Altered Muscle Research Articles

Obesity and the Importance of Breathing.

Obesity is a complex and non-communicable disease with a pandemic entity. Currently, multiple causes can lead to obesity, and it is not always easy to create a direct relationship between physical inactivity, poor quality of nutrients consumed, and calculation of excess calories. Among the associated comorbidities, obesity creates a dysfunctional environment of respiratory rhythms at the central and peripheral levels, with functional, morphological, and phenotypic alteration of the diaphragm muscle. This pathological adaptation of breathing is one of the most important causes of the dysregulation of the autonomic system, which will negatively affect the progression of comorbidities and chronic non-physiological adaptations in obese persons. Introducing a physical activity program involving diaphragm training could be a very valid strategy to restore the systemic autonomic response, delaying or avoiding the onset of pathologies in excess fat. This brief narrative review focuses on the importance of breathing in obese subjects.

Feruloylacetone and Its Analog Demethoxyferuloylacetone Mitigate Obesity-Related Muscle Atrophy and Insulin Resistance in Mice.

Obesity-induced muscle alterations, such as inflammation, metabolic dysregulation, and myosteatosis, lead to a decline in muscle mass and function, often resulting in sarcopenic obesity. Currently, there are no definitive treatments for sarcopenic obesity beyond lifestyle changes and dietary supplementation. Feruloylacetone (FER), a thermal degradation product of curcumin, and its analog demethoxyferuloylacetone (DFER), derived from the thermal degradation of bisdemethoxycurcumin, have shown potential antiobesity effects in previous studies. This study investigates the impact of FER and DFER on obesity-related glucose intolerance and muscle atrophy. High-fat diet (HFD) feeding resulted in muscle mass reduction and increased intramuscular triglyceride accumulation, both of which were mitigated by FER and DFER supplementation. The supplements activated the PI3K/Akt/mTOR signaling pathway, enhanced muscle protein synthesis, and decreased markers of muscle protein degradation. Additionally, FER and DFER supplementation improved glucose homeostasis in HFD-fed mice. The supplements also promoted the formation of a gut microbial consortium comprising Blautia intestinalis, Dubosiella newyorkensis, Faecalicatena fissicatena, Waltera intestinalis, Clostridium viride, and Caproiciproducens galactitolivorans, which contributed to the reduction of obesity-induced chronic inflammation. These findings suggest, for the first time, that FER and DFER may prevent obesity-related complications, including muscle atrophy and insulin resistance, thereby warranting further research into their long-term efficacy and safety.

Hazardous effects of heavy metal pollution on Nile tilapia in the aquatic ecosystem of the Eastern Delta in Egypt

IntroductionHeavy metal pollution threatens the biodiversity and ecological equilibrium of the Nile River. This study investigates the impact of heavy metal pollution on aquatic animals such as Nile tilapia (Oreochromis niloticus) in the Damietta branch of the River Nile and El-Rayah El-Tawfeeky canal in Benha City in Egypt.MethodsFish and water samples were collected from the Damietta branch and El-Rayah El-Tawfeeky during the fall of 2022. The concentrations of heavy metals in fish muscle tissues were analyzed using inductively coupled plasma atomic emission spectroscopy (ICP-OES). Histopathological examinations were performed on gill, liver, spleen, and muscle tissues, following standard histological procedures, to assess tissue damage and morphological alterations. Additionally, gene expression analysis was conducted using real-time polymerase chain reaction (RT-qPCR) to evaluate the expression levels of muscle growth (MyoD, IGF-1) and immune response (TNFa, IL6) genes.ResultsHistopathological examinations revealed noteworthy alterations in tilapia gill, liver, spleen, and muscle, suggesting potential health risks. Gene expression analysis using Real-time polymerase chain reaction (RT-qPCR) indicated significant changes in genes related to muscle growth (MyoD, IGF-1) and immune response (TNFa, IL6) in fish from the Damietta branch relative to fish of El-Rayah El-Tawfeeky.ConclusionThe findings raise concerns about bioaccumulation of heavy, some of which surpass international safety limits, posing potential health risks to consumers. The study underscores the significance of continuous monitoring, utilizing chemical, histopathological, and molecular tools as bioindicators for environmental protection measures against aquatic pollution.

