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Stochastic optimal open-loop control as a theory of force and impedance planning via muscle co-contraction.

ABSTRACT: Understanding the underpinnings of biological motor control is an important issue in movement neuroscience. Optimal control theory is a leading framework to rationalize this problem in computational terms. Previously, optimal control models have been devised either in deterministic or in stochastic settings to account for different aspects of motor control (e.g. average behavior versus trial-to-trial variability). While these approaches have yielded valuable insights about motor control, they typically fail in explaining muscle co-contraction. Co-contraction of a group of muscles associated to a motor function (e.g. agonist and antagonist muscles spanning a joint) contributes to modulate the mechanical impedance of the neuromusculoskeletal system (e.g. joint viscoelasticity) and is thought to be mainly under the influence of descending signals from the brain. Here we present a theory suggesting that one primary goal of motor planning may be to issue feedforward (open-loop) motor commands that optimally specify both force and impedance, according to noisy neuromusculoskeletal dynamics and to optimality criteria based on effort and variance. We show that the proposed framework naturally accounts for several previous experimental findings regarding the regulation of force and impedance via muscle co-contraction in the upper-limb. Stochastic optimal (closed-loop) control, preprogramming feedback gains but requiring on-line state estimation processes through long-latency sensory feedback loops, may then complement this nominal feedforward motor command to fully determine the limb's mechanical impedance. The proposed stochastic optimal open-loop control theory may provide new insights about the general articulation of feedforward/feedback control mechanisms and justify the occurrence of muscle co-contraction in the neural control of movement.

SUBMITTER: Berret B

PROVIDER: S-EPMC7065824 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Stochastic optimal open-loop control as a theory of force and impedance planning via muscle co-contraction.

Berret Bastien B Jean Frédéric F

PLoS computational biology 20200228 2

Understanding the underpinnings of biological motor control is an important issue in movement neuroscience. Optimal control theory is a leading framework to rationalize this problem in computational terms. Previously, optimal control models have been devised either in deterministic or in stochastic settings to account for different aspects of motor control (e.g. average behavior versus trial-to-trial variability). While these approaches have yielded valuable insights about motor control, they ty ...[more]

PMID: 32109941

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Project description:BackgroundThe role of Numb, a protein that is important for cell fate and development and that, in human muscle, is expressed at reduced levels with advanced age, was investigated; adult mice skeletal muscle and its localization and function within myofibres were determined.MethodsNumb expression was evaluated by western blot. Numb localization was determined by confocal microscopy. The effects of conditional knock out (cKO) of Numb and the closely related gene Numb-like in skeletal muscle fibres were evaluated by in situ physiology, transmission and focused ion beam scanning electron microscopy, three-dimensional reconstruction of mitochondria, lipidomics, and bulk RNA sequencing. Additional studies using primary mouse myotubes investigated the effects of Numb knockdown on cell fusion, mitochondrial function, and calcium transients.ResultsNumb protein expression was reduced by ~70% (P < 0.01) at 24 as compared with 3 months of age in gastrocnemius and tibialis anterior muscle. Numb was localized within muscle fibres as bands traversing fibres at regularly spaced intervals in close proximity to dihydropyridine receptors. The cKO of Numb and Numb-like reduced specific tetanic force by 36% (P < 0.01), altered mitochondrial spatial relationships to sarcomeric structures, increased Z-line spacing by 30% (P < 0.0001), perturbed sarcoplasmic reticulum organization and reduced mitochondrial volume by over 80% (P < 0.01). Only six genes were differentially expressed in cKO mice: Itga4, Sema7a, Irgm2, Vezf1, Mib1, and Tmem132a. Several lipid mediators derived from polyunsaturated fatty acids through lipoxygenases were up-regulated in Numb cKO skeletal muscle: 12-HEPE was increased by ~250% (P < 0.05) and 17,18-EpETE by ~240% (P < 0.05). In mouse primary myotubes, Numb knockdown reduced cell fusion (~20%, P < 0.01) and delayed the caffeine-induced rise in cytosolic calcium concentrations by more than 100% (P < 0.01).ConclusionsThese findings implicate Numb as a critical factor in skeletal muscle structure and function and suggest that Numb is critical for calcium release. We therefore speculate that Numb plays critical roles in excitation-contraction coupling, one of the putative targets of aged skeletal muscles. These findings provide new insights into the molecular underpinnings of the loss of muscle function observed with sarcopenia.

Project description:Action potential-driven Ca(2+) currents from the transverse tubules (t-tubules) trigger synchronous Ca(2+) release from the sarcoplasmic reticulum of cardiomyocytes. Loss of t-tubules has been reported in cardiac diseases, including heart failure, but the effect of uncoupling t-tubules from the sarcolemma on cardiac muscle mechanics remains largely unknown. We dissected intact rat right ventricular trabeculae and compared force, sarcomere length, and intracellular Ca(2+) in control trabeculae with trabeculae in which the t-tubules were uncoupled from the plasma membrane by formamide-induced osmotic shock (detubulation). We verified disconnection of a consistent fraction of t-tubules from the sarcolemma by two-photon fluorescence imaging of FM4-64-labeled membranes and by the absence of tubular action potential, which was recorded by random access multiphoton microscopy in combination with a voltage-sensitive dye (Di-4-AN(F)EPPTEA). Detubulation reduced the amplitude and prolonged the duration of Ca(2+) transients, leading to slower kinetics of force generation and relaxation and reduced twitch tension (1 Hz, 30°C, 1.5 mM [Ca(2+)]o). No mechanical changes were observed in rat left atrial trabeculae after formamide shock, consistent with the lack of t-tubules in rodent atrial myocytes. Detubulation diminished the rate-dependent increase of Ca(2+)-transient amplitude and twitch force. However, maximal twitch tension at high [Ca(2+)]o or in post-rest potentiated beats was unaffected, although contraction kinetics were slower. The ryanodine receptor (RyR)2 Ca-sensitizing agent caffeine (200 µM), which increases the velocity of transverse Ca(2+) release propagation in detubulated cardiomyocytes, rescued the depressed contractile force and the slower twitch kinetics of detubulated trabeculae, with negligible effects in controls. We conclude that partial loss of t-tubules leads to myocardial contractile abnormalities that can be rescued by enhancing and accelerating the propagation of Ca(2+)-induced Ca(2+) release to orphan RyR2 clusters.

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Stochastic optimal open-loop control as a theory of force and impedance planning via muscle co-contraction.

Publications

Stochastic optimal open-loop control as a theory of force and impedance planning via muscle co-contraction.

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