Muscular force production after concentric contraction

The steady-state force following active shortening does not reach the maximum isometric force associated with the final length. Isolated extensor digitorum longus and soleus muscles from mice (NMRI strain) were used to investigate the force produced by a muscle, and some parameters hypothetically influencing this shortening-induced force depression. The muscles were pre-stimulated at fixed length, shortened and then held isometrically to give maximum post-shortening forces, before de-stimulation. The shortening magnitude was 0.18, 0.36 or 0.72mm (about 2-7% of optimal length), time of shortening was chosen as 0.03, 0.06 and 0.12s, and final length as +0.72, 0 and -0.72mm, related to optimal length. The mechanical work during active shortening was evaluated by integrating the product of force and shortening velocity over the shortening period. The results show a positive correlation between the force depression and the mechanical work, whereas the force depression was not correlated to the velocity of shortening. Depression of the passive force component was also observed following all stimulations. Experiments show that the fully stimulated redevelopment of isometric force following concentric contraction follows a time function similar to the creation of force when isometric muscle is initially stimulated. The conclusion is that the isometric force development after active shortening can be well described by an asymptotic force which is decided by the produced work, and the initial isometric time constant.     

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 enhancement above the initial isometric force on the descending limb of the force-length relationship

Edman et al. (J. General Physiol. 80 (1982) 769) observed in single fibres of frog that the steady-state forces following active fibre stretch were greater than the purely isometric force obtained at the length from which the stretch was initiated. Operating on the descending limb of the force-length relationship, such a result can only be explained within the framework of the sarcomere length non-uniformity theory, if some fibre segments shortened during the fibre stretch. However, such a result was not found, leaving Edman's observation unexplained. Force enhancement above the initial isometric force has not been investigated systematically in whole muscle, and therefore it is not known whether this property is also part of whole muscle mechanics. The purpose of this study was to test if the steady-state forces following active stretch of cat semitendinosus were greater than the corresponding purely isometric forces at the muscle length from which the stretch was started. Cat semitendinosus was stretched by various amounts on the descending limb of the force-length relationship, and the steady-state forces following these stretches were compared to the corresponding isometric forces at the initial and final muscle lengths. In 109 of 131 tests, the steady-state forces following stretching were greater than the isometric forces at the initial muscle lengths. Force enhancement increased with increasing amounts of stretching, and force enhancement above the initial isometric force was more likely to occur following stretches of great compared to small amplitude. Passive forces following active muscle stretching were often significantly greater than the passive forces at the same muscle length following an isometric contraction or a passive stretching of the muscle. This observation was made consistently at the longest muscle lengths tested. It appears, therefore, that there is a passive force that accounts for part of the force enhancement above the isometric force at the initial muscle length, and that provides increased passive force when a muscle is actively, rather than passively, stretched at long muscle lengths. We conclude that cat semitendinosus demonstrates steady-state force enhancement above the corresponding purely isometric force at the initial muscle length on the descending limb of the force-length relationship for many contractile conditions, and that a unique, and so far undetected, passive, parallel element contributes to this force enhancement, particularly at long muscle lengths where muscle is assumed to be most vulnerable to injuries associated with sarcomere length instability.     

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.     

Stretch-induced,steady-state force enhancement in single skeletal muscle fibers exceeds the isometric force at optimum fiber length

Stretch-induced force enhancement has been observed in a variety of muscle preparations and on structural levels ranging from single fibers to in vivo human muscles. It is a well-accepted property of skeletal muscle. However, the mechanism causing force enhancement has not been elucidated, although the sarcomere-length non-uniformity theory has received wide support. The purpose of this paper was to re-investigate stretch-induced force enhancement in frog single fibers by testing specific hypotheses arising from the sarcomere-length non-uniformity theory. Single fibers dissected from frog tibialis anterior (TA) and lumbricals (n=12 and 22, respectively) were mounted in an experimental chamber with physiological Ringer's solution (pH=7.5) between a force transducer and a servomotor length controller. The tetantic force-length relationship was determined. Isometric reference forces were determined at optimum length (corresponding to the maximal, active, isometric force), and at the initial and final lengths of the stretch experiments. Stretch experiments were performed on the descending limb of the force-length relationship after maximal tetanic force was reached. Stretches of 2.5-10% (TA) and 5-15% lumbricals of fiber length were performed at 0.1-1.5 fiber lengths/s. The stretch-induced, steady-state, active isometric force was always equal or greater than the purely isometric force at the muscle length from which the stretch was initiated. Moreover, for stretches of 5% fiber length or greater, and initiated near the optimum length of the fiber, the stretch-enhanced active force always exceeded the maximal active isometric force at optimum length. Finally, we observed a stretch-induced enhancement of passive force. We conclude from these results that the sarcomere length non-uniformity theory alone cannot explain the observed force enhancement, and that part of the force enhancement is associated with a passive force that is substantially greater after active compared to passive muscle stretch.     

