BACKGROUND

Heart rate variability (HRV) is a common tool for assessing autonomic nervous system activity and monitoring training load in athletes. However, limited research has explored how HRV responds to different forms of resistance training, particularly in high-intensity intermittent sports like basketball and football.

This study aims to compare the acute HRV responses between neuromuscular and metabolic training in collegiate athletes involved in high-intensity intermittent sports.

A comparative cross-sectional study with a quasi-experimental crossover design will be employed.

Collegiate athletes will be randomly assigned to undergo both neuromuscular and metabolic training sessions with a one-week wash-out period in between. HRV data will be recorded using the Polar H10 chest strap during each session.

Descriptive statistics will summarize salient participant characteristics and HRV measurements. Inferential analysis will use paired t-tests or Wilcoxon signed-rank tests based on normality, assessed via the Kolmogorov-Smirnov test. All statistical analyses will be conducted using the IBM SPSS (ver.25) with a confidence interval set. at 95% and a critical α equal to 0.05.

Neuromuscular training is expected to elicit higher low-frequency (LF) power and an increased LF/HF ratio, reflecting greater sympathetic activation, while metabolic training is expected to show lower LF power and a decreased LF/HF ratio, indicating a more balanced autonomic response. These findings will offer insights into the differential autonomic impacts of these training modalities.

Background and Objective: Premature ventricular complex (PVC) burden exhibits one of three circadian types, classified as fast-type, slow-type, and independent-type PVC. It is unknown whether PVC circadian types have different heart rate variability (HRV) parameter values. Therefore, this study aimed to evaluate differences in HRV circadian rhythm among fast-, slow-, and independent-type PVC. Methods: This cross-sectional observational study consecutively recruited 65 idiopathic PVC subjects (23 fast-, 20 slow-, and 22 independent-type) as well as five control subjects. Each subject underwent a 24-hour Holter to examine PVC burden and HRV. HRV analysis included components that primarily reflect global, parasympathetic, and sympathetic activities. Repeated measures analysis of variance was used to compare differences in HRV circadian rhythm by PVC type. Results. The average PVC burden was 15.7%, 8.4%, and 13.6% in fast-, slow-, and independent-type idiopathic PVC subjects, respectively. Global, parasympathetic nervous system, and sympathetic nervous system HRV parameters were significantly lower in independenttype PVC versus fast- and slow-type PVC throughout the day and night. Furthermore, we unexpectedly found that tendency towards sympathetic activity dominance during nighttime was only in independent-type PVC. Conclusion The HRV parameters are reduced in patients with independent-type PVC compared to fast- and slowtype PVC. Future research is warranted to determine possible differences in the prognosis between the three PVC types.
Ventricular Premature Complexes ; Circadian Rhythm ; Autonomic Nervous System

Humans ; Lupus Vasculitis, Central Nervous System/pathology* ; Magnetic Resonance Imaging/methods* ; Diffusion Tensor Imaging/methods* ; Patients ; Lupus Erythematosus, Systemic/pathology* ; Brain/pathology*

Retrograde adeno-associated viruses (AAVs) are capable of infecting the axons of projection neurons and serve as a powerful tool for the anatomical and functional characterization of neural networks. However, few retrograde AAV capsids have been shown to offer access to cortical projection neurons across different species and enable the manipulation of neural function in non-human primates (NHPs). Here, we report the development of a novel retrograde AAV capsid, AAV-DJ8R, which efficiently labeled cortical projection neurons after local administration into the striatum of mice and macaques. In addition, intrastriatally injected AAV-DJ8R mediated opsin expression in the mouse motor cortex and induced robust behavioral alterations. Moreover, AAV-DJ8R markedly increased motor cortical neuron firing upon optogenetic light stimulation after viral delivery into the macaque putamen. These data demonstrate the usefulness of AAV-DJ8R as an efficient retrograde tracer for cortical projection neurons in rodents and NHPs and indicate its suitability for use in conducting functional interrogations.
Animals ; Haplorhini ; Axons ; Motor Neurons ; Interneurons ; Macaca ; Dependovirus/genetics* ; Genetic Vectors

Astrocytes are the largest glial population in the mammalian brain. However, we have a minimal understanding of astrocyte development, especially fate specification in different regions of the brain. Through lineage tracing of the progenitors of the third ventricle (3V) wall via in-utero electroporation in the embryonic mouse brain, we show the fate specification and migration pattern of astrocytes derived from radial glia along the 3V wall. Unexpectedly, radial glia located in different regions along the 3V wall of the diencephalon produce distinct cell types: radial glia in the upper region produce astrocytes and those in the lower region produce neurons in the diencephalon. With genetic fate mapping analysis, we reveal that the first population of astrocytes appears along the zona incerta in the diencephalon. Astrogenesis occurs at an early time point in the dorsal region relative to that in the ventral region of the developing diencephalon. With transcriptomic analysis of the region-specific 3V wall and lateral ventricle (LV) wall, we identified cohorts of differentially-expressed genes in the dorsal 3V wall compared to the ventral 3V wall and LV wall that may regulate astrogenesis in the dorsal diencephalon. Together, these results demonstrate that the generation of astrocytes shows a spatiotemporal pattern in the developing mouse diencephalon.
Mice ; Animals ; Astrocytes ; Neuroglia/physiology* ; Diencephalon ; Brain ; Neurons ; Mammals

