Steady-state Isometric Force Research Articles

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

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.

Activation-induced force enhancement in human adductor pollicis

It has been known for a long time that the steady-state isometric force after muscle stretch is bigger than the corresponding force obtained in a purely isometric contraction for electrically stimulated and maximal voluntary contractions (MVC). Recent studies using sub-maximal voluntary contractions showed that force enhancement only occurred in a sub-group of subjects suggesting that force enhancement for sub-maximal voluntary contractions has properties different from those of electrically-induced and maximal voluntary contractions. Specifically, force enhancement for sub-maximal voluntary contractions may contain an activation-dependent component that is independent of muscle stretching. To address this hypothesis, we tested for force enhancement using (i) sub-maximal electrically-induced contractions and stretch and (ii) using various activation levels preceding an isometric reference contraction at 30% of MVC (no stretch). All tests were performed on human adductor pollicis muscles. Force enhancement following stretching was found for all subjects ( n = 10) and all activation levels (10%, 30%, and 60% of MVC) for electrically-induced contractions. In contrast, force enhancement at 30% of MVC, preceded by 6 s of 10%, 60%, and 100% of MVC was only found in a sub-set of the subjects and only for the 60% and 100% conditions. This result suggests that there is an activation-dependent force enhancement for some subjects for sub-maximal voluntary contractions. This activation-dependent force enhancement was always smaller than the stretch-induced force enhancement obtained at the corresponding activation levels. Active muscle stretching increased the force enhancement in all subjects, independent whether they showed activation dependence or not. It appears that post-activation potentiation, and the associated phosphorylation of the myosin light chains, might account for the stretch-independent force enhancement observed here.

Mysteries of Muscle Contraction

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.

Cross-bridge induced force enhancement?

When a muscle is stretched while activated, its steady-state isometric force following stretch is greater than the corresponding purely isometric force. This so-called residual force enhancement (RFE) has been observed for half a century, yet its mechanism remains unknown. Recent experiments suggest that RFE is not caused by non-uniformities in sarcomere lengths, as had been assumed for a long time, and cannot be explained primarily with increases in passive force, but is directly related to the kinetics of the cross-bridge cycle. Specifically, it has been suggested that stretching an attached cross-bridge increases its dwell time and duty ratio; therefore, the proportion of attached cross-bridges in a muscle would be increased by stretch, thereby causing RFE. A three bead laser trap setup was used for testing single cross-bridge (myosin II) interactions with actin. Upon attachment of a cross-bridge, a stretch or shortening of the cross-bridge was applied with a force of about 1.0 pN. The hypothesis that stretching a single cross-bridge increases its dwell time and duty ratio was rejected. However, stretching caused an increase in the average steady-state force per cross-bridge (3.4±0.4 pN; n=433) compared to shortening (1.9±0.3 pN; n=689). Therefore, based on the results of this study, RFE cannot be explained by an increased duty ratio and the associated increase in proportion of attached cross-bridges, but might be associated with an increased force per cross-bridge.

근육 구조특성과 선행 신장성 수축에 의한 항정상태 등척성 근력 증대와의 연관성에 대한 연구

When an active muscle is stretched, its steady-state isometric force following stretch is greater than that of a purely isometric contraction as the corresponding muscle length, referred to as force enhancement (FE). The purpose of this study was to investigate possible effects of muscle architecture on the FE. While subject performed maximal isometric dorsiflexion (REF) and isometric-stretch-isometric dorsiflexion (ECC) contractions, ankle joint angle and dorsiflexion torque using a dynamometer and electromyography of the tibialis anterior and the medical gastrocnemius muscles were measure. Simultaneously, real-time ultrasound images of the tibialis anterior were acquired. Regardless of the speed of stretch of the ECC contractions. the torques produced during the isometric phase following stretch (<TEX>$37.3{\pm}1.5\;Nm$</TEX> (<TEX>$10{\pm}3%$</TEX> FE) and <TEX>$38.3{\pm}1.5$</TEX> (<TEX>$12{\pm}3%$</TEX> FE) for the ECC contractions with <TEX>$15^{\circ}$</TEX>/s and <TEX>$45^{\circ}$</TEX>/s stretch speeds, respectively) were greater than those of the REF contractions (<TEX>$34.5{\pm}2.5\;Nm$</TEX>). Moreover, the amount of FE was found to be stretch speed dependent. Angles of pennation (<TEX>$\alpha$</TEX>) during the isometric phase following stretch were the same for the REF (<TEX>$15{\pm}1^{\circ}$</TEX>) and the ECC (<TEX>$14{\pm}1^{\circ}$</TEX>(LS), <TEX>$15{\pm}1^{\circ}$</TEX>(LF)). During the same phase, muscle thicknesses were the same (<TEX>$14.9{\pm}0.6$</TEX>, and <TEX>$14.9{\pm}0.5\;mm$</TEX> for the REF and the ECC contractions, respectively). For a large limb muscle, the tibialis anterior muscle, a similar amount of force enhancement was observed as did for other human skeletal muscles. Architectural variables, pennation angle and thickness, were not systematically different between the REF and ECC contractions when FE occurred. Therefore, the results of this study suggest that muscle architecture may have little influence on the production of FE.

