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.

Perturbations in K+ have long been considered a key factor in skeletal muscle fatigue. However, the exercise-induced changes in K+ intra-to-extracellular gradient is by itself insufficiently large to be a major cause for the force decrease during fatigue unless combined to other ion gradient changes such as for Na+. Whilst several studies described K+-induced force depression at high extracellular [K+] ([K+]e), others reported that small increases in [K+]e induced potentiation during submaximal activation frequencies, a finding that has mostly been ignored. There is evidence for decreased Cl- ClC-1 channel activity at muscle activity onset, which may limit K+-induced force depression, and large increases in ClC-1 channel activity during metabolic stress that may enhance K+ induced force depression. The ATP-sensitive K+ channel (KATP channel) is also activated during metabolic stress to lower sarcolemmal excitability. Taking into account all these findings, we propose a revised concept in which K+ has two physiological roles: (1) K+-induced potentiation and (2) K+-induced force depression. During low-moderate intensity muscle contractions, the K+-induced force depression associated with increased [K+]e is prevented by concomitant decreased ClC-1 channel activity, allowing K+-induced potentiation of sub-maximal tetanic contractions to dominate, thereby optimizing muscle performance. When ATP demand exceeds supply, creating metabolic stress, both KATP and ClC-1 channels are activated. KATP channels contribute to force reductions by lowering sarcolemmal generation of action potentials, whilst ClC-1 channel enhances the force-depressing effects of K+, thereby triggering fatigue. The ultimate function of these changes is to preserve the remaining ATP to prevent damaging ATP depletion.

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.

Our purpose was to use small-angle X-ray diffraction to investigate the structural changes within sarcomeres at steady-state isometric contraction following active lengthening and shortening, compared to purely isometric contractions performed at the same final lengths. We examined force, stiffness, and the 1,0 and 1,1 equatorial and M3 and M6 meridional reflections in skinned rabbit psoas bundles, at steady-state isometric contraction following active lengthening to a sarcomere length of 3.0 µm (15.4% initial bundle length at 7.7% bundle length/s), and active shortening to a sarcomere length of 2.6 µm (15.4% bundle length at 7.7% bundle length/s), and during purely isometric reference contractions at the corresponding sarcomere lengths. Compared to the reference contraction, the isometric contraction after active lengthening was associated with an increase in force (i.e., residual force enhancement) and M3 spacing, no change in stiffness and the intensity ratio I1,1/I1,0, and decreased lattice spacing and M3 intensity. Compared to the reference contraction, the isometric contraction after active shortening resulted in decreased force, stiffness, I1,1/I1,0, M3 and M6 spacings, and M3 intensity. This suggests that residual force enhancement is achieved without an increase in the proportion of attached cross-bridges, and that force depression is accompanied by a decrease in the proportion of attached cross-bridges. Furthermore, the steady-state isometric contraction following active lengthening and shortening is accompanied by an increase in cross-bridge dispersion and/or a change in the cross-bridge conformation compared to the reference contractions.

Muscle force is enhanced during shortening when shortening is preceded by an active stretch. This phenomenon is known as the stretch-shortening cycle (SSC) effect. For some stretch-shortening conditions this increase in force during shortening is maintained following SSCs when compared to the force following a pure shortening contraction. It has been suggested that the residual force enhancement property of muscles, which comes into play during the stretch phase of SSCs may contribute to the force increase after SSCs. Knowing that residual force enhancement is associated with a substantial reduction in metabolic energy per unit of force, it seems reasonable to assume that the metabolic energy cost per unit of force is also reduced following a SSC. The purpose of this study was to determine the energy cost per unit of force at steady-state following SSCs and compare it to the corresponding energy cost following pure shortening contractions of identical speed and magnitude. We hypothesized that the energy cost per unit of muscle force is reduced following SSCs compared to the pure shortening contractions. For the SSC tests, rabbit psoas fibers (n = 12) were set at an average sarcomere length (SL) of 2.4 μm, activated, actively stretched to a SL of 3.2 μm, and shortened to a SL of 2.6 or 3.0 μm. For the pure shortening contractions, the same fibers were activated at a SL of 3.2 μm and actively shortened to a SL of 2.6 or 3.0 μm. The amount of ATP consumed was measured over a 40 s steady-state total isometric force following either the SSCs or the pure active shortening contractions. Fiber stiffness was determined in an additional set of 12 fibers, at steady-state for both experimental conditions. Total force, ATP consumption, and stiffness were greater following SSCs compared to the pure shortening contractions, but ATP consumption per unit of force was the same between conditions. These results suggest that the increase in total force observed following SSCs was achieved with an increase in the proportion of attached cross-bridges and titin stiffness. We conclude that muscle efficiency is not enhanced at steady-state following SSCs.

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.

UNASSIGNED: What is the central question of this study? The length dependence of activation (LDA) is typically explained by a length-dependent increase in calcium sensitivity, but recently calcium-independent mechanisms have been suggested: does active muscle shortening provided by a compliant in-series component impact the muscle length at which force output is maximized, thus contributing to LDA? What is the main finding and its importance? Using an in situ rat medial gastrocnemius set-up and varying the magnitude of muscle shortening via an artificial compliant series-elastic component, we were unable to observe any change in optimal length between conditions, contrary to some previous findings. More research is therefore required to explain these discrepancies.
UNASSIGNED: The force-length relationship dictates the amount of force a muscle can produce as a function of its length, during maximal isometric contractions. When activation is submaximal, it has been shown that the length at which force production is highest (the optimal length) is longer. This is typically explained by a length-dependent increase in Ca2+ sensitivity, known as the \'length dependence of activation\'. Recent reports have implicated shortening against in-series compliance to be a potential factor in the observed optimal length (L0 ) of muscle, via the phenomenon of shortening-induced force depression (a phenomenon which describes the relative reduction in muscle force when a muscle is actively shortening to a given length compared to contracting isometrically at that same length). In the current study, rat medial gastrocnemius was stimulated with single and triple pulses (200 Hz) over a range of lengths, both with and without additional in-series compliance provided by a small piece of silicon tubing in series with the muscle, which allowed greater fascicle shortening upon activation. Fascicle length was measured using sonomicrometry crystals, and peak force (Fpeak ) and L0 were estimated by curve-fitting of the force-length data. The additional in-series compliance significantly reduced Fpeak by approximately 14% and 25% for the single and triple pulses, respectively (P = 0.003, P < 0.001), yet L0 remained unchanged (P = 0.405), suggesting that in our model, shortening against in-series compliance does not affect L0 . We offer potential explanations for the discrepancies seen and discuss whether the velocity of shortening may have a role in the length dependence of force.

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.

Residual torque depression (rTD) is the reduction in steady-state isometric torque following an active shortening contraction when compared with an isometric contraction at the same muscle length and activation level. We have shown that spinal excitability increases in the rTD state, yet the mechanisms remains unknown. Percutaneous electrical tendon stimulation was used to induce tendon-evoked inhibitory reflexes. We demonstrated that in the rTD state, reduced torque contributes to a reduction in inhibitory afferent feedback, which indicates that the history-dependent properties of muscle can alter spinal excitability and the voluntary control of submaximal contractions through changes in peripheral afferent feedback. Novelty Residual force depression is a basic property of skeletal muscle, which can influence spinal and supraspinal excitability via inhibitory reflex activity. Residual force depression alters the voluntary control of force.