Frontiers in Physiology最新文献

Secondary lymphedema is a common complication following surgical treatment of solid tumors. Although more prevalent in women due to higher breast cancer rates, men also develop lymphedema, often with more severe manifestations. Despite these differences in clinical presentation, the cellular mechanisms underlying sex differences are poorly understood. Previous studies have shown that inducible nitric oxide synthase (iNOS) expression by inflammatory cells is an important regulator of lymphatic pumping and leakiness in lymphedema and that lymphatic endothelial cells are highly sensitive to nitrosative stress. Based on this rationale, we used a mouse tail model of lymphedema to study the role of nitric oxide in sex-related differences in disease severity. Consistent with clinical findings, we found that male mice have significantly worse tail edema and higher rates of tail necrosis compared with female mice following tail skin/lymphatic excision (p = 0.001). Our findings correlated with increased tissue infiltration of iNOS + inflammatory cells, increased iNOS protein expression, and increased nitrosative stress in male mouse lymphedematous skin tissues (p < 0.05). Importantly, transgenic male mice lacking the iNOS gene (iNOS-KO) displayed markedly reduced swelling, inflammation, and tissue necrosis rates, whereas no differences were observed between wild-type and iNOS-KO female mice. Overall, our results indicate that iNOS-mediated nitric oxide production contributes to sex-based differences in secondary lymphedema severity, emphasizing the need to consider sex as a biological variable in lymphedema research.

Purpose: This study aimed to examine the acute effects of static stretching (SS) and dynamic stretching (DS) on neuromuscular function and balance in recreationally active men.

Method: Sixty participants were randomly assigned to SS, DS, or no stretching (NS) groups. Before and after their respective stretching protocols, participants were assessed using the stork balance test (SBT), Y-balance test (YBT), T-change of direction test (CoD T-test), countermovement jump test (CMJT), squat jump test (SJT), and five-time jump test (FJT).

Results: Significant main effects of time were observed for the SBT, YBT, and CoD T-test. Significant interactions between time and group were found for the SBT, YBT, CoD T-test, and CMJT (P < 0.05). Compared to the NS group, the SS group showed significant improvement in the SBT (P < 0.05), while the DS group demonstrated significant improvements in the SBT, YBT (all directions), CoD T-test, CMJT, and SJT (P < 0.05). Post-training, the DS group showed greater improvements than the SS group in the YBT, CoD T-test, CMJT, and SJT (P < 0.05), with no significant differences in the SBT.

Conclusion: SS acutely improves static balance, while DS has a broader impact, enhancing both neuromuscular function and balance.

Introduction: Exhaustive exercise is a common training method in sports, but its impact on the autonomic nervous system of the human body remains unclear. Understanding the effects of exhaustive exercise on the body and its connection with the autonomic nervous system and central nervous system is crucial for guiding healthy training methods.

Methods: Twenty-three participants were selected, and exhaustive exercise intervention was performed using the Bruce Protocol. By measuring heart rate variability (HRV), the effects of exhaustive exercise on the autonomic nervous system function were analyzed.

Results: After exhaustive exercise, time-domain indices SDNN, RMSSD, and PNN50 all significantly decreased, with changes reaching significant levels (p < 0.01). Among them, the decrease in pNN50 was particularly pronounced, with a change rate of -94.55%. Frequency-domain indices VLF, LF, and HF also showed significant decreases (p < 0.01), but the ratio of LF to HF showed an upward trend (p < 0.01), with LF showing a greater decrease. Nonlinear indices SD1 and SD2 showed extremely significant decreases (p < 0.01), and the SD2/SD1 ratio showed a significant increase (p < 0.01), indicating significant changes in HRV nonlinear characteristics after exercise.

