A reduced muscle model and planar musculoskeletal model fit for the simulation of whole-body movements

Musculoskeletal models are made to reflect the capacities of the human body in general, and often a specific subject in particular. It remains challenging to both model the musculoskeletal system and then fit the modelled muscles to a specific human subject. We present a reduced muscle model, a planar musculoskeletal model, and a fitting method that can be used to find a feasible set of active and passive muscle parameters for a specific subject. At a minimum, the fitting method requires inverse dynamics data of the subject, a scalar estimate of the peak activation reached during the movement, and a plausible initial estimate for the strength and flexibility of that subject. While additional data can be used to result in a more accurate fit, this data is not required for the method solve for a feasible fit. The minimal input requirements of the proposed fitting method make it well suited for subjects who cannot undergo a maximum voluntary contraction trial, or for whom recording electromyographic data is not possible. To evaluate the model and fitting method we adjust the musculoskeletal model so that it can perform an experimentally recorded stoop-lift of a 15 kg box.     

Can altered muscle synergies control unimpaired gait?

Recent studies have postulated that the human motor control system recruits groups of muscles through low-dimensional motor commands, or muscle synergies. This scheme simplifies the neural control problem associated with the high-dimensional structure of the neuromuscular system. Several lines of evidence have suggested that neurological injuries, such as stroke or cerebral palsy, may reduce the dimensions that are available to the motor control system, and these altered dimensions or synergies are thought to contribute to impaired walking patterns. However, no study has investigated whether impaired low-dimensional control spaces necessarily lead to impaired walking patterns. In this study, using a two-dimensional model of walking, we developed a synergy-based control framework that can simulate the dynamics of walking. The simulation analysis showed that a synergy-based control scheme can produce well-coordinated movements of walking matching unimpaired gait. However, when the dimensions available to the controller were reduced, the simplified emergent pattern deviated from unimpaired gait. A system with two synergies, similar to those seen after neurological injury, could not produce an unimpaired walking pattern. These findings provide further evidence that altered muscle synergies can contribute to impaired gait patterns and may need to be directly addressed to improve gait after neurological injury.     

The effect of isokinetic dynamometer deceleration phase on maximum ankle joint range of motion and plantar flexor mechanical properties tested at different angular velocities

During range of motion (max-ROM) tests performed on an isokinetic dynamometer, the mechanical delay between the button press (by the participant to signal their max-ROM) and the stopping of joint rotation resulting from system inertia induces errors in both max-ROM and maximum passive joint moment. The present study aimed to quantify these errors by comparing data when max-ROM was obtained from the joint position data, as usual (max-ROM_POS), to data where max-ROM was defined as the first point of dynamometer arm deceleration (max-ROM_ACC). Fifteen participants performed isokinetic ankle joint max-ROM tests at 5, 30 and 60° s⁻¹. Max-ROM, peak passive joint moment, end-range musculo-articular (MAC) stiffness and area under the joint moment-position curve were calculated. Greater max-ROM was observed in max-ROM_POS than max-ROM_ACC (P < 0.01) at 5 (0.2 ± 0.15%), 30 (1.8 ± 1.0%) and 60° s⁻¹ (5.9 ± 2.3%), with the greatest error at the fastest velocity. Peak passive moment was greater and end-range MAC stiffness lower in max-ROM_POS than in max-ROM_ACC only at 60° s⁻¹ (P < 0.01), whilst greater elastic energy storage was found at all velocities. Max-ROM and peak passive moment are affected by the delay between button press and eventual stopping of joint rotation in an angular velocity-dependent manner. This affects other variables calculated from the data. When high data accuracy is required, especially at fast joint rotation velocities (≥30° s⁻¹), max-ROM (and associated measures calculated from joint moment data) should be taken at the point of first change in acceleration rather than at the dynamometer’s ultimate joint position.     

In vivo fascicle length measurements via B-mode ultrasound imaging with single vs dual transducer arrangements

Ultrasonography is a useful technique to study muscle contractions in vivo, however larger muscles like vastus lateralis may be difficult to visualise with smaller, commonly used transducers. Fascicle length is often estimated using linear trigonometry to extrapolate fascicle length to regions where the fascicle is not visible. However, this approach has not been compared to measurements made with a larger field of view for dynamic muscle contractions. Here we compared two different single-transducer extrapolation methods to measure VL muscle fascicle length to a direct measurement made using two synchronised, in-series transducers. The first method used pennation angle and muscle thickness to extrapolate fascicle length outside the image (extrapolate method). The second method determined fascicle length based on the extrapolated intercept between a fascicle and the aponeurosis (intercept method). Nine participants performed maximal effort, isometric, knee extension contractions on a dynamometer at 10° increments from 50 to 100° of knee flexion. Fascicle length and torque were simultaneously recorded for offline analysis. The dual transducer method showed similar patterns of fascicle length change (overall mean coefficient of multiple correlation was 0.76 and 0.71 compared to extrapolate and intercept methods respectively), but reached different absolute lengths during the contractions. This had the effect of producing force–length curves of the same shape, but each curve was shifted in terms of absolute length. We concluded that dual transducers are beneficial for studies that examine absolute fascicle lengths, whereas either of the single transducer methods may produce similar results for normalised length changes, and repeated measures experimental designs.     

