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Skeletal muscle is a very dynamic tissue, thus accurate quantification of skeletal muscle stiffness throughout its functional range is crucial to improve the physical functioning and independence following pathology. Shear wave elastography (SWE) is an ultrasound-based technique that characterizes tissue mechanical properties based on the propagation of remotely induced shear waves. The objective of this study is to validate SWE throughout the functional range of motion of skeletal muscle for three ultrasound transducer orientations. We hypothesized that combining traditional materials testing (MTS) techniques with SWE measurements will show increased stiffness measures with increasing tensile load, and will correlate well with each other for trials in which the transducer is parallel to underlying muscle fibers. To evaluate this hypothesis, we monitored the deformation throughout tensile loading of four porcine brachialis whole-muscle tissue specimens, while simultaneously making SWE measurements of the same specimen. We used regression to examine the correlation between Young′s modulus from MTS and shear modulus from SWE for each of the transducer orientations. We applied a generalized linear model to account for repeated testing. Model parameters were estimated via generalized estimating equations. The regression coefficient was 0.1944, with a 95% confidence interval of (0.1463–0.2425) for parallel transducer trials. Shear waves did not propagate well for both the 45° and perpendicular transducer orientations. Both parallel SWE and MTS showed increased stiffness with increasing tensile load. This study provides the necessary first step for additional studies that can evaluate the distribution of stiffness throughout muscle.

The vast majority of skeletal muscle biomechanical studies have rightly focused on its active contractile properties. However, skeletal muscle passive biomechanical properties have significant clinical impact in aging and disease and are yet incompletely understood. This review focuses on the passive biomechanical properties of the skeletal muscle extracellular matrix (ECM) and suggests aspects of its structural basis. Structural features of the muscle ECM such as perimysial cables, collagen cross-links and endomysial structures have been described, but the way in which these structures combine to create passive biomechanical properties is not completely known. We highlight the presence and organization of perimysial cables. We also demonstrate that the analytical approaches that define passive biomechanical properties are not necessarily straight forward. For example, multiple equations, such as linear, exponential, and polynomial are commonly used to fit raw stress–strain data. Similarly, multiple definitions of zero strain exist that affect muscle biomechanical property calculations. Finally, the appropriate length range over which to measure the mechanical properties is not clear. Overall, this review summarizes our current state of knowledge in these areas and suggests experimental approaches to measuring the structural and functional properties of skeletal muscle.

Titin, the largest protein known, forms an elastic myofilament in the striated muscle sarcomere. To establish titin’s contribution to skeletal muscle passive stiffness, relative to that of the extracellular matrix, a mouse model was created in which titin’s molecular spring region was shortened by deleting 47 exons, the TtnΔ112-158 model. RNA sequencing and super-resolution microscopy predicts a much stiffer titin molecule. Mechanical studies with this novel mouse model support that titin is the main determinant of skeletal muscle passive stiffness. Unexpectedly, the in vivo sarcomere length working range was shifted to shorter lengths in TtnΔ112-158 mice, due to a ~ 30% increase in the number of sarcomeres in series (longitudinal hypertrophy). The expected effect of this shift on active force generation was minimized through a shortening of thin filaments that was discovered in TtnΔ112-158 mice. Thus, skeletal muscle titin is the dominant determinant of physiological passive stiffness and drives longitudinal hypertrophy. Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter ).

The study investigated the potential for obtaining more accurate spine joint reaction force (JRF) estimates from musculoskeletal models by incorporating dynamic stereo X-ray imaging (DSX)-based in vivo lumbar vertebral rotational and translational kinematics compared to generic, rhythm (RHY)-based kinematics, while also observing the influence of accompanying inputs: intervertebral segment stiffness and neutral state. A full-body OpenSim® musculoskeletal model, constructed by combining existing lower- and upper-body models, was driven based on one volunteer’s (female; age 25; 60.8 kg; 176 cm) anthropometrics and kinematics from a series of upright standing and straight-legged dynamic lifting tasks. The lumbar spine portion was modified in a step-wise manner to observe effects of: (1) RHY vs. DSX lumbar kinematics; (2) No disc (bushing) stiffness (NBS); generic, linear bushing stiffness (LBS); subject-specific nonlinear bushing stiffness (NLBS); (3) Upright standing (UP) vs. Supine (SUP) neutral state; (4) Weight lifted: 4.5 kg vs. 13.6 kg. L4L5 JRF from 24 model variations based on combinations of aforementioned parameters were compared. Rhythm-based kinematics without translational components tends to over-predict JRF (31% and 39% for compression and shear, respectively) compared to DSX-based kinematics. Additionally, differences due to accompanying passive stiffness and neutral state choice combinations were even larger (>50%), indicating heightened demand on the quality of these accompanying inputs. The study not only highlights model sensitivity to choices made regarding the three primary inputs—kinematics, passive stiffness and neutral state— separately, but also how interactions between these choices can result in significant variability in joint loading estimates.

