Stretch Amplitude Research Articles

Systematic nonlinear relations between joint mechanics and the neural reflex response with changes in stretch amplitude at the wrist

The effects on both joint mechanics and the neural stretch reflex of changes in amplitude of stretch ranging from within the region of short range stiffness up to 3% of resting muscle length were quantified. The level of activation of the primary agonist was held constant but there was a small but systematic increase in activation of the other flexor and extensor muscles as stretch amplitude increased. The patterns of change with stretch amplitude in both the joint mechanics and stretch reflex properties were non-linear but systematic and were well described by power relationships that accounted for high proportions of variance. With an increase in stretch amplitude, joint stiffness, viscosity, damping ratio and natural frequency decreased. In parallel with these mechanical changes, the neural reflex coherence increased and the phase advance and gain decreased. Multiple regression analyses partitioned the variation in the joint mechanics that was attributable to the various factors and it was found that the variation of the mechanics was almost entirely attributable to the variation of the neural reflex gain, which accounted for 93% of the changes in the stiffness, viscosity and natural frequency and 82% of the changes in the damping ratio. It is concluded that joint mechanics are significantly affected by changes in the neural reflex gain.

Stretching Skeletal Muscle: Chronic Muscle Lengthening through Sarcomerogenesis

Skeletal muscle responds to passive overstretch through sarcomerogenesis, the creation and serial deposition of new sarcomere units. Sarcomerogenesis is critical to muscle function: It gradually re-positions the muscle back into its optimal operating regime. Animal models of immobilization, limb lengthening, and tendon transfer have provided significant insight into muscle adaptation in vivo. Yet, to date, there is no mathematical model that allows us to predict how skeletal muscle adapts to mechanical stretch in silico. Here we propose a novel mechanistic model for chronic longitudinal muscle growth in response to passive mechanical stretch. We characterize growth through a single scalar-valued internal variable, the serial sarcomere number. Sarcomerogenesis, the evolution of this variable, is driven by the elastic mechanical stretch. To analyze realistic three-dimensional muscle geometries, we embed our model into a nonlinear finite element framework. In a chronic limb lengthening study with a muscle stretch of 1.14, the model predicts an acute sarcomere lengthening from 3.09m to 3.51m, and a chronic gradual return to the initial sarcomere length within two weeks. Compared to the experiment, the acute model error was 0.00% by design of the model; the chronic model error was 2.13%, which lies within the rage of the experimental standard deviation. Our model explains, from a mechanistic point of view, why gradual multi-step muscle lengthening is less invasive than single-step lengthening. It also explains regional variations in sarcomere length, shorter close to and longer away from the muscle-tendon interface. Once calibrated with a richer data set, our model may help surgeons to prevent muscle overstretch and make informed decisions about optimal stretch increments, stretch timing, and stretch amplitudes. We anticipate our study to open new avenues in orthopedic and reconstructive surgery and enhance treatment for patients with ill proportioned limbs, tendon lengthening, tendon transfer, tendon tear, and chronically retracted muscles.

Frequency-dependent amplification of stretch-evoked excitatory input in spinal motoneurons.

Voltage-dependent calcium and sodium channels mediating persistent inward currents (PICs) amplify the effects of synaptic inputs on the membrane potential and firing rate of motoneurons. CaPIC channels are thought to be relatively slow, whereas the NaPIC channels have fast kinetics. These different characteristics influence how synaptic inputs with different frequency content are amplified; the slow kinetics of Ca channels suggest that they can only contribute to amplification of low frequency inputs (<5 Hz). To characterize frequency-dependent amplification of excitatory postsynaptic potentials (EPSPs), we measured the averaged stretch-evoked EPSPs in cat medial gastrocnemius motoneurons in decerebrate cats at different subthreshold levels of membrane potential. EPSPs were produced by muscle spindle afferents activated by stretching the homonymous and synergist muscles at frequencies of 5-50 Hz. We adjusted the stretch amplitudes at different frequencies to produce approximately the same peak-to-peak EPSP amplitude and quantified the amount of amplification by expressing the EPSP integral at different levels of depolarization as a percentage of that measured with the membrane hyperpolarized. Amplification was observed at all stretch frequencies but generally decreased with increasing stretch frequency. However, in many cells the amount of amplification was greater at 10 Hz than at 5 Hz. Fast amplification was generally reduced or absent when the lidocaine derivative QX-314 was included in the electrode solution, supporting a strong contribution from Na channels. These results suggest that NaPICs can combine with CaPICs to enhance motoneuron responses to modulations of synaptic drive over a physiologically significant range of frequencies.

