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        <title>Frontiers in Physiology | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology</link>
        <description>RSS Feed for Frontiers in Physiology | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-08T11:21:59.568+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1793768</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1793768</link>
        <title><![CDATA[Anatomical spatial-temporal distribution and multivariate risk of acute injuries in elite rugby: a cohort based on prospective surveillance]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zhuo Chen</author><author>Xue Wang</author><author>Xiaodong Mei</author>
        <description><![CDATA[BackgroundAcute injuries are common in rugby and threaten both player health and career longevity. Previous studies often focused on isolated risk factors, while limited research has comprehensively examined the interplay of physiological, environmental, and situational variables.MethodsStudy conducted A cohort study of 40 elite male players from the Tianjin Rugby Team was conducted, monitoring 575 match exposures across 2.5 consecutive seasons (2022–2025). Acute injuries were defined according to international consensus criteria and verified by medical staff. Spatiotemporal distributions (seasonal variation, match stage, playing position, and body site) were analyzed using chi-square and logistic regression. Multivariate models were applied to identify independent risk factors, including demographic, training, and environmental variables.ResultsA total of 143 acute injury events were recorded, with bone and joint injuries most prevalent (48.2%), and the majority classified as moderate-to-severe (78.3%). Injury incidence rate rose significantly across seasons (127.9 per 1,000 player-hours in 2024/25 vs. 43.3 in 2022/23, representing a 1.83-fold increase), and advanced competition stages showed higher risks (OR for finals = 7.06 vs. group stage, p<0.001). GEE analysis demonstrated that the 2023/24 season, semi-finals and finals, forward position, no previous injury history, and higher training load were associated with elevated acute injury risk among rugby players (all P<0.05), while higher temperature served as a protective factor (P<0.001); age, BMI, exercise level, fatigue, and training years showed no significant effects.ConclusionsAcute injury risk in rugby demonstrates clear spatiotemporal patterns and is strongly influenced by both individual and environmental factors. The model developed provides a practical basis for targeted prevention strategies, including load management, environmental adaptation, and individualized recovery protocols. These findings can serve as a reference for coaches and medical teams at elite Chinese rugby clubs—particularly those adopting training-competition models—to optimize training and competition management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1808008</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1808008</link>
        <title><![CDATA[A study on brain waves with electroencephalogram through the appreciation of virtual reality K-pop: a revised analysis with multiple comparison corrections]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Taeseung Park</author><author>Hyunsoo Kim</author><author>Deok Su Yoo</author>
        <description><![CDATA[BackgroundKorean popular culture (K-pop) has become increasingly popular worldwide and the convergence of K-pop and virtual reality (VR) has contributed to the popularity of metaverse technologies. Previous studies on K-pop and VR were largely conducted in the fields of cognitive psychology and qualitative research. Recently, the use of functional magnetic resonance imaging (MRI), electroencephalogram (EEG), and eye-trackers have gained attention.MethodsIn this study, EEG analysis was used to evaluate alpha waves, beta waves, and theta/beta ratios of 20 participants who had experienced VR or normal K-pop music video content, and the data analyzed based on the Media Richness Theory. Statistical analyses employed paired t-tests with False Discovery Rate (FDR) correction for multiple comparisons using the Benjamini-Hochberg procedure, and effect sizes (Cohen’s d) were calculated to assess practical significance.ResultsThe results revealed differences in alpha wave (p <.05), beta wave (p <.05), and theta/beta ratios between the general and VR music video groups. After FDR correction, 11 electrodes showed significant alpha wave differences (d = 0.54-1.51), 13 electrodes showed significant beta wave differences (d = 0.50-1.04), and 8 electrodes showed significant theta/beta ratio differences (d = 0.63-0.87). Alpha waves were higher in the normal music video group, whereas beta waves and the theta/beta ratio were higher in the VR music video group.ConclusionThe EEG results suggest that VR K-pop music videos are rich in media content, providing more information than normal K-pop music videos. The robustness of findings was confirmed through rigorous statistical correction, with medium to large effect sizes indicating substantial practical significance beyond statistical significance. This approach has the potential to develop a strategy for metaverse K-pop content.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1785061</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1785061</link>
        <title><![CDATA[A theoretic predictive model to simulate the interference effects of acute aerobic exercise on rate of force development in weightlifters]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Emidio E. Pistilli</author><author>Alan D. Mizener</author><author>Stuart A. Clayton</author>