Discussion: Exhaustive exercise leads to a decrease in autonomic nervous system activity and an increase in sympathetic nervous system activity. These findings underscore the profound impact of exhaustive exercise on the autonomic nervous system, with implications for understanding the physiological responses to intense physical exertion. Further research is warranted to explore the long-term effects of exhaustive exercise on autonomic regulation and its potential implications for training methodologies and athlete health.

Introduction: As adolescent smoking rates rise, its impact on cognitive function has drawn greater attention. This study explores whether exercise can mitigate the negative effects of smoking on executive function in male college students.

Methods: Sixty male college students were divided into four groups (n = 15 each): sedentary smokers, sedentary nonsmokers, athletic smokers, and athletic nonsmokers. All participants completed the Eriksen flanker task, with prefrontal cortex activation measured using functional near-infrared spectroscopy. After the baseline test, all sedentary students engaged in 33 min of high-intensity interval training, followed by the same procedures as in the pre-test.

Results: In the flanker task, college athletes exhibited superior executive function compared to sedentary students, with higher accuracy (p = 0.042), faster reaction times (p = 0.002), and more pronounced brain activation (p = 0.048). Post-exercise, reaction times improved significantly in sedentary groups (p < 0.05). Smoking impaired executive function both before and after exercise, with smokers showing lower accuracy (p < 0.001), slower reaction times (p < 0.001), and diminished brain activation (p < 0.001) compared to nonsmokers.

Discussion: Engaging in acute aerobic exercise may improve executive function in sedentary smokers. Exercise may help mitigate smoking-related declines in executive function among college students.

Background: The relationship between conduction system pacing (CSP) and the incidence of atrial fibrillation (AF) in patients with heart failure and preserved ejection fraction (HFpEF) remains uncertain. This study aims to investigate the occurrence of atrial high-rate episodes (AHREs) following CSP in patients with HFpEF, in comparison to right ventricular pacing (RVP).

Methods: Patients with HFpEF who received dual-chamber pacemakers for atrioventricular block were retrospectively enrolled from January 2018 to January 2023. Both new-onset and progressive AHREs were recorded, along with other clinical data, including cardiac performance and lead outcomes.

Results: A total of 498 patients were enrolled, comprising 387 patients with RVP and 111 patients with CSP, with a follow-up duration of 44.42 ± 10.41 months. In patients without a prior history of AF, CSP was associated with a significantly lower incidence of new-onset AHREs when the percentage of ventricular pacing was ≥20% (9.52% vs. 29.70%, P = 0.001). After adjusting for confounding factors, CSP exhibited a lower hazard ratio for new-onset AHREs compared to RVP (HR 0.336; [95% CI: 0.142-0.795]; P = 0.013), alongside left atrial diameter (LAD) (HR 1.109; [95% CI: 1.048-1.173]; P < 0.001). In patients with a history of AF, the progression of AHREs in CSP and RVP did not differ significantly (32.35% vs. 34.75%, P = 0.791). Cardiac performance metrics, including left ventricular end-diastolic diameter (LVEDD) (49.09 ± 4.28 mm vs. 48.08 ± 4.72 mm; P = 0.015), LAD (40.68 ± 5.49 mm vs. 39.47 ± 5.24 mm; P = 0.001), and NYHA class (2.31 ± 0.46 vs. 1.59 ± 0.73; P < 0.001), improved obviously following CSP, while LVEDD (48.37 ± 4.57 mm vs. 49.30 ± 5.32 mm; P < 0.001), LAD (39.77 ± 4.58 mm vs. 40.83 ± 4.80 mm; P < 0.001), NYHA class (2.24 ± 0.43 vs. 2.35 ± 0.83; P = 0.018), and left ventricular ejection fraction (LVEF) (57.41 ± 2.42 vs. 54.24 ± 6.65; P < 0.001) deteriorated after RVP.

Conclusion: Our findings suggest that CSP may be associated with improvements in cardiac performance and a reduction in new-onset AHREs compared to RVP in patients with HFpEF. However, prospective randomized trials are anticipated to confirm these potential benefits.

