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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>
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        <pubDate>2026-08-14T00:05:02.439+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1852707</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1852707</link>
        <title><![CDATA[Sternocleidomastoid muscle morphology is independently associated with neck strength and endurance in athletes and para-athletes]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sandra Rozenstoka</author><author>Elena Comadran de Barnola</author><author>Santa Kauzena</author><author>Gundega Akuratere</author><author>Zinta Galeja</author><author>Daira Deicmane</author>
        <description><![CDATA[BackgroundNeck functional capacity is clinically relevant in sports medicine for performance support, screening, and injury prevention in sports characterized by acceleration, contact, and sustained precision demands. Ultrasound can quantify local muscle morphology and may improve interpretation of neck performance beyond crude anthropometry (e.g., neck girth) and global strength indicators.ObjectiveTo determine whether sternocleidomastoid (SCM) cross-sectional area (CSA) and neck anthropometry are associated with neck function (strength, endurance, range of motion), and whether SCM morphology explains function beyond age, BMI, general strength (handgrip), and sport-domain context in a male cohort of athletes, para-athletes, and physically active controls.MethodsCross-sectional comparative study (n=195 men) including athletes across sport domains, para-athletes, and controls. Outcomes were isometric neck strength (flexor and extensor), neck flexor endurance, and active neck ROM. SCM CSA was assessed by standardized musculoskeletal ultrasound; neck girth served as an anthropometric comparator. Analyses included Pearson correlations and adjusted linear regression models controlling for age and BMI. Explanatory value beyond general strength was evaluated by adding handgrip strength, and independence from sport-domain context by adding sport domain as a covariate.ResultsSCM CSA correlated positively with flexor strength (r=0.34, p<0.001), extensor strength (r=0.25, p<0.001), and flexor endurance (r=0.28, p<0.001), and showed a weak inverse association with extension ROM (r=−0.17, p=0.017). In adjusted models (age, BMI), SCM CSA was independently associated with flexor strength (β=1.32 kg per cm²; p<0.001) and flexor endurance (β=0.53 min per cm²; p<0.001), but not extensor strength. SCM CSA remained associated with flexor strength and endurance after adjustment for handgrip strength and sport domain. Additional within- versus between-domain analysis supported a within-domain SCM association for flexor strength and endurance rather than a purely between-domain aggregation effect. Neck girth did not provide comparable independent explanatory value for strength or endurance outcomes.ConclusionsSCM morphology is independently associated with neck performance, particularly flexor strength and endurance. Ultrasound-based SCM assessment provides measurable but limited additional information beyond neck girth, handgrip strength, and sport-domain context. These findings support its cautious use as an adjunct measure alongside objective cervical functional testing, rather than as a stand-alone screening tool.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1835158</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1835158</link>
        <title><![CDATA[Quantifying gravity-dependent and gravity-independent ventilation distribution by hyperpolarized 129Xe MRI in restrictive and airway diseases]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kunyu (Kimi) Du</author><author>David Mummy</author><author>Robert Tighe</author><author>Loretta Que</author><author>Bastiaan Driehuys</author><author>Yuh-Chin T. Huang</author>
        <description><![CDATA[RationaleHyperpolarized 129XeMRI can be used to quantify ventilation heterogeneity. The radio-frequency bias correction method has been shown to preserve the physiological ventilation gradient in healthy individuals. In this study, we tested the hypothesis that idiopathic pulmonary fibrosis (IPF) and obese asthma would have worsened gravity-dependent and gravity-independent ventilation distribution gradients.MethodsWe analyzed 3-dimensional HPXeMRI ventilation images from our databank using both the conventional N4ITK and the RF bias correction methods. We divided the lung regions equally into apical/middle/basal compartments (gravity independent) and anterior/middle/posterior compartments (gravity dependent). We averaged the ventilation signals within each compartment