        <description><![CDATA[IntroductionCompelling data supports the concept that concurrent strength and aerobic training can interfere with adaptations to strength training related to speed, power, and rate of force development (RFD). Studies on this topic have primarily utilized non-athlete participants, with data subsequently extrapolated to athlete populations. Since there may be hesitancy to have athletes involved in research on the interference effects of aerobic exercise on strength specific adaptations, we built a model to simulate these effects and developed an equation to predict interference. The hypothesis tested in this project was that aerobic exercise is the main driver of interference on weightlifting-associated RFD, and that this interference can be modeled to generate an equation to predict changes to RFD. MethodsPython software was used to generate the model, perform the simulation, and optimize variables that contribute to the interference effect. A theoretical nonlinear exponential interference model was created that simulates the changes in RFD from a force-time curve in response to acute aerobic exercise lasting from 2-minutes to 60-minutes in duration. ResultsRFD sensitivity to aerobic exercise was modeled such that maximal RFD values were predicted to be reduced by approximately 70% after aerobic exercise less than 10 minutes, with further predicted reductions of 80% with durations greater than 10-minutes.DiscussionThe prediction equation includes variables that can be adjusted by coaches, such as the rate of decay and the RFD scaling factor, to predict the interference of acute aerobic exercise on RFD in strength athletes. This would theoretically allow the coach to make informed decisions on training program design if there is a need to include aerobic exercise in a strength and/or power-based periodized plan. The simulation model described herein is theoretical and has not yet been empirically validated.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1794886</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1794886</link>
        <title><![CDATA[Transcriptomic profiling of the sex-linked biological pathways of severe pulmonary arterial hypertension associated with endothelial cell caveolin-1 depletion and chronic hypoxia]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Joseph W. Leasure</author><author>Samuel M. Lee</author><author>Kayla L. Yerlioglu</author><author>Maricela Castellon</author><author>Haibin Li</author><author>Andrés Fantauzzi</author><author>Sunny Chen</author><author>Sami B. Muslmani</author><author>Arnav Sharma</author><author>Jiwang Chen</author><author>Richard D. Minshall</author>
        <description><![CDATA[IntroductionPulmonary arterial hypertension (PAH) is distinguished by elevated blood pressure and vascular resistance in the arteries of the lungs. Patients with PAH demonstrate pulmonary vascular remodeling, wall thickening, and a high rate of morbidity due to right heart failure. Notably, while female patients are more likely to develop PAH, male patients suffer from higher morbidity rates after diagnosis. The molecular mechanism(s) underlying PAH development is poorly understood, though heritable PAH linked to mutations in bone morphogenic protein receptor 2 (Bmpr2) and caveolin-1 (Cav1) may provide novel insights into the disease’s pathophysiology.MethodsTo interrogate this dynamic, we utilized a global Cav1 knockout (Cav1-KO) mouse model (Cav1-/-) in conjunction with chronic hypoxia to induce symptoms of PAH as demonstrated by hemodynamic and ECHO cardiography recordings.ResultsBoth female and male Cav1-/- mice in chronic hypoxia demonstrated elevated right ventricular systolic pressure (RVSP) of 48.49 mmHg and 47.78 mmHg respectively. Female knockout mice began dying earlier in hypoxic conditions (4 wks), though male mice showed greater total mortality by the end of the 8 wks of hypoxia. In addition to wildtype controls, we compared this knockout mouse to endothelial-specific Cav1 reconstituted (Cav1-RC) knockouts and found that restoration of Cav1 expression only in endothelial cells (ECs) is sufficient to ameliorate PAH symptoms, highlighting the importance of vascular Cav1 in maintaining pulmonary artery function. RNA-sequencing of the lungs revealed that Cav1-/- is associated with downregulation of biological process gene pathways involved in cilium assembly in normoxic conditions for both sexes. In hypoxic conditions, Cav1 knockout in females leads to downregulation of bone morphogenetic protein (BMP) signaling, while male hypoxic Cav1-/- led to a significant increase in muscle cell development genes. Reconstitution of Cav1 in ECs leads to upregulation of immune signaling pathways, muscle cell development, and various cell differentiation pathways in both sexes; females showed a unique upregulation of cilia-related pathways, while males demonstrated increased BMP signaling.DiscussionThese data indicate that muscle cell development, angiogenesis, cilia assembly, immune response, and BMP signaling pathways undergo sex-specific transcriptional regulation during PAH development that may underlie sex differences in PAH patient outcome.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1830278</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1830278</link>
        <title><![CDATA[Sex differences in endothelial cell biology: cellular phenotypes and molecular regulators]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Alexandra Pislaru</author><author>Tara L. Haas</author>
        <description><![CDATA[Endothelial cells (EC) line all blood vessels and are central to maintaining vascular homeostasis by regulating barrier integrity, angiogenesis, inflammation and other key processes. Although EC share core functions, they exhibit substantial heterogeneity across vascular beds and tissues, reflecting differences in local metabolic and microenvironmental conditions. Emerging evidence indicates that endothelial biology is also shaped by sex. Male and female EC differ in multiple aspects of cellular physiology, including metabolic activity, nitric oxide signaling, angiogenic capacity, oxidative stress responses, inflammatory signaling, and susceptibility to senescence. In this review, we summarize the current knowledge of these sex-dependent EC phenotypes and discuss how they vary by vascular location, as well as across age and disease context. Increasing evidence suggests that these differences arise from a complex interplay between sex hormones, sex chromosome complement, epigenetic regulation, and transcription factor networks. We discuss recent advances in understanding these mechanisms and their contributions to EC heterogeneity. Recognizing sex-specific EC functional characteristics and vulnerabilities is critical for a comprehensive understanding of vascular physiology and pathology, with important implications for improved knowledge of vascular disease mechanisms and development of more precise, sex-informed therapeutic strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1741526</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1741526</link>