Residual force enhancement and force depression in human single muscle fibres

Residual force depression (rFD) and residual force enhancement (rFE) are intrinsic contractile properties of muscle. rFD is characterized as a decrease in steady-state isometric force following active shortening compared with a purely isometric contraction at the same muscle length and level of activation. By contrast, isometric force is increased following active lengthening compared to a reference isometric contraction at the same muscle length and level of activation; this is termed rFE. To date, there have been no investigations of rFD and rFE in human muscle fibres, therefore the purpose of this study was to determine whether rFD and rFE occur at the single muscle fibre level in humans. rFD and rFE were investigated in maximally activated single muscle fibres biopsied from the vastus lateralis of healthy adults. To induce rFD, fibres were activated and shortened from an average sarcomere length (SL) of 3.2–2.6 μm. Reference isometric contractions were performed at an average SL of 2.6 μm. To induce rFE, fibres were actively lengthened from an average SL of 2.6–3.2 μm and a reference isometric contraction was performed at an average SL of 3.2 μm. Isometric steady-state force was lower following active shortening (p < 0.05), and higher following active lengthening (p < 0.05), as compared to the reference isometric contractions. We demonstrated rFD and rFE in human single fibres which is consistent with previous animal models. The non-responder phenomenon often reported in rFE studies involving voluntary contractions at the whole human level was not observed at the single fibre level.     

Residual force enhancement in myofibrils and sarcomeres

Residual force enhancement has been observed following active stretch of skeletal muscles and single fibres. However, there has been intense debate whether force enhancement is a sarcomeric property, or is associated with sarcomere length instability and the associated development of non-uniformities. Here, we studied force enhancement for the first time in isolated myofibrils (n=18) that, owing to the strict in series arrangement, allowed for evaluation of this property in individual sarcomeres (n=79). We found consistent force enhancement following stretch in all myofibrils and each sarcomere, and forces in the enhanced state typically exceeded the isometric forces on the plateau of the force-length relationship. Measurements were made on the plateau and the descending limb of the force-length relationship and revealed gross sarcomere length non-uniformities prior to and following active myofibril stretching, but in contrast to previous accounts, revealed that sarcomere lengths were perfectly stable under these experimental conditions. We conclude that force enhancement is a sarcomeric property that does not depend on sarcomere length instability, that force enhancement varies greatly for different sarcomeres within the same myofibril and that sarcomeres with vastly different amounts of actin-myosin overlap produce the same isometric steady-state forces. This last finding was not explained by differences in the amount of contractile proteins within sarcomeres, vastly different passive properties of individual sarcomeres or (half-) sarcomere length instabilities, suggesting that the basic mechanical properties of muscles, such as force enhancement, force depression and creep, which have traditionally been associated with sarcomere instabilities and the corresponding dynamic redistribution of sarcomere lengths, are not caused by such instabilities, but rather seem to be inherent properties of the mechanisms of contraction.     

