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Anconeus Muscle

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Charles L Rice – 1st expert on this subject based on the ideXlab platform

  • Rate modulation of human Anconeus motor units during high-intensity dynamic elbow extensions
    Journal of Applied Physiology, 2016
    Co-Authors: Brianna L Cowling, Brad Harwood, David B. Copithorne, Charles L Rice

    Abstract:

    We recorded single MUFRs during a high-intensity fatiguing dynamic elbow extension task. Because of unique features, the Anconeus Muscle (an accessory elbow extensor) facilitates tracking of units …

  • in vivo measurement of fascicle length and pennation of the human Anconeus Muscle at several elbow joint angles
    Journal of Anatomy, 2014
    Co-Authors: Daniel E Stevens, Cameron B Smith, Brad Harwood, Charles L Rice

    Abstract:

    Ultrasound imaging has facilitated the reliable measure of the architectural variables fascicle length (LF) and pennation angle (PA), at rest and during static and dynamic contractions in many human skeletal Muscles in vivo. Despite its small size and very modest contribution to elbow extension torque, the Anconeus Muscle has proven a useful model for the study of neuromuscular function in health and disease. Recent single motor unit (MU) studies in the Anconeus have reported discrete and identifiable individual trains of MU potentials from intramuscular electromyography (EMG) recordings during dynamic elbow extensions. It is unknown whether the Anconeus has unique architectural features related to alterations in LF and PA throughout the elbow joint range of motion that may help explain these high-quality recordings. Previous anatomical studies have investigated this Muscle in cadavers and at mainly one elbow joint angle. The purpose of this study was to measure in vivo PA and LF of the Anconeus Muscle in a relaxed state at different degrees of elbow flexion using ultrasonography. Ultrasound images were collected from 10 healthy males (25 ± 3 years) at 135°, 120°, 90°, 45°, and 0° of elbow flexion. Average values of LF decreased by 6 mm (10%), 6 mm (12%), and 4 mm (9%) from 135–120°, 120–90°, and 90–45° of elbow flexion, respectively, whereas average PA values increased by 1° (9%), 1° (8%), and 2° (14%) from 135–120°, 120–90°, and 45–0°, respectively. The results indicate that Anconeus Muscle architecture is dynamic, undergoing moderate changes with elbow joint excursion that are similar to other limb Muscles reported elsewhere. The data obtained here are more comprehensive and representative of architectural changes at various elbow joint positions than those data reported in cadaveric studies. Furthermore, the results of this study indicate that despite experiencing similar relative changes in Muscle architecture to other skeletal Muscles about the elbow joint, the minimal absolute changes in LF of the Anconeus likely contribute to the clarity of intramuscular EMG previously reported in this Muscle.

  • Reduced motor unit discharge rates of maximal velocity dynamic contractions in response to a submaximal dynamic fatigue protocol
    Journal of Applied Physiology, 2012
    Co-Authors: Brad Harwood, I. Choi, Charles L Rice

    Abstract:

    Fatigability is highly task dependent wherein motor unit (MU) discharge rates and recruitment thresholds are affected differently depending on whether contractions are performed at maximal or submaximal intensities. Although much is described for isometric tasks, the behavior of MU properties during the production of maximal velocity dynamic contractions following submaximal fatiguing contractions is unknown. In seven young men, we evaluated changes in MU recruitment thresholds and MU discharge rates of the Anconeus Muscle during both submaximal and maximal dynamic elbow extensions following a submaximal dynamic fatiguing protocol of moderate intensity to velocity task failure. Velocity and power of the maximal dynamic contractions declined ∼45 and ∼55%, respectively, but these variables were unchanged for the submaximal target velocity contractions. Discharge rates of the 12 MUs at task failure were unchanged for submaximal dynamic contractions, but were decreased ∼20% for maximal dynamic and ballistic i…

Ricardo A Maselli – 2nd expert on this subject based on the ideXlab platform

  • Novel delta subunit mutation in slow‐channel syndrome causes severe weakness by novel mechanisms
    Annals of Neurology, 2020
    Co-Authors: Christopher M. Gomez, Ricardo A Maselli, Bhupinder P. S. Vohra, Manuel F. Navedo, Joel R. Stiles, Pierre Charnet, Kelly Schott, Legier V. Rojas, John Keesey, Anthony Verity

    Abstract:

    We investigated the basis for a novel form of the slow-channel congenital myasthenic syndrome presenting in infancy in a single individual as progressive weakness and impaired neuromuscular transmission without overt degeneration of the motor endplate. Prolonged low-amplitude synaptic currents in biopsied Anconeus Muscle at 9 years of age suggested a kinetic disorder of the Muscle acetylcholine receptor. Ultrastructural studies at 16 months, at 9 years, and at 15 years of age showed none of the typical degenerative changes of the endplate associated with the slow-channel congenital myasthenic syndrome, and acetylcholine receptor numbers were not significantly reduced. We identified a novel C-to-T substitution in exon 8 of the δ-subunit that results in a serine to phenylalanine mutation in the region encoding the second transmembrane domain that lines the ion channel. Using Xenopus oocyte in vitro expression studies we confirmed that the δS268F mutation, as with other slow-channel congenital myasthenic syndrome mutations, causes delayed closure of acetylcholine receptor ion channels. In addition, unlike other mutations in slow-channel congenital myasthenic syndrome, this mutation also causes delayed opening of the channel, a finding that readily explains the marked congenital weakness in the absence of endplate degeneration. Finally, we used serial morphometric analysis of electron micrographs to explore the basis for the progressive weakness and decline of amplitude of endplate currents over a period of 14 years. We demonstrated a progressive widening and accumulation of debris in the synaptic cleft, resulting in loss of efficacy of released neurotransmitter and reduced safety factor. These studies demonstrate the role of previously unrecognized mechanisms of impairment of synaptic transmission caused by a novel mutation and show the importance of serial in vitro studies to elucidate novel disease mechanisms.

  • Exome sequencing detection of two untranslated GFPT1 mutations in a family with limb-girdle myasthenia
    Clinical Genetics, 2013
    Co-Authors: Ricardo A Maselli, Juan Arredondo, Joanna Nguyen, Marian Lara, Fiona Ng, J. M. Pham, Q. Yi, Jeffrey M. Stajich, Kristin K. Mcdonald

    Abstract:

    The term ‘limb-girdle myasthenia’ (LGM) was first used to describe three siblings with proximal limb weakness without oculobulbar involvement, but with EMG decrement and responsiveness to anticholinesterase medication. We report here that exome sequencing in the proband of this family revealed several sequence variations in genes linked to proximal limb weakness. However, the only mutations that cosegregated with disease were an intronic IVS7-8A>G mutation and the previously reported 3′-UTR c.*22C>A mutation in GFPT1, a gene linked to LGM. A minigene assay showed that IVS7-8A>G activates an alternative splice acceptor that results in retention of the last seven nucleotides of intron 7 and a frameshift leading to a termination codon 13 nucleotides downstream from the new splice site. An Anconeus Muscle biopsy revealed mild reduction of the axon terminal size and postsynaptic fold simplification. The amplitudes of miniature endplate potentials and quantal release were also diminished. The DNA of the mildly affected father of the proband showed only the intronic mutation along with sequence variations in other genes potentially relevant to LGM. Thus, this study performed in the family originally described with LGM showed two GFPT1 untranslated mutations, which may cause disease by reducing GFPT1 expression and ultimately impairing protein glycosylation.

  • Congenital myasthenic syndrome associated with epidermolysis bullosa caused by homozygous mutations in PLEC1 and CHRNE
    Clinical Genetics, 2010
    Co-Authors: Ricardo A Maselli, Juan Arredondo, Órla Cagney, Tahseen Mozaffar, S. Skinner, S. Yousif, Rr Davis, Jeffrey P. Gregg, Mark Sivak, Thomas Konia

    Abstract:

    Maselli RA, Arredondo J, Cagney O, Mozaffar T, Skinner S, Yousif S, Davis RR, Gregg JP, Sivak M, Konia TH, Thomas K, Wollmann RL. Congenital myasthenic syndrome associated with epidermolysis bullosa caused by homozygous mutations in PLEC1 and CHRNE.

