Search Results (58)

Background/Objectives: This study aims to investigate the effects of caffeinated chewing gum on maximal strength, muscular power, and neural drive to the prime movers during bench press and back squat in resistance-trained men. Methods: Sixteen resistance-trained males participated in a double-blind, randomized trial, chewing either caffeinated gum (4 mg/kg) or placebo gum on two separate occasions, seven days apart. After chewing for 5 min, participants performed a maximal strength test followed by muscular power assessments at 25%, 50%, 75%, and 90% of their one-repetition maximum (1RM), completing with 3, 2, 1, and 1 repetition (s), respectively, for bench press and back squat. Surface electromyography data were recorded for each repetition. Results: Caffeinated gum did not significantly improve one-repetition maximum (1RM) for bench press (p > 0.05), but increased mean frequency (MF) and median frequency (MDF) in anterior deltoid, pectoralis major, and biceps brachii (all p < 0.05) compared to placebo. For back squat, 1RM increased with caffeinated gum, along with higher MF and MDF in vastus medialis (all p < 0.05). Caffeinated gum also improved mean and peak velocities, and mean and peak power outputs at 25–75% 1RM during the bench press (all p < 0.05), along with elevated MDF in pectoralis major and biceps brachii (all p < 0.05). Similar improvements were seen in mean and peak velocities during the back squat at 25–90% 1RM (all p < 0.05), along with higher MF and MDF in vastus medialis and increased normalized root mean square activity in gluteus maximus (all p < 0.05). Conclusions: Caffeinated chewing gum (4 mg/kg) enhanced muscular power (25–75% 1RM) in the bench press and improved maximal strength and muscular power (25–90% 1RM) in the back squat by increasing muscle recruitment in resistance-trained men. Full article

Background: Within recent years, there has been a notable lack of research examining the factors associated with adolescent use of anabolic–androgenic steroids (AASs) in Australia, meaning information regarding risk factors of Australian adolescent AAS use is outdated and potentially inaccurate. Methods: To address this omission, the present study examined the prevalence and correlates of adolescent (aged 11 to 19 years) AAS use within the EveryBODY study, a large-scale representative survey of adolescents’ disordered eating behaviours and body image concerns, involving 5071 adolescents across thirteen schools within the Sydney and Newcastle/Hunter region of New South Wales, Australia. Results: A total of 1.1% of adolescents reported lifetime use of AAS to increase muscularity. In univariate analyses, increased prevalence of AAS use was associated with male sex (OR = 5.67), identifying as Aboriginal or Torres Strait Islander (OR = 3.80), identifying as same-sex or questioning sexual attraction (OR = 3.17), higher drive for muscularity (OR = 2.19) and weight/shape concerns in the past month (OR = 1.28), and higher frequency of purging (OR = 1.11) and binge eating (OR = 1.09) in the past month. In multivariate analysis, only drive for muscularity (OR = 2.44) and purging behaviours (OR = 1.10) remained as significant correlates. Finally, adolescents who reported lifetime AAS use also reported feeling significantly higher levels of distress and physical and psychosocial impairment compared to adolescents who reported never having used AAS to increase muscularity. Conclusions: Positive correlations between disordered eating and weight and shape concerns with AAS use suggests that adolescent AAS use may be conceptualised within the spectra of disordered eating among youth. These findings provide clinicians, carers, and educators with prototypical factors that should assist in the screening of adolescent AAS use to facilitate early intervention. Full article