Evaluating the Impact of Multimodal Prehabilitation with High Protein Oral Nutritional Supplementation (HP ONS) with Beta-Hydroxy Beta-Methylbutyrate (HMB) on Sarcopenic Surgical Patients-Interim Analysis of the HEROS Study.

Multimodal prehabilitation programs, which may incorporate nutritional supplementation and exercise, have been developed to combat sarcopenia in surgical patients to enhance post-operative outcomes. However, the optimal regime remains unknown. The use of beta-hydroxy beta-methylbutyrate (HMB) has beneficial effects on muscle mass and strength. However, its effect on muscle quality in the perioperative setting has yet to be established. This study aims to explore the impact of a multimodal prehabilitation program using a bundle of care that includes high-protein oral nutritional supplementation (HP ONS) with HMB and resistance exercise on muscle quality and functional outcomes in sarcopenic surgical patients. Sarcopenic adult patients undergoing elective major gastrointestinal surgeries were recruited for this pilot interventional cohort study. They were enrolled in a 2-4-week multimodal prehabilitation program comprising resistance exercise, nutritional supplementation, vitamin supplementation, comorbid optimization and smoking cessation. Participants were provided three units of HP ONS with HMB per day pre-operatively. The primary outcome was changes in intramuscular adipose tissue (IMAT) as a proxy of muscle quality, assessed using Artificial Intelligence (AI)-aided ultrasonography. Secondary outcomes include changes in anthropometric measurements and functional characteristics. Outcomes were measured before prehabilitation, after prehabilitation and 1 month post-operatively. A total of 36 sarcopenic patients, with a median age of 71.5 years, were included in this study. There was an increase in the IMAT index after two weeks of prehabilitation (p = 0.032) to 1 month after surgery (p = 0.028). Among functional parameters, improvement was observed in gait speed (p = 0.01) after two weeks of prehabilitation, which returned to baseline post-operatively. The median length of hospital stay was 7 (range: 2-75) days. The increase in the IMAT index in a sarcopenic surgical cohort undergoing prehabilitation may be due to altered muscle metabolism in elderly sarcopenic patients. A prehabilitation regime in sarcopenic patients incorporating HP ONS with HMB and resistance exercise is feasible and is associated with increased gait speed.

Effects of botulinum toxin on paraspinal muscle imbalance during spinal motions in adolescents with idiopathic scoliosis: Assessment using high-density electromyography

Background The pathogenesis of adolescent idiopathic scoliosis (AIS) remains unclear, with muscle imbalance being a widely discussed hypothesis. Objective This study examined the impact of muscle imbalance on AIS by injecting botulinum toxin A (BTX) into patients’ unilateral muscles and investigating altered back muscle synergies. Methods Three AIS patients received BTX injections in the concave-side paraspinal muscles. High-density electromyogram arrays placed from T8 to L4 recorded signals during five spinal motions at four timepoints (one pre-BTX and three post-BTX). Muscle synergies were extracted using non-negative matrix factorization and compared with data from ten healthy and ten AIS subjects from our previous studies. Results Post-BTX, muscle activity maps during flexion/extension, sitting, and standing exhibited reduced symmetry, with concave/convex ratios decreasing and being statistically lower than those of healthy subjects at post-2 and post-3 follow-ups ( p < 0.01). Muscles on the dominant side during lateral bending or axial rotation demonstrated decreased activation and differently distributed center of gravity positions on synergy maps compared to healthy subjects at all timepoints ( p < 0.05). Post-BTX changes were particularly notable for the patient with mild deformity. Conclusions BTX affected the activation of paraspinal muscles, providing insights into the role of muscle imbalance in AIS and informing future therapeutic strategies.