Residual force enhancement following eccentric induced muscle damage

During lengthening of an activated skeletal muscle, the force maintained following the stretch is greater than the isometric force at the same muscle length. This is termed residual force enhancement (RFE), but it is unknown how muscle damage following repeated eccentric contractions affects RFE. Using the dorsiflexors, we hypothesised muscle damage will impair the force generating sarcomeric structures leading to a reduction in RFE. Following reference maximal voluntary isometric contractions (MVC) in 8 young men (26.5±2.8y) a stretch was performed at 30°/s over a 30° ankle excursion ending at the same muscle length as the reference MVCs (30° plantar flexion). Surface electromyography (EMG) of the tibialis anterior and soleus muscles was recorded during all tasks. The damage protocol involved 4 sets of 25 isokinetic (30°/s) lengthening contractions. The same measures were collected at baseline and immediately post lengthening contractions, and for up to 10min recovery. Following the lengthening contraction task, there was a 30.3±6.4% decrease in eccentric torque (P<0.05) and 36.2±9.7% decrease in MVC (P<0.05) compared to baseline. Voluntary activation using twitch interpolation and RMS EMG amplitude of the tibialis anterior remained near maximal without increased coactivation for MVC. Contrary to our hypothesis, RFE increased (～100-250%) following muscle damage (P<0.05). It appears stretch provided a mechanical strategy for enhanced muscle function compared to isometric actions succeeding damage. Thus, active force of cross-bridges is decreased because of impaired excitation-contraction coupling but force generated during stretch remains intact because force contribution from stretched sarcomeric structures is less impaired.     

Force recovery after activated shortening in whole skeletal muscle: transient and steady-state aspects of force depression.

The depression of isometric force after active shortening is a well-accepted characteristic of skeletal muscle, yet 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 depression (FD). To identify the transient aspects of FD and its relation to shortening speed, shortening amplitude, and muscle mechanical work, in situ experiments were conducted in soleus muscle-tendon units of anesthetized cats. The period immediately after shortening, in which force recovers toward steady state, was fit by using an exponential recovery function (R2 > 0.99). Statistical analyses revealed that steady-state FD (FD(ss)) increased with shortening amplitude and mechanical work. This FD(ss) increase was always accompanied by a significant decrease in force recovery rate. Furthermore, a significant reduction in stiffness was observed after all activated shortenings, presumably because of a reduced proportion of attached cross bridges. These results were interpreted with respect to the two most prominent proposed mechanisms of force depression: sarcomere length nonuniformity theory (7, 32) and a stress-induced inhibition of cross-bridge binding in the newly formed actin-myosin overlap zone (14, 28). We hypothesized that the latter could describe both steady-state and transient aspects of FD using a single scalar variable, the mechanical work done during shortening. As either excursion (overlap) or force (stress) is increased, mechanical work increases, and cross-bridge attachment would become more inhibited, as supported by this study in which an increase in mechanical work resulted in a slower recovery to a more depressed steady-state force.     

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 15mM 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.     

The effect of shortening history on isometric and dynamic muscle function

Despite numerous reports on isometric force depression, few reports have quantified force depression during active muscle shortening (dynamic force depression). The purpose of this investigation was to determine the influence of shortening history on isometric force following active shortening, force during isokinetic shortening, and velocity during isotonic shortening. The soleus muscles of four cats were subjected to a series of isokinetic contractions at three shortening velocities and isotonic contractions under three loads. Muscle excursions initiated from three different muscle lengths but terminated at a constant length. Isometric force produced subsequent to active shortening, and force or shortening velocity produced at a specific muscle length during shortening, were compared across all three conditions. Results indicated that shortening history altered isometric force by up to 5%, force during isokinetic shortening up to 30% and shortening velocity during isotonic contractions by up to 63%. Furthermore, there was a load by excursion interaction during isotonic contractions such that excursion had the most influence on shortening velocity when the loads were the greatest. There was not a velocity by excursion interaction during isokinetic contractions. Isokinetic and isotonic power–velocity relationships displayed a downward shift in power as excursions increased. Thus, to discuss force depression based on differences in isometric force subsequent to active shortening may underestimate its importance during dynamic contractions. The presence of dynamic force depression should be realized in sport performance, motor control modeling and when controlling paralyzed limbs through artificial stimulation.     