EFFECTS OF SEGMENTAL MOTION ON GROUND REACTION FORCE DURING DROP LANDINGS

It is well-recognised that steady-state isometric muscle force is decreased following active shortening (force depression, FD) and increased following active stretch (force enhancement, FE). It has also been demonstrated that passive muscle force is increased following active stretch (passive FE). Several studies have reported that FD increases with shortening amplitude and that FE and passive FE increase with stretch amplitude. Here, we investigate whether these trends continue with further increases in shortening or stretch amplitude. Experiments were performed using in situ cat soleus muscles (n=8 for FD; n=7 for FE and passive FE). FD, FE and passive FE were measured after shortening or stretch contractions that covered as wide a range of amplitudes as practically possible without damaging the muscles. FD increased approximately linearly with shortening amplitude, over the full range of amplitudes investigated. This is consistent with the hypothesis that FD arises from a stress-induced inhibition of crossbridges. FE increased with stretch amplitude only up to a point, and then levelled off. Passive FE, and the transient increase in force at the end of stretch, showed relationships to stretch amplitude that were qualitatively very similar to the relationship for FE, increasing only until the same critical stretch amplitude had been reached. We conclude that FE and passive FE do not increase with stretch amplitude under all circumstances. This finding has important consequences for determining the mechanisms underlying FE and passive FE because any mechanism that is proposed to explain them must be able to predict it.

New insights into the passive force enhancement in skeletal muscles

The steady-state isometric force following active stretching of a muscle is always greater than the steady-state isometric force obtained in a purely isometric contraction at the same length. This phenomenon has been termed “residual force enhancement” and it is associated with an active and a passive component. The origin of these components remains a matter of scientific debate. The purpose of this work was to test the hypothesis that the passive component of the residual force enhancement is caused by a passive structural element. In order to achieve this purpose, single fibers ( n = 6 ) from the lumbrical muscles of frog ( Rana pipiens) were isolated and attached to a force transducer and a motor that could produce computer-controlled length changes. The passive force enhancement was assessed for three experimental conditions: in a normal Ringer's solution, and after the addition of 5 and 15 mM 2,3-butanedione monoxime (BDM) which inhibits force production in a dose-dependent manner. If our hypothesis was correct, one would expect the passive force enhancement to be unaffected following BDM application. However, we found that increasing concentrations of BDM decreased the isometric forces, increased the normalized residual force enhancement, and most importantly for this study, increased the passive force enhancement. Furthermore, BDM decreased the rate of force relaxation after deactivation following active stretching of fibers, passive stretching in the Ringer's and BDM conditions produced the same passive force–sarcomere length relationship, and passive force enhancement required activation and force production. These results led to the conclusion that the passive force enhancement cannot be caused by a structural component exclusively as had been assumed up to date, but must be associated, directly or indirectly, with cross-bridge attachments upon activation and the associated active force.