Objectives: The objective of this paper is to introduce a method to measure the force or pressure over the carpal tunnel indirectly, using a new device to drive the pointer of a computer system. The measurements were compared with those obtained using an ergonomic mouse. Simultaneously, measurements of muscular stress on the digitorum extensor muscle were performed to correlate the applied force against muscle activity. Methods: An experimental setup was constructed using an infrared static receiver plus two wearable moving light emitters, which can be displaced inside a rectangular projected region. The pointer functions are performed through two finger gestures, while the hand is naturally extended. A microcontroller was used to communicate with the computer, which works as a human interface device and possesses firmware to associate the position of each light source with the pointer functions. Meanwhile, force and electromyography sensing circuits were developed to transmit and measure carpal tunnel strength and muscular stress. The system was tested on five healthy volunteers, who were encouraged to solve the same computational tasks using this new device and a trademark ergonomic mouse. Results: Our results show great differences (greater than one magnitude) between the efforts of the same volunteers performing the same predefined tasks using both pointer controllers. Only when the new device was used did the Pearson’s correlation coefficients show a higher correlation between the effort measured on the carpal tunnel and the muscular activity. Conclusions: The optic pointer driver diminishes the strength on the carpal tunnel, causing slightly increased stress on the digitorum extensor muscle. Full article

Background: Appropriate wheelchair and seating systems are key to allow for the participation of people with Duchenne Muscular Dystrophy. There is little research that focuses on their long-term seating issues and what topics they want studied. Methods: This mixed-method study with adults with Duchenne used an Internet-based survey about wheelchair mobility and discomfort, followed by in-depth interviews. Unanticipated remarks in the interviews led to a second survey regarding the effects of cold weather on wheelchair driving. Descriptive and qualitative analyses were performed. Results: Thirty-seven individuals completed the original survey: 78% used a powered wheelchair, 58% were uncomfortable in their wheelchair, and 94% felt the need to change their seating position. In-depth interviews (N = 9) revealed three themes: seating and pain management, caregiver cooperation, and temperature sensitivity. Almost all (8/9) interviewees explained that cold was a barrier to their participation. In the second survey (N = 13), 11 reported that cold affected their driving, with 10 remarking that it prevented them from participating in daily life activities and 11 stating that the effects of cold on wheelchair driving should be studied. Conclusions: It is essential to ask end-users to identify key issues to ensure the relevance of research to people with disabilities. Full article

Dysregulated RNA metabolism caused by SMN deficiency leads to motor neuron disease spinal muscular atrophy (SMA). Current therapies improve patient outcomes but achieve no definite cure, prompting renewed efforts to better understand disease mechanisms. The calcium channel blocker flunarizine improves motor function in Smn-deficient mice and can help uncover neuroprotective pathways. Murine motor neuron-like NSC34 cells were used to study the molecular cell-autonomous mechanism. Following RNA and protein extraction, RT-qPCR and immunodetection experiments were performed. The relationship between flunarizine mRNA targets and RNA-binding protein GEMIN5 was explored by RNA-immunoprecipitation. Flunarizine increases demethylase Kdm6b transcripts across cell cultures and mouse models. It causes, in NSC34 cells, a temporal expression of GEMIN5 and KDM6B. GEMIN5 binds to flunarizine-modulated mRNAs, including Kdm6b transcripts. Gemin5 depletion reduces Kdm6b mRNA and protein levels and hampers responses to flunarizine, including neurite extension in NSC34 cells. Moreover, flunarizine increases the axonal extension of motor neurons derived from SMA patient-induced pluripotent stem cells. Finally, immunofluorescence studies of spinal cord motor neurons in Smn-deficient mice reveal that flunarizine modulates the expression of KDM6B and its target, the motor neuron-specific transcription factor HB9, driving motor neuron maturation. Our study reveals GEMIN5 regulates Kdm6b expression with implications for motor neuron diseases and therapy. Full article

