Sustained low-intensity muscle fatigue (SULMF) refers to the phenomenon that skeletal muscle continues to contract at less than 10% of maximum voluntary contraction during work activities, resulting in decreased muscle contractile function, which is one of the main causes of occupational neck, shoulder, waist and back discomfort and pain symptoms. Although surface electromyography is a key physiological technique for assessing the efficiency of neuromuscular activity, its effectiveness in objectively detecting SULMF remains controversial. Therefore, this paper describes the neurophysiological mechanism and related hypotheses of SULMF, and reviews the research progress of electromyography detection indicators and detection methods of SULMF, which is of great significance for the early prevention and accurate detection of work-related musculoskeletal disorders.
长时间-低强度肌肉疲劳指作业活动中骨骼肌以低于10%最大随意等长收缩力持续收缩导致肌肉收缩功能下降的现象，是职业性颈、肩、腰、背部不适与疼痛症状高发的主要诱因之一。尽管表面肌电图是评估神经肌肉活动效率的关键生理技术，但在客观检测长时间-低强度肌肉疲劳方面，其有效性仍存在争议。因此，本文阐述长时间-低强度肌肉疲劳的神经生理机制及相关假说，并综述长时间-低强度肌肉疲劳肌电检测指标与检测方法的研究进展，对工作相关肌肉骨骼疾患的早期预防与精准检测有重要意义。.

OBJECTIVE: Aging frequently causes changes in body composition, such as a loss of strength and muscular mass and an increase in fat mass. Exercise training programs have been suggested as effective strategies to mitigate or prevent age-related declines in body composition. Therefore, this study examined the effects of a sixteen-week High-Speed Resistance Training (HSRT) program on body composition parameters in community-dwelling independent older adults.
METHODS: The present clinical trial included 79 older adults, who were divided into two groups: intervention group (IG, N = 40, age, 68.50 ± 3.54 years; weight, 68.65 ± 11.36 kg) and control group (CG, N = 39, age, 72.08 ± 5.89 years; weight, 67.04 ± 10.69 kg). IG performed the supervised HSRT for 16 weeks, with 3 sessions per week of 60-70min, each session of 5-6 exercises, 2-3 sets, and 6-10 reps/exercise, while CG did not perform any exercise training program. Body composition parameters were assessed using a multifrequency tetrapolar bioelectrical impedance analyzer (InBody® S10). The level of physical activity and the dietary intake were evaluated by the International Physical Activity Questionnaire (IPAQ-SF) and the Food Frequency Questionnaire, respectively. Statistical analyses were performed using the analysis of covariance (ANCOVA), and effect size (Cohen\'s dunbiased).
RESULTS: The analysis showed significant effects of the group factor for IG on phase angle (F(1) = 14.39, p < 0.001, η2p = 0.159). Additionally, results from Δ changes (post-minus pre-values) revealed small and medium effects in favor to IG for body cell mass (t(77) = 1.21, p = 0.230, dunb = 0.27 [-0.17, 0.71]) and phase angle (t(77) = 2.82, p = 0.006, dunb = 0.63 [0.18, 1.08]), respectively.
CONCLUSIONS: The HSRT could effectively prevent the decline in cellular health and cell integrity in older adults, as evidenced by the significant improvements in the phase angle.
BACKGROUND: Clinicaltrial.gov (ID: NCT05586087).

The influence of accelerated electrons on neuronal structures is scarcely explored compared to gamma and X-rays. This study aims to investigate the effects of accelerated electron radiation on some pivotal neurotransmitter circuits (cholinergic and serotonergic) of rats\' myenteric plexus. Male Wistar rats were irradiated with an electron beam (9 MeV, 5 Gy) generated by a multimodality linear accelerator. The contractile activity of isolated smooth muscle samples from the gastric corpus was measured. Furthermore, an electrical stimulation (200 μs, 20 Hz, 50 s, 60 V) was performed on the samples and an assessment of the cholinergic and serotonergic circuits was made. Five days after irradiation, the recorded mechanical responses were biphasic-contraction/relaxation in controls and contraction/contraction in irradiated samples. The nature of the contractile phase of control samples was cholinergic with serotonin involvement. The relaxation phase involved ACh-induced nitric oxide release from gastric neurons. There was a significant increase in serotonergic involvement during the first and second contractile phases of the irradiated samples, along with a diminished role of acetylcholine in the first phase. This study demonstrates an increased involvement of serotonergic neurotransmitter circuits in the gastric myenteric plexus caused by radiation with accelerated electrons.

