Frontiers in Physiology最新文献

In athletic competitions, athletes continually challenge the limits of human performance. Exercise limitation refers to a state in which fatigue accumulates during prolonged activity, preventing the maintenance of the required power output despite maximal voluntary effort. High-intensity endurance exercise compromises muscle performance due to the accumulation of metabolic by-products in the peripheral tissues. Sympathetic nerve activation during exercise increases blood flow to the working muscles and aids in fatigue-inducing substance removal. However, excessive sympathetic activity may lead to peripheral muscular vasoconstriction, limiting exercise capacity. The present review explored the roles of the central autonomic regions, including the central nucleus of the amygdala (CeA), the paraventricular nucleus of the hypothalamus (PVN), and nucleus tractus solitarii (NTS) of the medulla in endurance limitation. The CeA is selectively activated during high-intensity exercises and contributes to the sympathetic drive. CeA lesions prolong exercise duration and delay blood pressure surges before exhaustion, suggesting that the CeA may act as a central "brake" on performance. Moreover, the co-activation pattern of the CeA-PVN-NTS circuits appears to shift dynamically depending on the exercise intensity. Understanding this emotion-autonomic circuits may provide new insights into exercise limitation and suggest novel strategies for enhancing endurance performance.

[This corrects the article DOI: 10.3389/fphys.2025.1709093.].

Introduction: Helicobacter pylori (H. pylori) infection is a primary etiological factor in gastric mucosal injury. High-altitude hypoxic environments are suspected to exacerbate this damage, although the precise mechanisms remain poorly defined. This study aimed to investigate the impact of high-altitude hypoxia on the gastric mucosal barrier and the Nrf2 signaling pathway in H. pylori-infected mice.

Methods: Male C57BL/6 mice were randomly divided into four groups: the control group (Con), the hypoxia group (H), the H. pylori infection group (Hp), and the combined H. pylori infection with hypoxia group (HpH), with 10 mice per group. A mouse model of H. pylori infection under hypoxic conditions was established by combining a hypobaric chamber simulating an altitude of 5000 m with H. pylori gavage. Pathological changes in the gastric mucosa were observed by HE staining. The expression of tight junction proteins, apoptosis-related proteins, oxidative stress markers, inflammatory factors, and key molecules of the Nrf2 pathway in gastric tissues were evaluated using qRT-PCR, immunohistochemistry, Western blot, and biochemical analysis.

Results: Compared to the H and Hp groups, mice in the HpH group exhibited significantly higher gastric mucosal epithelial damage scores. This group also showed decreased expression of ZO-1, Occludin, and Bcl-2 in gastric tissues, along with increased expression of Bax and Caspase-3. Furthermore, in the HpH group, the gastric levels of MDA, TNF-α, IL-1β, and IL-6 were elevated, while the activities of SOD and GSH-Px were reduced. Additionally, the HpH group displayed increased expression levels of Keap1 in gastric tissues, along with decreased levels of Nrf2 and its downstream target genes HO-1 and NQO1.

Discussion: High-altitude hypoxia exacerbates oxidative stress and inflammatory responses induced by H. pylori infection, reduces tight junction protein expression, and triggers changes in apoptosis-related protein expression, exacerbating the disruption of the gastric mucosal barrier, consequently leading to more severe gastric mucosal damage. The underlying mechanism may be associated with the inhibition of the Nrf2 signaling pathway in the gastric tissues.

[This corrects the article DOI: 10.3389/fphys.2025.1700313.].

Introduction: The purpose of this study was to assess whether bench press load-velocity (L-V) relationship variables serving as indicators of maximal theoretical force capacity (L ₀), maximal theoretical velocity capacity (v ₀ ), and maximal theoretical power capacity (A_line), as well as the softball-specific performance metrics (hit and throw distance), could be used to effectively monitor the selective fatigue induced by two different bench press training protocols.

