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Spinal mechanisms may provide a combination of intermittent and continuous control of human posture: predictions from a biologically based neuromusculoskeletal model.

Elias LA, Watanabe RN, Kohn AF - PLoS Comput. Biol. (2014)

Bottom Line: Simulation results showed that the neuromechanical outputs generated by the NMS model resemble experimental data from subjects standing on a stable surface.These results suggest that the spinal cord anatomy and neurophysiology (e.g., motor unit types, synaptic connectivities, ordered recruitment), along with the modulation of afferent activity, may account for the mixture of intermittent and continuous control that has been a subject of debate in recent studies on postural control.Another finding was the occurrence of the so-called "paradoxical" behaviour of muscle fibre lengths as a function of postural sway.

View Article: PubMed Central - PubMed

Affiliation: Biomedical Engineering Laboratory, Escola Polit├ęcnica, University of Sao Paulo, Sao Paulo, Brazil.

ABSTRACT
Several models have been employed to study human postural control during upright quiet stance. Most have adopted an inverted pendulum approximation to the standing human and theoretical models to account for the neural feedback necessary to keep balance. The present study adds to the previous efforts in focusing more closely on modelling the physiological mechanisms of important elements associated with the control of human posture. This paper studies neuromuscular mechanisms behind upright stance control by means of a biologically based large-scale neuromusculoskeletal (NMS) model. It encompasses: i) conductance-based spinal neuron models (motor neurons and interneurons); ii) muscle proprioceptor models (spindle and Golgi tendon organ) providing sensory afferent feedback; iii) Hill-type muscle models of the leg plantar and dorsiflexors; and iv) an inverted pendulum model for the body biomechanics during upright stance. The motor neuron pools are driven by stochastic spike trains. Simulation results showed that the neuromechanical outputs generated by the NMS model resemble experimental data from subjects standing on a stable surface. Interesting findings were that: i) an intermittent pattern of muscle activation emerged from this posture control model for two of the leg muscles (Medial and Lateral Gastrocnemius); and ii) the Soleus muscle was mostly activated in a continuous manner. These results suggest that the spinal cord anatomy and neurophysiology (e.g., motor unit types, synaptic connectivities, ordered recruitment), along with the modulation of afferent activity, may account for the mixture of intermittent and continuous control that has been a subject of debate in recent studies on postural control. Another finding was the occurrence of the so-called "paradoxical" behaviour of muscle fibre lengths as a function of postural sway. The simulations confirmed previous conjectures that reciprocal inhibition is possibly contributing to this effect, but on the other hand showed that this effect may arise without any anticipatory neural control mechanism.

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Neuromechanical outputs of the postural control model (Model 2) for a typical simulation.(A) Anteroposterior centre of mass (COM; gray curve) and centre of pressure (COP; black curve) displacements. (B) Muscular torque produced during postural sway. The negative value represents a plantar-flexion torque produced by the leg muscles (activation of the Triceps Surae muscle group) (C-E) Electromyogram (EMG) envelopes from Soleus (SO), Medial Gastrocnemius (MG), and Lateral Gastrocnemius (LG) muscles.
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pcbi-1003944-g001: Neuromechanical outputs of the postural control model (Model 2) for a typical simulation.(A) Anteroposterior centre of mass (COM; gray curve) and centre of pressure (COP; black curve) displacements. (B) Muscular torque produced during postural sway. The negative value represents a plantar-flexion torque produced by the leg muscles (activation of the Triceps Surae muscle group) (C-E) Electromyogram (EMG) envelopes from Soleus (SO), Medial Gastrocnemius (MG), and Lateral Gastrocnemius (LG) muscles.

Mentions: Typical biomechanical and neuronal outputs of the NMS model are presented in Figure 1. The model's responses resemble qualitatively those frequently reported in postural control studies (e.g., [9], [29], [36]). Irrespective of model structure (i.e., Model 1 or Model 2 - see Methods for details), the inverted pendulum leaned about 5 deg forward (equilibrium point), so that COM and COP displacements oscillated around a basal value of 80 mm (see Figure 1A). The basal plantar-flexion torque (negative torque) was 10% of the maximum isometric torque produced by the model. One can notice that COM and COP (Figure 1A) oscillated in anti-phase with respect to the muscle torque (Figure 1B), i.e. when the body leaned forward from its equilibrium position the plantar-flexion torque increased (more negative). Conversely, muscle activations (EMG envelopes in Figure 1C-E) were modulated approximately in phase with postural sway. In the simulations, TA muscle was silent during postural sway (not shown).