Spatially explicit, nano-mechanical models of the muscle half-sarcomere: Implications for biomechanical tuning in atrophy and fatigue

Astronaut biomechanical performance depends on a wide variety of factors. Results from computational modelling suggest that muscle function—a key component of performance—could be modulated by compliance of the contractile filaments in muscle, especially when force is low such as transient Ca 2 + activation in a twitch, reduced activation in muscle fatigue encountered during EVA, or perhaps atrophy during prolonged space flight. We used Monte-Carlo models to investigate the hypotheses that myofilament compliance influences muscle function during a twitch, and also modulates the effects of cooperative interactions between contractile proteins on force generation. Peak twitch force and the kinetics of force decay were both decreased, while tension cost was increased, when myofilament compliance was increased relative to physiological values. Both the apparent Ca 2 + sensitivity and cooperativity of activation of steady-state isometric force were altered by myofilament compliance even when there were no explicit interactions included between binding sites. The effects of cooperative interactions between adjacent regulatory units were found to be greater than either the effect of myofilament compliance on apparent cooperativity of activation or that due to myosin cross-bridge-induced cooperativity. These results indicate that muscle function may be “tuned” at the molecular level, particularly under conditions of reduced Ca 2 + activation.

Hand dominance and multi-finger synergies

Recent studies of arm movement reaching to a target have provided support for the Dynamic Dominance model of handedness, which proposes that each hemisphere/limb system is specialized for controlling different features of performance: The dominant system for control of the trajectory, and the nondominant system for control of the steady state final position. We now examine a more general form of this hypothesis by investigating differences between the right and left hands of right-handed persons in their ability to stabilize the combined action of a set of fingers. The subjects produced very quick pulses and steps of force from a low background force level while pressing with four fingers of one hand. An index of force stabilizing synergy showed a strong multi-finger synergy during steady-state force production followed by a small anticipatory drop in the index prior to the force increase. Hand differences emerged during the force increase: The left (non-dominant) hand showed a significantly larger drop in the synergy index. While our findings support the idea that the dominant system is specialized for stabilizing quick changes in performance variables, we failed to support a nondominant specialization for stabilizing steady-state isometric force. This may be a ceiling effect due to the simplicity of the task for either hand, or it might indicate that this aspect of the dynamic dominance hypothesis does not generalize to isometric conditions.

History-dependence of isometric muscle force: Effect of prior stretch or shortening amplitude

It is well-recognised that steady-state isometric muscle force is decreased following active shortening (force depression, FD) and increased following active stretch (force enhancement, FE). It has also been demonstrated that passive muscle force is increased following active stretch (passive FE). Several studies have reported that FD increases with shortening amplitude and that FE and passive FE increase with stretch amplitude. Here, we investigate whether these trends continue with further increases in shortening or stretch amplitude. Experiments were performed using in situ cat soleus muscles ( n=8 for FD; n=7 for FE and passive FE). FD, FE and passive FE were measured after shortening or stretch contractions that covered as wide a range of amplitudes as practically possible without damaging the muscles. FD increased approximately linearly with shortening amplitude, over the full range of amplitudes investigated. This is consistent with the hypothesis that FD arises from a stress-induced inhibition of crossbridges. FE increased with stretch amplitude only up to a point, and then levelled off. Passive FE, and the transient increase in force at the end of stretch, showed relationships to stretch amplitude that were qualitatively very similar to the relationship for FE, increasing only until the same critical stretch amplitude had been reached. We conclude that FE and passive FE do not increase with stretch amplitude under all circumstances. This finding has important consequences for determining the mechanisms underlying FE and passive FE because any mechanism that is proposed to explain them must be able to predict it.

Urotensin-II Upregulation in Human Heart Failure: Direct Effects on Contractility and Sarcoplasmic Reticulum Calcium Load

