Biomedical subjects

Walter Herzog

Publications and source records attributed to Walter Herzog.

At least 19 recordsLinked to original sources

PubMed2006

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.

Animals↗

PubMed2006

Model-based estimation of muscle forces exerted during movements.

Estimation of individual muscle forces during human movement can provide insight into neural control and tissue loading and can thus contribute to improved diagnosis and management of both neurological and orthopaedic conditions. Direct measurement of muscle forces is generally not feasible in a clinical setting, and non-invasive methods based on musculoskeletal modeling should therefore be considered. The current state of the art in clinical movement analysis is that resultant joint torques can be reliably estimated from motion data and external forces (inverse dynamic analysis). Static optimization methods to transform joint torques into estimates of individual muscle forces using musculoskeletal models, have been known for several decades. To date however, none of these methods have been successfully translated into clinical practice. The main obstacles are the lack of studies reporting successful validation of muscle force estimates, and the lack of user-friendly and efficient computer software. Recent advances in forward dynamics methods have opened up new opportunities. Forward dynamic optimization can be performed such that solutions are less dependent on measured kinematics and ground reaction forces, and are consistent with additional knowledge, such as the force-length-velocity-activation relationships of the muscles, and with observed electromyography signals during movement. We conclude that clinical applications of current research should be encouraged, supported by further development of computational tools and research into new algorithms for muscle force estimation and their validation.

Algorithms↗

PubMed2006

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.

Animals↗

PubMed2006

The dependence of force enhancement on activation in human adductor pollicis.

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

Adaptation, Physiological↗

PubMed2006

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

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

Adult↗

PubMed2006

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

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

Adult↗

PubMed2006

Effect of altering starting length and activation timing of muscle on fiber strain and muscle damage.

Muscle strain injuries are some of the most frequent injuries in sports and command a great deal of attention in an effort to understand their etiology. These injuries may be the culmination of a series of subcellular events accumulated through repetitive lengthening (eccentric) contractions during exercise, and they may be influenced by a variety of variables including fiber strain magnitude, peak joint torque, and starting muscle length. To assess the influence of these variables on muscle injury magnitude in vivo, we measured fiber dynamics and joint torque production during repeated stretch-shortening cycles in the rabbit tibialis anterior muscle, at short and long muscle lengths, while varying the timing of activation before muscle stretch. We found that a muscle subjected to repeated stretch-shortening cycles of constant muscle-tendon unit excursion exhibits significantly different joint torque and fiber strains when the timing of activation or starting muscle length is changed. In particular, measures of fiber strain and muscle injury were significantly increased by altering activation timing and increasing the starting length of the muscle. However, we observed differential effects on peak joint torque during the cyclic stretch-shortening exercise, as increasing the starting length of the muscle did not increase torque production. We conclude that altering activation timing and muscle length before stretch may influence muscle injury by significantly increasing fiber strain magnitude and that fiber dynamics is a more important variable than muscle-tendon unit dynamics and torque production in influencing the magnitude of muscle injury.

Animals↗

PubMed2006

Lower leg muscle atrophy in ankle osteoarthritis.

The aim of this study was to determine changes in the lower leg muscles associated with ankle osteoarthritis. Fifteen unilateral ankle osteoarthritis patients and fifteen age-gender-matched normal subjects were assessed with clinical [osteoarthritis latency time, pain, alignment, AOFAS ankle score, ankle range of motion (ROM), calf circumference], radiological (ankle osteoarthritis grading), and muscular-physiological parameters [isometric maximal voluntary ankle torque, surface electromyography of the anterior tibial (AT), medial gastrocnemius (MG), soleus (SO), and peroneus longus (PL) muscle]. The osteoarthritis patients had increased pain (6.8 points) and reduced AOFAS score (33.7 points) compared to the control group. Compared to the contralateral healthy leg, the arthritic leg showed reduced mean dorsi-/plantar flexion ROM (16.0 degrees), reduced mean calf circumference (2.1 cm), smaller mean dorsiflexion (16.4 Nm) and plantar flexion (15.8 Nm) torques, lower mean electromyography frequency for all muscles (AT -22.6 Hz; MG -27.3 Hz; SO -25.9 Hz; PL -28.5 Hz), and lower mean electromyography intensity in the AT [-28.0x10(3) (microv)2], MG [-13.3x10(3) (microv)2], and PL [-12.8x10(3) (microv)2]. SO mean electromyography intensity was not significantly changed [+2.0x10(3) (microv)2]. Unilateral ankle osteoarthritis is associated with atrophic changes of the lower leg muscles. This study supports previous observations on muscle dysfunction in knee osteoarthritis.

