Passive Mechanical Properties of Human Medial Gastrocnemius and Soleus Musculotendinous Unit

The in vivo characterization of the passive mechanical properties of the human triceps surae musculotendinous unit is important for gaining a deeper understanding of the interactive responses of the tendon and muscle tissues to loading during passive stretching. This study sought to quantify a comprehensive set of passive muscle-tendon properties such as slack length, stiffness, and the stress-strain relationship using a combination of ultrasound imaging and a three-dimensional motion capture system in healthy adults. By measuring tendon length, the cross-section areas of the Achilles tendon subcompartments (i.e., medial gastrocnemius and soleus aspects), and the ankle torque simultaneously, the mechanical properties of each individual compartment can be specifically identified. We found that the medial gastrocnemius (GM) and soleus (SOL) aspects of the Achilles tendon have similar mechanical properties in terms of slack angle (GM: − 10.96 ° ± 3.48 ° ; SOL: − 8.50 ° ± 4.03 ° ), moment arm at 0° of ankle angle (GM: 30.35 ± 6.42 mm; SOL: 31.39 ± 6.42 mm), and stiffness (GM: 23.18 ± 13.46 Nmm-1; SOL: 31.57 ± 13.26 Nmm-1). However, maximal tendon stress in the GM was significantly less than that in SOL (GM: 2.96 ± 1.50 MPa; SOL: 4.90 ± 1.88 MPa, p = 0.024 ), largely due to the higher passive force observed in the soleus compartment (GM: 99.89 ± 39.50 N; SOL: 174.59 ± 79.54 N, p = 0.020 ). Moreover, the tendon contributed to more than half of the total muscle-tendon unit lengthening during the passive stretch. This unequal passive stress between the medial gastrocnemius and the soleus tendon might contribute to the asymmetrical loading and deformation of the Achilles tendon during motion reported in the literature. Such information is relevant to understanding the Achilles tendon function and loading profile in pathological populations in the future.

SENSITIVITY OF MODEL-PREDICTED MUSCLE FORCES OF PATIENTS WITH CEREBRAL PALSY TO VARIATIONS IN MUSCLE-TENDON PARAMETERS

Computational musculoskeletal modeling and simulation platforms are efficient tools to gain insight into the muscular coordination of patients with motor disabilities such as cerebral palsy (CP). Muscle force predictions from simulation programs are influenced by the architectural and contractile properties of muscle-tendon units. In this study, we aimed to evaluate the sensitivity of major lower limb muscle forces in patients with CP to changes in muscle-tendon parameters. Open-access datasets of children with CP ([Formula: see text]) and healthy children ([Formula: see text]) were considered. Monte Carlo analysis was executed to specify how sensitive the muscle forces to perturbations between [Formula: see text]% and [Formula: see text]% of the nominal value of the maximum isometric muscle force, optimal muscle fiber length, muscle pennation angle, tendon slack length, and maximum contraction velocity of muscle. The sensitivity analysis revealed that muscle forces of CP patients and healthy individuals were most sensitive to perturbations in the tendon slack length ([Formula: see text]), while forces of CP patients were more sensitive to tendon slack length when compared to the healthy group ([Formula: see text]). Muscle forces of patients and healthy individuals were insensitive to the other four parameters ([Formula: see text]), except for the gracilis and sartorius muscles in which the proportion of optimal muscle fiber length to tendon slack length is higher than 1; forces of these two muscles were also sensitive to the optimal muscle fiber length. The results of this study are expected to contribute to our understanding of which parameters should be personalized when conducting musculoskeletal modeling and simulation of patients with CP.