Electrical impedance myography detects progressive pathological alterations in the hindlimb muscle of the PMP22-C3 mice, an animal model of CMT1A.

Charcot-Marie-Tooth type 1A (CMT1A) is the most common inherited peripheral dysmyelinating neuropathy. Although lower limb muscle weakness is the most important factor affecting the quality of life of patients with CMT1A, existing clinical measures for its evaluation have limitations, including low sensitivity in detecting disease progression. Electrical impedance myography (EIM) is a newer tool that enables noninvasive evaluation of muscle state by measuring muscle composition, and potentially supports the evaluation of neuromuscular disease progression and treatment effects. To determine the potential of EIM as a CMT1A biomarker, we obtained natural history data for EIM from the gastrocnemius muscle of the PMP22-C3 mice, an animal model of CMT1A. Alterations in the EIM parameters, weak hindlimb grip strength, decreased muscle fiber size, and changes in the mRNA expression of genes related to neuromuscular junction dysfunction were found. These changes were more pronounced at later stages (12 and 18weeks of age) than at earlier stage (6weeks of age), indicating that EIM can detect disease progression in PMP22-C3 mice. Our preclinical findings support the use of EIM as a potential translational biomarker for assessing progressive changes in the pathological muscle state in CMT1A.

Muscular strength, endothelial function and cognitive disorders: state of the art.

In recent years, the ageing population has increasingly grown. This process carries a range of pathophysiological changes involving alterations in the skeletal muscle, vascular endothelium and brain function, becoming an important risk factor for developing cognitive disorders and cardiovascular diseases. With ageing, there is a decrease in muscle mass and muscle strength, and a relationship between muscle strength decrease and cognitive decline has been shown. Lower handgrip strength has been linked to memory impairment, lower global cognitive function, decreased attention and reduced visuospatial abilities in the elderly, but understanding of the underlying mechanisms that explain the link between altered skeletal muscle function and structure, endothelial dysfunction, and the role of endothelial dysfunction in the onset of cognitive disorders has been scarcely explored. This review aims to detail the cellular and molecular mechanisms by which the progressive changes associated with ageing can alter healthy skeletal muscle and endothelial function, creating an environment of oxidative stress, inflammation and mitochondrial dysfunction. These changes can lead to reduced muscle strength, and the secretion of detrimental endothelial factors, resulting in endothelial dysfunction, blood-brain barrier disruption, and damage to neurons and microglia, ultimately accelerating the onset of cognitive disorders in the elderly. In addition, we aimed to describe the mechanisms that potentially explain how preserving muscular function with resistance training could prevent brain function deterioration, including the production of different factors that allow an improved endothelial function, haemodynamic parameters and brain plasticity, ultimately delaying the onset of cognitive impairment and chronic diseases.

Analysis of Added Postoperative Diplopia After Transnasal Endoscopic Inferomedial Wall Decompression for Thyroid-Associated Ophthalmopathy.

The authors retrospectively analyzed the reported rate of added diplopia and associated factors in patients with thyroid-associated ophthalmopathy (TAO) after transnasal endoscopic inferomedial wall decompression, to illuminate the issue and look for ways to improve prognosis. Retrospective analysis was done on the medical records of patients with moderate-to-severe TAO between 2023-01 and 2024-01. Under general anesthesia, transnasal endoscopic inferomedial wall decompression was carried out on each subject. Clinical outcomes included postoperative added diplopia (including new-onset and aggravated), strabismus, and alterations in the extraocular muscles. Sixty-five eyes in 65 patients received treatment. Nineteen patients (29.3%) had new-onset horizontal diplopia at 1 month and 10 patients (15.4%) at 6 months postoperatively; 9 patients (13.8%) experienced aggravated horizontal diplopia at 1 month and 6 patients (9.2%) at 6 months (C2=4.947, P<0.05). The average volume of the medial rectus muscle was the only one to increase in the extraocular muscles (F=34.131, P<0.001), and the preoperative medial rectus muscle volume was higher in the added diplopia patients than in the no-added diplopia patients (F=267.405, P<0.001). Postoperative diplopia (both new-onset and aggravated) increased in TAO with transnasal endoscopic inferomedial wall decompression. Most added diplopia was horizontal and most added strabismus was esotropia. They were closely associated with changes in the medial rectus's thickness, displacement, and structural alterations. The preoperative medial rectus volume is one of the possible markers of further postoperative diplopia.