Evaluation of Mechanical Properties of Skeletal Muscle with Strain Injury

To discuss the mechanism of muscle strain injury from biomechanical viewpoints, the change of mechanical properties of injured skeletal muscle was evaluated experimentally. We induced strain injury to rabbit tibialis anterior muscle by applying a single tension loading/unloading process under the conditions of various stretch amplitude, stretch rate, and muscle activation in situ. The results showed that isometric contractile force decreased with increasing stretch amplitude during the injury-induction process. Multiple regression analyses were conducted for the results and they showed that the stretch amplitude played a dominant role in the decrease of the contractility. The failure stress decreased significantly with the increasing stretch amplitude and dissipation energy during the injury-induction process. Moreover, the failure stresses of the muscle injured under unstimulated conditions obviously decreased in comparison with those of the muscles in intact and injured under stimulated conditions. On the basis of these results and previous experimental studies, we concluded that muscle activity played a significant roll to prevent the decrease of the failure stress and that the damage mechanism of strain injury depended on the muscle activity during injury-induction process.

Calcium Dependence of Titin-Regulated Passive Forces in Skeletal Muscle Fibers

There is evidence that the passive forces produced by titin in skeletal muscles may be regulated by Ca2+. Studies have shown an upwards shift in the passive force-sarcomere length (SL) relation when muscle fibres are tested with a high concentration of Ca2+ and the myosin-actin interaction is abolished. In this study we tested the hypothesis that there is a direct relation between the concentrations of Ca2+ and the cross-bridge independent increase in passive forces. Single fibres were isolated from the rabbit psoas muscle and transferred into an experimental chamber, between a force transducer and a motor arm. Fibres were activated in a range of Ca2+ concentrations (pCa2+ between 4.5 and 9.0), before and after administration of the myosin inhibitor blebbistatin, which caused the maximal isometric force to decrease by 93.5%. After blebbistatin administration, the fibres were submitted to a protocol in which they underwent consecutive step-stretches, starting at an initial SL of 2.5μm (amplitude of stretch: 5% initial SL, duration 300 ms, pauses between stretches: 30 sec). We observed an upwards shift in the passive force-SL relation when pCa2+ was lower than 6.4 (increase from 1.06 mN/mm2 to 4.28 mN/mm2 at SL of 2.8μm and from 14.99 mN/mm2 to 27.85 mN/mm2 at SL of 3.8μm). Decreasing the pCa2+ below 6.4 did not change the forces further. The results suggest that there is not a direct relation between passive forces and Ca2+ concentrations; instead there is a threshold for Ca2+ regulation of passive forces via titin (in the condition investigated, a pCa2+ of 6.4), beyond which force does not change significantly.

Optimizing an Intermittent Stretch Paradigm Using ERK1/2 Phosphorylation Results in Increased Collagen Synthesis in Engineered Ligaments

Dynamic mechanical input is believed to play a critical role in the development of functional musculoskeletal tissues. To study this phenomenon, cyclic uniaxial mechanical stretch was applied to engineered ligaments using a custom-built bioreactor and the effects of different stretch frequency, amplitude, and duration were determined. Stretch acutely increased the phosphorylation of p38 (3.5±0.74-fold), S6K1 (3.9±0.19-fold), and ERK1/2 (2.45±0.32-fold). The phosphorylation of ERK1/2 was dependent on time, rather than on frequency or amplitude, within these constructs. ERK1/2 phosphorylation was similar following stretch at frequencies from 0.1 to 1 Hz and amplitudes from 2.5% to 15%, whereas phosphorylation reached maximal levels at 10 min of stretch and returned toward basal within 60 min of stretch. Following a single 10-min bout of cyclic stretch, the cells remained refractory to a second stretch for up to 6 h. Using the phosphorylation of ERK1/2 as a guide, the optimum stretch paradigm was hypothesized to be 10 min of stretch at 2.5% of resting length repeated every 6 h. Consistent with this hypothesis, 7 days of stretch using this optimized intermittent stretch program increased the collagen content of the grafts more than a continuous stretch program (CTL=3.1%±0.44%; CONT=4.8%±0.30%; and INT=5.9%±0.56%). These results suggest that short infrequent bouts of loading are optimal for improving engineered tendon and ligament physiology.