        <title><![CDATA[Is there a link between fascia and cancer? From potential mechanisms to future treatment options]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Stephanie Otto</author><author>Werner Klingler</author>
        <description><![CDATA[Fascia, the connective tissue network enveloping muscles, organs, nerves, and vasculature, plays an important role in maintaining structural integrity, biomechanical function, and integrative physiological processes. Traditionally considered a passive support structure, fascia is increasingly discussed as an active component in cancer biology, particularly within the tumor microenvironment (TME), although many mechanistic pathways remain incompletely characterized. Experimental and clinical studies suggest that tumor-associated remodeling of the extracellular matrix (ECM) within fascial tissues can increase tissue stiffness, fibrosis, and desmoplasia, changes that may facilitate tumor progression, invasion, metastasis, and immune escape, and could contribute to resistance against conventional therapies in at least some tumor entities. Cancer-associated fibroblasts (CAFs) appear to be central mediators of these processes by producing collagen, enzymatically modifying ECM structure, and influencing mechanotransduction pathways involving transcriptional regulators such as YAP/TAZ and integrins, thereby promoting pro-malignant cellular phenotypes in model systems. Fascia also interfaces closely with immune and nervous systems, potentially influencing immune cell trafficking, neuroinflammatory signaling, and systemic stress responses via the hypothalamic pituitary adrenal axis and vagal pathways, but these interactions are only partly understood in the context of cancer. Emerging preclinical and early clinical data indicate that physical exercise and movement-based interventions, including controlled stretching and other mechanical therapies, may modulate fascial stiffness and low-grade inflammation, with possible effects on tumor biology and patient-reported outcomes that appear at least partly distinct from those of aerobic exercise, yet this requires confirmation in larger, well-controlled trials. Clinically, patterns of fascial involvement and ECM remodeling correlate with aggressive behavior and poorer outcome in several cancers, suggesting potential prognostic value, although standardized assessment and validation across entities are still lacking. Targeting fascia- and ECM-related components, such as collagen cross-linking enzymes (for example lysyl oxidase), is being explored as a translational strategy to enhance drug delivery and immunotherapy responses, but these approaches remain largely experimental. Priority areas for future research include the development of imaging and molecular tools for more precise fascia assessment, mechanobiological interventions tailored to individual patients, and rigorous clinical trials evaluating fascia-modulating therapies as adjuncts in integrative oncology. In summary, current evidence supports a view of fascia as a dynamic, multifunctional tissue that is likely implicated in cancer progression and therapy response while highlighting substantial knowledge gaps and the need for cautious, hypothesis-driven translation into clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1796624</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1796624</link>
        <title><![CDATA[Exercise evokes retained motor performance without neuroprotection in a mouse model of Parkinson’s disease]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Henry M. Skelton</author><author>Nathaniel Hyman</author><author>Alejandra M. Fernandez</author><author>Emma Acerbo</author><author>Madison Scott</author><author>Ken Berglund</author><author>Claire-Anne Gutekunst</author><author>Robert E. Gross</author>
        <description><![CDATA[Exercise has been extensively studied in Parkinson’s Disease, with a particular focus on the potential for neuroprotection that has been demonstrated in animal models. While this preclinical work has provided insight into the underlying molecular mechanisms, it has not addressed the neurophysiological changes during exercise. Here, first, we tested for neuroprotective effects of adaptive wheel running exercise in the 6-hydroxydopamine mouse model of Parkinson’s disease, assessing for dopamine cell preservation. Finding none, despite running performance that equaled the pre-parkinsonian state, we probed the neurophysiology of running exercise as a transient state of high motor function amidst an unameliorated Parkinsonian lesion. Exercise was associated with characteristic, excitatory changes in the dopamine-depleted substantia nigra, which could be suppressed along with running itself by dopamine receptor blockade. Going forward, the functional state evoked by exercise merits further study, as it has parallels in human disease and may represent an optimal physiologic target for neuromodulation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1808663</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1808663</link>
        <title><![CDATA[Lacticaseibacillus rhamnosus HN001 enhances intestinal barrier function and protects the blood-brain barrier from inflammatory disruption in vitro]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dulantha Ulluwishewa</author><author>Ajitpal Purba</author><author>Vincent Fegan</author><author>Narsaa Na</author><author>Simon J. O’Carroll</author><author>Rachel C. Anderson</author>
