force ◽  
Residual Force Enhancement ◽  
Isometric Forces

Residual force enhancement (FE) following stretch of an activated muscle is a well accepted property of skeletal muscle contraction. However, the mechanism underlying FE remains unknown. A crucial assumption on which some proposed mechanisms are based is the idea that forces in the enhanced state cannot exceed the steady-state isometric force at a sarcomere length associated with optimal myofilament overlap. Although there are a number of studies in which forces in the enhanced state were compared with the corresponding isometric forces on the plateau of the force-length relationship, these studies either did not show enhanced forces above the plateau or, if they did, they lacked measurements of sarcomere lengths confirming the plateau region. Here, we revisited this question by optimizing stretch conditions and measuring the average sarcomere lengths in isolated fibers, and we found that FE exceeded the maximal isometric reference force obtained at the plateau of the force-length relationship consistently (mean ± SD: 4.8 ± 2.1%) and by up to 10%. When subtracting the passive component of FE from the total FE, the enhanced forces remained greater than the isometric plateau force (mean ± SD: 4.3 ± 2.0%). Calcium-induced increases in passive forces, known to be present in single fibers and myofibrils, are too small to account for the FE observed here. We conclude that FE cannot be explained exclusively with a stretch-induced development of sarcomere length nonuniformities, that FE in single fibers may be associated with the recruitment of additional contractile force, and that isometric steady-state forces in the enhanced state are not uniquely determined by sarcomere lengths.

scholarly journals Active force inhibition and stretch-induced force enhancement in frog muscle treated with BDM

2004 ◽  
Vol 97 (4) ◽  
pp. 1395-1400 ◽  
Author(s):  
Dilson E. Rassier ◽  
Walter Herzog
Keyword(s):  
Fiber Length ◽  
Isometric Force ◽  
Ringer Solution ◽  
Total Force ◽  
Passive Force ◽  
Force Enhancement ◽  
Cross Bridge ◽  
Length Relationship ◽  
Cross Bridges ◽  
Lumbrical Muscles

There is evidence that the stretch-induced residual force enhancement observed in skeletal muscles is associated with 1) cross-bridge dynamics and 2) an increase in passive force. The purpose of this study was to characterize the total and passive force enhancement and to evaluate whether these phenomena may be associated with a slow detachment of cross bridges. Single fibers from frog lumbrical muscles were placed at a length 20% longer than the plateau of the force-length relationship, and active and passive stretches (amplitudes of 5 and 10% of fiber length and at a speed of 40% fiber length/s) were performed. Experiments were conducted in Ringer solution and with the addition of 2, 5, and 10 mM of 2,3-butanedione monoxime (BDM), a cross-bridge inhibitor. The steady-state active and passive isometric forces after stretch of an activated fiber were higher than the corresponding forces measured after isometric contractions or passive stretches. BDM decreased the absolute isometric force and increased the total force enhancement in all conditions investigated. These results suggest that total force enhancement is directly associated with cross-bridge kinetics. Addition of 2 mM BDM did not change the passive force enhancement after 5 and 10% stretches. Addition of 5 and 10 mM did not change (5% stretches) or increased (10% stretches) the passive force enhancement. Increasing stretch amplitudes and increasing concentrations of BDM caused relaxation after stretch to be slower, and because passive force enhancement is increased at the greatest stretch amplitudes and the highest BDM concentrations, it appears that passive force enhancement may be related to slow-detaching cross bridges.

scholarly journals Variation in isometric force after active shortening and lengthening and their mechanisms: a review

2014 ◽  
Vol 27 (1) ◽  
pp. 141-153
Author(s):  
Rodrigo Troyack de Lima ◽  
Paulo Farinatti ◽  
Walace Monteiro ◽  
Carlos Gomes de Oliveira
Keyword(s):  
Skeletal Muscle ◽  
Literature Review ◽  
Systematic Literature Review ◽  
Isometric Force ◽  
Force Enhancement ◽  
Literature Searching ◽  
History Dependence ◽  
Force Depression ◽  
Key Variables ◽  
Cross Bridges