Introduction: In failing (F) hearts, rate and adrenergic dependent contractile reserve are impaired and the ability to increase contractility (CY) in response to physiologic stress is diminished. The inability to increase CY in response to increases in heart rate has been linked to a reduced ability of the SR to sequester Ca2þ. The goal of this research was to determine whether alterations in the competition between SERCA and the NCX contribute to impaired rate-dependent reserve and whether CY could be restored in F muscle by increasing extracellular bath Ca2þ. Methods: Steady state isometric force was measured (1.75 mM Ca2þ, 37 C, 80% Lmax-Lo) in control (C) (n 5 9) and F (via pulmonary artery banding) right ventricular trabeculae (n 5 11) at varying stimulation frequencies (0.5e2.5Hz). Altered bath Ca2þ experiments (1.0e7.0mM) were also performed in these trabeculae (0.5Hz). Single and paired rapid cooling contractures (RCCs) were employed to define SR Ca2þ load and the competition between SERCA and the NCX, respectively. Results: C trabeculae exhibited a positive forcefrequency response which was paralleled by a rate-dependent increase in RCC amplitude and the RCC2/RCC1 ratio. F trabeculae exhibited a blunted response to increases in stimulation frequency which was paralleled by a reduced RCC amplitude and RCC2/ RCC1 ratio. Increases in extracellular bath Ca2þ evoked similar increases in both RCC amplitude and developed tension (DT) in F trabeculae compared to C, although DTwas not normalized. Conclusion: This data suggests that under basal conditions (0.5Hz), supraphysiologic application of Ca2þ can evoke similar increases in both SR Ca2þ load and DT in F compared to C trabeculae. This implies that the blunted forcefrequency response representative of F hearts is largely due to an alteration in the functional competition between SERCA and the NCX during relaxation. During increased rates of stimulation, SERCA is not able to adequately compete with the NCX for Ca2þ due to an increase in the NCX/SERCA activity ratio. Thus, Ca2þ extrusion exceeds SR re-sequestration in failing myocardium.

The dependence of force enhancement on activation in human adductor pollicis

It has been well recognized that the steady-state isometric force after active muscle/fiber stretch is greater than the corresponding isometric force for electrically stimulated muscles and maximal voluntary contractions (MVC). However, recent evidence obtained for sub-MVC suggests that force enhancement properties are different from those observed for electrically induced and MVC. Specifically, it appears that force enhancement is activation-dependent and that there is a subject-specific threshold for force enhancement in sub-MVC. To address these suggestions, the relationship between force enhancement and voluntary activation during stretch was investigated in 11 healthy subjects. Human adductor pollicis muscles were studied and force enhancement was measured while muscle activation during the steady-state isometric phase was controlled at a level of 30% of MVC. In order to study the effects of activation on force enhancement, subjects performed stretch contractions at 0, 10, 30, 60, and 100% of maximal voluntary effort while the steady-state isometric force after stretch, obtained at 30% of activation in all cases, was compared to the corresponding values measured in the isometric reference contractions. There was no force enhancement if muscle stretching occurred passively but all subjects showed force enhancement when muscle stretching occurred at maximal voluntary effort. When increasing the level of activation during the stretch phase, force enhancement increased, and the number of subjects who showed force enhancement increased as well. We conclude from these results that force enhancement during voluntary contractions is activation-dependent with a threshold that is subject-specific.

Force enhancement at different levels of voluntary contraction in human adductor pollicis

There is substantial evidence that the steady-state isometric force following active muscle stretch is greater than the corresponding isometric force for sub-maximal and maximal electrically induced contractions, and for maximal voluntary contractions (MVC). This so-called force enhancement (FE) has not been investigated systematically for sub-MVC. Recently, we found that FE only occurred in about half of all tested subjects at 30% of MVC in the adductor pollicis muscle, suggesting that FE for voluntary contractions might depend on the level of activation. Therefore, the purpose of this study was to determine if FE during voluntary contractions is associated with activation. We hypothesized that FE increases with increasing levels of activation, and thus increasing levels of effort. Subjects (n=12) performed voluntary contractions of the adductor pollicis using a custom-built dynamometer at 10 and 60% of maximal effort. There was consistent FE in 4 of 12 subjects at 10% and in 10 of 12 subjects at 60% of maximal voluntary effort. Furthermore, the absolute FE increased from 10 to 60% of maximal voluntary effort. The results of this study, together with previous results on the same subject group at 30% and other subjects at 100% of maximal voluntary effort, suggest that FE systematically increases with increasing levels of voluntary contraction. The mechanisms responsible for this increased FE remain unclear.

Force depression following muscle shortening in sub-maximal voluntary contractions of human adductor pollicis

