Stretch-shortening cycles (SSCs) outperform shortening contractions preceded by isometric contractions in terms of enhanced force/torque, work, and power production during shortening. This so-called SSC effect is presumably related to the active muscle stretch before shortening in SSCs. However, it remains unclear whether the effects of stretch-induced higher preload level or stretch-induced history dependence maximize the SSC effect. Therefore, we analyzed fascicle behavior, muscle-tendon unit (MTU) shortening work, and torque/force (n = 12 participants) via ultrasound and dynamometry during electrically stimulated submaximal plantar flexion contractions from 10° plantarflexion to 15° dorsiflexion. To elucidate the effects of preload level and preload modality (i.e., contraction type) on shortening performance, muscle-tendon unit shortening was preceded by fixed-end (SHO), active stretch (SSC), and preload-matched fixed-end (MATCHED) contractions. Before shortening, MATCHED and SCC had the same preload level (1% torque difference), similar joint position, and muscle fascicle lengths. Compared with SHO, shortening work was significantly (P < 0.001, partial η2 = 0.749) increased by 85% and 55% for SSC and MATCHED, respectively, with SSC shortening work being significantly higher than MATCHED (P = 0.016). This indicates that preload contributes by 65% to the overall SSC effect so that 35% needs to be referred to stretched-induced history-dependent mechanisms. In addition, SSC showed larger fascicle forces at the end of shortening (P < 0.001) and 20% less depressed isometric torque following shortening compared with MATCHED (P < 0.001). As potential decoupling effects by the series elastic element were controlled by matching the preload levels, we conclude that the difference between SSC and MATCHED is related to stretch-induced long-lasting history-dependent effects.NEW & NOTEWORTHY Using a torque-matched preload protocol, we found that 2/3 of the performance enhancement in muscle-tendon unit stretch-shortening cycles (SSCs) is caused by the increased preload level. The remaining 1/3 is owed to the long-lasting history-dependent effects triggered during the stretch in SSCs. This increased performance output is attributed to passive elastic structures within the contractile element that do not require additional muscle activation, therefore contributing to the higher efficiency of the neuromuscular system in SSCs.

BACKGROUND: Following active lengthening or shortening contractions, isometric steady-state torque is increased (residual force enhancement; rFE) or decreased (residual force depression; rFD), respectively, compared to fixed-end isometric contractions at the same muscle length and level of activation. Though the mechanisms underlying this history dependence of force have been investigated extensively, little is known about the influence of exercise-induced muscle weakness on rFE and rFD.
OBJECTIVE: Assess rFE and rFD in the dorsiflexors at 20%, 60%, and 100% maximal voluntary torque (MVC) and activation matching, and electrically stimulated at 20% MVC, prior to, 1 h following, and 24 h following 150 maximal eccentric dorsiflexion contractions.
METHODS: Twenty-six participants (13 male, 24.7 ± 2.0y; 13 female, 22.5 ± 3.6y) were seated in a dynamometer with their right hip and knee angle set to 110° and 140°, respectively, with an ankle excursion set between 0° and 40° plantar flexion (PF). MVC torque, peak twitch torque, and prolonged low frequency force depression were used to assess eccentric exercise-induced neuromuscular impairments. History-dependent contractions consisted of a 1 s isometric (40°PF or 0°PF) phase, a 1 s shortening or lengthening phase (40°/s), and an 8 s isometric (0°PF or 40°PF) phase.
RESULTS: Following eccentric exercise; MVC torque was decreased, prolonged low frequency force depression was present, and both rFE and rFD increased for all maximal and submaximal conditions.
CONCLUSIONS: The history dependence of force during voluntary torque and activation matching, and electrically stimulated contractions is amplified following eccentric exercise. It appears that a weakened neuromuscular system amplifies the magnitude of the history-dependence of force.

The steady-state isometric force produced by skeletal muscle after active shortening and stretching is depressed and enhanced, respectively, compared to purely isometric force produced at corresponding final lengths and level of activation. One hypothesis proposed to account for these force depression (FD) and force enhancement (FE) properties is a change in cross-bridge cycling kinetics. The rate of cross-bridge attachment (f) and/or cross-bridge detachment (g) may be altered following active shortening and active stretching, leading to FD and FE respectively. Experiments elucidating cross-bridge kinetics in actively shortened and stretched muscle preparations and their corresponding purely isometric contractions have yet to be performed. The aim of this study was to investigate cross-bridge cycling kinetics of muscle fibres at steady-state following active shortening and stretching. This was done by determining muscle fibre stiffness and rate of active force redevelopment following a quick release - re-stretch protocol (kTR). Applying these measures to equations previously used in the literature for a two-state cross-bridge cycling model (attached/detached cross-bridges) allowed us to determine apparent f and g, the proportion of attached cross-bridges, and the force produced per cross-bridge. kTR, apparent f and g, the proportion of attached cross-bridges and the force produced per cross-bridge were significantly decreased following active shortening compared to corresponding purely isometric contractions, indicating a change in cross-bridge cycling kinetics. Additionally, we showed no change in cross-bridge cycling kinetics following active stretch compared to corresponding purely isometric contractions. These findings suggest FD is associated with changes in cross-bridge kinetics, while FE is not.