Introduction The isometric force history dependence of skeletal muscle has been studied along the last one hundred years. Several theories have been formulated to explain and establish the causes of the phenomenon, but not successfully, as they have not been fully accepted and demonstrated, and much controversy on such a subject still remains. Objective To present a systematic literature review on the dynamics of the mechanisms of force depression and force enhancement after active shortening and lengthening, respectively, identifying the key variables involved in the phenomenon, and to date to present the main theories and hypothesis developed trying to explaining it. Method The procedure of literature searching complied the major databases, including articles either, those which directly investigated the phenomena of force depression and force enhancement or those which presented possible causes and mechanisms associated with their respective events, from the earliest studies published until the year of 2010. Results 97 references were found according to the criteria used. Conclusion Based on this review, it is suggested that the theory of stress inhibition of actin-myosin cross-bridges is that better explain the phenomenon of force depression. Whereas regarding the force enhancement phenomenon, one theory have been well accepted, the increased number of actin-myosin cross-bridges in strong binding state influenced by the recruitment of passive elastic components, which hole is attributed to the titin filament.

Mysteries of Muscle Contraction

2008 ◽  
Vol 24 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Walter Herzog ◽  
Timothy R. Leonard ◽  
Venus Joumaa ◽  
Ashi Mehta
Keyword(s):  
Steady State ◽  
Experimental Evidence ◽  
Active Component ◽  
Isometric Force ◽  
Force Production ◽  
Myosin Filament ◽  
Passive Component ◽  
Cross Bridge ◽  
The Cross ◽  
State Force

According to the cross-bridge theory, the steady-state isometric force of a muscle is given by the amount of actin–myosin filament overlap. However, it has been known for more than half a century that steady-state forces depend crucially on contractile history. Here, we examine history-dependent steady-state force production in view of the cross-bridge theory, available experimental evidence, and existing explanations for this phenomenon. This is done on various structural levels, ranging from the intact muscle to the myofibrillar and isolated contractile protein level, so that advantages and limitations of the various preparations can be fully exploited and overcome. Based on experimental evidence, we conclude that steady-state force following active muscle stretching is enhanced, and this enhancement has a passive and an active component. The active component is associated with the cross-bridge kinetics, and the passive component is associated with a calcium-dependent increase in titin stiffness.

The origin of passive force enhancement in skeletal muscle

2008 ◽  
Vol 294 (1) ◽  
pp. C74-C78 ◽  
Author(s):  
V. Joumaa ◽  
D. E. Rassier ◽  
T. R. Leonard ◽  
W. Herzog
Keyword(s):  
Calcium Concentration ◽  
Force Production ◽  
Primary Source ◽  
Passive Force ◽  
Active Force ◽  
Force Enhancement ◽  
Bridge Formation ◽  
Calcium Dependent ◽  
Cross Bridge ◽  
High Calcium

The aim of the present study was to test whether titin is a calcium-dependent spring and whether it is the source of the passive force enhancement observed in muscle and single fiber preparations. We measured passive force enhancement in troponin C (TnC)-depleted myofibrils in which active force production was completely eliminated. The TnC-depleted construct allowed for the investigation of the effect of calcium concentration on passive force, without the confounding effects of actin-myosin cross-bridge formation and active force production. Passive forces in TnC-depleted myofibrils ( n = 6) were 35.0 ± 2.9 nN/ μm2 when stretched to an average sarcomere length of 3.4 μm in a solution with low calcium concentration (pCa 8.0). Passive forces in the same myofibrils increased by 25% to 30% when stretches were performed in a solution with high calcium concentration (pCa 3.5). Since it is well accepted that titin is the primary source for passive force in rabbit psoas myofibrils and since the increase in passive force in TnC-depleted myofibrils was abolished after trypsin treatment, our results suggest that increasing calcium concentration is associated with increased titin stiffness. However, this calcium-induced titin stiffness accounted for only ∼25% of the passive force enhancement observed in intact myofibrils. Therefore, ∼75% of the normally occurring passive force enhancement remains unexplained. The findings of the present study suggest that passive force enhancement is partly caused by a calcium-induced increase in titin stiffness but also requires cross-bridge formation and/or active force production for full manifestation.

scholarly journals Force enhancement after stretch of isolated myofibrils is increased by sarcomere length non-uniformities

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ricarda M. Haeger ◽  
Dilson E. Rassier
Keyword(s):  
Steady State ◽  
Sarcomere Length ◽  
Isometric Force ◽  
Force Production ◽  
Force Enhancement ◽  
Residual Force ◽  
Residual Force Enhancement ◽  
State Force ◽  
Isometric Forces