Adult↗

PubMed2006

Analysis of the mechanical behavior of chondrocytes in unconfined compression tests for cyclic loading.

Experimental evidence indicates that the biosynthetic activity of chondrocytes is associated with the mechanical environment. For example, excessive, repetitive loading has been found to induce cell death, morphological and cellular damage, as seen in degenerative joint disease, while cyclic, physiological-like loading has been found to trigger a partial recovery of morphological and ultrastructural aspects in osteoarthritic human articular chondrocytes. Mechanical stimuli are believed to influence the biosynthetic activity via the deformation of cells. However, the in situ deformation of chondrocytes for cyclic loading conditions has not been investigated experimentally or theoretically. The purpose of the present study was to simulate the mechanical response of chondrocytes to cyclic loading in unconfined compression tests using a finite element model. The material properties of chondrocytes and extracellular matrix were considered to be biphasic. The time-histories of the shape and volume variations of chondrocytes at three locations (i.e., surface, center, and bottom) within the cartilage were predicted for static and cyclic loading conditions at two frequencies (0.02 and 0.1 Hz) and two amplitudes (0.1 and 0.2 MPa). Our results show that cells at different depths within the cartilage deform differently during cyclic loading, and that the depth dependence of cell deformation is influenced by the amplitude of the cyclic loading. Cell deformations under cyclic loading of 0.02 Hz were found to be similar to those at 0.1 Hz. We conclude from the simulation results that, in homogeneous cartilage layers, cell deformations are location-dependent, and further are affected by load magnitude. In physiological conditions, the mechanical environment of cells are even more complex due to the anisotropy, depth-dependent inhomogeneity, and tension-compression non-linearity of the cartilage matrix. Therefore, it is feasible to speculate that biosynthetic responses of chondrocytes to cyclic loading depend on cell location and load magnitude.

Animals↗

PubMed2005

Control of ground reaction forces by hindlimb muscles during cat locomotion.

It has been proposed that biarticular muscles are primarily responsible for the control of the direction of external forces, as their activation is closely related and highly sensitive to the direction of external forces. This functional role for biarticular muscles has been supported qualitatively by experimental evidence, but has never been tested quantitatively for lack of a mathematical/mechanical formulation of this theory and the difficulty of measuring individual muscle forces during voluntary movements. The purposes of this study were: (1) to define rules for muscular coordination based on the control of external forces; (2) to develop a model of the cat hindlimb that allows for the calculation of the magnitude and direction of the ground reaction forces (GRFs) produced by individual hindlimb muscles; and (3) to test if the coordination of mono- and biarticular cat hindlimb muscles is related to the control of the resultant GRF. We measured the GRF, hindlimb kinematics, selected muscle forces and activations during cat locomotion. Then, the measured muscle forces were used as input to the hindlimb model to compute the muscle-induced GRF. We assume that if activation (and possibly force) increased as the muscle-induced component of GRF approximated the resultant GRF, then that muscle was used by the central nervous system (CNS) to help control the direction of the external GRF. During cat walking, medial gastrocnemius (MG) and plantaris (PL) forces increased with increasing proximity to the GRF, while soleus (SOL) forces and vastus lateralis (VL) activations did not. SOL and VL activation were most strongly related to the vertical and parallel (braking/accelerating) component of the GRF, respectively. We concluded from these results that MG and PL are primarily responsible for the control of the direction of the GRF, while SOL primarily functions as an anti-gravity muscle, and VL as an acceleration/deceleration muscle.

Acceleration↗

PubMed2005

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.

Animals↗

PubMed2005

The magnitude of muscle strain does not influence serial sarcomere number adaptations following eccentric exercise.