Background: Vitamin B12 is one of the common drugs used by physicians to treat peripheral neuropathy (PN), although many patients have a good response, however, overdose and toxicity aggravate the condition and worsen the patient’s symptoms. The purpose of this paper is to highlight association between Vitamin B12 toxicity and deterioration of PN symptoms. Case Summary: An elder Sudanese man with acute onset of sensory PN, the patient’s symptoms started by tingling sensations and paresthesia affecting both hands and feet. After patient received cobalamin (vitamin B 12) prescribed by his doctor, the patient symptoms were markedly aggravated and his condition worsened to extend that impaired the normal patient ordinary work. No symptoms related to motor system. Other possible etiologies were studied and excluded. Investigations of his condition revealed blood level of B12 was 1900 pg/mL, the patient condition improved dramatically with discontinuation of the drug. Conclusion Cobalamin toxicity aggravate sensory PN symptoms. Clinicians are advised to adjust the dose and check Cobalamin level before and during treatment to avoid its toxicity.
Peripheral Nervous System Diseases ; Vitamin B 12

In the last decade, it has become increasingly recognized that a balanced gut microbiota plays an important role in maintaining the health of the host. Numerous clinical and preclinical studies have shown that changes in gut microbiota composition are associated with a variety of neurological diseases, e.g., Parkinson's disease, Alzheimer's disease, and myasthenia gravis. However, the underlying molecular mechanisms are complex and remain unclear. Behavioral phenotypes can be transmitted from humans to animals through gut microbiota transplantation, indicating that the gut microbiota may be an important regulator of neurological diseases. However, further research is required to determine whether animal-based findings can be extended to humans and to elucidate the relevant potential mechanisms by which the gut microbiota regulates neurological diseases. Such investigations may aid in the development of new microbiota-based strategies for diagnosis and treatment and improve the clinical management of neurological disorders. In this review, we describe the dysbiosis of gut microbiota and the corresponding mechanisms in common neurological diseases, and discuss the potential roles that the intestinal microbiome may play in the diagnosis and treatment of neurological disorders.
Animals ; Humans ; Gastrointestinal Microbiome/physiology* ; Nervous System Diseases ; Parkinson Disease ; Microbiota ; Brain

Serum and glucocorticoid-regulated kinase 1 (SGK1) plays an important role in the physiological processes of hormone release, neuronal excitation and cell proliferation. SGK1 also participates in the pathophysiological processes of inflammation and apoptosis in the central nervous system (CNS). Increasing evidence demonstrates that SGK1 may serve as a target of the intervention of neurodegenerative diseases. In this article, we summarize the recent progress on the role and molecular mechanisms of SGK1 in the regulation of the function of the CNS. We also discuss the potential of newly discovered SGK1 inhibitors in the treatment of CNS diseases.
Humans ; Cell Proliferation ; Central Nervous System Diseases/drug therapy* ; Inflammation ; Protein Serine-Threonine Kinases/physiology*

Neurological diseases include a variety of neurodegenerative diseases and other brain damage diseases.The treatment schemes for neurological diseases are still in research.The existing clinical and basic studies have confirmed that traditional estrogen therapy has certain protective effect on the nervous system,while it increases the risk of breast or endometrial cancer.The emergence of the selective estrogen receptor modulators (SERMs) can avoid the above mentioned problems.The available studies have confirmed the protective effect of tamoxifen as a SERM on the nervous system.This paper reviews the role and functioning mechanisms of tamoxifen in the nervous system and cognitive function,aiming to provide guidance for the future application of tamoxifen in the treatment of neurological diseases and the improvement of cognitive function.
Tamoxifen/therapeutic use* ; Selective Estrogen Receptor Modulators/therapeutic use* ; Cognition ; Nervous System

Tripterygium glycosides liposome(TPGL) were prepared by thin film-dispersion method, which were optimized accor-ding to their morphological structures, average particle size and encapsulation rate. The measured particle size was(137.39±2.28) nm, and the encapsulation rate was 88.33%±1.82%. The mouse model of central nervous system inflammation was established by stereotaxic injection of lipopolysaccharide(LPS). TPGL and tripterygium glycosides(TPG) were administered intranasally for 21 days. The effects of intranasal administration of TPG and TPGL on behavioral cognitive impairment of mice due to LPS-induced central ner-vous system inflammation were estimated by animal behavioral tests, hematoxylin-eosin(HE) staining of hippocampus, real-time quantitative polymerase chain reaction(RT-qPCR) and immunofluorescence. Compared with TPG, TPGL caused less damage to the nasal mucosa, olfactory bulb, liver and kidney of mice administered intranasally. The behavioral performance of treated mice was significantly improved in water maze, Y maze and nesting experiment. Neuronal cell damage was reduced, and the expression levels of inflammation and apoptosis related genes [tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), BCL2-associated X(Bax), etc.] and glial activation markers [ionized calcium binding adaptor molecule 1(IBA1) and glial fibrillary acidic protein(GFAP)] were decreased. These results indicated that liposome technique combined with nasal delivery alleviated the toxic side effects of TPG, and also significantly ameliorated the cognitive impairment of mice induced by central nervous system inflammation.
Mice ; Animals ; Tripterygium ; Liposomes ; Glycosides/therapeutic use* ; Administration, Intranasal ; Lipopolysaccharides ; Central Nervous System ; Cognitive Dysfunction/drug therapy* ; Inflammation/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Cardiac Glycosides