Parameter interdependence and success of skeletal muscle modelling

In muscle and movement modelling it is almost invariably assumed that force actually exerted is determined by several independent factors. This review considers the fact that length force characteristics are not a relatively fixed property of muscle but should be considered the product of a substantial number of interacting factors. Level of activation and recruitment are influential factors in relation to aspects of muscle architecture. For the level of activation effects of its short term history (potentiation, fatigue in sustained contractions) have to be taken into account and are reviewed on the basis of recent experimental results as well as available literature. History is also an important determinant for the effect of length changes. This concept is introduced on the basis of recent experimental evidence as well as available literature. Regarding effects of muscle architecture, the concepts of primary and secondary distribution of fibre mean sarcomere length are introduced as well as effects of muscle geometry for mono- and bi-articular muscles on those distributions. Implications for motor control are discussed and the need for intramuscular coordination indicated

FIM: A fatigued-injured muscle model based on the sliding filament theory

Skeletal muscle modeling has a vital role in movement studies and the development of therapeutic approaches. In the current study, a Huxley-based model for skeletal muscle is proposed, which demonstrates the impact of impairments in muscle characteristics. This model focuses on three identified ions: H + , inorganic phosphate Pi and Ca 2+. Modifications are made to actin-myosin attachment and detachment rates to study the effects of H + and Pi. Additionally, an activation coefficient is included to represent the role of calcium ions interacting with troponin, highlighting the importance of Ca 2+. It is found that maximum isometric muscle force decreases by 9.5% due to a reduction in pH from 7.4 to 6.5 and by 47.5% in case of the combination of a reduction in pH and an increase of Pi concentration up to 30 mM, respectively. Then the force decline caused by a fall in the active calcium ions is studied. When only 15% of the total calcium in the myofibrillar space is able to interact with troponin, up to 80% force drop is anticipated by the model. The proposed fatigued-injured muscle model is useful to study the effect of various shortening velocities and initial muscletendon lengths on muscle force; in addition, the benefits of the model go beyond predicting the force in different conditions as it can also predict muscle stiffness and power. The power and stiffness decrease by 40% and 6.5%, respectively, due to the pH reduction, and the simultaneous accumulation of H + and Pi leads to a 50% and 18% drop in power and stiffness

Design of human surrogates for the study of biomechanical injury: a review

Human surrogates are representations of living human structures employed to replicate “real-life” injurious scenarios in artificial environments. They are used primarily to evaluate personal protective equipment (PPE) or integrated safety systems (e.g., seat belts) in a wide range of industry sectors (e.g., automotive, military, security service, and sports equipment). Surrogates are commonly considered in five major categories relative to their form and functionality: human volunteers, postmortem human surrogates, animal surrogates, anthropomorphic test devices, and computational models. Each surrogate has its relative merits. Surrogates have been extensively employed in scenarios concerning “life-threatening” impacts (e.g., penetrating bullets or automotive accidents). However, more frequently occurring nonlethal injuries (e.g., fractures, tears, lacerations, contusions) often result in full or partial debilitation in contexts where optimal human performance is crucial (e.g., military, sports). Detailed study of these injuries requires human surrogates with superior biofidelity to those currently available if PPE designs are to improve. The opportunities afforded by new technologies, materials, instrumentation, and processing capabilities should be exploited to develop a new generation of more sophisticated human surrogates. This paper presents a review of the current state of the art in human surrogate construction, highlighting weaknesses and opportunities, to promote research into improved surrogates for PPE development

Functional Effects of Calcium Regulation of Thin Filaments at Single Particle Resolution