Muscle recruitment and coordination with an ankle exoskeleton

Exoskeletons have the potential to assist and augment human performance. Understanding how users adapt their movement and neuromuscular control in response to external assistance is important to inform the design of these devices. The aim of this research was to evaluate changes in muscle recruitment and coordination for ten unimpaired individuals walking with an ankle exoskeleton. We evaluated changes in the activity of individual muscles, cocontraction levels, and synergistic patterns of muscle coordination with increasing exoskeleton work and torque. Participants were able to selectively reduce activity of the ankle plantarflexors with increasing exoskeleton assistance. Increasing exoskeleton net work resulted in greater reductions in muscle activity than increasing exoskeleton torque. Patterns of muscle coordination were not restricted or constrained to synergistic patterns observed during unassisted walking. While three synergies could describe nearly 95% of the variance in electromyography data during unassisted walking, these same synergies could describe only 85–90% of the variance in muscle activity while walking with the exoskeleton. Synergies calculated with the exoskeleton demonstrated greater changes in synergy weights with increasing exoskeleton work versus greater changes in synergy activations with increasing exoskeleton torque. These results support the theory that unimpaired individuals do not exclusively use central pattern generators or other low-level building blocks to coordinate muscle activity, especially when learning a new task or adapting to external assistance, and demonstrate the potential for using exoskeletons to modulate muscle recruitment and coordination patterns for rehabilitation or performance.     

The effect of starvation on the ultrastructure of the red and white myotomal muscles of the crucian carp (Carassius carassius)

Summary The effect of 16 weeks total starvation on the ultrastructure of the red and white myotomal muscles of the crucian carp (Carassius Carassius) has been investigated. In the white fibres the amount of myofibrillar material fell from 89.6% to 70.7% of the total fibre volume whilst in the red fibres the fall was from 72.2% to 70.3%. The sarcoplasmic reticulum appeared to have become swollen during starvation in both fibre types. In the white fibres the terminal cisternae of some triads seem to have fused. The volume of the red fibres occupied by mitochondria was reduced from 16.2 % to 5.9 %. The concentration of mitochondria in the white fibres was too low to detect any quantitative changes. A marked reduction in the amount of euchromatin material was observed in most white fibre nuclei and many red fibre nuclei. Many of the ultrastructural changes noted in the present study can be correlated with biochemical changes known to occur in the red and white myotomal muscles of fish during starvation. This work was supported by a grant from the Natural Environmental Research Council.     

Reduced sexual dimorphism in upper arm muscle circumference associated with protein-deficient diet in a South American population

Animal experiments have demonstrated that individuals exhibit differing tendencies to arrest growth and resorb muscle tissue under nutritional stress. Since placental and adrenocortical hormones are active in promoting muscle tissue resorption, sex differences may exist. In order to identify such sex differences, the upper arm circumferences of 362 individuals, aged one to 60 years, living in an area of chronic protein-calorie malnutrition were compared by age and sex with published data collected from U.S. and highland Peruvian populations. Sexual dimorphism for arm muscle circumference in the malnourished population is less than in U.S. samples of comparable age-categories. The highland population is closer to U.S. samples in the degree of dimorphism. The reduction in muscle circumference of males in the malnourished population appears to be the cause of the comparatively greater similarity of the sexes where protein-calorie malnutrition is experienced from infancy through adolescence. High muscle relief and excellent tonus in these same males indicate that reduced muscle circumference is not the result of flaccidity or higher ratios of compressible fat to muscle tissue. Reduction of muscle tissue in undernourished males is a reduction in total metabolic demand. Such reductions are adaptive in areas of chronic nutritional stress.     