Methods: The bench press L-V relationship variables and softball-specific performance metrics of 12 professional female softball players were measured on three separate occasions: (I) following passive rest (non-fatigue condition), (II) after light-load ballistic bench press throw (LLB), and (III) after heavy-load traditional bench press (HLT). Additionally, blood lactate and rating of perceived exertion (RPE) were assessed after LLB and HLT training protocols.

Results: A significantly lower v ₀ , A_line and hit distance were found after both training protocols (p ≤ 0.008), with the LLB protocol revealing a higher fatigue compared with the HLT protocol. However, the change of L-V relationship variables and softball-specific performance metrics (0.15 ≤ ES ≤ 1.05) were not as sensitive as that of blood lactate and RPE (1.30 ≤ ES ≤ 1.78).

Discussion: Hence, changes in mechanical performance could be applied as a supplementary monitoring tool to be integrated into athletes' daily routines, but should not be considered replacements for traditional fatigue indicators.

The coexistence of osteoporosis and sarcopenia is recognized as a syndrome known as osteosarcopenia. As an aging-related disease, research into the molecular mechanisms of osteosarcopenia has gradually shifted from the study of single-organ pathology to the elucidation of multidimensional interactions. This review aims to construct a hierarchical framework of "intracellular - intercellular - systemic" to systematically elaborate on the pathogenesis of osteosarcopenia. Based on this foundation, it explores frontier interventions and their prospects for clinical transformation, including bone-targeting F6-(DSS)6-exo nanoparticles, miR-495, natural active compounds (resveratrol, nuciferine), Clostridium butyricum, and bimagrumab. Future research should focus on analyzing the microenvironment of the musculoskeletal interface, utilizing deep learning CT analysis for early risk identification, and exploring the application of biomaterials in osteomuscular regeneration. This review aims to provide a reference for the field of mechanism research in osteosarcopenia and offer new insights for its precision prevention and treatment.

Introduction: Avian influenza virus (AIV) infections, even with low-pathogenic strains (LPAIVs), can severely disrupt reproduction in turkey breeder hens. Although the vagina and uterovaginal junction (UVJ) are among the earliest mucosal sites exposed to pathogens, their early transcriptomic responses to LPAIV infection are uncharacterized.

Methods: This study investigated early transcriptomic changes in these tissues during both presymptomatic and symptomatic stages of LPAIV infection (n = 4/group/tissue). Flocks for sampling were classified as presymptomatic or symptomatic based on drinker swab LPAIV testing and egg production records. Presymptomatic group consisted of infected hens from LPAIV-negative barns. These flocks had stable egg production at the time of collection but with a subsequent egg drop. The symptomatic group included infected hens from LPAIV-positive barns with reduced egg production and sampled 2-3 days post-detection.

Results: Principal component analysis of high-throughput RNA-seq data, identified symptomatic status as the primary driver of gene expression variance, followed by tissue origin. In the UVJ, 4,683 genes were differentially expressed (adjusted P-value < 0.05; Log2fold change ≥ 1.5), with symptomatic birds showing upregulation of genes involved in cellular remodeling and transport, and downregulation of those related to protein synthesis and metabolic pathways. Gene Set Enrichment Analysis (GSEA) confirmed significant upregulation of the insulin signaling pathway and downregulation of cytokine-cytokine receptor interaction, ribosome, and peroxisome proliferator-activated receptor signaling, indicating metabolic disruption and immune system alteration. The vagina presented a distinct transcriptomic profile, with 701 differentially expressed genes identified between the symptomatic vs. presymptomatic groups. In the symptomatic vagina, upregulated pathways were linked to gene regulation and biosynthesis, while downregulated pathways involved protein synthesis, metabolism, energy production, and vascular development.

Discussion: These findings reveal early, tissue-specific molecular vulnerabilities to LPAIV. The UVJ shows disruptions in cellular maintenance and metabolism, potentially impairing fertility, while the vaginal response suggests heightened early immune activation but later compromised barrier integrity. This study offers potential mechanistic insights into LPAIV-induced reproductive pathologies, providing a foundation for targeted strategies to reduce viral impact on flock health and maintain production efficiency.