It is generally accepted that eccentric exercise, when performed by a muscle that is unaccustomed to that type of contraction, results in a delayed onset of muscle soreness (DOMS). A prolonged exposure to eccentric exercise leads to the disappearance of the signs and symptoms associated with DOMS, which has been referred to as the repeated bout effect (RBE). Although the mechanisms underlying the RBE remain unclear, several mechanisms have been proposed, including the serial sarcomere number addition following exercise induced muscle damage. In the traditional DOMS and RBE protocols, muscle injury has been treated as a global parameter, with muscle force and strain assumed to be uniform throughout the muscle. To assess the effects of muscle-tendon unit strain, fiber strain, torque and injury on serial sarcomere number adaptations, three groups of New Zealand White (NZW) rabbits were subjected to chronic repetitive eccentric exercise bouts of the ankle dorsiflexors for 6 weeks. These eccentric exercise protocols consisted of identical muscle tendon unit (MTU) strain, but other mechanical factors were systematically altered. Following chronic eccentric exercise, serial sarcomere number adaptations were not identical between the three eccentric exercise protocols, and serial sarcomere number adaptations were not uniform across all regions of the muscle. Peak torque and relaxation fiber strain were the best predictors of serial sarcomere number across all three protocols. Therefore, MTU strain does not appear to be the primary cause for sarcomerogenesis, and differential adaptations within the muscle may be explained by the nonuniform architecture of the muscle, resulting in differential local fiber strains.

Adaptation, Physiological↗

PubMed2005

Should tendon and aponeurosis be considered in series?

Fibres, aponeuroses, and tendons are often considered mechanically "in series" in skeletal muscles. This notion has led to oversimplified calculations of fibre forces from tendon forces, to incorrect derivations of constitutive laws for aponeuroses, and to misinterpretations of the recovery of elastic energy in stretch-shortening cycles of muscles. Here, we demonstrate theoretically, using examples of increasing complexity, that tendon and aponeurosis are not in series in a muscle fibre-aponeurosis-tendon complex. We then demonstrate that assuming the tendon and aponeurosis to be in series can lead to the appearance of mechanical work creation in these passive viscoelastic structures, a result that is mechanically impossible. Finally, we explain the mechanical role of the incompressible muscle matrix in force transmission from fibres to aponeuroses and tendon, and emphasize that incompressibility necessitates the introduction of extra forces necessary to maintain this constraint. Unfortunately, this requirement eliminates, for all but the simplest cases, a theoretical approach of muscle modeling based on intuitive free-body diagrams.

Animals↗

PubMed2005

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.

Animals↗

PubMed2005

Differential serial sarcomere number adaptations in knee extensor muscles of rats is contraction type dependent.

Sarcomerogenesis, or the addition of sarcomeres in series within a fiber, has a profound impact on the performance of a muscle by increasing its contractile velocity and power. Sarcomerogenesis may provide a beneficial adaptation to prevent injury when a muscle consistently works at long lengths, accounting for the repeated-bout effect. The association between eccentric exercise, sarcomerogenesis and the repeated-bout effect has been proposed to depend on damage, where regeneration allows sarcomeres to work at shorter lengths for a given muscle-tendon unit length. To gain additional insight into this phenomenon, we measured fiber dynamics directly in the vastus lateralis (VL) muscle of rats during uphill and downhill walking, and we measured serial sarcomere number in the VL and vastus intermedius (VI) after chronic training on either a decline or incline grade. We found that the knee extensor muscles of uphill walking rats undergo repeated active concentric contractions, and therefore they suffer no contraction-induced injury. Conversely, the knee extensor muscles during downhill walking undergo repeated active eccentric contractions. Serial sarcomere numbers change differently for the uphill and downhill exercise groups, and for the VL and VI muscles. Short muscle lengths for uphill concentric-biased contractions result in a loss of serial sarcomeres, and long muscle lengths for downhill eccentric-biased contractions result in a gain of serial sarcomeres.

Adaptation, Physiological↗

PubMed2005

Proposed model of botulinum toxin-induced muscle weakness in the rabbit.