Mechanical properties of skeletal muscles are often studied for controlled, electrically induced, maximal, or supra-maximal contractions. However, many mechanical properties, such as the force–length relationship and force enhancement following active muscle stretching, are quite different for maximal and sub-maximal, or electrically induced and voluntary contractions. Force depression, the loss of force observed following active muscle shortening, has been observed and is well documented for electrically induced and maximal voluntary contractions. Since sub-maximal voluntary contractions are arguably the most important for everyday movement analysis and for biomechanical models of skeletal muscle function, it is important to study force depression properties under these conditions. Therefore, the purpose of this study was to examine force depression following sub-maximal, voluntary contractions. Sets of isometric reference and isometric-shortening-isometric test contractions at 30% of maximal voluntary effort were performed with the adductor pollicis muscle. All reference and test contractions were executed by controlling force or activation using a feedback system. Test contractions included adductor pollicis shortening over 10°, 20°, and 30° of thumb adduction. Force depression was assessed by comparing the steady-state isometric forces (activation control) or average electromyograms (EMGs) (force control) following active muscle shortening with those obtained in the corresponding isometric reference contractions. Force was decreased by 20% and average EMG was increased by 18% in the shortening test contractions compared to the isometric reference contractions. Furthermore, force depression was increased with increasing shortening amplitudes, and the relative magnitudes of force depression were similar to those found in electrically stimulated and maximal contractions. We conclude from these results that force depression occurs in sub-maximal voluntary contractions, and that force depression may play a role in the mechanics of everyday movements, and therefore may have to be considered in biomechanical models of human movement.

Observations on force enhancement in submaximal voluntary contractions of human adductor pollicis muscle

It has been observed consistently and is well accepted that the steady-state isometric force after active muscle stretch is greater than the corresponding isometric force for electrically stimulated muscles and maximal voluntary contractions. However, this so-called force enhancement has not been studied for submaximal voluntary efforts; therefore, it is not known whether this property affects everyday movements. The purpose of this study was to determine whether there was force enhancement during submaximal voluntary contractions. Human adductor pollicis muscles (n = 17) were studied using a custom-built dynamometer, and both force and activation were measured while muscle activation and force were controlled at a level of 30% of maximal voluntary contraction. The steady-state isometric force and activation after active stretch were compared with the corresponding values obtained during isometric reference contractions. There was consistent and reliable force enhancement in 8 of the 17 subjects, whereas there was no force enhancement in the remaining subjects. Subjects with force enhancement had greater postactivation potentiation and a smaller resistance to fatigue in the adductor pollicis. We conclude from these results that force enhancement exists during submaximal voluntary contractions in a subset of the populations and suggest that it may affect everyday voluntary movements in this subset. On the basis of follow-up testing, it appears that force enhancement during voluntary contractions is linked to potentiation and fatigue resistance and therefore possibly to the fiber-type distribution in the adductor pollicis muscle.

A Spatially Explicit Nanomechanical Model of the Half-Sarcomere: Myofilament Compliance Affects Ca2+-Activation

The force exerted by skeletal muscle is modulated by compliance of tissues to which it is connected. Force of the muscle sarcomere is modulated by compliance of the myofilaments. We tested the hypothesis that myofilament compliance influences Ca2+ regulation of muscle by constructing a computational model of the muscle half sarcomere that includes compliance of the filaments as a variable. The biomechanical model consists of three half-filaments of myosin and 13 thin filaments. Initial spacing of motor domains of myosin on thick filaments and myosin-binding sites on thin filaments was taken to be that measured experimentally in unstrained filaments. Monte-Carlo simulations were used to determine transitions around a three-state cycle for each cross-bridge and between two-states for each thin filament regulatory unit. This multifilament model exhibited less "tuning" of maximum force than an earlier two-filament model. Significantly, both the apparent Ca(2+)-sensitivity and cooperativity of activation of steady-state isometric force were modulated by myofilament compliance. Activation-dependence of the kinetics of tension development was also modulated by filament compliance. Tuning in the full myofilament lattice appears to be more significant at submaximal levels of thin filament activation.

Considerations on the history dependence of muscle contraction.

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.

The effects of muscle stretching and shortening on isometric forces on the descending limb of the force–length relationship

The purpose of this study was to examine the effects of stretching and shortening on the isometric forces at different lengths on the descending limb of the force–length relationship. Cat soleus ( N=10) was stretched and shortened by various amounts on the descending limb of the force–length relationship, and the steady-state forces following these dynamic contractions were compared to the isometric forces at the corresponding muscle lengths. We found a shift of the force–length relationship to greater force values following muscle stretching, and to smaller force values following muscle shortening. Shifts in both directions critically depended on the magnitude of stretching/shortening and the final muscle length. We confirm recent findings that the steady-state isometric force following some stretch conditions clearly exceeded the maximal isometric forces at optimum muscle length, and that force enhancement was associated with an increase in the passive force, i.e., a passive force enhancement. When the passive force enhancement was subtracted from the total force enhancement, forces following stretch were always equal to or smaller than the isometric force at optimum muscle length. Together, these findings led to the conclusions: (a) that force enhancement is composed of an “active and a “passive” component; (b) that the “passive” component of force enhancement allows for forces greater than the maximal isometric forces at the muscle's optimum length; and (c) that force enhancement and force depression are critically affected by muscle length and stretch/shortening amplitude.