The aim of this study was to compare the correlation between electromyography (EMG) activity and vehicle motion during double lane change driving. This study measured five vehicle motions: the steering wheel angle, steering wheel torque, lateral acceleration, roll angle, and yaw velocity. The EMG activity for 19 muscles and vehicle motions was applied for envelope detection. There was a significantly high positive correlation between muscles (mean correlation coefficient) for sternocleidomastoid (0.62) and biceps brachii (0.71) and vehicle motions for steering wheel angle, steering wheel torque, lateral acceleration, and yaw velocity, but a negative correlation between the muscles for middle deltoid (−0.75) and triceps brachii long head (−0.78) and these vehicle motions. The ANOVA test was used to analyze statistically significant differences in the main and interaction effects of muscle and vehicle speed. The mean absolute correlation coefficient exhibited an increasing trend with the increasing vehicle speed for the muscles (increasing rate%): upper trapezius (30.5%), pectoralis major sternal (38.7%), serratus anterior (13.3%), and biceps brachii (11.0%). The mean absolute correlation coefficient showed a decreasing trend with increasing vehicle speed for the masseter (−9.6%), sternocleidomastoid (−12.9%), middle deltoid (−5.5%), posterior deltoid (−20.0%), pectoralis major clavicular (−13.4%), and triceps brachii long head (−6.3%). The sternocleidomastoid muscle may decrease with increasing vehicle speed as the neck rotation decreases. As shoulder stabilizers, the upper trapezius, pectoralis major sternal, and serratus anterior muscles are considered to play a primary role in maintaining body balance. This study suggests that the primary muscles reflecting vehicle motions include the sternocleidomastoid, deltoid, upper trapezius, pectoralis major sternal, serratus anterior, biceps, and triceps muscles under real driving conditions. Full article

Dynamic muscle fatigue during repetitive movements can lead to changes in communication between the central nervous system and peripheral muscles. This study investigated these changes by examining electromyogram (EMG) characteristics from agonist and antagonist muscles during a fatiguing task. Twenty-two healthy male university students (age: 22.92 ± 2.19 years) performed heel raises until fatigue. EMG signals from lateral gastrocnemius (GL) and tibialis anterior (TA) muscles were processed using synchrosqueezed wavelet transform (SST). Root mean square (RMS), mean frequency (MF), power across frequency ranges, wavelet coherence, and co-activation ratio were computed. During the initial 80% of the task, RMS and EMG power increased for both muscles, while MF declined. In the final 20%, GL parameters stabilized, but TA showed significant decreases. Beta and gamma intermuscular coherence increased upon reaching 60% of the task. Alpha coherence and co-activation ratio remained constant. Results suggest that the central nervous system adopts a differentiated control strategy for agonist and antagonist muscles during fatigue progression. Initially, a coordinated “common drive” mechanism enhances both muscle groups’ activity. Later, despite continued increases in muscle activity, neural-muscular coupling remains stable. This asynchronous, differentiated control mechanism enhances our understanding of neuromuscular adaptations during fatigue, potentially contributing to the development of more targeted fatigue assessment and management strategies. Full article

Nuclear lamins, a type V intermediate filament, are crucial components of the nuclear envelope’s inner layer, maintaining nuclear integrity and mediating interactions between the nucleus and cytoplasm. Research on human iPSC-derived cells and animal models has demonstrated the importance of lamins in cardiac and skeletal muscle development and function. Mutations in lamins result in laminopathies, a group of diseases including muscular dystrophies, Hutchison–Gilford progeria syndrome, and cardiomyopathies with conduction defects. These conditions have been linked to disrupted autophagy, mTOR, Nrf2-Keap, and proteostasis signaling pathways, indicating complex interactions between the nucleus and cytoplasm. Despite progress in understanding these pathways, many questions remain about the mechanisms driving lamin-induced pathologies, leading to limited therapeutic options. This review examines the current literature on dysregulated pathways in cardiac and skeletal muscle laminopathies and explores potential therapeutic strategies for these conditions. Full article

Duchenne muscular dystrophy (DMD) is a progressive neuromuscular disease caused by mutations to the dystrophin gene, resulting in deficiency of dystrophin protein, loss of myofiber integrity in skeletal and cardiac muscle, and eventual cell death and replacement with fibrotic tissue. Pathologic cardiac manifestations occur in nearly every DMD patient, with the development of cardiomyopathy—the leading cause of death—inevitable by adulthood. As early cardiac abnormalities are difficult to detect, timely diagnosis and appropriate treatment modalities remain a challenge. There is no cure for DMD; treatment is aimed at delaying disease progression and alleviating symptoms. A comprehensive understanding of the pathophysiological mechanisms is crucial to the development of targeted treatments. While established hypotheses of underlying mechanisms include sarcolemmal weakening, upregulation of pro-inflammatory cytokines, and perturbed ion homeostasis, mitochondrial dysfunction is thought to be a potential key contributor. Several experimental compounds targeting the skeletal muscle pathology of DMD are in development, but the effects of such agents on cardiac function remain unclear. The synergistic integration of small molecule- and gene-target-based drugs with metabolic-, immune-, or ion balance-enhancing compounds into a combinatorial therapy offers potential for treating dystrophin deficiency-induced cardiomyopathy, making it crucial to understand the underlying mechanisms driving the disorder. Full article