Early life lipid overload in Native American Myopathy is phenocopied by stac3 knockout in zebrafish

Understanding the early stages of human congenital myopathies is critical for proposing strategies for improving musculoskeletal muscle performance, such as restoring the functional integrity of the cytoskeleton. SH3 and cysteine-rich domain 3 (STAC3) are proteins involved in nutrient regulation and are an essential component of the excitation–contraction (EC) coupling machinery for Ca2+ releasing. A mutation in STAC3 causes debilitating Native American Myopathy (NAM) in humans, while loss of this gene in mice and zebrafish (ZF) results in premature death. Clinically, NAM patients demonstrated increased lipids in skeletal muscle, but it is unclear if neutral lipids are associated with altered muscle function in NAM. Using a CRISPR/Cas9 induced stac3-/- knockout (KO) zebrafish model, we determined that loss of stac3 leads to delayed larval hatching which corresponds with muscle weakness and decreased whole-body Ca2+ level during early skeletal development. Specifically, we observed defects in the cytoskeleton in F-actin and slow muscle fibers at 5 and 7 days post-fertilizations (dpf). Myogenesis regulators such as myoD and myf5, mstnb were significantly altered in stac3-/- larvae. These muscle alterations were associated with elevated neutral lipid levels starting at 5 dpf and persisting beyond 7 dpf. Larva lacking stac3 had reduced viability with no larva knockouts surviving past 11 dpf. This data suggests that our stac3-/- zebrafish serve as an alternative model to study the diminished muscle function seen in NAM patients. The data gathered from this new model over time supports a mechanistic view of lipotoxicity as a critical part of the pathology of NAM and the associated loss of function in muscle.

Skeletal Muscle 31P MR Spectroscopy Surpasses CT in Predicting Patient Survival After Liver Transplantation.

Skeletal muscle alterations are associated with higher mortality and morbidity in patients with liver cirrhosis. Assessing these changes seems to be a promising method for identifying patients at a high risk of poor outcomes following liver transplantation (LT). This is particularly important given the current global shortage of organ donors. However, evidence of the impact of these alterations on the prognosis of patients undergoing LT is inconclusive. The aim of our prospective study was to evaluate the impact of skeletal muscle changes, reflected in sarcopenia, myosteatosis and metabolic changes in the calf muscles, on perioperative outcomes and long-term survival after LT. We also sought to determine the posttransplant evolution of the resting muscle metabolism. We examined 134 adult LT candidates. Of these, 105 underwent LT. Sarcopenia and myosteatosis were diagnosed by measuring the skeletal muscle index and mean psoas muscle radiation attenuation, respectively, which were obtained from computed tomography (CT) scans taken during pretransplant assessment. Additionally, patients underwent 31P MR spectroscopy (MRS) of the calf muscles at rest before LT and 6, 12 and 24 months thereafter. The median follow-up was 6 years. Patients with abnormal 31P MRS results and CT-diagnosed myosteatosis prior to LT had significantly worse long-term survival after LT (hazard ratio (HR), 3.36; 95% confidence interval (CI), 1.48-7.60; p = 0.0021 and HR, 2.58; 95% CI, 1.06-6.29; p = 0.03, respectively). Multivariable analysis showed that abnormal 31P MR spectra (HR, 3.40; 95% CI, 1.50-7.71; p = 0.003) were a better predictor of worse long-term survival after LT than myosteatosis (HR, 2.78; 95% CI, 1.14-6.78; p = 0.025). Patients with abnormal 31P MR spectra had higher blood loss during LT (p = 0.038), required a higher number of red blood cell transfusions (p = 0.006) and stayed longer in ICU (p = 0.041) and hospital (p = 0.007). Myosteatosis was associated with more revision surgeries following LT (p = 0.038) and a higher number of received red blood cell transfusion units (p = 0.002). Sarcopenia had no significant effect on posttransplant patient survival. An improvement in the resting metabolism of the calf muscles was observed at 12 and 24 months after LT. Abnormal 31P MRS results of calf muscles were superior to CT-based diagnosis of myosteatosis and sarcopenia in predicting perioperative complications and long-term survival after LT. Resting muscle metabolism normalized 1 year after LT in most recipients.

Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action

Type 2 diabetes is preceded by a defective insulin response, yet our knowledge of the precise mechanisms is incomplete. Here, we investigate how insulin resistance alters skeletal muscle signaling and how exercise partially counteracts this effect. We measured parallel phenotypes and phosphoproteomes of insulin-resistant (IR) and insulin-sensitive (IS) men as they responded to exercise and insulin (n= 19, 114 biopsies), quantifying over 12,000 phosphopeptides in each biopsy. Insulin resistance involves selective and time-dependent alterations to signaling, including reduced insulin-stimulated mTORC1 and non-canonical signaling responses. Prior exercise promotes insulin sensitivity even in IR individuals by "priming" a portion of insulin signaling prior to insulin infusion. This includes MINDY1 S441, which we show is an AKT substrate. We found that MINDY1 knockdown enhances insulin-stimulated glucose uptake in rat myotubes. This work delineates the signaling alterations in IR skeletal muscle and identifies MINDY1 as a regulator of insulin action.

SMN Deficiency Induces an Early Non-Atrophic Myopathy with Alterations in the Contractile and Excitatory Coupling Machinery of Skeletal Myofibers in the SMN∆7 Mouse Model of Spinal Muscular Atrophy.

Spinal muscular atrophy (SMA) is caused by a deficiency of the ubiquitously expressed survival motor neuron (SMN) protein. The main pathological hallmark of SMA is the degeneration of lower motor neurons (MNs) with subsequent denervation and atrophy of skeletal muscle. However, increasing evidence indicates that low SMN levels not only are detrimental to the central nervous system (CNS) but also directly affect other peripheral tissues and organs, including skeletal muscle. To better understand the potential primary impact of SMN deficiency in muscle, we explored the cellular, ultrastructural, and molecular basis of SMA myopathy in the SMNΔ7 mouse model of severe SMA at an early postnatal period (P0-7) prior to muscle denervation and MN loss (preneurodegenerative [PND] stage). This period contrasts with the neurodegenerative (ND) stage (P8-14), in which MN loss and muscle atrophy occur. At the PND stage, we found that SMN∆7 mice displayed early signs of motor dysfunction with overt myofiber alterations in the absence of atrophy. We provide essential new ultrastructural data on focal and segmental lesions in the myofibrillar contractile apparatus. These lesions were observed in association with specific myonuclear domains and included abnormal accumulations of actin-thin myofilaments, sarcomere disruption, and the formation of minisarcomeres. The sarcoplasmic reticulum and triads also exhibited ultrastructural alterations, suggesting decoupling during the excitation-contraction process. Finally, changes in intermyofibrillar mitochondrial organization and dynamics, indicative of mitochondrial biogenesis overactivation, were also found. Overall, our results demonstrated that SMN deficiency induces early and MN loss-independent alterations in myofibers that essentially contribute to SMA myopathy. This strongly supports the growing body of evidence indicating the existence of intrinsic alterations in the skeletal muscle in SMA and further reinforces the relevance of this peripheral tissue as a key therapeutic target for the disease.