Human plantar fascial dimensions and shear wave velocity change in vivo as a function of ankle and metatarsophalangeal joint positions

The plantar fascia (PF), a primary contributor of the foot arch elasticity, may experience slack, taut, and stretched states depending on the ankle and metatarsophalangeal (MTP) joint positions. Since PF has proximodistal site-difference in its dimensions and stiffness, the response to applied tension can also be site-specific. Furthermore, PF can contribute to supporting the foot arch while being stretched beyond the slack length, but it has never been quantitatively evaluated in vivo. This study investigated the effects of ankle and MTP joint positions on PF length and localized thickness and shear wave velocity (SWV) at three different sites from its proximal to distal end using magnetic resonance and supersonic shear imaging techniques. During passive ankle dorsiflexion, rise of SWV, an indication of slack length, was observed at the proximal site when the ankle was positioned by 10˚-0˚ ankle plantar flexion with up to 3 mm (+1.5%) increase in PF length. On the other hand, SWV increased at the distal site when MTP joint dorsiflexed 40˚ with the ankle 30˚-20˚ plantar flexion, and in this position, PF was lengthened up to 4 mm (+2.3%). Beyond the slack length, SWV curvi-linearly increased at all measurement sites toward the maximal dorsiflexion angle while PF lengthened up to 9 mm (+7.6%) without measurable changes in its thickness. This study provides evidence that the dimensions and SWV of PF change in a site-specific manner depending on the ankle and MTP joint positions, which can diversify foot arch elasticity during human locomotion.

History-dependence of muscle slack length in humans: effects of contraction intensity, stretch amplitude, and time

The slack length of a relaxed human skeletal muscle is not fixed; it can be modified by contraction and stretch. Contraction of the human vastus lateralis muscle at short lengths reduces the muscle’s slack length. Even very weak contractions are sufficient to induce this effect. The effect persists for at least 5 min but can be reduced or abolished with a large-amplitude passive stretch.

Transient receptor potential vanilloid-4 contributes to stretch-induced hypercontractility and time-dependent dysfunction in the aged heart

Aims Cardiovascular disease remains the greatest cause of mortality in Americans over 65. The stretch-activated transient receptor potential vanilloid-4 (TRPV4) ion channel is expressed in cardiomyocytes of the aged heart. This investigation tests the hypothesis that TRPV4 alters Ca2+ handling and cardiac function in response to increased ventricular preload and cardiomyocyte stretch. Methods and results Left ventricular maximal pressure (PMax) was monitored in isolated working hearts of Aged (24–27 months) mice following preload elevation from 5 to 20mmHg, with and without TRPV4 antagonist HC067047 (HC, 1 µmol/L). In preload responsive hearts, PMax prior to and immediately following preload elevation (i.e. Frank–Starling response) was similar between Aged and Aged+HC. Within 1 min following preload elevation, Aged hearts demonstrated secondary PMax augmentation (Aged>Aged+HC) suggesting a role for stretch-activated TRPV4 in cardiac hypercontractility. However, after 20 min at 20 mmHg Aged exhibited depressed PMax (Aged<Aged+HC) suggestive of TRPV4-dependent contractile dysfunction with sustained stretch. To examine stretch-induced Ca2+ homeostasis at the single-cell level, isolated cardiomyocytes were stretched 10–15% of slack length while measuring intracellular Ca2+ with fura-2. Uniaxial longitudinal stretch increased intracellular Ca2+ levels and triggered Ca2+ overload and terminal cellular contracture in Aged, but not Aged+HC. Preload elevation in hearts of young/middle-age (3–12 months) mice produced an initial PMax increase (Frank–Starling response) without secondary PMax augmentation, and cardiomyocyte stretch did not affect intracellular Ca2+ levels. Hearts of transgenic mice with cardiac-specific TRPV4 expression exhibited PMax similar to 3- to 12-month control mice prior to and immediately following preload elevation but displayed secondary PMax augmentation. Cardiomyocytes of mice with transgenic TRPV4 expression were highly sensitive to mechanical stimulation and exhibited elevated Ca2+ levels, Ca2+ overload, and terminal contracture upon cellular attachment and stretch. Conclusion TRPV4 contributes to a stretch-induced increase in cardiomyocyte Ca2+ and cardiac hypercontractility, yet sustained stretch leads to cardiomyocyte Ca2+ overload and contractile dysfunction in the aged heart.