Over the past couple of decades, it has become apparent that skeletal muscles might be engaged in endocrine signaling, mostly as a result of exercise or physical activity in general. The importance of this phenomenon is currently studied in terms of the impact that exercise- or physical activity -induced signaling factors have, in the interaction of the "muscle-brain crosstalk." So far, skeletal muscle-derived myokines were demonstrated to intercede in the connection between muscles and a plethora of various organs such as adipose tissue, liver, or pancreas. However, the exact mechanism of muscle-brain communication is yet to be determined. It is speculated that, in particular, brain-derived neurotrophic factor (BDNF), irisin, cathepsin B (CTSB), interleukin 6 (IL-6), and insulin-like growth factor-1 (IGF-1) partake in this crosstalk by promoting neuronal proliferation and synaptic plasticity, also resulting in improved cognition and ameliorated behavioral alterations. Researchers suggest that myokines might act directly on the brain parenchyma via crossing the blood-brain barrier (BBB). The following article reviews the information available regarding rodent studies on main myokines determined to cross the BBB, specifically addressing the association between exercise-induced myokine release and central nervous system (CNS) impairments. Although the hypothesis of skeletal muscles being critical sources of myokines seems promising, it should not be forgotten that the origin of these factors might vary, depending on the cell types engaged in their synthesis. Limited amount of research providing information on alterations in myokines expression in various organs at the same time, results in taking them only as circumstantial evidence on the way to determine the actual involvement of skeletal muscles in the overall state of homeostasis. The following article reviews the information available regarding rodent studies on main myokines determined to cross the BBB, specifically addressing the association between exercise-induced myokine release and CNS impairments.

This study addresses the limitations of traditional sports rehabilitation, emphasizing the need for improved accuracy and response speed in real-time action detection and recognition in complex rehabilitation scenarios. We propose the STA-C3DL model, a deep learning framework that integrates 3D Convolutional Neural Networks (C3D), Long Short-Term Memory (LSTM) networks, and spatiotemporal attention mechanisms to capture nuanced action dynamics more precisely. Experimental results on multiple datasets, including NTU RGB + D, Smarthome Rehabilitation, UCF101, and HMDB51, show that the STA-C3DL model significantly outperforms existing methods, achieving up to 96.42% accuracy and an F1 score of 95.83% on UCF101, with robust performance across other datasets. The model demonstrates particular strength in handling real-time feedback requirements, highlighting its practical application in enhancing rehabilitation processes. This work provides a powerful, accurate tool for action recognition, advancing the application of deep learning in rehabilitation therapy and offering valuable support to therapists and researchers. Future research will focus on expanding the model's adaptability to unconventional and extreme actions, as well as its integration into a wider range of rehabilitation settings to further support individualized patient recovery.

Red blood cells (RBCs) play a role in the regulation of vascular tone via release of adenosine triphosphate (ATP) into the vasculature in response to various stimuli. Interestingly, ApoE/LDLR double-deficient (ApoE/LDLR^-/-) mice, a murine model of atherosclerosis, display a higher exercise capacity compared to the age-matched controls. However, it is not known whether increased exercise capacity in ApoE/LDLR^-/- mice is linked to the altered ATP release from RBCs. In this work, we characterized the ATP release feature of RBCs from ApoE/LDLR^-/- mice by exposing them to various stimuli in vitro. The results are linked to the previously reported mechanical and biochemical alterations in RBCs. 3V-induced ATP release from RBCs was at comparable levels for all groups, which indicated that the activity of adenylyl cyclase and the components of upstream signal-transduction pathway were intact. Moreover, hypoxia- and low pH-induced ATP release from RBCs was higher in ApoE/LDLR^-/- mice compared to their age-matched controls, a potential contributing factor and a finding in line with the higher exercise capacity. Taken together, augmented hypoxia-induced ATP release from RBCs in ApoE/LDLR^-/- mice indicates a possible deterioration in the ATP release pathway. This supports our previous reports on the role of the protein structure alterations of RBC cytosol in hypoxia-induced ATP release from RBCs in ApoE/LDLR^-/- mice. Thus, we emphasize that the presented herein results are the first step to future pharmacological modification of pathologically impaired microcirculation.