Aberrant expression of the double homeobox 4 (DUX4) gene in skeletal muscle predominantly drives the pathogenesis of facioscapulohumeral muscular dystrophy (FSHD). We recently demonstrated that berberine, an herbal extract known for its ability to stabilize guanine–quadruplex structures, effectively downregulates DUX4 expression in FSHD patient-derived myoblasts and in mice overexpressing exogenous DUX4 after viral vector-based treatment. Here, we sought to confirm berberine’s inhibitory efficacy on DUX4 in the widely used FSHD-like transgenic mouse model, ACTA1-MCM/FLExDUX4, where DUX4 is induced at pathogenic levels using tamoxifen. Animals repeatedly treated with berberine via intraperitoneal injections for 4 weeks exhibited significant reductions in both mRNA and protein levels of DUX4, and in mRNA expression of murine DUX4-related genes. This inhibition translated into improved forelimb muscle strength and positive alterations in important FSHD-relevant cellular pathways, although its impact on muscle mass and histopathology was less pronounced. Collectively, our data confirm the efficacy of berberine in downregulating DUX4 expression in the most relevant FSHD mouse model. However, further optimization of dosing regimens and new studies to enhance the bioavailability of berberine in skeletal muscle are warranted to fully leverage its therapeutic potential for FSHD treatment. Full article

This article is a continuation of research on the possibility of using artificial pneumatic muscles to drive a parallel manipulator with six degrees of freedom. The authors present an artificial pneumatic muscle they have developed. The article contains a description of the research methodology and a description of the authors’ research position. The article presents the results of a comparison of the developed pneumatic muscle with an existing commercial solution. Then, the dynamic characteristics of the authors’ muscle are presented. A mathematical model is proposed that contains two inputs—the force generated by the muscle and the position of the muscle—and one output—the value of the signal controlling the pressure valve. The results of verification of the developed model are presented. The model is then presented in two versions. The first one contains the full dynamic model. The second one is its simplified version: the static model. The authors compare both models and present the comparison results. A servo drive is then synthesized and consists of a pair of muscles capable of generating the desired angular position and intended to drive a single arm of a parallel manipulator. The developed servo drive is verified on a test stand, and its behavior is assessed and analyzed in the context of its use in the manipulator. Full article

Muscular atrophy is a complex catabolic condition that develops due to several inflammatory-related disorders, resulting in muscle loss. Tumor necrosis factor alpha (TNF-α) is believed to be one of the leading factors that drive inflammatory response and its progression. Until now, the link between inflammation and muscle wasting has been thoroughly investigated, and the non-coding RNA machinery is a potential connection between the candidates. This study aimed to identify specific miRNAs for muscular atrophy induced by TNF-α in the C2C12 murine myotube model. The difference in expression of fourteen known miRNAs and two newly identified miRNAs was recorded by next-generation sequencing between normal muscle cells and treated myotubes. After validation, we confirmed the difference in the expression of one novel murine miRNA (nov-mmu-miRNA-1) under different TNF-α-inducing conditions. Functional bioinformatic analyses of nov-mmu-miRNA-1 revealed the potential association with inflammation and muscle atrophy. Our results suggest that nov-mmu-miRNA-1 may trigger inflammation and muscle wasting by the downregulation of LIN28A/B, an anti-inflammatory factor in the let-7 family. Therefore, TNF-α is involved in muscle atrophy through the modulation of the miRNA cellular machinery. Here, we describe for the first time and propose a mechanism for the newly discovered miRNA, nov-mmu-miRNA-1, which may regulate inflammation and promote muscle atrophy. Full article