        <description><![CDATA[The integrity of the intestinal epithelial and blood-brain barriers is critical for maintaining homeostasis along the gut-brain axis as these interfaces regulate the passage of inflammatory mediators into systemic circulation and their access to the brain. Disruption of these barriers can lead to neuroinflammatory processes implicated in mood disturbances. Lacticaseibacillus rhamnosus HN001 has been associated with improved mood outcomes in clinical and preclinical studies, however the mechanistic basis for these effects is unclear. Here, we investigated whether HN001 enhances intestinal and blood-brain barrier function in a two-stage in vitro gut-brain axis model. Differentiated Caco-2 epithelial monolayers were co-cultured with HN001 (Stage-1; intestinal epithelial barrier), and the conditioned basal medium from this stage was subsequently applied to hCMEC/D3 endothelial monolayers (Stage-2; blood-brain barrier). HN001 increased transepithelial electrical resistance in Caco-2 monolayers under both aerobic and apical-anaerobic conditions. This was accompanied by transcriptional modulation of tight-junction signaling, including upregulation of OCLN and sealing claudins, and downregulation of the pore-forming claudin CLDN2. Conditioned basal medium collected from HN001-treated Caco-2 intestinal epithelial monolayers improved barrier resistance in hCMEC/D3 brain endothelial monolayers and mitigated IL-1β-induced barrier disruption. The protective effect was not accompanied by changes in IL-1β-stimulated secretion of IL-6, IL-8, MCP-1, TNF-α or IL-1β, indicating that HN001-derived signals regulate blood-brain barrier function independently of the cytokines measured here. Together, these findings indicate that HN001 supports both the intestinal barrier and the blood-brain barrier integrity within the gut-brain axis. By regulating these barrier interfaces, HN001 may reduce susceptibility to neuroinflammation, suggesting a potential mechanistic basis for its previously reported psychobiotic benefits.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1820135</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1820135</link>
        <title><![CDATA[Biomechanical effects of squatting movements in Tai Chi on the knee joint]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Haibin Liu</author><author>Wenxiao He</author><author>Guang Yang</author><author>Suheng Li</author><author>Liqing Liu</author><author>Fan Gao</author><author>Shudong Yan</author><author>Ziyang Wang</author><author>Fengjie Ran</author>
        <description><![CDATA[BackgroundSquatting is essential for daily activities but may risk knee injury due to excessive loads. Tai Chi squatting (TCS), characterized by slow, controlled movements, is hypothesized to reduce joint load compared to standard squatting (SS), though biomechanical comparisons remain scarce. This study aimed to biomechanically compare TCS and SS, with a focus on knee joint kinematics, kinetics, muscle activation, and internal stress distribution.MethodsTwelve experienced Tai Chi practitioners (6 males, 6 females) participated in this study. Participants performed TCS and SS in a controlled laboratory setting. Three-dimensional kinematics were captured with a VICON system, ground reaction forces were measured using AMTI force platforms, and muscle activation was recorded via surface electromyography (sEMG) using the Noraxon Ultium EMG system. The data were processed with an OpenSim musculoskeletal model, and finite element analysis was conducted using Ansys SpaceClaim and Ansys Workbench to evaluate internal knee joint stress distributions.Results(1) Kinematics and Kinetics: Compared with SS, TCS produced a markedly smoother knee flexion–extension angle time profile (p < 0.001). TCS elicited significantly greater peak knee extension moments compared with SS (p < 0.001), particularly in male participants, and was associated with significantly elevated activation of the biceps femoris and sartorius, reflecting a shift toward posterior chain co-activation, resulting in a more balanced quadriceps-to-hamstring co-activation pattern. This tendency was particularly pronounced in female participants (p < 0.05). (2) Finite Element Stress Analysis: While the absolute difference in peak Von Mises stress on the femoral cartilage between SS and TCS was modest, TCS produced a qualitatively more homogeneous stress distribution across the articular surface, with the focal high-stress concentration pattern observed under SS notably attenuated. This improvement in load distribution morphology may carry greater functional relevance for long-term cartilage health than peak stress magnitude alone.ConclusionTCS promotes more balanced muscle co-activation and a more homogeneous intra-articular stress distribution compared with SS, potentially reducing the risk of localized cartilage fatigue, particularly in female practitioners. These findings support the integration of TCS into rehabilitation and conditioning programs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1789909</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1789909</link>
        <title><![CDATA[Effects of long-term functional training combined with blood flow restriction training on athletic performance and body composition in basketball athletes]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Di Wang</author><author>Moran Lyu</author><author>Zhiheng Li</author><author>Ming Li</author><author>Yuliu Tao</author><author>Aisong Zhu</author>
        <description><![CDATA[BackgroundThis study examined the effects of a 24-week functional training (FT) and blood flow restriction combined with FT (BFR-FT) on athletic performance and body composition in athletes.MethodsTwenty-six male basketball players were randomly assigned to either the experimental group (EG) or the control group (CG). The CG performed FT, while the EG performed BFR-FT, both for 24 weeks. Assessments were conducted at seven time points, every 4 weeks, measuring 1RM half-squat, 1RM squat, vertical jump, 30m sprint, agility, 17-return shuttle run, body weight, and limb circumference and skinfold thickness.Results(1) Significant time × group interactions were observed for 1RM half−squat and speed (P < 0.01). The EG showed superior speed (weeks 12, 20, P < 0.01) and 1RM half−squat (week 8, P = 0.02; weeks 12–24, P < 0.01). For 1RM squat and endurance, both interaction and time effects were significant (P < 0.05). For explosive power and agility, only time effects were significant (P < 0.01). (2) Significant interactions were found for body weight (P = 0.04), thigh circumference (P < 0.01), and calf skinfold thickness (P = 0.02), and the main effects of time were also significant (P < 0.01). For calf circumference and thigh skinfold thickness, only time effects were significant (P < 0.01).]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1776903</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1776903</link>