PurposeThe acute effects of static stretching have been frequently studied, but the chronic effects have not been studied concurrently. Thus, this study aimed to investigate both the acute and chronic effects of static stretching at different intensities on flexibility.MethodsTwenty-three healthy men were randomly assigned to perform 1 min of static stretching 3 days/week for 4 weeks at 100% intensity (n = 12) or 120% intensity (n = 11). The acute effects of stretching were assessed by measuring the range of motion (ROM), peak passive torque, and passive stiffness before and after every stretching session; the chronic effects of stretching were assessed by measuring these outcomes at baseline and after 2 and 4 weeks of stretching.ResultsCompared with the 100% intensity group, the 120% intensity group had significantly greater acute increases in ROM after all 12 sessions, a significantly greater decrease in passive stiffness after 11 of 12 sessions, and a significantly greater increase in peak passive torque after six of 12 sessions. Regarding the chronic effects, ROM was significantly increased in both groups after 2 and 4 weeks of stretching. Peak passive torque significantly increased in the 100% intensity group after 2 and 4 weeks of stretching, and after 4 weeks in the 120% intensity group.ConclusionStretching at 120% intensity resulted in significantly greater acute improvements in ROM, peak passive torque, and stiffness than stretching at 100% intensity. Four weeks of stretching increased ROM and peak passive torque but did not decrease passive stiffness, regardless of the stretching intensity.

Background Previous studies showed that repetitive transcranial magnetic stimulation (rTMS) reduces spasticity after stroke. However, clinical assessments like the modified Ashworth scale, cannot discriminate stretch reflex-mediated stiffness (spasticity) from passive stiffness components of resistance to muscle stretch. The mechanisms through which rTMS might influence spasticity are also not understood. Methods We measured the effects of contralesional motor cortex 1 Hz rTMS (1200 pulses + 50 min physiotherapy: 3×/week, for 4–6 weeks) on spasticity of the wrist flexor muscles in 54 chronic stroke patients using a hand-held dynamometer for objective quantification of the stretch reflex response. In addition, we measured the excitability of three spinal mechanisms thought to be related to post-stroke spasticity: post-activation depression, presynaptic inhibition and reciprocal inhibition before and after the intervention. Effects on motor impairment and function were also assessed using standardized stroke-specific clinical scales. Results The stretch reflex-mediated torque in the wrist flexors was significantly reduced after the intervention, while no change was detected in the passive stiffness. Additionally, there was a significant improvement in the clinical tests of motor impairment and function. There were no significant changes in the excitability of any of the measured spinal mechanisms. Conclusions We demonstrated that contralesional motor cortex 1 Hz rTMS and physiotherapy can reduce the stretch reflex-mediated component of resistance to muscle stretch without affecting passive stiffness in chronic stroke. The specific physiological mechanisms driving this spasticity reduction remain unresolved, as no changes were observed in the excitability of the investigated spinal mechanisms.

Abstract In mammals, prolonged mechanical unloading results in a significant decrease in passive stiffness of postural muscles. The nature of this phenomenon remains unclear. The aim of the present study was to investigate possible causes for a reduction in rat soleus passive stiffness after 7 and 14 days of unloading (hindlimb suspension, HS). We hypothesized that HS-induced decrease in passive stiffness would be associated with calpain-dependent degradation of cytoskeletal proteins or a decrease in actomyosin interaction. Wistar rats were subjected to HS for 7 and 14 days with or without PD150606 (calpain inhibitor) treatment. Soleus muscles were subjected to biochemical analysis and ex vivo measurements of passive tension with or without blebbistatin treatment (an inhibitor of actomyosin interactions). Passive tension of isolated soleus muscle was significantly reduced after 7- and 14-day HS compared to the control values. PD150606 treatment during 7- and 14-day HS induced an increase in alpha-actinin-2 and -3, desmin contents compared to control, partly prevented a decrease in intact titin (T1) content, and prevented a decrease in soleus passive tension. Incubation of soleus muscle with blebbistatin did not affect HS-induced reductions in specific passive tension in soleus muscle. Our study suggests that calpain-dependent breakdown of cytoskeletal proteins, but not a change in actomyosin interaction, significantly contributes to unloading-induced reductions in intrinsic passive stiffness of rat soleus muscle.