and calculated ventilation differences (ΔV˙) between basal and apical compartments (ΔV˙B-A) and between posterior and anterior compartments (ΔV˙P-A).ResultsWe included 10 younger (age: 23 ± 3 years), 10 older healthy subjects (age: 62 ± 7 years), 30 patients with idiopathic pulmonary fibrosis (IPF) (age: 74 ± 6 years) and 10 obese asthma patients (age: 40 ± 10 years). Younger and older healthy subjects had greater ventilation in the basal compartment (ΔV˙B-A=0.20 ± 0.17 and 0.11 ± 0.15 respectively) and the posterior compartment (ΔV˙P-A=0.08 ± 0.06 and 0.13 ± 0.16 respectively). Twenty-five IPF patients had positive ΔV˙B-A (0.17 ± 0.08) and ΔV˙P-A (0.11 ± 0.07). Five patients had negative ΔV˙P-A (-0.17 ± 0.09, p<0.0001) with three also having negative ΔV˙B-A (-0.04 ± 0.01, p=0.049). Six obese asthma patients had positive ΔV˙P-A (0.13 ± 0.08). Four patients had negative ΔV˙P-A (-0.11 ± 0.15, p=0.017) with two also having negative ΔV˙B-A (-0.17 and -0.09).ConclusionsWith the RF depolarization bias correction method, we showed physiological ventilation gradients in healthy subjects and detected abnormal (inverse) ventilation gradients in a subgroup of patients with IPF and obese asthma, despite low ventilation defect percentage (VDP), and mild or no spirometry abnormalities. The abnormal ventilation gradients may reflect the heterogeneity of the disease that may be associated with different treatment response and prognosis. These will need to be explored in future studies with a different design including larger populations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1889633</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1889633</link>
        <title><![CDATA[Beyond the apnea–hypopnea index in COPD–OSA overlap syndrome: a mechanism-informed framework for nocturnal oxygenation and ventilation]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xize Zhang</author><author>Xue Han</author><author>Shaodan Hu</author><author>Li Shi</author>
        <description><![CDATA[BackgroundIn chronic obstructive pulmonary disease (COPD)–obstructive sleep apnea (OSA) overlap syndrome, the apnea–hypopnea index (AHI) confirms and grades OSA but does not fully explain nocturnal hypoxemia or carbon dioxide retention.ObjectiveWe propose a post-diagnostic, mechanism-informed framework for interpreting nocturnal oxygenation and ventilation after both COPD and OSA have been objectively confirmed.MethodsThis targeted narrative review synthesized PubMed literature and major guideline sources through 20 May 2026. Reporting followed established narrative-review quality principles, and evidence use was categorized as guideline-supported, direct overlap-syndrome observational evidence, indirect COPD or OSA evidence, or physiological inference.ResultsThe framework separates three baseline mechanisms: event-related upper-airway obstruction, sustained low-baseline oxygenation or gas-exchange impairment, and sleep-related hypoventilation or chronic hypercapnia. Residual hypoxemia after optimized positive airway pressure or noninvasive ventilation is treated as a post-treatment reassessment scenario rather than a baseline phenotype. Suggested core reporting includes the AHI measurement method, hypopnea rule, oxygen desaturation threshold, time spent below specified oxygen saturation thresholds, mean and verified minimum oxygen saturation, rapid eye movement and supine exposure, treatment context, oximetry settings, and carbon dioxide monitoring when indicated.ConclusionAHI remains essential for diagnosing OSA, but oxygenation and ventilation in overlap syndrome may be better interpreted by mechanism. The proposed framework is an interpretive and reporting scaffold rather than a treatment algorithm, and its clinical utility, reproducibility, and prognostic value require prospective validation in well-characterized cohorts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1695483</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1695483</link>
        <title><![CDATA[Psychological monitoring in isolated, confined, and extreme environments: promise and challenges of ecological momentary assessment]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Clara Richard</author>
