Evidence map›Paper›PMID 39451824›Full record

ArticleBiomimetics (Basel, Switzerland)2024

Antagonistic Feedback Control of Muscle Length Changes for Efficient Involuntary Posture Stabilization.

Masami Iwamoto, Noritoshi Atsumi, Daichi Kato

Abstract read
In one paragraph

Article in Biomimetics (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Masami IwamotoHuman Science Research-Domain, Toyota Central R&D Labs., Inc., 41-1, Yokomichi, Nagakute, Aichi 480-1192, Japan.ORCID 0000-0002-0738-521X
Noritoshi AtsumiHuman Science Research-Domain, Toyota Central R&D Labs., Inc., 41-1, Yokomichi, Nagakute, Aichi 480-1192, Japan.ORCID 0000-0001-5938-9557
Daichi KatoHuman Science Research-Domain, Toyota Central R&D Labs., Inc., 41-1, Yokomichi, Nagakute, Aichi 480-1192, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Simultaneous and cooperative muscle activation results in involuntary posture stabilization in vertebrates. However, the mechanism through which more muscles than joints contribute to this stabilization remains unclear. We developed a computational human body model with 949 muscle action lines and 22 joints and examined muscle activation patterns for stabilizing right upper or lower extremity motions at a neutral body posture (NBP) under gravity using actor-critic reinforcement learning (ACRL). Two feedback control models (FCM), muscle length change (FCM-ML) and joint angle differences, were applied to ACRL with a normalized Gaussian network (ACRL-NGN) or deep deterministic policy gradient. Our findings indicate that among the six control methods, ACRL-NGN with FCM-ML, utilizing solely antagonistic feedback control of muscle length change without relying on synergy pattern control or categorizing muscles as flexors, extensors, agonists, or synergists, achieved the most efficient involuntary NBP stabilization. This finding suggests that vertebrate muscles are fundamentally controlled without categorization of muscles for targeted joint motion and are involuntarily controlled to achieve the NBP, which is the most comfortable posture under gravity. Thus, ACRL-NGN with FCM-ML is suitable for controlling humanoid muscles and enables the development of a comfortable seat design.

Indexed as

actor-critic reinforcement learninghuman musculosketetal modelinvoluntary posture stabilizationmuscle length feedback controlneutral body posture

Identifiers

PMID39451824
PMCPMC11506834

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.