Cerebral palsy (CP) is a non-progressive motor disorder that affects posture and gait due to contracture development. The purpose of this study is to analyze a possible relation between muscle stiffness and gene expression levels in muscle tissue of children with CP. Next-generation sequencing (NGS) of gene transcripts was carried out in muscle biopsies from gastrocnemius muscle (n = 13 children with CP and n = 13 typical developed (TD) children). Passive stiffness of the ankle plantarflexors was measured. Structural changes of the basement membranes and the sarcomere length were measured. Twelve pre-defined gene target sub-categories of muscle function, structure and metabolism showed significant differences between muscle tissue of CP and TD children. Passive stiffness was significantly correlated to gene expression levels of HSPG2 (p = 0.02; R2 = 0.67), PRELP (p = 0.002; R2 = 0.84), RYR3 (p = 0.04; R2 = 0.66), C COL5A3 (p = 0.0007; R2 = 0.88), ASPH (p = 0.002; R2 = 0.82) and COL4A6 (p = 0.03; R2 = 0.97). Morphological differences in the basement membrane were observed between children with CP and TD children. The sarcomere length was significantly increased in children with CP when compared with TD (p = 0.04). These findings show that gene targets in the categories: calcium handling, basement membrane and collagens, were significantly correlated to passive muscle stiffness. A Reactome pathway analysis showed that pathways involved in DNA repair, ECM proteoglycans and ion homeostasis were amongst the most upregulated pathways in CP, while pathways involved in collagen fibril crosslinking, collagen fibril assembly and collagen turnover were amongst the most downregulated pathways when compared with TD children. These results underline that contracture formation and motor impairment in CP is an interplay between multiple factors.

PurposeWe investigated the immediate effects of neurodynamic nerve gliding (ND) on hamstring flexibility, viscoelasticity, and mechanosensitivity, compared with traditional static stretching (ST).MethodsTwenty-two physically active men aged 21.9 ± 1.9 years were divided randomly into two equal intervention groups using ST or ND. An isokinetic dynamometer was used to measure the active knee joint position sense, perform passive knee extension, record the passive extension range of motion (ROM) and the passive-resistive torque of hamstrings. Stiffness was determined from the slope of the passive torque–angle relationship. A stress relaxation test (SRT) was performed to analyze the viscoelastic behavior of the hamstrings. The passive straight leg raise (SLR) test was used to evaluate hamstring flexibility.ResultsA significant interaction was observed for ROM and passive ultimate stiffness, reflected by an increase in these indicators after ND but not after SD. SLR increased significantly in both groups. After ST, a significantly faster initial stress relaxation was observed over the first 4 s. than after ND. There was no significant change in the active knee joint position sense.ConclusionsND provided a slightly greater increase in hamstring extensibility and passive stiffness, possibly by decreasing nerve tension and increasing strain in connective tissues than ST. The ST mostly affected the viscoelastic behavior of the hamstrings, but neither intervention had a significant impact on proprioception.

To compare the effects of local-vibration and active warm-up on knee extensors muscle stiffness and neuromuscular performance. Experimental crossover study. Thirteen participants performed three 15-min warm-up protocols of control (CON), active (ACT) and local-vibration (LV) in separate testing session. Passive stiffness of vastus lateralis (VL) and vastus medialis (VM) by shear wave elastography and neuromuscular performance were assessed before and 2-min after each condition. A decrease in muscle stiffness was reported after ACT for VL (−16.0±6.6%; p<0.001) and VM (−10.2±8.7%; p=0.03) while no changes were reported after CON (p=0.46 and p=0.34 for VL and VM, respectively) and LV (p=0.07 and p=0.46 for VL and VM, respectively). Maximal jump performances increased during squat (+8.5±6.6%; p<0.001) and countermovement jump (+5.2±5.8%; p<0.001) after ACT while no changes were reported after CON and LV during squat (p=0.16 and p=0.81, respectively) and countermovement jump (p=0.18 and p=0.31, respectively). We further report that each condition was ineffective to inducing changes in maximal voluntary isometric contraction force (p=0.18), rate of force development (p=0.92), twitch parameters (p>0.05) as well as central modulations as reported by the unchanged voluntary activation level (p=0.24) and maximal electromyography (EMG) recorded from the VL (p=0.44). The active warm-up acutely reduced muscle stiffness and increased muscle performance during maximal dynamic tasks. With regard to LV, further studies are required to determine optimal parameters (frequency, amplitude, duration) to significantly increase muscle performance.