        <description><![CDATA[Personnel in Isolated, Confined, and Extreme (ICE) environments face unique psychological stressors that can compromise performance, safety, and mission success. Traditional psychological monitoring approaches, predominantly retrospective questionnaires and clinical interviews, may inadequately capture the dynamic nature of psychological adaptation in these demanding contexts. This mini-review examines the potential role of Ecological Momentary Assessment (EMA) as part of a comprehensive approach to psychological monitoring in ICE environments. We review current monitoring practices across spaceflight, polar, submarine, and remote field operations, and evaluate emerging technologies including EMA, wearable sensors, and digital biomarkers. While EMA offers theoretical advantages through real-time data collection and reduced recall bias, implementation faces substantial obstacles including technological constraints, participant burden, cultural considerations, and validation challenges. Limited empirical evidence suggests that hybrid approaches combining multiple assessment modalities may be most promising for operational implementation. We propose a framework for developing next-generation psychological monitoring systems that balance scientific rigor with operational feasibility, emphasizing environment-specific validation and the inherent sample-size constraints of ICE settings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1869905</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1869905</link>
        <title><![CDATA[Nutraceutical potential of prekese (Tetrapleura tetraptera) fruit extract: synergizing growth performance, oxidative stability, and economic viability in Nile tilapia (Oreochromis niloticus)]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Samuel B. Umma</author><author>Yetunde E. Agbeja</author><author>Raphael Z. Agu</author><author>Bilal A. Paray</author><author>Eijaz A. Bhat</author><author>Robert M. Iorhiin</author>
        <description><![CDATA[This study evaluated the effects of dietary Prekese (Tetrapleura tetraptera) fruit extract (PFE) on the growth, haemato-biochemical profile, antioxidant status, and economic efficiency of Nile tilapia (Oreochromis niloticus) fingerlings. Five isonitrogenous (35% crude protein) and isolipidic diets were formulated with graded PFE levels: 0.0 (control), 5.0, 10.0, 15.0, and 20.0 g/kg. Fish (5.20 ± 0.05 g) were fed twice daily to satiety for 60 days. Gas chromatography- mass spectral analysis of PFE identified 29 compounds, primarily linoleic (20.46%), myristic (14.53%), and oleic (12.49%) acids. Dietary PFE significantly enhanced growth in a dose-dependent manner (P< 0.05). The 20.0 g/kg inclusion yielded a higher final body weight (35.04 g) and weight gain (571.97%), a 121.9% increase over the control. Polynomial contrasts identified 20.0 g/kg as the upper limit for growth and feed efficiency in this study. Haematologically, PFE increased red and white blood cell counts, suggesting improved hematopoietic and immune function. Serum biochemistry showed elevations in aspartate aminotransferase, alanine aminotransferase, and alkaline phosphate at 15.0 – 20.0 g/kg PFE, though within physiological ranges. Importantly, PFE supplementation significantly reduced oxidative stress, evidenced by decreased superoxide dismutase, catalase, and malondialdehyde levels (P< 0.05), indicating enhanced systemic antioxidant capacity. Economic analysis revealed that despite a 96.73% increase in feed cost, 20.0 g/kg PFE increased net profit per fish by 136.8% and significantly improved the benefit-cost ratio. In conclusion, PFE is a viable nutraceutical for Nile tilapia. At a higher inclusion of 20.0 g/kg, PFE boosts growth, mitigates oxidative stress, and maximizes economic returns in sustainable aquaculture.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1863045</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1863045</link>
        <title><![CDATA[Associations of resting plasma adenosine triphosphate, antioxidant capacity, and oxidative stress biomarkers with cardiorespiratory fitness in combat sport athletes: a pilot cross-sectional study]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jinling Huang</author><author>Lüfeng Miao</author><author>Yangjun Liu</author>
        <description><![CDATA[Background and study aimCombat sports involve repeated high-intensity efforts separated by short recovery periods, creating substantial demands on aerobic function and recovery. However, little is known about whether resting metabolic and redox-related biomarkers are associated with cardiorespiratory fitness in combat sport athletes. This pilot cross-sectional study examined the associations of resting plasma adenosine triphosphate (ATP), total antioxidant capacity (T-AOC), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPX) with maximal oxygen uptake (VO2max) and relative VO2max.Materials and methodsResting venous blood samples were collected once after at least 8 h of fasting and before a graded treadmill exercise test; no post-exercise samples were obtained. Cardiorespiratory fitness was evaluated using a graded treadmill exercise test, with VO2max, relative