Heart failure with preserved ejection fraction (HFpEF) is characterized by biomechanically dysfunctional cardiomyocytes. Underlying cellular changes include perturbed myocardial titin expression and titin hypophosphorylation leading to titin filament stiffening. Beside these well-studied alterations at the cardiomyocyte level, exercise intolerance is another hallmark of HFpEF caused by molecular alterations in skeletal muscle (SKM). Currently, there is a lack of data regarding titin modulation in the SKM of HFpEF. Therefore, the aim of the present study was to analyze molecular alterations in limb SKM (tibialis anterior (TA)) and in the diaphragm (Dia), as a more central SKM, with a focus on titin, titin phosphorylation, and contraction-regulating proteins. This study was performed with muscle tissue, obtained from 32-week old female ZSF-1 rats, an established a HFpEF rat model. Our results showed a hyperphosphorylation of titin in limb SKM, based on enhanced phosphorylation at the PEVK region, which is known to lead to titin filament stiffening. This hyperphosphorylation could be reversed by high-intensity interval training (HIIT). Additionally, a negative correlation occurring between the phosphorylation state of titin and the muscle force in the limb SKM was evident. For the Dia, no alterations in the phosphorylation state of titin could be detected. Supported by data of previous studies, this suggests an exercise effect of the Dia in HFpEF. Regarding the expression of contraction regulating proteins, significant differences between Dia and limb SKM could be detected, supporting muscle atrophy and dysfunction in limb SKM, but not in the Dia. Altogether, these data suggest a correlation between titin stiffening and the appearance of exercise intolerance in HFpEF, as well as a differential regulation between different SKM groups.

Volumetric muscle loss (VML) injury causes irreversible deficits in muscle mass and function, often resulting in permanent disability. The current standard of care is physical therapy, but it is limited in mitigating functional deficits. We have previously optimized a rehabilitation technique using electrically stimulated eccentric contraction training (EST) that improved muscle mass, strength, and size in VML-injured rats. A biosponge scaffold composed of extracellular matrix proteins has previously enhanced muscle function postVML. This study aimed to determine whether combining a regenerative therapy (i.e., biosponge) with a novel rehabilitation technique (i.e., EST) could enhance recovery in a rat model of VML. A VML defect was created by removing ~20% of muscle mass from the tibialis anterior muscle in adult male Lewis rats. Experimental groups included VML-injured rats treated with biosponge with EST or biosponge alone (n = 6/group). EST was implemented 2 weeks postinjury at 150 Hz and was continued for 4 weeks. A linear increase in eccentric torque over 4 weeks showed the adaptability of the VML-injured muscle to EST. Combining biosponge with EST improved peak isometric torque by ~52% compared with biosponge treatment alone at 6 weeks postinjury. Application of EST increased MyoD gene expression and the percentage of large (>2000 μm2) type 2B myofibers but reduced fibrotic tissue deposition in VML-injured muscles. Together, these changes may provide the basis for improved torque production. This study demonstrates the potential for combined regenerative and rehabilitative therapy to improve muscle recovery following VML.

Filamins are mechanosensitive actin crosslinking proteins that organize the actin cytoskeleton in a variety of shapes and tissues. In muscles, filamin crosslinks actin filaments from opposing sarcomeres, the smallest contractile units of muscles. This happens at the Z-disc, the actin-organizing center of sarcomeres. In flies and vertebrates, filamin mutations lead to fragile muscles that appear ruptured, suggesting filamin helps counteract muscle rupturing during muscle contractions by providing elastic support and/or through signaling. An elastic region at the C-terminus of filamin is called the mechanosensitive region and has been proposed to sense and counteract contractile damage. Here we use molecularly defined mutants and microscopy analysis of the Drosophila indirect flight muscles to investigate the molecular details by which filamin provides cohesion to the Z-disc. We made novel filamin mutations affecting the C-terminal region to interrogate the mechanosensitive region and detected three Z-disc phenotypes: dissociation of actin filaments, Z-disc rupture, and Z-disc enlargement. We tested a constitutively closed filamin mutant, which prevents the elastic changes in the mechanosensitive region and results in ruptured Z-discs, and a constitutively open mutant which has the opposite elastic effect on the mechanosensitive region and gives rise to enlarged Z-discs. Finally, we show that muscle contraction is required for Z-disc rupture. We propose that filamin senses myofibril damage by elastic changes in its mechanosensory region, stabilizes the Z-disc, and counteracts contractile damage at the Z-disc.