Force depression following muscle shortening of voluntarily activated and electrically stimulated human adductor pollicis.

The purpose of this study was to investigate steady-state force depression following active muscle shortening in human adductor pollicis during voluntary and electrically induced contractions. Subjects (n = 12; age 28 +/- 5 years; 7 males and 5 females) performed isometric reference contractions and isometric-shortening-isometric contractions, using maximal voluntary effort and near-maximal electrical stimulation. Force depression was assessed by comparing the steady-state isometric forces produced following active muscle shortening with the purely isometric reference forces obtained at the corresponding muscle length. In order to test for effects of the shortening conditions on the steady-state force depression, the amplitude and speed of shortening were changed systematically in a random order but balanced design. Thumb adduction force and carpometacarpal joint angle were continuously measured using a custom-designed dynamometer. During voluntary contractions, muscle activation was recorded using electromyography and the superimposed twitch technique. During electrically induced contractions, muscle stiffness was assessed using a quick-stretch method. Force depression during voluntary contractions, with a constant level of muscle activation, was similar to that obtained during electrically induced contractions. Force depression increased with increasing amplitudes of shortening (9.9 +/- 1.6%, 15.6 +/- 2.4% and 22.4 +/- 2.4% for 10, 20 and 30 deg of shortening, respectively) and decreased with increasing speeds of shortening (27.1 +/- 2.5%, 19.3 +/- 1.6% and 15.6 +/- 1.8% for 20, 60 and 300 deg s(-1) of shortening, respectively), regardless of the activation method. Muscle stiffness was significantly lower in the force-depressed state (5.9 +/- 0.2 N deg(-1)) compared with that of the isometric reference contractions (7.2 +/- 0.3 N deg(-1)), and decreased with increasing force depression (6.6 +/- 0.5, 6.0 +/- 0.5 and 5.3 +/- 0.4 N deg(-1) for the 10, 20 and 30 deg of shortening test contractions, respectively). Force depression appeared to be fully established at the end of the shortening phase. The results of this study suggest that steady-state force depression for voluntary movements is similar to that observed using electrical stimulation. Furthermore, it appears that force depression is established at the end of the shortening phase and is associated with a reduction in muscle stiffness and thus, presumably, a decrease in the proportion of attached cross-bridges.

Force enhancement following muscle stretch of electrically stimulated and voluntarily activated human adductor pollicis.

For electrically stimulated muscles, it has been observed that maximal muscle force during and after stretch is substantially greater than the corresponding isometric force. However, this observation has not been made for human voluntary contractions. We investigated the effects of active muscle stretch on muscle force production for in vivo human adductor pollicis (n = 12) during maximal voluntary contractions and electrically induced contractions. Peak forces during stretch, steady-state isometric forces following stretch, and passive forces following muscle deactivation were compared to the corresponding isometric forces obtained at optimal muscle length. Contractions with different stretch magnitudes (10, 20, and 30 deg at a constant speed of 10 deg s(-1)) and different speeds (10, 20, and 60 deg s(-1) over a range of 30 deg) were performed in triplicate in a random order, balanced design. We found three novel results: (i) there was steady-state force enhancement following stretch in voluntarily contracted muscles; (ii) some force enhancement persisted following relaxation of the muscle and (iii) force enhancement, for some stretch conditions, exceeded the maximum isometric force at optimal muscle length. We conclude from these results that voluntary muscle contraction produces similar force enhancement to that observed in the past with electrically stimulated preparations. Therefore, steady-state force enhancement may play a role in everyday movements. Furthermore, these results suggest that non-uniformities in sarcomere length do not, at least not exclusively, account for the force enhancement following active muscle stretch, and that the stretch magnitude-dependent passive force enhancement observed here may be responsible for the enhancement of force above the isometric reference force at optimal muscle length.