Cyclic Stress at mHz Frequencies Aligns Fibroblasts in Direction of Zero Strain

Recognition of external mechanical signals is vital for mammalian cells. Cyclic stretch, e.g. around blood vessels, is one such signal that induces cell reorientation from parallel to almost perpendicular to the direction of stretch. Here, we present quantitative analyses of both, cell and cytoskeletal reorientation of umbilical cord fibroblasts. Cyclic strain of preset amplitudes was applied at mHz frequencies. Elastomeric chambers were specifically designed and characterized to distinguish between zero strain and minimal stress directions and to allow accurate theoretical modeling. Reorientation was only induced when the applied stretch exceeded a specific amplitude, suggesting a non-linear response. However, on very soft substrates no mechanoresponse occurs even for high strain. For all stretch amplitudes, the angular distributions of reoriented cells are in very good agreement with a theory modeling stretched cells as active force dipoles. Cyclic stretch increases the number of stress fibers and the coupling to adhesions. We show that changes in cell shape follow cytoskeletal reorientation with a significant temporal delay. Our data identify the importance of environmental stiffness for cell reorientation, here in direction of zero strain. These in vitro experiments on cultured cells argue for the necessity of rather stiff environmental conditions to induce cellular reorientation in mammalian tissues.

Alignment dependent chemisorption of vibrationally excited CH4(ν3) on Ni(100), Ni(110), and Ni(111)

We present a stereodynamics study of the dissociative chemisorption of vibrationally excited methane on the (100), (110), and (111) planes of a nickel single crystal surface. Using linearly polarized infrared excitation of the antisymmetric C-H stretch normal mode vibration (ν(3)), we aligned the angular momentum and C-H stretch amplitude of CH(4)(ν(3)) in the laboratory frame and measured the alignment dependence of state-resolved reactivity of CH(4) for the ν(3) = 1, J = 0-3 quantum states over a range of incident translational energies. For all three surfaces studied, in-plane alignment of the C-H stretch results in the highest dissociation probability and alignment along the surface normal in the lowest reactivity. The largest alignment contrast between the maximum and minimum reactivity is observed for Ni(110), which has its surface atoms arranged in close-packed rows separated by one layer deep troughs. For Ni(110), we also probed for alignment effects relative to the direction of the Ni rows. In-plane C-H stretch alignment perpendicular to the surface rows results in higher reactivity than parallel to the surface rows. The alignment effects on Ni(110) and Ni(100) are independent of incident translational energy between 10 and 50 kJ/mol. Quantum state-resolved reaction probabilities are reported for CH(4)(ν(3)) on Ni(110) for translational energies between 10 and 50 kJ/mol.

Rhythmic arm cycling differentially modulates stretch and H-reflex amplitudes in soleus muscle

During rhythmic arm cycling, soleus H-reflex amplitudes are reduced by modulation of group Ia presynaptic inhibition. This suppression of reflex amplitude is graded to the frequency of arm cycling with a threshold of 0.8Hz. Despite the data on modulation of the soleus H-reflex amplitude induced by rhythmic arm cycling, comparatively little is known about the modulation of stretch reflexes due to remote limb movement. Therefore, the present study was intended to explore the effect of arm cycling on stretch and H-reflex amplitudes in the soleus muscle. In so doing, additional information on the mechanism of action during rhythmic arm cycling would be revealed. Although both reflexes share the same afferent pathway, we hypothesized that stretch reflex amplitudes would be less suppressed by arm cycling because they are less inhibited by presynaptic inhibition. Failure to reject this hypothesis would add additional strength to the argument that Ia presynaptic inhibition is the mechanism modulating soleus H-reflex amplitude during rhythmic arm cycling. Participants were seated in a customized chair with feet strapped to footplates. Three motor tasks were performed: static control trials and arm cycling at 1 and 2Hz. Soleus H-reflexes were evoked using single 1ms pulses of electrical stimulation delivered to the tibial nerve at the popliteal fossa. A constant M-wave and ~6% MVC activation of soleus were maintained across conditions. Stretch reflexes were evoked using a single sinusoidal pulse at 100Hz given by a vibratory shaker placed over the triceps surae tendon and controlled by a custom-written LabView program. Results demonstrated that rhythmic arm cycling that was effective for conditioning soleus H-reflexes did not show a suppressive effect on the amplitude of the soleus stretch reflex. We suggest this indicates that stretch reflexes are less sensitive to conditioning by rhythmic arm movement, as compared to H-reflexes, due to the relative insensitivity to Ia presynaptic inhibition.