Multi-channel EMG manifestations of upper-extremity muscle coordination imbalance among community-dwelling sarcopenic seniors

BackgroundSarcopenia is an age-related, insidious, crippling but curable degenerative disease if diagnosed and treated early. However, no accessible and accurate early screening method is available for community settings that does not require specialized personnel. One of the hallmarks of sarcopenia is the pathological changes of muscle fiber type composition and motor unit firing patterns. Surface electromyography (sEMG) may serve as an effective tool for detecting differences between healthy and sarcopenic individuals due to its superior wearability and accessibility compared to other screening methods such as medical imaging and bioimpedance measurements, making it ideal for community-based sarcopenic screening. Our study aims to explore sEMG biomarkers that can be used for screening or diagnosis of sarcopenia.ResultsWe collected multi-channel sEMG signals from six forearm muscles of 98 healthy and 55 sarcopenic community-dwelling older adults. Participants performed grasp tasks at 20% and 50% of maximum voluntary contraction (MVC). Hexagons created by various EMG features, normalized with respect to respective MVC, and symmetry analyses were performed to estimate multi-muscle coordination patterns. An innovative index, namely incenter–circumcenter distance of muscle coordination (ICDMC), is proposed to discriminate between the healthy and sarcopenic groups. We utilized non-parametric tests to compare the ICDMC between the two groups, considering a p-value less than 0.05 statistically significant. The results showed that at 20% MVC, ICDMCs from root mean square (RMS), mean absolute value (MAV), slope sign changes (SSC) and wavelength (WL) showed statistically significant differences. More insights of this sEMG manifestation of sarcopenia were revealed by gender- and age-stratifications analyses.ConclusionsOur results demonstrated that there are clear sEMG manifestations of altered muscle coordination in sarcopenic patients. More consistent force generation patterns were observed in the sarcopenic group, especially at lower contraction intensities. The novel ICDMC can quantify differences between sarcopenic and healthy muscle. These results warrant further research to further develop more accessible sarcopenia screening strategies in community settings based on electrophysiological measurements such as sEMG.

Sex-differences in neuromuscular control of hip abductors during isometric submaximal tasks

BackgroundOne key focus in the literature is the need to better understand how males and females perform neuromuscular control, which requires consideration of muscle morphology, as it may change neural drive during force production. Although previous studies focused on muscles around the knee and ankle, it is crucial to explore the behavior of other muscles, such as the hip abductors, since many lower limb conditions more common in females have been associated with alterations in hip muscles. Research questionsAre electromyography (EMG) variables (amplitude and low- and high frequency bands) of hip abductors during submaximal isometric tasks different between males and females? How is muscle size associated with EMG responses during these tasks? MethodsThirty-six participants (males, n = 18; females, n = 18) had muscle and subcutaneous thickness of gluteus medius (GMed) and tensor fascia latae (TFL) measured. They then performed an estimated one-repetition maximum (1RM) test in a side-lying hip abduction exercise, followed by two 10-s submaximal tasks: (i) side-lying hip abduction with 50 % 1RM and (ii) with 20 % 1RM. GMed and TFL EMG amplitude and frequency bands (low and high frequency components) were analyzed. ResultsFemales had higher GMed EMG amplitude, lower low-frequency, and higher high-frequency components than males in both tasks (p = 0.001–0.040). No differences were observed in TFL EMG variables. Greater GMed thickness was associated with lower amplitudes in the 50 % 1RM task (r = − 0.35; p = 0.03), while greater TFL thickness was associated with lower low-frequency [20 % 1RM: r = − 0.70; p = 0.002; 50 %-1RM: r = − 0.65; p = 0.005] and higher high-frequency components [20 % 1RM: r = 0.74; p = 0.001; 50 %-1RM: r = 0.76; p < 0.001] only in females. SignificanceMales and females employ different neuromuscular control strategies, which vary among the synergists for hip abduction.

Exploring the interplay between body mass index and passive muscle properties in relation to grip strength and jump performance in female university students.