The history dependence of force production in mammalian skeletal muscle following stretch-shortening and shortening-stretch cycles

The purpose of this study was to determine the history dependence of force production during and following stretch-shortening and shortening-stretch cycles in mammalian skeletal muscle. Thirty-three different isometric, stretch, shortening, stretch-shortening and shortening-stretch experiments were preformed in cat soleus (n=8) using previously established methods. Stretch-shortening and shortening-stretch cycles are not commutative with respect to the isometric forces following the length changes. Whereas force depression following shortening is virtually unaffected by previous stretching of the muscle, force enhancement following stretch depends in a dose-dependent manner on the amount of muscle shortening preceding the stretch. The history dependence of isometric force following shortening-stretch cycles can conveniently be modelled using an elastic (compressive and tensile) element that engages at the length of muscle activation. Such an "elastic" mechanism has been proposed by Edman and Tsuchiya (1996) (Edman, K.A. P., Tsuchiya, T., 1996. Strain of passive elements during force enhancement by stretch in frog mucle fibres. Journal of Physiology 490. 1, 191-205) based on experimental observations, and has been implemented theoretically in a rheological model of muscle (Forcinito et al., 1997) (Forcinito, M., Epstein, M., Herzog, W., 1997. Theoretical considerations on myofibril stiffness. Biophysics Journal 72, 1278-1286). The history dependence of isometric force following stretch-shortening cycles appears independent of the stretch preceding the shortening, except perhaps, if stretching occurs at very high speeds (i.e. 6-10 times fibre length per second). The results of this study are hard to reconcile with the two major mechanisms associated with history dependence of force production: sarcomere length non-uniformity (Edman et al., 1993) and stress-induced cross-bridge inhibition (Maréchal and Plaghki, 1979) (Maréchal, G., Plaghki, L., 1979. The deficit of the isometric tetanic tension redeveloped after a relase of frog muscle at a constant velocity. Journal of General Physiology 73, 453-467). It appears that studying the history dependence of force production under more functionally relevant conditions than has been done to date may provide new information that contributes to our understanding of possible mechanisms associated with force depression and force enhancement following muscular length changes.     

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.     

Relationship between force and stiffness in muscle fibers after stretch.

The purpose of this study was to evaluate the relationship between force and stiffness after stretch of activated fibers, while simultaneously changing contractility by interfering with the cross-bridge kinetics and muscle activation. Single fibers dissected from lumbrical muscles of frogs were placed at a length 20% longer than the plateau of the force-length relationship, activated, and stretched by 5 and 10% of fiber length (speed: 40% fiber length/s). Experiments were conducted with maximal and submaximal stimulation in Ringer solution and with the addition of 2 and 5 mM of the myosin inhibitor 2,3-butanedione monoxime (BDM) to the solution. The steady-state force after stretch of an activated fiber was higher than the isometric force produced at the corresponding length in all conditions investigated. Lowering the frequency of stimulation decreased the force and stiffness during isometric contractions, but it did not change force enhancement and stiffness enhancement after stretch. Administration of BDM decreased the force and stiffness during isometric contractions, but it increased the force enhancement and stiffness enhancement after stretch. The relationship between force enhancement and stiffness suggests that the increase in force after stretch may be caused by an increase in the proportion of cross bridges attached to actin. Because BDM places cross bridges in a weakly bound, pre-powerstroke state, our results further suggest that force enhancement is partially associated with a recruitment of weakly bound cross bridges into a strongly bound state.     

Evidence of residual force enhancement for multi-joint leg extension

Force enhancement is a well accepted property of skeletal muscle and has been observed at all structural levels ranging from single myofibrils to voluntarily activated m. quadriceps femoris in vivo. However, force enhancement has not been studied for multi-joint movements like human leg extension; therefore knowledge about its relevance in daily living remains limited. The purpose of this study was to determine whether there is force enhancement during maximal voluntary multi-joint leg extension. Human leg extension was studied (n=22) on a motor driven leg press dynamometer where external reaction forces under the feet as well as activity of 8 lower extremity muscles were measured. In addition, torque in the ankle and knee joints was calculated using inverse dynamics. The steady-state isometric force, joint torques, and muscle activation after active stretch (20° stretch amplitude at 60°/s) were compared with the corresponding values obtained during isometric reference contractions. There was consistent force enhancement during and following stretch for both forces and joint torques. Potentiation during stretch reached values between 26% and 30%, while a significant force enhancement of 10.5–12.3% and 4.3–7.4% remained 0.5–1 and 2.5–3 s after stretch, respectively. During stretch, EMG signals of m. gastrocnemius medialis and lateralis were significantly increased, while following stretch all analyzed muscles showed the same activity as during the reference contractions. We conclude from these results that force enhancement exists in everyday movements and should be accounted for when analyzing or modelling human movement.     