Background: the precision agriculture field optimizes resource use, enhancing performance. However, this leads to exposure to ergonomic risks for operators, in particular, tractor drivers, potentially causing musculoskeletal disorders (MSDs). This study investigates how the display position in a semi-automatic tractor system influences operator comfort and muscle activation during harrowing operations. Methods: the assessment of muscular strain involved the use of surface electromyographic devices, while posture was evaluated throughout the analysis of the distribution of pressure exerted by the operator’s body on the seat, which was observed using two barometric pads, each positioned on the backrest and base of the seat. Finally, infrared thermography (IRT), a non-invasive tool to assess muscle activation, was used to measure the surface temperature of the driver’s back. The results showed a significantly greater muscular activation display for the position of display in semi-automatic driving at 50° and 80°. Conclusions: this study showed how the position of the display on the vehicle negatively influences posture, exposing workers to the risk of developing fatigue and, therefore, discomfort, with the potential onset of MSDs. The combined use of sEMG and IRT allowed for a non-invasive, cheap, and repeatable mechanical and functionality analysis. Full article

While studying myoblast methylomes and transcriptomes, we found that CDH15 had a remarkable preference for expression in both myoblasts and cerebellum. To understand how widespread such a relationship was and its epigenetic and biological correlates, we systematically looked for genes with similar transcription profiles and analyzed their DNA methylation and chromatin state and accessibility profiles in many different cell populations. Twenty genes were expressed preferentially in myoblasts and cerebellum (Myob/Cbl genes). Some shared DNA hypo- or hypermethylated regions in myoblasts and cerebellum. Particularly striking was ZNF556, whose promoter is hypomethylated in expressing cells but highly methylated in the many cell populations that do not express the gene. In reporter gene assays, we demonstrated that its promoter’s activity is methylation sensitive. The atypical epigenetics of ZNF556 may have originated from its promoter’s hypomethylation and selective activation in sperm progenitors and oocytes. Five of the Myob/Cbl genes (KCNJ12, ST8SIA5, ZIC1, VAX2, and EN2) have much higher RNA levels in cerebellum than in myoblasts and displayed myoblast-specific hypermethylation upstream and/or downstream of their promoters that may downmodulate expression. Differential DNA methylation was associated with alternative promoter usage for Myob/Cbl genes MCF2L, DOK7, CNPY1, and ANK1. Myob/Cbl genes PAX3, LBX1, ZNF556, ZIC1, EN2, and VAX2 encode sequence-specific transcription factors, which likely help drive the myoblast and cerebellum specificity of other Myob/Cbl genes. This study extends our understanding of epigenetic/transcription associations related to differentiation and may help elucidate relationships between epigenetic signatures and muscular dystrophies or cerebellar-linked neuropathologies. Full article

Gene therapy holds promise as a life-changing option for individuals with genetic variants that give rise to disease. FDA-approved gene therapies for Spinal Muscular Atrophy (SMA), cerebral adrenoleukodystrophy, β-Thalassemia, hemophilia A/B, retinal dystrophy, and Duchenne Muscular Dystrophy have generated buzz around the ability to change the course of genetic syndromes. However, this excitement risks over-expansion into areas of genetic disease that may not fit the current state of gene therapy. While in situ (targeted to an area) and ex vivo (removal of cells, delivery, and administration of cells) approaches show promise, they have a limited target ability. Broader in vivo gene therapy trials have shown various continued challenges, including immune response, use of immune suppressants correlating to secondary infections, unknown outcomes of overexpression, and challenges in driving tissue-specific corrections. Viral delivery systems can be associated with adverse outcomes such as hepatotoxicity and lethality if uncontrolled. In some cases, these risks are far outweighed by the potentially lethal syndromes for which these systems are being developed. Therefore, it is critical to evaluate the field of genetic diseases to perform cost–benefit analyses for gene therapy. In this work, we present the current state while setting forth tools and resources to guide informed directions to avoid foreseeable issues in gene therapy that could prevent the field from continued success. Full article