        <title><![CDATA[Science policies and practice of including and excluding women from clinical studies: focus on cardiovascular research]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Anton Kovalsky</author><author>Irena Levitan</author>
        <description><![CDATA[The under-representation of women in clinical studies remains a major issue, recognized by researchers, patients, and legislators alike. In this review, we examine the key legislative documents that have shaped policies governing the exclusion and inclusion of women in clinical research over the past several decades, and their impact on seminal cardiovascular studies. We focus on early federal human-subject regulations codified as the Common Rule, which initially contributed to the near-complete exclusion of women, and trace the gradual recognition of the need for women’s inclusion and the progress achieved to date. Key trials discussed include the Framingham Heart Study, the Multiple Risk Factor Intervention Trial (MRFIT), and the Physicians’ Health Study (PHS), as well as a meta-analysis of over 1, 000 cardiovascular trials conducted between 2017 and 2023. We also discuss the critiques of the legislation including the current reliance on informed consent from a bioethics perspective.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1802284</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1802284</link>
        <title><![CDATA[Advances in quantitative ultrasound for metabolic dysfunction-associated steatotic liver disease diagnosis]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Zejun Ma</author><author>Bo Liu</author><author>Shuyi Zhou</author><author>Shuai Yang</author><author>Xiaojie Sun</author><author>Xinping Jiang</author><author>Xiaofeng Sun</author>
        <description><![CDATA[Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasing worldwide, underscoring the need for noninvasive, repeatable biomarkers for accurate clinical stratification. This review synthesizes recent advances in quantitative ultrasound (QUS) for MASLD phenotyping, spanning attenuation-based metrics (e.g., controlled attenuation parameter, tissue attenuation imaging, ultrasound-guided attenuation parameter), shear-wave elastography, backscatter analysis, sound-speed imaging, and artificial-intelligence–enabled multiparametric models. Unlike conventional B-mode ultrasound, which relies on subjective echogenicity, QUS derives biophysical parameters from radiofrequency signals that correlate with hepatic fat content, stiffness and viscoelasticity, microstructure, and perfusion. Across recent evidence, attenuation techniques show strong performance for detecting early steatosis, whereas shear-wave elastography better stages clinically significant fibrosis; shear-wave dispersion and microvascular imaging provide emerging surrogates of necroinflammatory activity. Integrating multiple QUS features with clinical covariates improves robustness and reduces diagnostic error relative to single-parameter tools. We summarize technical principles, acquisition considerations, and sources of variability, and discuss harmonization, cross-platform comparability, and the role of open protocols. Remaining challenges include vendor heterogeneity, the absence of unified thresholds, limited multicenter outcome data, and the need for explainable and generalizable AI. Overall, QUS is evolving from a screening adjunct to a physiologically grounded, multiparametric platform. However, current challenges such as cross-platform harmonization, vendor variability, and the need for unified diagnostic thresholds remain significant barriers. The future of QUS lies in the integration of artificial intelligence (AI) to enhance diagnostic accuracy, improve reproducibility, and address these limitations. Further research should focus on large-scale validation studies and the development of multi-parametric approaches that combine QUS with other non-invasive diagnostic tools for a more comprehensive assessment of MASLD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1822610</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1822610</link>
        <title><![CDATA[Effects of low-load blood flow restriction resistance training on lower limb morphology and functional performance in male college table tennis athletes: a three-arm randomized controlled trial]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hongjian Qu</author><author>Hong Wang</author><author>Lei Zhao</author><author>Rui Sun</author>
        <description><![CDATA[BackgroundHigh-load resistance training (HL-RT) is commonly utilized to enhance performance in competitive table tennis athletes. Low-load blood flow restriction training (BFR-RT) has emerged as an alternative approach under lower mechanical loads. Considering the importance of explosive power and rapid movements in table tennis, it is essential to evaluate how BFR-RT compares with traditional HL-RT in terms of strength, muscle hypertrophy, jump, and sprint performance. This study aimed to directly compare the effects of HL-RT and BFR-RT in male college table tennis players.Methods24 male college table tennis players were randomly divided into a BFR-RT group (n=8), HL-RT group (n=8), or control group (CON, n=8). Both BFR-RT and HL-RT groups performed RT, including squats, leg presses, and leg extensions, twice weekly for eight weeks. The BFR-RT group performed training at 30% of one-repetition maximum (1RM) with blood flow restriction, while the HL-RT group trained at 80% 1RM. The CON group engaged solely in regular table tennis training. Outcome measures—1RM, quadriceps cross-sectional area (QCSA), countermovement jump (CMJ) height, and 10-meter sprint time (T10m)—were assessed at baseline and post-intervention.ResultsSignificant group × time interaction effects were observed for 1RM, QCSA, CMJ height, and T10m (all p < 0.01). The HL-RT group demonstrated a significantly greater increase in 1RM than the BFR-RT group (20.5% vs. 12.9%, p < 0.01). In contrast, improvements in QCSA (+10.1% vs. +9.5%), CMJ height (+11.2% vs. +10.5%), and T10m (−5.1% vs. −4.8%) did not differ significantly between groups (p > 0.05). The CON group showed no significant changes in any variable.ConclusionHL-RT appears to be effective for promoting strength development, while low-load BFR-RT may serve as a potential alternative to traditional HL-RT for enhancing muscle hypertrophy, as well as jump and sprint performance in competitive table tennis athletes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1788389</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1788389</link>
