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A computational model of torque generation: neural, contractile, metabolic and musculoskeletal components.

ABSTRACT: The pathway of voluntary joint torque production includes motor neuron recruitment and rate-coding, sarcolemmal depolarization and calcium release by the sarcoplasmic reticulum, force generation by motor proteins within skeletal muscle, and force transmission by tendon across the joint. The direct source of energetic support for this process is ATP hydrolysis. It is possible to examine portions of this physiologic pathway using various in vivo and in vitro techniques, but an integrated view of the multiple processes that ultimately impact joint torque remains elusive. To address this gap, we present a comprehensive computational model of the combined neuromuscular and musculoskeletal systems that includes novel components related to intracellular bioenergetics function. Components representing excitatory drive, muscle activation, force generation, metabolic perturbations, and torque production during voluntary human ankle dorsiflexion were constructed, using a combination of experimentally-derived data and literature values. Simulation results were validated by comparison with torque and metabolic data obtained in vivo. The model successfully predicted peak and submaximal voluntary and electrically-elicited torque output, and accurately simulated the metabolic perturbations associated with voluntary contractions. This novel, comprehensive model could be used to better understand impact of global effectors such as age and disease on various components of the neuromuscular system, and ultimately, voluntary torque output.

SUBMITTER: Callahan DM

PROVIDER: S-EPMC3566067 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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A computational model of torque generation: neural, contractile, metabolic and musculoskeletal components.

Callahan Damien M DM Umberger Brian R BR Kent-Braun Jane A JA

PloS one 20130206 2

The pathway of voluntary joint torque production includes motor neuron recruitment and rate-coding, sarcolemmal depolarization and calcium release by the sarcoplasmic reticulum, force generation by motor proteins within skeletal muscle, and force transmission by tendon across the joint. The direct source of energetic support for this process is ATP hydrolysis. It is possible to examine portions of this physiologic pathway using various in vivo and in vitro techniques, but an integrated view of t ...[more]

PMID: 23405245

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Project description:Assessment of metabolic cost as a metric for human performance has expanded across various fields within the scientific, clinical, and engineering communities. As an alternative to measuring metabolic cost experimentally, musculoskeletal models incorporating metabolic cost models have been developed. However, to utilize these models for practical applications, the accuracy of their metabolic cost predictions requires improvement. Previous studies have reported the benefits of using personalized musculoskeletal models for various applications, yet no study has evaluated how model personalization affects metabolic cost estimation. This study investigated the effect of musculoskeletal model personalization on estimates of metabolic cost of transport (CoT) during post-stroke walking using three commonly used metabolic cost models. We analyzed walking data previously collected from two male stroke survivors with right-sided hemiparesis. The three metabolic cost models were implemented within three musculoskeletal modeling approaches involving different levels of personalization. The first approach used a scaled generic OpenSim model and found muscle activations via static optimization (SOGen). The second approach used a personalized electromyographic (EMG)-driven musculoskeletal model with personalized functional axes but found muscle activations via static optimization (SOCal). The third approach used the same personalized EMG-driven model but calculated muscle activations directly from EMG data (EMGCal). For each approach, the muscle activation estimates were used to calculate each subject's CoT at different gait speeds using three metabolic cost models (Umberger et al., 2003; Bhargava et al., 2004; Umberger, 2010). The calculated CoT values were compared with published CoT data as a function of walking speed, step length asymmetry, stance time asymmetry, double support time asymmetry, and severity of motor impairment (i.e., Fugl-Meyer score). Overall, only SOCal and EMGCal with the Bhargava metabolic cost model were able to reproduce accurately published experimental trends between CoT and various clinical measures of walking asymmetry post-stroke. Tuning of the parameters in the different metabolic cost models could potentially resolve the observed CoT magnitude differences between model predictions and experimental measurements. Realistic CoT predictions may allow researchers to predict human performance, surgical outcomes, and rehabilitation outcomes reliably using computational simulations.

Project description:Normal functioning of the brain relies on a continual and efficient delivery of energy by a vast network of cerebral blood vessels. The bidirectional coupling between neurons and blood vessels consists of vasodilatory energy demand signals from neurons to blood vessels, and the retrograde flow of energy substrates from the vessels to neurons, which fuel neural firing, growth and other housekeeping activities in the neurons. Recent works indicate that, in addition to the functional coupling observed in the adult brain, the interdependence between the neural and vascular networks begins at the embryonic stage, and continues into subsequent developmental stages. The proposed Vascular Arborization Model (VAM) captures the effect of neural cytoarchitecture and neural activity on vascular arborization. The VAM describes three important stages of vascular tree growth: (i) The prenatal growth phase, where the vascular arborization depends on the cytoarchitecture of neurons and non-neural cells, (ii) the post-natal growth phase during which the further arborization of the vasculature depends on neural activity in addition to neural cytoarchitecture, and (iii) the settling phase, where the fully grown vascular tree repositions its vascular branch points or nodes to ensure minimum path length and wire length. The vasculature growth depicted by VAM captures structural characteristics like vascular volume density, radii, mean distance to proximal neurons in the cortex. VAM-grown vasculature agrees with the experimental observation that the neural densities do not covary with the vascular density along the depth of the cortex but predicts a high correlation between neural areal density and microvascular density when compared over a global scale (across animals and regions). To explore the influence of neural activity on vascular arborization, the VAM was used to grow the vasculature in neonatal rat whisker barrel cortex under two conditions: (i) Control, where the whiskers were intact and (ii) Lesioned, where one row of whiskers was cauterized. The model captures a significant reduction in vascular branch density in lesioned animals compared to control animals, concurring with experimental observation.

Dataset Information

A computational model of torque generation: neural, contractile, metabolic and musculoskeletal components.

Publications

A computational model of torque generation: neural, contractile, metabolic and musculoskeletal components.

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