Odegard, Gregory M.

Clinical treatments of skeletal muscle weakness are hindered by a lack of an approach to evaluate individual muscle force. Intramuscular pressure (IMP) has shown a correlation to muscle force in vivo, but patient to patient and muscle to muscle variability results in difficulty of utilizing IMP to estimate muscle force. The goal of this work was to develop a finite element model of whole skeletal muscle that can predict IMP under passive and active conditions to further investigate the mechanisms of IMP variability. A previously validated hypervisco-poroelastic constitutive approach was modified to incorporate muscle activation through an inhomogeneous geometry. Model parameters were optimized to fit model stress to experimental data, and the resulting model fluid pressurization data were utilized for validation. Model fitting was excellent (root-mean-square error or RMSE <1.5 kPa for passive and active conditions), and IMP predictive capability was strong for both passive (RMSE 3.5 mmHg) and active (RMSE 10 mmHg at in vivo lengths) conditions. Additionally, model fluid pressure was affected by length under isometric conditions, as increases in stretch yielded decreases in fluid pressurization following a contraction, resulting from counteracting Poisson effects. Model pressure also varied spatially, with the highest gradients located near aponeuroses. These findings may explain variability of in vivo IMP measurements in the clinic, and thus help reduce this variability in future studies. Further development of this model to include isotonic contractions and muscle weakness would greatly benefit this work.

Since Blix noted that force varies with muscle length [1], many investigators have worked to characterize the passive length-tension properties of skeletal muscle in the tissue’s fiber direction [2]. However, few reports have examined the properties of muscle in either transverse extension or in longitudinal shear [3–4]. Material properties in these three directions are needed to fully characterize computational models, which generally describe muscle as being transversely isotropic, hyperelastic, and isovolumetric [3–6]. Further, previous studies reporting tri-planar material properties indicate that muscle tissue is stiffer in the transverse direction compared to the longitudinal direction [3–4]. This counters conventional notions of transversely isotropic materials, which are generally stiffer in the fiber direction.

The main functions of the human musculoskeletal system are to sustain loads and provide mobility. Bones and joints themselves cannot produce movement; skeletal muscles provide the ability to move. Knowledge of muscle forces during given activities can provide insight into muscle mechanics, muscle physiology, musculoskeletal mechanics, neurophysiology, and motor control. However, clinical examinations or instrumented strength testing only provides information regarding muscle groups. Musculoskeletal models are typically needed to calculate individual muscle forces.

Intramuscular pressure (IMP) has been put forth as a surrogate measure for muscle force. As technological advancements have lead to the creation of smaller IMP microsensors, obtaining IMP readings in the clinic has come closer to becoming a minimally-invasive reality. However, appropriate use of data from these sensors relies upon an understanding of the mechanism of pressure changes within skeletal muscle. To that end, a constitutive model, representing muscle as a transversely isotropic, hyperelastic, and isovolumetric was created [1] for implementation in a finite element simulation. The purpose of this study was to validate this constitutive muscle model with passive elongation tests of skeletal muscle tissue from New Zealand White (NZW) rabbits. Reaction forces and hydrostatic pressures resulting from applied deformations were determined with the finite element modeling (FEM) approach and were compared with previously published experimental data [2].

Many single-phase, solid mechanics computational models of skeletal muscle have been created based on the assumptions that skeletal muscle is hyperelastic, transversely isotropic,1,2 and isovolumic. However, muscle has also been observed to have non-linear time-dependent behaviors that can be modeled using viscoelasticity or poroelasticity. The inherent viscoelasticity of muscle may not fully explain the time-dependent nature that may arise from extracellular fluid filtration3 and redistribution4 within the tissue. Further, intramuscular pressure (IMP) has been shown to have a heterogeneous distribution in muscle. This may be attributable to the movement of extracellular fluid, but the mechanisms of fluid redistribution are not completely understood. While a viscoelastic model may predict time-dependent responses of skeletal muscle, viscoelastic theory does not explain underlying causative tissue behaviors.5

A fully 3D, continuum mechanics based model of skeletal muscle, validated against experimental force data, can be used to computationally solve for individual muscle forces. A constitutive formulation, representing muscle as a transversely isotropic, hyperelastic, and isovolumetric material [1] has been implemented in a finite element model (FEM) of passive skeletal muscle and validated against experimental tension measurements [2]. Of further interest is an expanded formulation that will allow for the addition of muscle activation levels on the overall skeletal muscle force generation. The purpose of this study was to expand the FEA model to include muscle activation and validate it with tests of active skeletal muscle tissue at varied lengths.

Intraneural ganglion cysts have been considered a curiosity for 2 centuries. Based on a unifying articular (synovial) theory, recent evidence has provided a logical explanation for their formation and propagation. The fundamental principle is that of a joint origin and a capsular defect through which synovial fluid escapes following the articular branch, typically into the parent nerve. A stereotypical, reproducible appearance has been characterized that suggests a shared pathogenesis. In the present report the authors will provide a mechanistic explanation that can then be mathematically tested using a preliminary model created by finite element analysis.

While much work has previously been done in the modeling of skeletal muscle, no model has, to date, been developed that describes the mechanical behavior with an explicit strain-energy function associated with the active response of skeletal muscle tissue. A model is presented herein that has been developed to accommodate this design consideration using a robust dynamical approach. The model shows excellent agreement with a previously published model of both the active and passive length-tension properties of skeletal muscle.