When an active muscle is stretched and kept isometrically active, the resulting force is enhanced compared to a purely isometric reference contraction at the same muscle length and activity; a generally accepted muscle property called residual force enhancement (rFE). Interestingly, studies on voluntary muscle action regularly identify a significant number of participants not showing rFE. Therefore, the aim was to unmask possible confounders for this non-responsive behavior. Ten participants performed maximum voluntary isometric plantarflexion contractions with and without preceding stretch. Contractions were accompanied by the assessment of voluntary activation using the twitch-interpolation technique. The same test protocol was repeated four additional times with a least on day rest in-between. Additionally, at the first and fifth sessions, a submaximal tetanic muscle-stimulation condition was added. At both muscle-stimulation sessions mean rFE higher 10% (p < 0.028) was found. In contrast, during voluntary muscle action, individual participants showed inconsistent rFE across sessions and only one session (#3) had significant rFE (5%; p = 0.023) in group means. As all participants clearly had rFE in electrical stimulation conditions, structural deficits cannot explain the missing rFE in voluntary muscle action. However, we also did not find variability in voluntary activation levels or muscle activity as the confounding characteristics of \"non-responders.\"

Active state titin\'s effects have been studied predominantly in sarcomere or muscle fiber segment level and an understanding of its functional effects in the context of a whole muscle, and the mechanism of those is lacking. By representing experimentally observed calcium induced stiffening and actin-titin interaction induced reduced free spring length effects of active state titin in our linked fiber-matrix mesh finite element model, our aim was to study the mechanism of effects and particularly to determine the functionally more effective active state titin model. Isolated EDL muscle of the rat was modeled and three cases were studied: passive state titin (no change in titin constitutive equation in the active state), active state titin-I (constitutive equation involves a higher stiffness in the active state) and active state titin-II (constitutive equation also involves a strain shift coefficient accounting for titin\'s reduced free spring length). Isometric muscle lengthening was imposed (initial to long length, lm = 28.7 mm to 32.7 mm). Compared to passive state titin, (i) active state titin-I and II elevates muscle total (lm = 32.7 mm: 14% and 29%, respectively) and active (lm = 32.7 mm: 37.5% and 77.4%, respectively) forces, (ii) active state titin-II also shifts muscle\'s optimum length to a longer length (lm = 29.6 mm), (iii) active state titin-I and II limits sarcomere shortening (lm = 32.7 mm: up to 10% and 20%, respectively). Such shorter sarcomere effect characterizes active state titin\'s mechanism of effects. These effects become more pronounced and functionally more effective if not only calcium induced stiffening but also a reduced free spring length of titin is accounted for.

In everyday muscle action or exercises, a stretch-shortening cycle (SSC) is performed under different levels of intensity. Thereby, compared to a pure shortening contraction, the shortening phase in a SSC shows increased force, work, and power. One mechanism to explain this performance enhancement in the SSC shortening phase is, besides others, referred to the phenomenon of stretch-induced increase in muscle force (known as residual force enhancement; rFE). It is unclear to what extent the intensity of muscle action influences the contribution of rFE to the SSC performance enhancement. Therefore, we examined the knee torque, knee kinematics, m. vastus lateralis fascicle length, and pennation angle changes of 30 healthy adults during isometric, shortening (CON) and stretch-shortening (SSC) conditions of the quadriceps femoris. We conducted maximal voluntary contractions (MVC) and submaximal electrically stimulated contractions at 20%, 35%, and 50% of MVC. Isometric trials were performed at 20° knee flexion (straight leg: 0°), and dynamic trials followed dynamometer-driven ramp profiles of 80°-20° (CON) and 20°-80°-20° (SSC), at an angular velocity set to 60°/s. Joint mechanical work during shortening was significantly (p < 0.05) enhanced by up to 21% for all SSC conditions compared to pure CON contractions at the same intensity. Regarding the steady-state torque after the dynamic phase, we found significant torque depression for all submaximal SSCs compared to the isometric reference contractions. There was no difference in the steady-state torque after the shortening phases between CON and SSC conditions at all submaximal intensities, indicating no stretch-induced rFE that persisted throughout the shortening. In contrast, during MVC efforts, the steady-state torque after SSC was significantly less depressed compared to the steady-state torque after the CON condition (p = 0.034), without significant differences in the m. vastus lateralis fascicle length and pennation angle. From these results, we concluded that the contribution of the potential enhancing factors in SSCs of the m. quadriceps femoris is dependent on the contraction intensity and the type of activation.