Heart disease is the leading cause of death in the United States. Understanding heart function at the molecular level is critical for developing of more effective treatments. In the cardiac muscle, the thin filament is composed by troponin (Tn), tropomyosin (Tm), and F-actin. It provides Ca2+-dependent regulation of contraction by modulating myosin attachment and force generation in a cooperative scheme. However, this mechanism remains unclear. To understand thin filament activation, we studied the binding and functional properties of Tn and Tm to F-actin at single particle resolution by employing fluorescence image colocalization, in vitro motility assays, and Förster resonance energy transfer based on fluorescence lifetime imaging (FLIM-FRET). Our results suggest that under physiologically relevant conditions, Tn and Tm binding to Factin is not cooperative and it is not affected by Ca2+. This suggests that one single type of interaction is involved in fully regulated thin filaments. Thin filament activation has been confirmed by in vitro motility assays, where phosphorylation of serine 23 and 24 in TnI, truncation of TnT C-terminal region, and incorporation of a Ca2+ desensitizer altered the Ca2+ response to filament sliding. FLIM-FRET measurements revealed an allosteric dependence on thin filament activation as a function of myosin and Ca2+. Our results provide evidence of multiple allosteric elements within thin filaments responsible for the molecular modulation of cardiac muscle activation

Modelling Human Locomotion

This report is a coverage of my 16 weeks practical training at the Center for Sensori-Motor Interaction of the Aalborg University (Denmark). One of their research topics is on the ?eld of the biomedical modelling, where they want to answer the question of the functional behavior of the proprioceptive feedback system of the human body. A valid/good biomedical model could support their hypotheses which are results from different measurements. The original intention of the project was to build a complete walking lower body model to ?nd the reason for proprioceptive feedback during walking. In the middle of the project this original goal was a too high, because of the additional work of redesigning previous work of Huber [26]. The goal is adjusted to design the mechanical and muscle model and a well documented report, so a next project can continue immediately. The mechanical and muscle model appeared to work correct and are veri?ed with measured data. The forward activation of the muscle/mechanical model is not completely the same as expected. This is because the used method does not take co-activation of antagonistic muscle into account. For the continuation of this project a complete measured data set is necessary, because the veri?cation is not 100% valid. This performed veri?cation uses data that is not correlated in the sense that is measured at the same conditions and persons

Measurement of central and peripheral fatigue during whole body exercise : a new method