In Situ Joint Stiffness Increases During Skeletal Growth but Decreases Following Partial and Complete Anterior Cruciate Ligament Injury

Partial and complete anterior cruciate ligament (ACL) injuries occur in both pediatric and adult populations and can result in loss of joint stability and function. The sigmoidal shape of knee joint function (load-translation curve) under applied loads includes a low-load region (described by slack length) followed by a high-load region (described by stiffness). However, the impact of age and injury on these parameters is not fully understood. The current objective was to measure the effects of age and injury on the shape of joint function in a porcine model. In response to an applied anterior–posterior tibial load, in situ slack did not change (p > 0.05), despite sevenfold increases in joint size with increasing age. Joint stiffness increased from an average of 10 N/mm in early youth to 47 N/mm in late adolescence (p < 0.05). In situ ACL stiffness increased similarly, and changes in in situ joint stiffness and ACL stiffness were highly correlated across ages. With complete ACL injury, in situ slack length increased by twofold to fourfold and in situ stiffness decreased threefold to fourfold across ages (p < 0.05). Partial ACL injury resulted in less dramatic, but statistically significant, increases in joint slack and significant decreases in in situ joint stiffness in the adolescent age groups (p < 0.05). This work furthers our understanding of the interaction between joint biomechanics and ACL function throughout growth and the impact of ACL injury in the skeletally immature joint.

Plantarflexor fiber length and tendon slack length are the strongest determinates of simulated single-leg heel raise function

Achilles tendon ruptures lead to reduced ankle function and often limits recreational activity. Single-leg heel raises are often used clinically to characterize patient function. However, it is unclear how the structure of the Achilles tendon and plantarflexor muscles affects single-leg heel raise function. Therefore, the purpose of this study was to develop a musculoskeletal model in order to simulate the effects of muscle-tendon unit (MTU) parameters on peak plantarflexion during this clinically-relevant task. The ankle joint was plantarflexed by two MTUs that represented the soleus and gastrocnemius muscles. The optimal fiber length, maximal muscle force, muscle pennation, tendon stiffness, and resting ankle angle – a surrogate measure of tendon slack length – were iteratively adjusted to test the combined effects of each of these MTU parameters. Single-leg heel raises were simulated by maximally exciting the two plantarflexor MTUs for each model configuration (N = 161,051 simulations). Optimal muscle fiber and tendon slack lengths had the greatest effect on peak plantarflexion during simulated single-leg heel raises. Simulations that were unable to produce at least 30 degrees of plantarflexion had muscle fibers that were shorter than healthy muscle and longer tendon slack lengths. These findings highlight the importance of preserving muscle fascicle and tendon length following Achilles tendon injuries.Funding no funding has been provided for this researchAcknowledgements the Authors have no acknowledgementsConflict of interest the Authors have no conflicts of interest that are relevant to this work

Early Shortening of Wrist Flexor Muscles Coincides With Poor Recovery After Stroke

Background. The mechanism and time course of increased wrist joint stiffness poststroke and clinically observed wrist flexion deformity is still not well understood. The components contributing to increased joint stiffness are of neural reflexive and peripheral tissue origin and quantified by reflexive torque and muscle slack length and stiffness coefficient parameters. Objective. To investigate the time course of the components contributing to wrist joint stiffness during the first 26 weeks poststroke in a group of patients, stratified by prognosis and functional recovery of the upper extremity. Methods. A total of 36 stroke patients were measured on 8 occasions within the first 26 weeks poststroke using ramp-and-hold rotations applied to the wrist joint by a robot manipulator. Neural reflexive and peripheral tissue components were estimated using an electromyography-driven antagonistic wrist model. Outcome was compared between groups cross-sectionally at 26 weeks poststroke and development over time was analyzed longitudinally. Results. At 26 weeks poststroke, patients with poor recovery (Action Research Arm Test [ARAT] ≤9 points) showed a higher predicted reflexive torque of the flexors ( P < .001) and reduced predicted slack length ( P < .001) indicating shortened muscles contributing to higher peripheral tissue stiffness ( P < .001), compared with patients with good recovery (ARAT ≥10 points). Significant differences in peripheral tissue stiffness between groups could be identified around weeks 4 and 5; for neural reflexive stiffness, this was the case around week 12. Conclusions. We found onset of peripheral tissue stiffness to precede neural reflexive stiffness. Temporal identification of components contributing to joint stiffness after stroke may prompt longitudinal interventional studies to further evaluate and eventually prevent these phenomena.