Spinal mechanisms may provide a combination of intermittent and continuous control of human posture: predictions from a biologically based neuromusculoskeletal model.

Elias LA, Watanabe RN, Kohn AF - PLoS Comput. Biol. (2014)

Neuromechanical outputs of the postural control model (Model 2) for a typical simulation.(A) Anteroposterior centre of mass (COM; gray curve) and centre of pressure (COP; black curve) displacements. (B) Muscular torque produced during postural sway. The negative value represents a plantar-flexion torque produced by the leg muscles (activation of the Triceps Surae muscle group) (C-E) Electromyogram (EMG) envelopes from Soleus (SO), Medial Gastrocnemius (MG), and Lateral Gastrocnemius (LG) muscles.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230754&req=5

pcbi-1003944-g001: Neuromechanical outputs of the postural control model (Model 2) for a typical simulation.(A) Anteroposterior centre of mass (COM; gray curve) and centre of pressure (COP; black curve) displacements. (B) Muscular torque produced during postural sway. The negative value represents a plantar-flexion torque produced by the leg muscles (activation of the Triceps Surae muscle group) (C-E) Electromyogram (EMG) envelopes from Soleus (SO), Medial Gastrocnemius (MG), and Lateral Gastrocnemius (LG) muscles.
Mentions: Typical biomechanical and neuronal outputs of the NMS model are presented in Figure 1. The model's responses resemble qualitatively those frequently reported in postural control studies (e.g., [9], [29], [36]). Irrespective of model structure (i.e., Model 1 or Model 2 - see Methods for details), the inverted pendulum leaned about 5 deg forward (equilibrium point), so that COM and COP displacements oscillated around a basal value of 80 mm (see Figure 1A). The basal plantar-flexion torque (negative torque) was 10% of the maximum isometric torque produced by the model. One can notice that COM and COP (Figure 1A) oscillated in anti-phase with respect to the muscle torque (Figure 1B), i.e. when the body leaned forward from its equilibrium position the plantar-flexion torque increased (more negative). Conversely, muscle activations (EMG envelopes in Figure 1C-E) were modulated approximately in phase with postural sway. In the simulations, TA muscle was silent during postural sway (not shown).

Bottom Line: Simulation results showed that the neuromechanical outputs generated by the NMS model resemble experimental data from subjects standing on a stable surface.These results suggest that the spinal cord anatomy and neurophysiology (e.g., motor unit types, synaptic connectivities, ordered recruitment), along with the modulation of afferent activity, may account for the mixture of intermittent and continuous control that has been a subject of debate in recent studies on postural control.Another finding was the occurrence of the so-called "paradoxical" behaviour of muscle fibre lengths as a function of postural sway.

View Article: PubMed Central - PubMed

Affiliation: Biomedical Engineering Laboratory, Escola Polit├ęcnica, University of Sao Paulo, Sao Paulo, Brazil.

ABSTRACT
Several models have been employed to study human postural control during upright quiet stance. Most have adopted an inverted pendulum approximation to the standing human and theoretical models to account for the neural feedback necessary to keep balance. The present study adds to the previous efforts in focusing more closely on modelling the physiological mechanisms of important elements associated with the control of human posture. This paper studies neuromuscular mechanisms behind upright stance control by means of a biologically based large-scale neuromusculoskeletal (NMS) model. It encompasses: i) conductance-based spinal neuron models (motor neurons and interneurons); ii) muscle proprioceptor models (spindle and Golgi tendon organ) providing sensory afferent feedback; iii) Hill-type muscle models of the leg plantar and dorsiflexors; and iv) an inverted pendulum model for the body biomechanics during upright stance. The motor neuron pools are driven by stochastic spike trains. Simulation results showed that the neuromechanical outputs generated by the NMS model resemble experimental data from subjects standing on a stable surface. Interesting findings were that: i) an intermittent pattern of muscle activation emerged from this posture control model for two of the leg muscles (Medial and Lateral Gastrocnemius); and ii) the Soleus muscle was mostly activated in a continuous manner. These results suggest that the spinal cord anatomy and neurophysiology (e.g., motor unit types, synaptic connectivities, ordered recruitment), along with the modulation of afferent activity, may account for the mixture of intermittent and continuous control that has been a subject of debate in recent studies on postural control. Another finding was the occurrence of the so-called "paradoxical" behaviour of muscle fibre lengths as a function of postural sway. The simulations confirmed previous conjectures that reciprocal inhibition is possibly contributing to this effect, but on the other hand showed that this effect may arise without any anticipatory neural control mechanism.

Show MeSH
Related in: MedlinePlus