Amplitude- and velocity-dependency of rigidity measured at the wrist in Parkinson’s disease

ObjectiveQuantify the effects of increased amplitude and rate of muscle stretch on parkinsonian rigidity. MethodsEighteen subjects with Parkinson’s disease participated in this study. Subjects’ tested hand was passively displaced through 60° and 90° ranges of wrist flexion and extension at velocities of 50°/s and 280°/s in both treated and untreated conditions. Joint angular position, resistance torque, and surface electromyography (EMG) of the wrist flexors and extensors were recorded. Rigidity was quantified by normalized work scores and normalized angular impulses for flexion and extension, separately. Reflex responses of stretched and shortened muscles were quantified by mean EMG and EMG ratio. A series of ANOVAs was performed to determine the effect of amplitude, velocity and medication on selected variables. ResultsBoth work scores and angular impulses revealed that the larger displacement amplitude and the higher velocity were associated with significantly greater rigidity, increased EMG ratio and mean EMG of stretched muscles. Dopaminergic medication was not associated with a reduction in rigidity. ConclusionsParkinsonian rigidity is modulated by the amplitude and rate of muscle stretch. SignificanceThese findings shed light on the biomechanical underpinnings and physiological characteristics of rigidity and may inform clinical rigidity assessment in Parkinson’s disease.

A continuum damage model for the high-cycle fatigue life prediction of styrene-butadiene rubber under multiaxial loading

In the present contribution, the relationship between the fatigue life of styrene-butadiene rubber (SBR) and the stretch amplitude was established. Focusing on the multiaxial loading effect on the life duration of SBR, experimental tests were conducted using cylindrical specimens subjected to tension and torsion loadings under constant and variable amplitudes. Based upon the continuum damage mechanics approach, a three-dimensional model was derived and coupled with the cracking energy density criterion to predict the fatigue life of SBR. The capabilities of the model, which requires only three damage parameters to be identified, were analysed and a good agreement between predicted values and experimental data were clearly highlighted for tension and torsion loadings both in constant and variable amplitudes.

Monitoring markers of muscle damage during a 3 week periodized drop-jump exercise programme

The aim of this study was to examine changes in indirect markers of muscle damage during 3 weeks of stretch–shortening exercise with a progressively increasing load and continued modulation of various key training variables. Eight healthy untrained men performed a drop-jump programme involving a progressive increase in load impact with respect to the number of jumps performed, drop (platform) height, squat depth amplitude, and addition of weights. Maximal concentric and isometric knee extensor strength were assessed immediately before and 10 min after each training session. Voluntary and 100 Hz-stimulation-evoked torque decreased acutely after each training session relative to pre-exercise values (P < 0.05) but recovered before the subsequent training session. Post-exercise plasma creatine kinase activity increased from 162.2 ± 56.2 IU · l−1 to 284.3 ± 116.3 IU · l−1 at 48 h after the first training session (P < 0.05) and remained marginally elevated throughout the training period. The present results indicate that detrimental muscle damage can be avoided with drop-jump training even with the gradual introduction of more demanding exercise induced by increasing the volume, intensity, and muscle stretch amplitude. These findings suggest that the human neuromuscular system is highly adaptable to progressively varied loading demands during stretch–shortening exercise training.