    Mutations in the plectin gene (PLEC1) cause epidermolysis bullosa simplex (EBS), which may associate with muscular dystrophy (EBS–MD) or pyloric atresia (EBS–PA). The association of EBS with congenital myasthenic syndrome (CMS) is also suspected to result from PLEC1 mutations. We report here a consanguineous patient with EBS and CMS for whom mutational analysis of PLEC1 revealed a homozygous 36 nucleotide insertion (1506_1507ins36) that results in a reduced expression of PLEC1 mRNA and plectin in the patient Muscle. In addition, mutational analysis of CHRNE revealed a homozygous 1293insG, which is a well-known low-expressor receptor mutation. A skin biopsy revealed signs of EBS, and an Anconeus Muscle biopsy showed signs of a mild myopathy. Endplate studies showed fragmentation of endplates, postsynaptic simplification, and large collections of thread-like mitochondria. Amplitudes of miniature endplate potentials were diminished, but the endplate quantal content was actually increased. The complex phenotype presented here results from mutations in two separate genes. While the skin manifestations are because of the PLEC1 mutation, footprints of mutations in PLEC1 and CHRNE are present at the neuromuscular junction of the patient indicating that abnormalities in both genes contribute to the CMS phenotype.

Brad Harwood – 3rd expert on this subject based on the ideXlab platform

  • Rate modulation of human Anconeus motor units during high-intensity dynamic elbow extensions
    Journal of Applied Physiology, 2016
    Co-Authors: Brianna L Cowling, Brad Harwood, David B. Copithorne, Charles L Rice

    Abstract:

    We recorded single MUFRs during a high-intensity fatiguing dynamic elbow extension task. Because of unique features, the Anconeus Muscle (an accessory elbow extensor) facilitates tracking of units …

  • in vivo measurement of fascicle length and pennation of the human Anconeus Muscle at several elbow joint angles
    Journal of Anatomy, 2014
    Co-Authors: Daniel E Stevens, Cameron B Smith, Brad Harwood, Charles L Rice

    Abstract:

    Ultrasound imaging has facilitated the reliable measure of the architectural variables fascicle length (LF) and pennation angle (PA), at rest and during static and dynamic contractions in many human skeletal Muscles in vivo. Despite its small size and very modest contribution to elbow extension torque, the Anconeus Muscle has proven a useful model for the study of neuromuscular function in health and disease. Recent single motor unit (MU) studies in the Anconeus have reported discrete and identifiable individual trains of MU potentials from intramuscular electromyography (EMG) recordings during dynamic elbow extensions. It is unknown whether the Anconeus has unique architectural features related to alterations in LF and PA throughout the elbow joint range of motion that may help explain these high-quality recordings. Previous anatomical studies have investigated this Muscle in cadavers and at mainly one elbow joint angle. The purpose of this study was to measure in vivo PA and LF of the Anconeus Muscle in a relaxed state at different degrees of elbow flexion using ultrasonography. Ultrasound images were collected from 10 healthy males (25 ± 3 years) at 135°, 120°, 90°, 45°, and 0° of elbow flexion. Average values of LF decreased by 6 mm (10%), 6 mm (12%), and 4 mm (9%) from 135–120°, 120–90°, and 90–45° of elbow flexion, respectively, whereas average PA values increased by 1° (9%), 1° (8%), and 2° (14%) from 135–120°, 120–90°, and 45–0°, respectively. The results indicate that Anconeus Muscle architecture is dynamic, undergoing moderate changes with elbow joint excursion that are similar to other limb Muscles reported elsewhere. The data obtained here are more comprehensive and representative of architectural changes at various elbow joint positions than those data reported in cadaveric studies. Furthermore, the results of this study indicate that despite experiencing similar relative changes in Muscle architecture to other skeletal Muscles about the elbow joint, the minimal absolute changes in LF of the Anconeus likely contribute to the clarity of intramuscular EMG previously reported in this Muscle.

  • Reduced motor unit discharge rates of maximal velocity dynamic contractions in response to a submaximal dynamic fatigue protocol
    Journal of Applied Physiology, 2012
    Co-Authors: Brad Harwood, I. Choi, Charles L Rice

    Abstract:

    Fatigability is highly task dependent wherein motor unit (MU) discharge rates and recruitment thresholds are affected differently depending on whether contractions are performed at maximal or submaximal intensities. Although much is described for isometric tasks, the behavior of MU properties during the production of maximal velocity dynamic contractions following submaximal fatiguing contractions is unknown. In seven young men, we evaluated changes in MU recruitment thresholds and MU discharge rates of the Anconeus Muscle during both submaximal and maximal dynamic elbow extensions following a submaximal dynamic fatiguing protocol of moderate intensity to velocity task failure. Velocity and power of the maximal dynamic contractions declined ∼45 and ∼55%, respectively, but these variables were unchanged for the submaximal target velocity contractions. Discharge rates of the 12 MUs at task failure were unchanged for submaximal dynamic contractions, but were decreased ∼20% for maximal dynamic and ballistic i…