        <title><![CDATA[From body composition to reflux esophagitis: an interpretable machine learning model based on CT-derived features]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tianyi Wang</author><author>Lu Chen</author><author>Yajie Li</author><author>Qi Zhang</author><author>Xilong Ou</author><author>Qin Lu</author>
        <description><![CDATA[BackgroundThe prevalence of gastroesophageal reflux disease (GERD) has been increasing in China. Previous studies link sarcopenia and visceral adiposity to GERD, but most models lack CT-based body composition data. This study aims to improve the identification of Reflux esophagitis (RE) by applying machine learning (ML) to third lumbar vertebra cross-sectional CT (L3-CT) images for quantitative analysis of muscle and fat mass.MethodsParticipants underwent comprehensive abdominal CT and gastroscopy. Body composition parameters, including skeletal muscle mass (SM), total fat mass (FM), fat-free mass (FFM), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and intermuscular adipose tissue (IMAT), were derived from the L3-CT images. Six ML models were developed: Random Forest (RF), Extreme Gradient Boosting (XGBoost), Logistic Regression (LR), K-Nearest Neighbors (KNN), Support Vector Machine (SVM), and Artificial Neural Network (ANN). Model performance was evaluated using the area under the receiver operating characteristic curve (AUROC). Shapley Additive exPlanations (SHAP) values were used to interpret the RF model.ResultsA total of 324 subjects were included, with 135 diagnosed with RE. The prevalence of low skeletal muscle mass index (low SMI) was significantly higher in the RE group compared to controls (52.6% vs. 36.5%, P < 0.01). The top six variables in the RF importance matrix were IMAT, visceral-to-subcutaneous fat ratio (VSR), age, VAT, SAT, and hiatal hernia. In the validation set, RF (AUC = 0.829, 95% CI: 0.731–0.905) and LR (AUC = 0.829, 95% CI: 0.736–0.909) demonstrated the best discriminative performance for RE. SHAP summary plots illustrated the positive and negative contributions of the top 20 features, while SHAP dependence plots explained the impact of individual variables on the RF model output.ConclusionThis study reveals a significant association between low SMI and RE. ML models identified key body composition factors, providing insights for targeted screening and clinical assessment.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1800941</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1800941</link>
        <title><![CDATA[HPRNet: a hierarchical pyramidal residual network for ECG arrhythmia classification]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiayan Huang</author><author>Miaomiao Huang</author><author>Hanling Zheng</author><author>Yongyi Xiao</author><author>Yolanda Bolea</author><author>Antoni Grau</author><author>Shaoye Luo</author>
        <description><![CDATA[Accurate classification of electrocardiogram (ECG) signals plays a critical role in the automated diagnosis of cardiac arrhythmias. However, ECG recordings are often non-stationary and susceptible to various types of noise, which makes robust feature extraction challenging for many existing deep learning models. To address these challenges, this paper proposes a hierarchical pyramidal residual network (HPRNet) for ECG arrhythmia classification. HPRNet incorporates a hierarchical pyramidal REB-based backbone (HRB) to capture multi-scale morphological characteristics of ECG signals. In the HRB, the temporal resolution is progressively reduced while the number of feature channels is gradually increased, allowing the network to effectively learn multi-scale ECG representations. Furthermore, a multi-level pruning optimization (MLPO) strategy is incorporated, including network-level pruning and block-level pruning, to reduce redundant parameters and improve computational efficiency while preserving classification capability. Experiments on two public benchmark datasets show that HPRNet achieves superior performance compared with five representative methods on MIT-BIH, reaching an F1-score of 92.05%, while obtaining 91.98% on the INCART binary classification task with an average inference latency of 0.031 s. Moreover, visualization analysis highlights the intrinsic difficulty of distinguishing challenging beat classes, and ablation studies confirm the effectiveness of the proposed HRB and MLPO. These findings support the robustness of HPRNet for automated arrhythmia classification. The source code is publicly available at: https://github.com/jyanhuang/HPRNet-ECG.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1807587</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1807587</link>
        <title><![CDATA[Effectiveness of non-pharmacological therapies in complementary and alternative medicine on improving fatigue levels, oxidative stress, inflammation, and endocrine levels in animal models of chronic fatigue-like conditions: a systematic review and network meta-analysis]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Shumeng Ren</author><author>Jingyuan Wei</author><author>Shan Zhao</author><author>Linghua Li</author><author>Jingshi Zhang</author><author>Chaoqun Yan</author><author>Jun Wang</author>