Isoenzyme studies of whole muscle grafts and movement of muscle precursor cells

Summary Isoenzymes of glucose-6-phosphate isomerase (GPI: E.C. 5.3.1.9) were used as markers to determine the origin of cells which give rise to new muscle formed in allografts of whole intact muscle. GPI isoenzymes were also employed to see whether host precursor cells, which have been shown to contribute to muscle formation in grafts of minced muscle, can be derived from muscle lying adjacent to grafts.Excellent muscle regeneration was found in allografts of extensor digitorum longus (EDL) muscle examined after 58 days: 12 of 16 grafts contained 80% or more new muscle. Isoenzyme analysis showed that most, and in 2 instances all, new muscle was derived from implanted donor cells; however, there was strong evidence that in 5 grafts some, or all, new muscle must have resulted from host cells moving into the graft. Although hybrid isoenzyme was not detected this was attributed to factors associated with host tolerance which appear to interfere with fusion between host and donor myoblasts.Isografts of minced muscle were placed next to whole EDL muscle allografts to see if cells from allografts moved into adjacent regenerating tissue. Unfortunately, muscle regeneration in minced isografts was poor; only 3 contained 50% or more new muscle and most contained large amounts of fibrous connective tissue. Only a single isoenzyme band was detected in 11 isografts, but in five instances, the presence of a second band showed that cells from EDL allografts were also present. As no hybrid isoenzyme was detected, it is not known whether these cells which had moved into the regenerating minced grafts were muscle precursors, fibroblasts or some other cell types.     

Asymmetric and Globular Forms of AChE in Slow and Fast Muscles of 129/ReJ Normal and Dystrophic Mice

Abstract: Acetylcholinesterase activities and molecular forms were studied in normal and dystrophic 129/ReJ mice, focusing on four predominantly fast-twitch muscles and the slow-twitch soleus. The asymmetric and globular forms were analyzed separately so that the effect of dystrophy on each form could be determined. This comparative study showed the following. (1) In the normal condition, each muscle exhibited a distinct distribution of the molecular forms. (2) The diversity among the fast muscles resulted mainly from variations in the proportions of the three globular forms; in contrast, these muscles showed a constant and precise A₁₂/A₈/A₄ ratio. (3) The slow-twitch soleus clearly differed from the other muscles in its low acetylcholinesterase activity and distinct distribution of the molecular forms, characterized by a low level of G₄ and a peculiar ratio among its asymmetric forms, resulting from a relative increase of the A₈ and A₄ forms. (4) In dystrophic mice, the diversity of the acetylcholin esterase distribution was lost; all the fast muscles displayed profiles exhibiting the characteristics typical of the soleus. The fast-twitch extensor digitorum longus, sternomastoid, and plantaris converged towards an identical set of acetylcholinesterase molecules. (5) In contrast, the acetylcholinesterase activity and molecular forms of the soleus were only slightly affected by the disease. These results reveal that the dystrophy modifies both categories of molecular forms of acetylcholinesterase in a very precise manner. Such complex changes, which are highly reproducible in a variety of different muscles, are unlikely to result from nonspecific reactions secondary to the disease.     

Cardiac Restricted Overexpression of Membrane Type-1 Matrix Metalloproteinase Causes Adverse Myocardial Remodeling following Myocardial Infarction

The membrane type-1 matrix metalloproteinase (MT1-MMP) is a unique member of the MMP family, but induction patterns and consequences of MT1-MMP overexpression (MT1-MMPexp), in a left ventricular (LV) remodeling process such as myocardial infarction (MI), have not been explored. MT1-MMP promoter activity (murine luciferase reporter) increased 20-fold at 3 days and 50-fold at 14 days post-MI. MI was then induced in mice with cardiac restricted MT1-MMPexp (n = 58) and wild type (WT, n = 60). Post-MI survival was reduced (67% versus 46%, p < 0.05), and LV ejection fraction was lower in the post-MI MT1-MMPexp mice compared with WT (41 ± 2 versus 32 ± 2%,p < 0.05). In the post-MI MT1-MMPexp mice, LV myocardial MMP activity, as assessed by radiotracer uptake, and MT1-MMP-specific proteolytic activity using a specific fluorogenic assay were both increased by 2-fold. LV collagen content was increased by nearly 2-fold in the post-MI MT1-MMPexp compared with WT. Using a validated fluorogenic construct, it was discovered that MT1-MMP proteolytically processed the pro-fibrotic molecule, latency-associated transforming growth factor-1 binding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activity was increased by 4-fold in the post-MI MT1-MMPexp group. Early and persistent MT1-MMP promoter activity occurred post-MI, and increased myocardial MT1-MMP levels resulted in poor survival, worsening of LV function, and significant fibrosis. A molecular mechanism for the adverse LV matrix remodeling with MT1-MMP induction is increased processing of pro-fibrotic signaling molecules. Thus, a proteolytically diverse portfolio exists for MT1-MMP within the myocardium and likely plays a mechanistic role in adverse LV remodeling.