Cholesterol is one of the major components of plasma membrane, where its distribution is nonhomogeneous and it participates in lipid raft formation. In skeletal muscle cholesterol and lipid rafts seem to be important for excitation-contraction coupling and for neuromuscular transmission, involving cholesterol-rich synaptic vesicles. In the present study, nerve and muscle stimulation-evoked contractions were recorded to assess the role of cholesterol in contractile function of mouse diaphragm. Exposure to cholesterol oxidase (0.2 U/ml) and cholesterol-depleting agent methyl-β-cyclodextrin (1 mM) did not affect markedly contractile responses to both direct and indirect stimulation at low and high frequency. However, methyl-β-cyclodextrin at high concentration (10 mM) strongly decreased the force of both single and tetanus contractions induced by phrenic nerve stimulation. This decline in contractile function was more profoundly expressed when methyl-β-cyclodextrin application was combined with phrenic nerve activation. At the same time, 10 mM methyl-β-cyclodextrin had no effect on contractions upon direct muscle stimulation at low and high frequency. Thus, strong cholesterol depletion suppresses contractile function mainly due to disturbance of the neuromuscular communication, whereas muscle fiber contractility remains resistant to decline.

The paramount importance of mechanical forces in morphogenesis and embryogenesis is widely recognized, but understanding the mechanism at the cellular and molecular level remains challenging. Because of its simple internal organization, Caenorhabditis elegans is a rewarding system of study. As demonstrated experimentally, after an initial period of steady elongation driven by the actomyosin network, muscle contractions operate a quasi-periodic sequence of bending, rotation, and torsion, that leads to the final fourfold size of the embryos before hatching. How actomyosin and muscles contribute to embryonic elongation is investigated here theoretically. A filamentary elastic model that converts stimuli generated by biochemical signals in the tissue into driving forces, explains embryonic deformation under actin bundles and muscle activity, and dictates mechanisms of late elongation based on the effects of energy conversion and dissipation. We quantify this dynamic transformation by stretches applied to a cylindrical structure that mimics the body shape in finite elasticity, obtaining good agreement and understanding of both wild-type and mutant embryos at all stages.

Our previous study showed that daily six maximal eccentric contractions that were performed 5 days a week for 4 weeks increased maximal voluntary isometric (MVC-ISO), concentric (MVC-CON), and eccentric contraction (MVC-ECC) strength of the elbow flexors and muscle thickness of biceps brachii and brachialis (MT) by 8.3 ± 4.9%, 11.1 ± 7.4%, 13.5 ± 11.5%, and 10.6 ± 5.1%, respectively. In the present study, we tested the hypothesis that the muscle strength and MT would still increase when the training intensity was reduced to 2/3 or 1/3 of the peak MVC-ECC torque. Thirty-six healthy young (19-24 years) adults who had not performed resistance training were placed to three groups (n = 12/group): 2/3MVC or 1/3MVC that performed six eccentric contractions with 2/3 or 1/3 MVC-ECC load using a dumbbell 5 days a week for 4 weeks or control group that did not perform any training. Changes in the MVC-ISO, MVC-CON, MVC-ECC torque, and MT before and after the 4-week period were compared among the groups and with the group of the previous study in which six maximal eccentric contractions were performed 5 days a week for 4 weeks (MVC group; n = 12). The control and 1/3MVC groups showed no significant changes in any measures. Significant (p < 0.05) increases in MVC-ISO (10.3 ± 11.4%), MVC-CON (10.9 ± 9.5%), and MVC-ECC (9.3 ± 8.8%) torque and MT (10.1 ± 9.2%) were observed for the 2/3MVC group. These changes were not significantly different from those of the MVC group. These results suggest that the 2/3-intensity eccentric contractions with a dumbbell are as effective as maximal-intensity isokinetic eccentric contractions to induce muscle adaptations.

We sought to determine the physiological relevance of pannexin/purinergic-dependent signaling in mediating conducted vasodilation elicited by capillary stimulation through skeletal muscle contraction. Using hamster cremaster muscle and intravital microscopy we stimulated capillaries through local muscle contraction while observing the associated upstream arteriole. Capillaries were stimulated with muscle contraction at low and high contraction (6 and 60CPM) and stimulus frequencies (4 and 40 Hz) in the absence and presence of pannexin blocker mefloquine (MEF; 10-5 M), purinergic receptor antagonist suramin (SUR 10-5 M) and gap-junction uncoupler halothane (HALO, 0.07%) applied between the capillary stimulation site and the upstream arteriolar observation site. Conducted vasodilations elicited at 6CPM were inhibited by HALO while vasodilations at 60CPM were inhibited by MEF and SUR. The conducted response elicited at 4 Hz was inhibited by MEF while the vasodilation at 40 Hz was unaffected by any blocker. Therefore, upstream vasodilations resulting from capillary stimulation via muscle contraction are dependent upon a pannexin/purinergic-dependent pathway that appears to be stimulation parameter-dependent. Our data highlight a physiological importance of the pannexin/purinergic pathway in facilitating communication between capillaries and upstream arteriolar microvasculature and, consequently, indicating that this pathway may play a crucial role in regulating blood flow in response to skeletal muscle contraction.