Background: This thesis sought to establish a new method for instantaneous measurement of central and peripheral fatigue during whole-body exercise up to maximal aerobic capacity in humans. Until now, measurement of central and peripheral fatigue has been limited to isolated muscle tasks or to time points after exercise where the physiological conditions that brought about the limiting symptoms for exercise have subsided. Thus, development of a method to overcome this would allow the first demonstration of the relative contributions of central and peripheral fatigue to limiting exercise that elicited maximal strain of the combined neuromuscular and cardiopulmonary systems. Objective: To develop and validate a method for quantifying peripheral muscle fatigue (MF, defined as the power produced for a given muscle stimulation), activation fatigue (AF, defined as the maximal evocable muscle activity), their sum, performance fatigue (PF, defined as the decline in maximal voluntary isokinetic power compared to the fresh, baseline, state) during cycling exercise at maximal aerobic capacity. In addition, this thesis aimed to determine the rate with which MF, AF and PF recovered to baseline after intolerance during whole-body exercise in humans. Methods: To quantify fatigue during whole-body exercise, a method was developed to allow a rapid switch from standard cycling (where the relationship between power and cadence is hyperbolic) to isokinetic cycling (where power is independent of cadence, and cadence is fixed) to be implemented. By asking the participant to give a maximal isokinetic effort at any point during exercise or recovery, allowed the velocity-specific decline in maximal isokinetic power (PISO) to be measured. The difference in PISO between baseline and exercise quantified PF. It was tested whether the baseline relationship between PISO and electromyographic power in 5 leg muscles (RMS EMG) was velocity dependent, linear and reproducible, such that the relative contributions to PF could be isolated from: 1) the decline in muscle activation (AF); and 2) the decline in PISO at a given activation (MF). Results: Healthy participants (n=13, 29 to 72 years old, ranging in aerobic capacity from 23.5 to 62.4 ml/min/kg) completed short (5 s) variable-effort isokinetic bouts at 50, 70, and 100 rpm to characterize the baseline relationship between RMS EMG and isokinetic power. Individual baseline EMG-PISO relationships were linear (r2 = 0.95 ± 0.04) and velocity dependent (analysis of covariance). Subsequently, repeated ramp incremental exercise tests were performed on a cycle ergometer and breath-by-breath gas exchange and ventilation was measured. Exercise was terminated with a maximal isokinetic effort (5 s) at 70 rpm. PISO at intolerance (two legs, 335 ± 88 W) was ~45% less than baseline (630 ± 156 W, p < 0.05). Following intolerance, PISO recovered within 3 minutes (p < 0.05). AF and MF (measured in one leg) were 97 ± 55 and 60 ± 50 W, respectively. Mean bias (± limits of agreement) for reproducibility were as follows: PISO at baseline 1 ± 30 W; PISO at 0-min recovery 3 ± 35 W; and EMG at PISO 3 ± 14%. Conclusions: The baseline EMG-PISO relationship was well modelled by a linear function, which was reproducible day-to-day. The variability of the individual EMG-PISO measurements between ~25% and 100% effort, around the linear model, was sufficiently tight that the baseline linear relationship allowed for a precise quantification of AF and MF at the limit of tolerance and in recovery from a maximal aerobic exercise task. It was also demonstrated that the EMG-PISO relationship was velocity dependent, as expected from the parabolic nature power-velocity curve. As such, this provides a valuable new method to identify the contributions of central and peripheral fatigue to limiting whole-body exercise in humans.Contexto: Esta tese procurou estabelecer um novo método de mensuração instantânea de fadiga central e periférica durante o exercício de corpo inteiro até a capacidade aeróbica máxima em seres humanos. Até agora, a mensuração da fadiga central e periférica tem sido limitada a tarefas musculares isoladas ou a momentos específicos após o exercício, nos quais as condições fisiológicas que levaram aos sintomas limitantes do exercício já estão abrandadas. Assim, desenvolver um método que supere estas limitações permitiria demonstrar pela primeira vez as contribuições relativas da fadiga central e periférica na limitação ao exercício, no qual haja estimulação máxima dos sistemas neuromuscular e cardiovascular. Objetivo: Desenvolver e validar um método para quantificar a fadiga muscular periférica (MF, definida como a potência produzida para uma determinada estimulação muscular), fadiga de ativação (AF, definida como a atividade muscular evocável máxima), sua soma, fadiga de desempenho (PF, definida como a perda de potência isocinética voluntária máxima em comparação com a basal) durante o exercício realizado no cicloergômetro em capacidade aeróbica máxima. Além disso, esta tese teve como objetivo determinar as taxas de recuperação nas quais MF, AF e PF retornaram à linha de base após a intolerância durante o exercício de corpo inteiro em seres humanos. Métodos: Para quantificar a fadiga durante o exercício de corpo inteiro, foi desenvolvido um método para permitir uma rápida transição do ciclismo padrão (em que a relação entre potência e cadência é hiperbólica) para o ciclismo isocinético (em que a potência é independente da cadência, e a cadência é fixa). Assim, ao pedir para o participante realizar um esforço isocinético máximo em qualquer ponto durante o exercício ou na fase de recuperação, permitiu-se quantificar o declínio velocidade-específica da potência isocinética máxima (PISO). A diferença na PISO entre a linha de base e o exercício quantifica a PF. Foi testado se a relação de base entre PISO e potência eletromiográfica em 5 músculos da perna (RMS EMG) era velocidade dependente, linear e reprodutível, de tal modo que as contribuições relativas para PF pudessem ser isoladas a partir de: 1) a diminuição da ativação muscular (AF) ; e 2) o declínio na PISO num dado grau de ativação (MF). Resultados: Participantes saudáveis (n=13, 29-72 anos, variando em capacidade aeróbica de 23,5 até 62,4 ml/min/kg) completaram tiros isocinéticos esforço-variável de curta duração (5 s) a 50, 70 e 100 rpm para caracterizar a relação basal entre EMG RMS e potência isocinética. As correlações entre EMG-Piso basais foram lineares (r2= 0,95 ± 0,04) e velocidade dependente (análise de covariância). Posteriormente, testes de exercício incrementais repetidos foram realizados em uma bicicleta ergométrica e as trocas gasosas e a ventilação foram mensuradas respiração a respiração. O exercício encerrava com um esforço isocinético máximo (5 s) a 70 rpm. Na intolerância, PISO (duas pernas, 335 ± 88 W) foi ~ de 45% menos do que na linha de base (630 ± 156 W, p <0,05). Após a intolerância, houve recuperação da PISO em 3 minutos (p <0,05). AF e MF (medido em uma perna) foram de 97 ± 55 e 60 ± 50 W, respectivamente. As médias de viés (± limites de concordância) para a reprodutibilidade foram as seguintes: PISO na linha de base 1 ± 30 W; PISO na recuperação 0-min 3 ± 35 W; e EMG em PISO 3 ± 14%. Conclusões: A relação basal EMG-PISO foi bem modelada por uma função linear, que foi reprodutível no dia-a-dia. A variabilidade das mensurações EMG-PISO individuais entre ~ 25% e 100% de esforço, em torno do modelo linear, foi suficientemente forte de modo que a relação linear basal permitiu uma quantificação precisa de AF e MF no limite de tolerância e na recuperação do exercício aeróbico máximo. Foi também demonstrado que a relação EMG-PISO foi velocidade dependente, como esperado a partir da curva parabólica de potência-velocidade. Assim, esta tese apresenta um novo método útil para identificar as contribuições da fadiga central e periférica na limitação do exercício de corpo inteiro em seres humanos