Background: Changes in blood vessel properties have been identified with confinement, spaceflight, bedrest, and dry immersion. Subsequently, it was suspected that other organs may also be affected in these extreme environments. The purposes of the current study were to determine the effects of head-down bedrest (HDT) on cardiovascular and organ measurements made using ultrasound imaging similar to that currently available on the International Space Station, and to evaluate the efficacy of two different countermeasure protocols in preventing any observed changes in the ultrasound measurements with HDT.

Methods: Ultrasound measures were conducted on 24 individuals (3 groups of 8) pre HDT and on day 55 of the HDT. The control group (C°) remained in passive HDT for the 55 days, the C1 group performed aerobic exercise daily (EX), and the C2 group practiced aerobic exercise under artificial gravity conditions (EX-AG). Fifteen parameters were measured on 10 different organs and blood vessels including the right common carotid artery, abdominal aorta, right tibial artery, left ventricle, right jugular vein, portal vein, right kidney, cervical and lumbar vertebra, and the vastus intermedius muscle.

Results: HDT resulted in changes for many of the parameters investigated. Observed changes in carotid IMT and distensibility, cardiac ejection fraction, portal vein diameter, and vastus intermedius muscle thickness were attenuated with EX and EX-AG, with EX-AG having a greater effect than exercise alone on measures of carotid distensibility.

Conclusion: Results from this study indicate changes in many structures assessed with ultrasound imaging after 55 days of HDT bedrest with some changes being attenuated with the two investigated countermeasure protocols.

Objective: Although seizures are the cardinal feature, epilepsy is associated with other forms of brain dysfunction including impaired cognition, abnormal sleep, and increased risk of developing dementia. We hypothesized that, given the widespread neurologic dysfunction caused by epilepsy, accelerated brain aging would be seen. We measured the sleep-based brain age index (BAI) in a diverse group of patients with epilepsy. The BAI is a machine learning-based biomarker that measures how much the brain activity of a person during overnight sleep deviates from chronological age-based norms.

Methods: This case-control study drew information of age-matched controls without epilepsy from home sleep monitoring volunteers and from non-epilepsy patients with Sleep Lab testing. Patients with epilepsy underwent in-patient monitoring and were classified by epilepsy type and seizure burden. The primary outcomes measured were BAI, processed from electroencephalograms, and epilepsy severity metrics (years with epilepsy, seizure frequency standardized by year, and seizure burden [number of seizures in life]). Subanalyses were conducted on a subset with NIH Toolbox cognitive testing for total, fluid, and crystallized composite cognition.

Results: 138 patients with epilepsy (32 exclusively focal and 106 generalizable [focal seizures with secondary generalization]) underwent in-patient monitoring, and age-matched, non-epilepsy controls were analyzed. The mean BAI was higher in epilepsy patients vs controls and differed by epilepsy type: -0.05 years (controls) versus 5.02 years (all epilepsy, p < 0.001), 5.53 years (generalizable, p < 0.001), and 3.34 years (focal, p = 0.03). Sleep architecture was disrupted in epilepsy, especially in generalizable epilepsy. A higher BAI was positively associated with increased lifetime seizure burden in focal and generalizable epilepsies and associated with lower crystallized cognition. Lifetime seizure burden was inversely correlated with fluid, crystallized, and composite cognition.

Significance: Epilepsy is associated with accelerated brain aging. Higher brain age indices are associated with poorer cognition and more severe epilepsy, specifically generalizability and higher seizure burden. These findings strengthen the use of the sleep-derived, electroencephalography-based BAI as a biomarker for cognitive dysfunction in epilepsy.