The resulting muscular performance is considered notably higher during a stretch shortening cycle (SSC) compared to an isolated concentric contraction. Thus, the present study examined the occurrence and magnitude of rowing performance enhancement after a flexion-extension cycle (FEC) of the legs compared to both concentric contractions only and isometric pre-contraction. Therefore, 31 sub-elite male rowers (age: 25 ± 6 years, height: 1.90 ± 0.02 m, weight: 91 ± 10 kg, weekly training volume: 11.4 ± 5.3 h/week, rowing experience: 7.1 ± 2.7 years) randomly completed (a) isolated concentric rowing strokes (DRIVE), (b) single FEC-type rowing strokes (SLIDE-DRIVE), and (c) rowing strokes with an isometric pre-contraction (ISO-DRIVE). The resulting rowing power (Prow), leg power (Pleg), and work per stroke (WPS) were recorded using motion-capturing, force, and rotation sensors. Comparison of DRIVE and SLIDE-DRIVE revealed significantly (p < 0.05) higher Prow (+11.8 ± 14.0%), Pleg (+19.6 ± 26.7%), and WPS (+9.9 ± 10.5%) during SLIDE-DRIVE. Compared to ISO-DRIVE, Pleg (+9.8 ± 26.6%) and WPS (+6.1 ± 6.7%) are again significantly (p < 0.05) higher for SLIDE-DRIVE. In conclusion, notably higher work and power outputs (compared to an isolated concentric contraction) during FEC rowing referred to an underlying SSC. Future ultrasound studies should elucidate whether a real SSC on the muscle tendon unit level account for these performance enhancements.

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.

A systematic literature search was conducted to review the force-enhancing mechanisms caused by a stretch-shortening cycle (SSC). The review aims to yield an overview of the contraction modalities influencing the SSC performance in animals and single joint movements in humans. The search was executed in common with the PRISMA statement. CINAHL, MEDLINE (via ProQuest), PubMed, ScienceDirect, Scopus and Web of Science databases were used for the systematic search from its inception until February 2019. A quality assessment was conducted with a modified Downs and Black checklist. Twenty-five studies were included. SSC effects, leading to increased force/work during a SSC and a reduced force depression (FD) compared to a pure shortening contraction, are existent on different levels of the muscle, from single fiber experiments to the level of in vivo muscle-tendon complex. Muscle performance is dependent on shortening velocity, shortening distance, stretch distance, the time (transition phase) between stretch and shortening and the active prephase duration. Concerning stretch velocity we found conflicting results. The findings from this systematic review indicate that the mechanisms in the early phase of shortening are associated with pre-activation effects, elastic recoil and stretch reflex. Furthermore, we speculate that residual force enhancement (RFE) is mainly responsible for an increased steady-state force compared to a pure shortening contraction.

An exceptional property of skeletal muscles that distinguishes them from other soft tissues is their ability to contract by generating active forces, which in turn are initiated by an electrochemical trigger. Some of these so-called active material properties are generally characterised using isometric contraction experiments at various muscle lengths. In this context, experimental observations revealed that unlike the widespread assumption in muscle modelling, reaction forces indeed depend on so-called history effects, which can be classified into force enhancement and force depression. For the experimental settings of force enhancement, two subsequent isometric contractions are interrupted by an isokinetic extension. The isometric reaction force is increased after the isokinetic extension with respect to a reference measurement, while in the case of force depression, isokinetic shortening is responsible for forces below a certain isometric reference measurement. Most theoretical investigations of force enhancement and force depression use one-dimensional models to simulate the force response considering muscle deformation to be homogeneous. In contrast, the aim of the present study is to analyse history effects in skeletal muscle tissue using a three-dimensional geometry model of the whole muscle-tendon unit. Therefore, a purely phenomenological approach is presented. The model is implemented in the finite element framework to analyse history effects for the boundary value problem of the entire three-dimensional muscle-tendon geometry. The constitutive model shows good agreement with the experimental data. Furthermore, the simulations reveal information about the inhomogeneous stretch distributions within the muscle tissues.