Women typically have a higher body fat content than men. Fat accumulation is associated with muscle weakness and alterations in mechanical properties. This study aims to determine the relationship between BMI and weight status with the mechanical properties of muscle and tendon. It was hypothesized that the stiffness and tone of the forearm muscle and Achilles tendon would be correlated with weight status and BMI. A cross-sectional study was conducted with 136 female university students. Grip strength was assessed using a dynamometer, body composition was analyzed through bioimpedance, and countermovement jump performance was evaluated with a force platform. Stiffness and tone were measured using the MyotonPro device. ANOVA was used to compare grip strength and countermovement jump performance according to body composition. The Pearson correlation coefficient was used to examine bivariate associations. Relative grip strength decreased with an increase in fat content, while forearm muscle stiffness and tone decreased with rising weight status and BMI. Stiffness of the Achilles tendon increased with an increase in fat content and showed a significant positive correlation with BMI. Multiple regression analysis revealed a weak correlation between BMI, body composition, and stiffness of the forearm muscles. The results of this study support the notion that the stiffness of the forearm muscles and Achilles tendon is correlated with BMI in young adult women. Furthermore, an increase in body fat percentage is linked to a decrease in mechanical properties and poorer muscle function.

Effects of robot-assisted hand function therapy on brain functional mechanisms: a synchronized study using fNIRS and sEMG.

Robot-assisted hand function therapy is pivotal in the rehabilitation of patients with stroke; however, its therapeutic mechanism remains elusive. Currently, research examining the impact of robot-assisted hand function therapy on brain function in patients with stroke is scarce, and there is a lack of studies investigating the correlation between muscle activity and alterations in brain function. This study aimed to investigate the correlation between forearm muscle movement and brain functional activation by employing the synchronized use of functional near-infrared spectroscopy and surface electromyography methods. Moreover, it sought to compare neural activity patterns during different rehabilitation tasks and refine the mechanism of robot-assisted hand function therapy for post-stroke hand function impairments. Stroke patients with hand dysfunction underwent three sessions of robot-assisted hand function therapy within 2 weeks to 3 months of onset. The fNIRS-sEMG synchronous technique was used to observe brain function and forearm muscle activation. Ten participants were randomly assigned to receive mirror, resistance, or passive rehabilitation training. During the intervention, cortical and muscle activation information was obtained using fNIRS and electromyographic signals. The primary outcomes included changes in oxyhemoglobin concentration and root mean square of surface electromyography. Compared to the resting state, the Oxy-Hb concentration in the brain regions involved in three rehabilitation tasks with robot-assisted hand function therapy significantly increased (p < 0.05). Mirror therapy significantly enhanced the prefrontal cortex and the superior frontal cortex activation levels. In contrast, resistance therapy significantly promoted the activation of the supplementary motor area and the premotor cortex. Passive rehabilitation tasks showed some activation in the target brain area premotor cortex region. Robot-assisted hand function therapy has shown that forearm muscle movement is closely related to oxygenated hemoglobin concentration activity in specific brain regions during different rehabilitation tasks. The simultaneous sEMG-fNIRS study found a significant correlation between muscle movement and brain activity after stroke, which provides an important basis for understanding the treatment mechanism of hand function impairment.

Quantitative magnetic resonance imaging of paraspinal muscles for assessing chronic non-specific low back pain in young adults: a prospective case-control study