Articular human joint modelling

Copyright @ Cambridge University Press 2009.The work reported in this paper encapsulates the theories and algorithms developed to drive the core analysis modules of the software which has been developed to model a musculoskeletal structure of anatomic joints. Due to local bone surface and contact geometry based joint kinematics, newly developed algorithms make the proposed modeller different from currently available modellers. There are many modellers that are capable of modelling gross human body motion. Nevertheless, none of the available modellers offer complete elements of joint modelling. It appears that joint modelling is an extension of their core analysis capability, which, in every case, appears to be musculoskeletal motion dynamics. It is felt that an analysis framework that is focused on human joints would have significant benefit and potential to be used in many orthopaedic applications. The local mobility of joints has a significant influence in human motion analysis, in understanding of joint loading, tissue behaviour and contact forces. However, in order to develop a bone surface based joint modeller, there are a number of major problems, from tissue idealizations to surface geometry discretization and non-linear motion analysis. This paper presents the following: (a) The physical deformation of biological tissues as linear or non-linear viscoelastic deformation, based on spring-dashpot elements. (b) The linear dynamic multibody modelling, where the linear formulation is established for small motions and is particularly useful for calculating the equilibrium position of the joint. This model can also be used for finding small motion behaviour or loading under static conditions. It also has the potential of quantifying the joint laxity. (c) The non-linear dynamic multibody modelling, where a non-matrix and algorithmic formulation is presented. The approach allows handling complex material and geometrical nonlinearity easily. (d) Shortest path algorithms for calculating soft tissue line of action geometries. The developed algorithms are based on calculating minimum ‘surface mass’ and ‘surface covariance’. An improved version of the ‘surface covariance’ algorithm is described as ‘residual covariance’. The resulting path is used to establish the direction of forces and moments acting on joints. This information is needed for linear or non-linear treatment of the joint motion. (e) The final contribution of the paper is the treatment of the collision. In the virtual world, the difficulty in analysing bodies in motion arises due to body interpenetrations. The collision algorithm proposed in the paper involves finding the shortest projected ray from one body to the other. The projection of the body is determined by the resultant forces acting on it due to soft tissue connections under tension. This enables the calculation of collision condition of non-convex objects accurately. After the initial collision detection, the analysis involves attaching special springs (stiffness only normal to the surfaces) at the ‘potentially colliding points’ and motion of bodies is recalculated. The collision algorithm incorporates the rotation as well as translation. The algorithm continues until the joint equilibrium is achieved. Finally, the results obtained based on the software are compared with experimental results obtained using cadaveric joints