Osteoarthritic patients show only a weak association between radiographic signs of joint disease and joint pain and disability. Conversely, muscle weakness is one of the earliest and most common symptoms of patients with osteoarthritis (OA). However, while many experimental models of osteoarthritis include a component of muscular weakness, no model has isolated this factor satisfactorily. Therefore, the purpose of this study was to develop and validate an experimental animal model of muscle weakness for future use in the study of OA. Botulinum Type-A toxin (BTX-A) was uni-laterally injected into the quadriceps musculature of New Zealand white rabbits (3.5 units/kg). Isometric knee extensor torque at a range of knee angles and stimulation frequencies, and quadriceps muscle mass, were quantified for control animals, and at one- and six-months post-repeated injections, in both, the experimental and the contralateral hindlimb. Ground reaction forces were measured in all animals while hopping across two force platforms. Isometric knee extension torque and quadriceps muscle mass was systematically decreased in the experimental hindlimb. Vertical ground reaction forces in the push off phase of hopping were also decreased in the experimental compared to control hindlimbs. We conclude that BTX-A injection into the rabbit musculature creates functional and absolute muscle weakness in a reproducible manner. Therefore, this model may be used to systematically study the possible effects of muscle weakness on joint degeneration, either as an isolated intervention, or in combination with other interventions (anterior cruciate ligament transection, meniscectomy) known to create knee joint degeneration.

Animals↗

PubMed2005

Predictions of co-contraction depend critically on degrees-of-freedom in the musculoskeletal model.

In biomechanics, the calculation of individual muscle forces during movements is based on a model of the musculoskeletal system and a method for extracting a unique set of muscle forces. To obtain a unique set of muscle forces, non-linear, static optimisation is commonly used. However, the optimal solution is dependent on the musculoskeletal geometry, and single joints may be represented using one, two or three degrees-of-freedom. Frequently, a system with multiple degrees-of-freedom is replaced with a system that contains a subset of all the possible degrees-of-freedom. For example, the cat ankle joint is typically modelled as a planar joint with its primary degree-of-freedom (plantar-dorsiflexion), whereas, the actual joint has three rotational degrees-of-freedom. Typically, such simplifications are justified by the idea that the reduced case is contained as a specific solution of the more general case. However, here we demonstrate that the force-sharing solution space of a general, three degrees-of-freedom musculoskeletal system does not necessarily contain the solutions from the corresponding one or two degrees-of-freedom systems. Therefore, solutions of a reduced system, in general, are not sub-set solutions of the actual three degrees-of-freedom system, but are independent solutions that are often incompatible with solutions of the actual system. This result shows that representing a three degrees-of-freedom system as a one or two degrees-of-freedom system gives force-sharing solutions that cannot be extrapolated to the actual system, and vice-versa. These results imply that general solutions cannot be extracted from models with fewer degrees-of-freedom than the actual system. They further emphasise the need for precise geometric representation of the musculoskeletal system, if general force-sharing rules are to be derived.

Algorithms↗

PubMed2005

Quantification of muscle fiber strain during in vivo repetitive stretch-shortening cycles.

Muscles subjected to lengthening contractions exhibit evidence of subcellular disruption, arguably a result of fiber strain magnitude. Due to the difficulty associated with measuring fiber strains during lengthening contractions, fiber length estimates have been used to formulate relationships between the magnitude of injury and mechanical measures such as fiber strain. In such protocols, the series compliance is typically minimized by removing the distal tendon and/or preactivating the muscle. These in vitro and in situ experiments do not represent physiological contractions well where fiber strain and muscle strain may be disassociated; thus the mechanisms of in vivo muscle injury remain elusive. The purpose of this paper was to quantify fiber strains during lengthening contractions in vivo and assess the potential role of fiber strain in muscle injury following repetitive stretch-shortening cycles. Using intact New Zealand White rabbit dorsiflexors, fiber strain and joint torque were measured during 50 stretch-shortening cycles. We were able to show that fiber length changes are disassociated from muscle tendon unit length changes and that complex fiber dynamics during these cycles prevent easy estimates of fiber strains. In addition, fiber strains vary, depending on how they are defined, and vary from repetition to repetition, thereby further complicating the potential relationship between muscle injury and fiber strain. We conclude from this study that, during in vivo stretch-shortening cycles, the relationship between fiber strain and muscle injury is complex. This is due, in part, to temporal effects of repeated loading on fiber strain magnitude that may be explained by an increasing compliance of the contractile element as exercise progresses.

Adaptation, Physiological↗