PurposeThis study aimed to investigate the application of quantitative magnetic resonance imaging of paraspinal muscles in assessing the young CNLBP with unilateral symptom.MethodsThis prospective study enrolled 107 young individuals with unilateral symptomatic CNLBP (56 cases) and a normal cohort (51 cases). All subjects underwent conventional lumbar sequences, T2 mapping, and IDEAL-IQ scans at 3T. T2 values and fat fraction (FF) of bilateral multifidus (mid-levels of L2-L5 vertebrae) and erector spinae (mid-levels of L1-L4 vertebrae) were measured. CNLBP severity, Japanese Orthopedic Association (JOA) score, and Visual Analogue Scale (VAS) score were recorded. Wilcoxon signed-rank tests were used to compare parameter differences between painful and non-painful sides in the case group. Mann-Whitney U tests were employed to evaluate differences between the case and normal group. Logistic regression analysis was conducted to identify predictive factors and to establish a combined model.ResultsIn the case group, erector spinae FF values (L4 level), erector spinae T2 values (L1, L2, and L4 levels), and multifidus T2 values (L4 and L5 levels) were higher on the painful side (P<0.05). Multifidus T2 values (L5 level) and FF values (L2-L5 levels) were higher in the case group compared to the normal group (P<0.05). The optimal performance in differentiating young CNLBP was the combination of L5 level multifidus T2 value with FF (AUC = 91.81%). Negative correlation existed between T2 values and FF of multifidus at L5 level and JOA scores (r=-0.41, P < 0.05), and positive correlation with VAS scores (r = 0.46, P < 0.05).ConclusionThe combination of T2 value and FF may provide deeper insights into the pathological alterations of paraspinal muscles in young CNLBP, providing an important imaging basis for clinical judgment and preventive treatment of non-painful side in unilateral symptomatic patients.

Exploration of the triceps surae muscle in ambulatory children with cerebral palsy using instrumented measurements of stiffness and diffusion tensor magnetic resonance imaging for muscle architecture

BackgroundMusculoskeletal alterations causing reduced range of motion of the ankle joint are common in children with cerebral palsy (CP). Objective measurements of passive joint resistance and three-dimensional skeletal muscle volume and muscle architecture can lead to a comprehensive understanding of which factors influence joint range of motion.Research questionTo investigate the relation between the passive dorsiflexion of the ankle joint, biomechanical contributing factors to the passive joint resistance, and muscular architectural properties of the triceps surae muscle in children with CP.MethodsIn this cross-sectional observational study, 14 children with spastic CP (bilateral: 5, unilateral: 9, Gross Motor Function Classification System (GMFCS) level I:11, II:3) naïve to intramuscular tone reducing treatment, and 14 TD children were included. The passive dorsiflexion of the ankle was measured with a goniometer. Passive joint resistance and related parameters were estimated based on a biomechanical model and measurements using a motorized device, the Neuroflexor. Three-dimensional muscle architecture was quantified with diffusion tensor magnetic resonance imaging (DT-MRI).ResultsIn the CP group, the median [min, max] passive dorsiflexion was decreased in the most affected leg (MAL) compared to the less affected leg (LAL) (2.5° [-25°, 20°] vs. 12.5° [5°, 30°], p = 0.001). The stiffness coefficient (Nm/rad) in the MAL was significantly higher in children with CP compared to TD children (7.10 [3.39, 62.00] vs. 2.82 [1.24, 10.46], p = 0.015). Muscle architecture properties did not differ between CP and TD, except for pennation angle in the medial gastrocnemius (MG) of the MAL (CP 17.64° (2.29) vs. TD 21.46° (3.20), p = 0.017). The stiffness coefficient, in the MAL, correlated negatively to passive dorsiflexion (rs=-0.638) and pennation angle in medial gastrocnemius (rs=-0.964), and the non-linear coefficient (Non-linear 1) correlated negatively to the fascicle length of the medial gastrocnemius (rs=-0.857).ConclusionThis study shows that stiffness of the plantarflexors is related to decreased passive dorsiflexion of the ankle and muscle structure of the MG in high-functioning children with spastic CP. Assessments of how dynamic components as well as microscopic muscle alterations contribute to joint stiffness in the plantarflexors in individuals with CP are warranted.Trial registrationRetrospectively registered in ClinicalTrials.gov, NCT05447299. Observational study. Study start: 2019-01-15, register date: 2022-07-01.

648P MRI demonstrates altered skeletal muscle membrane permeability in Becker muscular dystrophy, representing a potential biomarker for disease activity

648P MRI demonstrates altered skeletal muscle membrane permeability in Becker muscular dystrophy, representing a potential biomarker for disease activity

Altered Muscle Bioenergetic in CKD: Focus on Inorganic Phosphate and Acidosis

Altered Muscle Bioenergetic in CKD: Focus on Inorganic Phosphate and Acidosis