        <description><![CDATA[ObjectiveTo systematically evaluate the effects of various complementary and alternative medicine (CAM) non-pharmacological therapies on fatigue levels, oxidative stress, inflammation, and endocrine indicators in chronic fatigue-like conditions animal models, and to rank the efficacy of these interventions.MethodsA computerized search was conducted across databases including PubMed, Cochrane Library, Embase, Web of Science, CNKI, Wanfang, VIP, and CBMdisc, to collect animal experiments on fatigue-like conditions treated with CAM non-pharmacological therapies published from the establishment of the databases to January 14, 2026. Two researchers independently screened the literature, extracted data, and assessed risk of bias. Stata 16.0 software was used for network meta-analysis, and SYRCLE’s risk of bias tool was employed to evaluate the quality of the included studies.ResultsA total of 77 studies involving nine types of CAM non-pharmacological therapies were included. In terms of improving fatigue levels, compared to the control group, electroacupuncture (MD = 347.00 s, 95% CI [144.70, 549.29]) and moxibustion (MD = 311.28 s, 95% CI [146.36, 476.20]) significantly prolonged exhaustive swimming time. In terms of improving oxidative stress damage, fire acupuncture (MD = -13.15 nmol/ml, 95% CI [-18.06, -8.24]), manual acupuncture (MD = -3.85 nmol/ml, 95% CI [-5.12, -2.58]), needle-pricking (MD = -11.43 nmol/ml, 95% CI [-16.54, -6.32]), and moxibustion (MD = -479.16 nmol/ml, 95% CI [-567.05, -391.27]) significantly reduced MDA levels. In terms of improving inflammatory damage, Tuina (MD = -552.03 pg/ml, 95% CI [-700.81, -403.25]) and electroacupuncture (MD = -156.59 pg/ml, 95% CI [-259.85, -53.34]) can significantly reduce the level of IL-1β. In terms of regulating endocrine, electroacupuncture (MD = -9.91 pg/ml, 95% CI [-14.77, -5.05]) and Tuina (MD = -16.96 pg/ml, 95% CI [-25.37, -8.55]) can significantly reduce the level of CRH.ConclusionNon-pharmacological therapies in complementary and alternative medicine have great potential in improving fatigue-related phenotypes, oxidative stress damage, inflammatory damage, and regulating endocrine levels in animal models of fatigue-like conditions. Future research should focus on developing animal models that better replicate the pathogenesis and core characteristics of CFS, and then extend them to randomized controlled trials involving CFS patients to verify the transformation potential.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420251177070.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1827919</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1827919</link>
        <title><![CDATA[Exercise-induced modulation of astrocyte in Alzheimer’s disease: mechanisms and therapeutic implications]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Lei Shi</author><author>Jiding Xie</author><author>Tianjiao Dai</author><author>Mingzheng Zhang</author><author>Taoshuo Yang</author><author>Limei Sheng</author><author>Qiguan Jin</author><author>Jingang Dai</author>
        <description><![CDATA[Alzheimer’s disease (AD) is characterized by extracellular amyloid-β (Aβ) deposition, tau pathology, and chronic neuroinflammatory responses, although the relative contribution of these processes varies across disease stage and patient population. Current pharmacological therapies provide limited symptomatic benefit or modest disease-slowing effects in selected populations, underscoring the need for safe and sustainable adjunctive interventions. Astrocytes are central regulators of synaptic homeostasis, metabolic support, vascular coupling, and perivascular solute clearance, and these functions are profoundly altered in AD. For heuristic purposes, reactive astrocytes are often described along an A1-like to A2-like spectrum, with the former associated with pro-inflammatory and neurotoxic programs and the latter with reparative and neurotrophic functions; however, emerging single-cell and spatial transcriptomic data indicate that astrocyte states in AD are heterogeneous and context dependent rather than strictly binary. Growing evidence, predominantly from preclinical studies, suggests that exercise may remodel astrocyte-associated inflammatory, metabolic, and clearance pathways, with potential benefits for AD-related pathology and cognition. In several rodent models, exercise has been associated with reduced expression of A1-like reactive markers, enhanced protective astrocyte-associated programs, improved astrocyte–neuron metabolic coupling, and better perivascular localization of aquaporin-4 (AQP4). These changes may contribute to reduced inflammatory signaling and more efficient clearance of Aβ and tau, although the extent to which AQP4-dependent perivascular clearance mechanisms mediate exercise benefits in humans remains uncertain. Here, we review current evidence on how exercise influences astrocyte biology in AD, distinguish preclinical from clinical findings, and discuss key translational modifiers—including exercise modality, disease stage, sex, and APOE genotype—to inform glia-aware therapeutic strategies and future exercise prescriptions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1791522</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1791522</link>
        <title><![CDATA[Clinical evidence of exercise intervention in improving adults with type 2 diabetes mellitus and frailty: a narrative literature review]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xiuli Mo</author><author>Zhengyu Duan</author><author>Weihong Zhang</author><author>Yongliang Jia</author>
        <description><![CDATA[BackgroundThe global aging process is accelerating with the increasing prevalence of diabetes mellitus in the elderly population. Frailty, a clinical syndrome closely related to age, is particularly prevalent in elderly with type 2 diabetes mellitus (T2DM). Previous studies indicated that some common mechanisms and exercise interventions may be an effective intervention for T2DM and frailty management.ObjectiveThis narrative literature review aimed to provide evidence to explore possible common mechanisms and the role of exercise in management of T2DM combined with frailty.MethodsPubMed was searched for mechanistic studies. PubMed and China National Knowledge Infrastructure were searched for randomized controlled trials (RCTs) exploring exercise for T2DM and frailty.ResultsMechanistic analysis on 33 studies identified overlapping pathophysiological pathways between T2DM and frailty including encompassing inflammaging, insulin resistance, β-cell dysfunction, mitochondrial impairment, and gut dysbiosis. Evidence synthesized from 20 RCTs demonstrates that multicomponent exercise interventions could reduce frailty, lower blood glucose levels, and improve muscle strength for patients with T2DM and frailty, potentially by modulating these shared pathways, and resistance training enhances insulin sensitivity and muscle synthesis via GLUT-4 upregulation and Akt/mTOR activation.ConclusionMulticomponent exercise and resistance training would be efficacy for elderly patients with T2DM and frailty through modulating the overlapping pathophysiological mechanisms.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1818589</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1818589</link>