Crossbridge recruitment by stretching does not invalidate force spectroscopy experiments in living skeletal muscle fibres

Crossbridge recruitment by stretching does not invalidate force spectroscopy experiments in living skeletal muscle fibres

Tactile spatial acuity is reduced by skin stretch at the human wrist

The skin is an elastic organ that is continuously distorted as our limbs move. The hypothesis that the precision of human tactile localisation is reduced when the skin is stretched, with concurrent expansion of receptive fields (RFs) was tested. Locognosic acuity over the dorsal wrist area was quantified during application of background stretch by (a) Wrist-Bend (skin stretch combined with non-cutaneous proprioceptor activation) and (b) Skin-Pull (skin stretch alone). Participants identified the perceived direction (distal or proximal) of brief test stimuli, applied along a 7-point linear array, relative to a central reference locus. Performance was significantly reduced during the large amplitude compared to the small amplitude of tonic skin stretch, but there was no effect of stretch mode (Wrist-Bend, Skin-Pull), nor was the effect of stretch amplitude modulated by the mode of stretch. Locognosic acuity was poorer than baseline accuracy for the large amplitude skin stretches, for both application modes, but did not differ significantly from baseline for either of the small amplitude stretches. We interpret these observations as corroborating the long-held assumption that tactile localisation is primarily dependent upon the RF dimensions, and associated innervation densities, of regional touch units. The finding that performance was reduced to a similar extent under Skin-Pull and Wrist-Bend conditions suggests that non-cutaneous proprioceptors had rather little tonic modulatory effect.

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 2.5–3s 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.

The influence of tendon compliance on muscle power output and efficiency during cyclic contractions

Muscle power output and efficiency during cyclical contractions are influenced by the timing and duration of stimulation of the muscle and the interaction of the muscle with its mechanical environment. It has been suggested that tendon compliance may reduce the energy required for power production from the muscle by reducing the required shortening of the muscle fibres. Theoretically this may allow the muscle to maintain both high power output and efficiency during cyclical contraction; however, this has yet to be demonstrated experimentally. To investigate how tendon compliance might act to increase muscle power output and/or efficiency, we attached artificial tendons of varying compliance to muscle fibre bundles in vitro and measured power output and mechanical efficiency during stretch-shorten cycles (2 Hz) with a range of stretch amplitudes and stimulation patterns. The results showed that peak power, average power output and efficiency (none of which can have direct contributions from the compliant tendon) all increased with increasing tendon compliance, presumably due to the tendon acting to minimise muscle energy use by allowing the muscle fibres to shorten at optimal speeds. Matching highly compliant tendons with a sufficiently large amplitude length change and appropriate stimulation pattern significantly increased the net muscle efficiency compared with stiff tendons acting at the same frequency. The maximum efficiency for compliant tendons was also similar to the highest value measured under constant velocity and force conditions, which suggests that tendon compliance can maximise muscle efficiency in the conditions tested here. These results provide experimental evidence that during constrained cyclical contractions, muscle power and efficiency can be enhanced with compliant tendons.

Effects of prolonged walking on neural and mechanical components of stretch responses in the human soleus muscle

After repeated passive stretching, tendinous tissue compliance increases in the human soleus (SOL) muscle-tendon unit. During movement, such changes would have important consequences for neural and mechanical stretch responses. This study examined the existence of such effects in response to a 75 min walking intervention. Eleven healthy subjects walked on a treadmill at 4 km h(1) with a robotic stretch device attached to the left leg. Ultrasonography was used to measure SOL fascicle lengths, and surface EMG activity was recorded in the SOL and tibialis anterior (TA) muscles. Perturbations of 6 deg were imposed at three different measurement intervals: Pre (immediately before the walking intervention), Mid (after approximately 30 min of walking) and Post (immediately after the intervention). Between the Pre-Mid and Mid-Post intervals, subjects walked for 30 min at a gradient of 3%. After the intervention, the amplitude and velocity of fascicle stretch both decreased (by 46 and 59%, respectively; P < 0.001) in response to a constant external perturbation, as did short (33%; P < 0.01) and medium (25%; P < 0.01) latency stretch reflex amplitudes. A faster perturbation elicited at the end of the protocol resulted in a recovery of fascicle stretch velocities and short latency reflex amplitudes to the pre-exercise values. These findings suggest that repeated stretching and shortening of a muscle-tendon unit can induce short-term structural changes in the tendinous tissues during human walking. The data also highlight the effect of these changes on neural feedback from muscle sensory afferents.