AbstractWhen a muscle is stretched during a contraction, the resulting steady-state force is higher than the isometric force produced at a comparable sarcomere length. This phenomenon, also referred to as residual force enhancement, cannot be readily explained by the force-sarcomere length relation. One of the most accepted mechanisms for the residual force enhancement is the development of sarcomere length non-uniformities after an active stretch. The aim of this study was to directly investigate the effect of non-uniformities on the force-producing capabilities of isolated myofibrils after they are actively stretched. We evaluated the effect of depleting a single A-band on sarcomere length non-uniformity and residual force enhancement. We observed that sarcomere length non-uniformity was effectively increased following A-band depletion. Furthermore, isometric forces decreased, while the percent residual force enhancement increased compared to intact myofibrils (5% vs. 20%). We conclude that sarcomere length non-uniformities are partially responsible for the enhanced force production after stretch.

scholarly journals Are Force Enhancement after Stretch and Muscle Fatigue Due to Effects of Elevated Inorganic Phosphate and Low Calcium on Cross Bridge Kinetics?

Medicina ◽  
2020 ◽  
Vol 56 (5) ◽  
pp. 249
Author(s):  
Hans Degens ◽  
David A. Jones
Keyword(s):  
Muscle Fatigue ◽  
Isometric Force ◽  
Force Enhancement ◽  
Shortening Velocity ◽  
Cross Bridge ◽  
Fatigued Muscle ◽  
Butanedione Monoxime ◽  
Combined Action ◽  
Cross Bridges ◽  
Muscle Contractile

Background and Objectives: Muscle fatigue is characterised by (1) loss of force, (2) decreased maximal shortening velocity and (3) a greater resistance to stretch that could be due to reduced intracellular Ca2+ and increased Pi, which alter cross bridge kinetics. Materials and Methods: To investigate this, we used (1) 2,3-butanedione monoxime (BDM), believed to increase the proportion of attached but non-force-generating cross bridges; (2) Pi that increases the proportion of attached cross bridges, but with Pi still attached; and (3) reduced activating Ca2+. We used permeabilised rat soleus fibres, activated with pCa 4.5 at 15 °C. Results: The addition of 1 mM BDM or 15 mM Pi, or the lowering of the Ca2+ to pCa 5.5, all reduced the isometric force by around 50%. Stiffness decreased in proportion to isometric force when the fibres were activated at pCa 5.5, but was well maintained in the presence of Pi and BDM. Force enhancement after a stretch increased with the length of stretch and Pi, suggesting a role for titin. Maximum shortening velocity was reduced by about 50% in the presence of BDM and pCa 5.5, but was slightly increased by Pi. Neither decreasing Ca2+ nor increasing Pi alone mimicked the effects of fatigue on muscle contractile characteristics entirely. Only BDM elicited a decrease of force and slowing with maintained stiffness, similar to the situation in fatigued muscle. Conclusions: This suggests that in fatigue, there is an accumulation of attached but low-force cross bridges that cannot be the result of the combined action of reduced Ca2+ or increased Pi alone, but is probably due to a combination of factors that change during fatigue.

Force Recovery After Activated Stretching in Whole Skeletal Muscle: Transient Aspects of Force Enhancement

2008 ◽  
Author(s):  
Ryan A. Koppes ◽  
David T. Corr
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Isometric Force ◽  
Underlying Mechanism ◽  
Mechanical Work ◽  
Force Enhancement ◽  
Transient Phenomena ◽  
Force Depression ◽  
Force Relaxation ◽  
In Situ Experiments

The enhancement of isometric force after active stretching is a well-accepted and demonstrated characteristic of skeletal muscle in both whole muscle [1,2] and single-fiber preparations [1,3], but its mechanisms remain unknown. Although traditionally analyzed at steady-state, transient phenomena caused, at least in part, by cross-bridge kinetics may provide novel insight into the mechanisms associated with force enhancement (FE). In order to identify the transient aspects of FE and its relation to stretching speed, stretching amplitude, and muscle mechanical work, a post hoc analysis of in situ experiments in soleus muscle tendon units of anesthetized cats [2] was conducted. The period immediately following stretching, at which the force returns to steady-state, was fit using an exponential decay function. The aims of this study were to analyze and quantify the effects of stretching amplitude, stretching speed, and muscle mechanical work on steady-state force enhancement (FEss) and transient force relaxation rate after active stretching. The results of this study were interpreted with respect to prior force depression (FD) experiments [4], to identify if the two phenomena exhibited similar transient and steady-state behaviors, and thus could be described by the same underlying mechanism(s).

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