[This corrects the article DOI: 10.3389/fphys.2025.1712471.].

Objective: In competitive rowing, the winter training phase is a conventional periodized block focused on foundational physiological development through land-based strength and power training. The primary aim of this phase is to enhance athletes' force-generating capabilities and metabolic resilience. This study investigated the effects of such a 16-week periodized winter training block on anaerobic capacity and energy expenditure during a 30-s all-out rowing test in elite female rowers.

Methods: Five elite female rowers (age: 20.0 ± 2.5 years; BMI: 20.8 ± 0.3 kg/m²; training experience: 4.8 ± 1.6 years) underwent pre- and post-training assessments. The winter training program consisted of three sequential phases focusing on aerobic endurance, anaerobic threshold, and race-pace intervals, with 5-6 sessions per week. Testing was conducted on the same day in the following order: (1) a 30-s all-out rowing test to assess anaerobic power output and metabolism; and (2) an incremental rowing test to exhaustion performed after a 10-min recovery, to establish individual oxygen uptake-power relationships for the maximal accumulated oxygen deficit (MAOD) method and to confirm maximal oxygen uptake (VO₂max).

Results: Following winter training, significant improvements were observed during the 30-s all-out rowing test in mean power output (+14.1%), anaerobic energy contribution (+22.0%), and total energy expenditure (+12.1%), alongside a reduction in aerobic contribution (-16.9%) and oxygen uptake (p < 0.05). Peak post-test blood lactate concentration also increased significantly (p < 0.05). No changes were detected in body mass or energy utilization efficiency (p > 0.05). The incremental test confirmed that V̇O₂max was maintained post-training (p > 0.05), ensuring that the calculated MAOD reflected true anaerobic adaptations.

Conclusion: Winter training markedly enhanced anaerobic capacity in elite female rowers, facilitated by a pronounced metabolic shift toward anaerobic pathways. Despite increased total energy expenditure, energy efficiency remained unchanged, suggesting improvements were driven primarily by physiological rather than technical adaptations. These findings underscore the importance of anaerobic development in competitive rowing performance.

Background: The gut microbiota has emerged as a key contributor to cardiovascular regulation. Acute stimulation of microbial fermentation with lactulose enhances hypoxic ventilatory response (HVR) in healthy subjects, indicating increased peripheral chemoreceptor (PCh) responsiveness. Given that heart failure (HF) is characterized by PCh hyperactivity, this study investigated whether enhancing intestinal fermentation could acutely modify chemoreceptor-driven responses in HF patients.

Methods: HF patients (n = 12; all males; age: 59.2[15.8]y; 67% in NYHA III) underwent transient hypoxia test twice: before and ∼120 min after ingesting a gut-fermentation-stimulating meal. Hydrogen in expired air was measured repeatedly and used to stratify the patients into high early fermentation (HEF) and low early fermentation (LEF) groups. Ventilatory (HVR) and cardiovascular (heart rate, blood pressure, systemic vascular resistance) responses to hypoxia were measured.

Results: HEF patients, as compared with the LEF group, displayed: (1) higher pre-lactulose HVR (mean ± SD, L/min/SpO₂: 0.680 ± 0.284 vs. 0.343 ± 0.122; p = 0.024), (2) pre- and post-lactulose SVR response (mean ± SD, dyn s/cm⁵/SpO₂: for pre-lactulose comparison, 35.40 ± 24.41 vs. 9.96 ± 1.80, p = 0.039; for post-lactulose comparison, 37.19 ± 25.75 vs. 9.22 ± 4.33, p = 0.026). HVR in the HEF group correlated with the net hydrogen excretion during the lactulose test (r = 0.85, p = 0.033).

Conclusion: Our preliminary results, derived from a small, uncontrolled physiological experiment conducted in 12 H F patients, imply a link between the upper gut microbial fermentation capacity and the baseline peripheral chemoreflex sensitivity in this population. Given the exploratory and non-randomized design, these findings should be interpreted with caution, and larger controlled studies are needed to confirm the nature and clinical relevance of this association.