        <title><![CDATA[The protective model of myofascial trigger points: a testable systems-level framework based on strain-repair mismatch]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Michael Strickland</author><author>Micheal J. Luera</author><author>Mandy E. Parra</author><author>Chris Riggs</author>
        <description><![CDATA[Myofascial trigger points (MTPs) are frequently identified in clinical practice, yet their underlying physiology remains conceptually fragmented across biochemical, mechanical, and neurophysiological domains. Commonly reported features, including spontaneous electrical activity, increased stiffness, nociceptive sensitization, hypoxia, and elevated inflammatory mediators, are well documented but are not consistently interpreted within established frameworks of tissue stress and repair biology. This paper proposes a systems-level integrative framework, the Protective Model of Myofascial Trigger Points, which conceptualizes MTPs as localized tissue responses emerging when cumulative mechanical strain exceeds local repair capacity. Within this model, increased stiffness, sustained motor endplate activity, nociceptive sensitization, and localized neuroimmune signaling are interpreted as coordinated responses to strain–repair imbalance rather than independent pathological abnormalities. Variability in clinical presentation, including atent and active classifications, is proposed to reflect differences in the magnitude and duration of mechanical overload rather than biologically distinct entities, with persistent MTPs representing indicators of unresolved load–recovery mismatch. Eight falsifiable predictions are outlined, addressing load modification, recurrence patterns, elastographic stiffness, electromyographic behavior, biochemical signatures, and temporal resolution dynamics, providing explicit criteria for empirical testing. By situating MTP-associated phenomena within established principles of tissue injury, repair, and neuromuscular stress physiology, the Protective Model offers a coherent framework to guide systematic experimental investigation of MTP formation, persistence, and resolution.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1822139</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1822139</link>
        <title><![CDATA[From homeostasis to pathology, organelle-specific autophagy in skeletal muscle: a PRISMA-ScR scoping review]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Chunxiao Wang</author><author>Guanghua Liu</author><author>Changsheng Guo</author><author>Qi Li</author><author>Feixiao Wang</author><author>Ming Zhang</author>
        <description><![CDATA[BackgroundAs the largest metabolic organ in the human body, skeletal muscle relies on the structural and functional integrity of its organelles for cellular viability and responsiveness. Organelle-specific autophagy, a major subtype of autophagy encompassing mitophagy, pexophagy, reticulophagy (ER-phagy), ribophagy, lysophagy, and nucleophagy, has been reported to exert a protective role in skeletal muscle by selectively eliminating damaged organelles and maintaining cellular homeostasis.ObjectiveThis scoping review aims to systematically map the current literature on organelle-specific autophagy in skeletal muscle, clarifying the molecular mechanisms, physiological and pathological roles, and research gaps for the six types of organelle-specific autophagy.MethodsFollowing the PRISMA-ScR guidelines and the Joanna Briggs Institute framework, we searched PubMed, Embase, Web of Science, and Cochrane Library up to 21 March 2026 using keywords for skeletal muscle combined with mitophagy, pexophagy, ER-phagy, ribophagy, lysophagy, and nucleophagy. Studies involving humans, mice, rats, or skeletal muscle cells were included.ResultsAmong 113 included studies, human studies accounted for 15%, animal models 56%, and skeletal muscle cell lines 29%. By autophagy type, mitophagy dominated (87%, 98 studies), reticulophagy and lysophagy each accounted for 4% (five studies each), and lysophagy, pexophagy, ribophagy, and nucleophagy together comprised less than 5%. Regarding evidence level, among 24 human studies, 18 (75%) were cross-sectional observational studies or small case series (level 4), only three were randomized controlled trials (RCTs) (level 2b), and one was an individual RCT (level 1b); the overall evidence was predominantly low-level observational, with a lack of high-quality interventional clinical trials. For autophagic flux methodology, 53% of studies performed dual detection of LC3B and p62, 17% used lysosomal inhibitor blocking experiments, 64% used transmission electron microscopy (TEM) or tandem fluorescent probes, 23% combined bidirectional verification of autophagic function, and 18% examined intervention reversibility. Among 88 animal studies, low risk of bias (RoB) was found in 14 (16%), moderate RoB in 43 (49%), and high RoB in 30 (35%). For 46 cell experiments assessed by five self-established criteria, 83% used TEM to confirm autophagosomes, 28% used lysosomal inhibitors to validate flux, 72% used gene knockout/knockdown to verify mechanisms, 91% used skeletal muscle-derived cell lines, and 41% performed multi-time-point dynamic autophagy detection.ConclusionsCurrent research is severely lacking in nonmitophagy mechanisms, standardized dynamic flux assays, and high-quality clinical studies. Furthermore, systematic investigations of sex differences and muscle fiber type specificity are persistently absent, constraining the development of precise intervention strategies. Future efforts should strengthen multiorganelle autophagy network research and clinical translation to provide new targets for preventing and treating skeletal muscle disorders.]]></description>
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