Mechanical and neural stretch responses of the human soleus muscle at different walking speeds

During human walking, a sudden trip may elicit a Ia afferent fibre mediated short latency stretch reflex. The aim of this study was to investigate soleus (SOL) muscle mechanical behaviour in response to dorsiflexion perturbations, and to relate this behaviour to short latency stretch reflex responses. Twelve healthy subjects walked on a treadmill with the left leg attached to an actuator capable of rapidly dorsiflexing the ankle joint. Ultrasound was used to measure fascicle lengths in SOL during walking, and surface electromyography (EMG) was used to record muscle activation. Dorsiflexion perturbations of 6 deg were applied during mid-stance at walking speeds of 3, 4 and 5 km h(-1). At each walking speed, perturbations were delivered at three different velocities (slow: approximately 170 deg s(-1), mid: approximately 230 deg s(-1), fast: approximately 280 deg s(-1)). At 5 km h(-1), fascicle stretch amplitude was 34-40% smaller and fascicle stretch velocity 22-28% slower than at 3 km h(-1) in response to a constant amplitude perturbation, whilst stretch reflex amplitudes were unchanged. Changes in fascicle stretch parameters can be attributed to an increase in muscle stiffness at faster walking speeds. As stretch velocity is a potent stimulus to muscle spindles, a decrease in the velocity of fascicle stretch at faster walking speeds would be expected to decrease spindle afferent feedback and thus stretch reflex amplitudes, which did not occur. It is therefore postulated that other mechanisms, such as altered fusimotor drive, reduced pre-synaptic inhibition and/or increased descending excitatory input, acted to maintain motoneurone output as walking speed increased, preventing a decrease in short latency reflex amplitudes.

Does residual force enhancement increase with increasing stretch magnitudes?

It is generally accepted that force enhancement in skeletal muscles increases with increasing stretch magnitudes. However, this property has not been tested across supra-physiological stretch magnitudes and different muscle lengths, thus it is not known whether this is a generic property of skeletal muscle, or merely a property that holds for small stretch magnitudes within the physiological range. Six cat soleus muscles were actively stretched with magnitudes varying from 3 to 24mm at three different parts of the force–length relationship to test the hypothesis that force enhancement increases with increasing stretch magnitude, independent of muscle length. Residual force enhancement increased consistently with stretch amplitudes on the descending limb of the force–length relationship up to a threshold value, after which it reached a plateau. Force enhancement did not increase with stretch amplitude on the ascending limb of the force–length relationship. Passive force enhancement was observed for all test conditions, and paralleled the behavior of the residual force enhancement. Force enhancement increased with stretch magnitude when stretching occurred at lengths where there was natural passive force within the muscle. These results suggest that force enhancement does not increase unconditionally with increasing stretch magnitude, as is generally accepted, and that increasing force enhancement with stretch appears to be tightly linked to that part of the force–length relationship where there is naturally occurring passive force.

Titin-induced force enhancement and force depression: A ‘sticky-spring’ mechanism in muscle contractions?

The sliding filament and crossbridge theories do not suffice to explain a number of muscle experiments. For example, from the entire muscle to myofibrils, predictions of these theories were shown to underestimate the force output during and after active tissue stretch. The converse applies to active tissue shortening. In addition to the crossbridge cycle, we propose that another molecular mechanism is effective in sarcomere force generation. We suggest that, when due to activation, myosin binding sites are available on actin, the giant protein titin's PEVK region attaches itself to the actin filament at those sites. As a result, the molecular spring length is dramatically reduced. This leads to increased passive force when the sarcomere is stretched and to decreased or even negative passive force when the sarcomere shortens. Moreover, during shortening, the proposed mechanism interferes with active-force production by inhibiting crossbridges. Incorporation of a simple ‘sticky-spring’ mechanism model into a Hill-type model of sarcomere dynamics offers explanations for several force-enhancement and force-depression effects. For example, the increase of the sarcomere force compared to the force predicted solely by the sliding filament and crossbridge theories depends on the stretch amplitude and on the working range. The same applies to the decrease of sarcomere force during and after shortening. Using only literature data for its parameterization, the model predicts forces similar to experimental results.