Modulation of passive force in single skeletal muscle fibres

In this study, we investigated the effects of activation and stretch on the passive force-sarcomere length relationship in skeletal muscle. Single fibres from the lumbrical muscle of frogs were placed at varying sarcomere lengths on the descending limb of the force-sarcomere length relationship, and tetanic contractions, active stretches and passive stretches (amplitudes of ca 10% of fibre length at a speed of 40% fibre length/s) were performed. The passive forces following stretch of an activated fibre were higher than the forces measured after isometric contractions or after stretches of a passive fibre at the corresponding sarcomere length. This effect was more pronounced at increased sarcomere lengths, and the passive force-sarcomere length relationship following active stretch was shifted upwards on the force axis compared with the corresponding relationship obtained following isometric contractions or passive stretches. These results provide strong evidence for an increase in passive force that is mediated by a length-dependent combination of stretch and activation, while activation or stretch alone does not produce this effect. Based on these results and recently published findings of the effects of Ca2+ on titin stiffness, we propose that the observed increase in passive force is caused by the molecular spring titin.     

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

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.     

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.     

Residual force enhancement contributes to increased performance during stretch-shortening cycles of human plantar flexor muscles in vivo

It is well known that muscular force production is history-dependent, which results in enhanced (RFE) and depressed (RFD) steady-state forces after stretching and shortening, respectively. However, it remains unclear if force-enhancing mechanisms can contribute to increased performance during in vivo stretch-shortening cycles (SSCs) of human locomotor muscles. The purpose of this study was to investigate whether RFE-related mechanisms contribute to enhanced force and power output during SSCs of the human plantar flexor muscles. Net ankle torques of fourteen participants were measured during and after pure isometric, pure stretch, pure shortening, and SSC contractions when the triceps surae muscles were electrically stimulated at a submaximal level that resulted in 30% of their maximum isometric torque. Dynamic contractions were performed over an amplitude of 15°, from 5° plantar flexion to 10° dorsiflexion, at a speed of 120° s⁻¹. External ankle work during shortening was 11.6% greater during SSCs compared to pure shortening contractions (p = .003). Additionally, RFD after SSCs (8.6%) was reduced compared to RFD after pure shortening contractions (12.0%; p < .05). It is therefore concluded that RFE-related mechanisms contribute to increased performance following SSCs of human locomotor muscles. Since RFD after SSCs decreased although work during shortening was increased, we speculate that the relevant mechanism lies outside actin-myosin interaction. Finally, our data suggests that RFE might be relevant and beneficial for human locomotion whenever a muscle is stretched, but this needs to be confirmed.     

Effects of shortening on stretch-induced force enhancement in single skeletal muscle fibers

The main purpose of this study was to evaluate the effects of shortening on the stretch-induced force enhancement in single muscle fibers, and indirectly test the hypothesis that force enhancement may be associated with the engagement of a passive element upon activation. Fibers were placed on the descending limb of the force-length relationship, and stretch and shortening contractions were performed. Fibers underwent two sets of shortening-stretch cycles. First, fibers were shortened by a fixed amplitude and speed (10% fiber length, and at 40% fiber length/s), and then were stretched (10% fiber length, and at 40% fiber length/s) immediately following shortening, or 500 or 1000 ms following the shortening. Second, fibers were shortened by varying amounts (5%, 10% and 15% fiber length) and at a constant speed (40% fiber length/s) immediately preceding a given fiber stretch (10% fiber length, and at 40% fiber length/s). When stretching was immediately preceded by shortening, force enhancement was decreased proportionally with the shortening magnitude. When intervals were introduced between shortening and stretch, the effects of shortening on the stretch-induced force enhancement became less prominent. We concluded that, in contrast to published suggestions, shortening affects the stretch-induced force enhancement in an amplitude-dependent manner in single fibers, as it does in whole muscles, but this effect is diminished by increasing the time period between the shortening and stretch phases.