VO2max, respiratory exchange ratio, exercise heart rate, and exercise duration recorded. Statistical analyses included descriptive statistics, Spearman and partial correlations, multiple linear regression, and decision tree modeling, with additional robustness checks using Bootstrap confidence intervals and permutation tests.ResultsTwenty-one combat sport athletes were included. Mean VO2max was 2937.19 ± 643.93 mL/min, and mean relative VO2max was 42.38 ± 8.80 mL/kg/min.s. T-AOC was strongly positively correlated with both VO2max (Spearman’s ρ = 0.723, p < 0.01) and relative VO2max (Spearman’s ρ = 0.678, p < 0.01), and these associations remained significant in partial correlation analyses adjusted for age, sex, height, and body mass. MDA was moderately correlated with relative VO2max (ρ = 0.454, p < 0.05). In multivariable models, T-AOC was the only biomarker significantly associated with VO2max and, together with MDA, was associated with relative VO2max. Partial correlation, decision tree, Bootstrap, and permutation analyses consistently supported T-AOC as the most stable signal across analytical approaches, suggesting that its association with cardiorespiratory fitness was not model-specific. By contrast, ATP, SOD, and GPX showed limited independent explanatory value.ConclusionsCombat sport athletes in this pilot sample demonstrated high cardiorespiratory fitness. In this pilot sample, resting T-AOC showed the most consistent positive association with VO2max and relative VO2max, while MDA showed an exploratory association with relative VO2max. Because biomarkers were measured once before exercise, these results represent baseline cross-sectional associations and do not establish causality, acute exercise responses, or recovery status. Larger longitudinal studies are needed to confirm these findings.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1833719</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1833719</link>
        <title><![CDATA[Study-level age patterns in cardiometabolic response to high-intensity interval training among adults with overweight or obesity: a systematic review and meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Ping Lin</author><author>Gang Xu</author><author>Xia Li</author>
        <description><![CDATA[BackgroundHIIT is a time-efficient exercise strategy for adults with overweight or obesity, but trial findings are heterogeneous and whether age independently modifies cardiometabolic response remains uncertain.MethodsPubMed, Embase, the Cochrane Library, and Web of Science were searched from inception to December 2025. Random-effects meta-analyses estimated weighted mean differences for SBP and DBP in mmHg and standardized mean differences for lipid and anthropometric outcomes, with 95% confidence intervals and prediction intervals where available. Additional Stata analyses included funnel plots, Egger tests for all six outcomes, trim-and-fill analysis for BW and BMI, exploratory study-level meta-regression using continuous mean age and intervention duration, and GRADE assessment.ResultsNineteen trials involving 570 participants were included. HIIT was associated with reductions in SBP, DBP, TG, BW, and BMI and an increase in HDL-C; overall heterogeneity was moderate to substantial (I² range, 46.77%–87.07%). Egger tests suggested small-study effects for BW and BMI, but not SBP, DBP, HDL-C and TG. Trim-and-fill imputed no studies for BW and BMI. Mean age was associated with TG effects and duration was associated with HDL-C effects in univariable models. Certainty of evidence was low for SBP and very low for the remaining outcomes.ConclusionHIIT was associated with favorable average cardiometabolic changes in adults with overweight or obesity, but substantial heterogeneity, low-to-very-low certainty and possible small-study effects findings require cautious interpretation. The available evidence supports the hypothesis that trial-level mean age may be associated with differential responses, rather than proving age as a definitive individual-level effect modifier.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420261279689.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1903705</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1903705</link>
        <title><![CDATA[Effects of exercise interventions on fall-related functional performance in postmenopausal women with osteoporosis or low bone mass: a systematic review and meta-analysis with an exploratory analysis of reported consistency with ACSM recommendations]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Shixian Li</author><author>Neng Pan</author><author>Lulu Niu</author><author>Min Yao</author><author>Shuai Zhao</author><author>Chenming Liu</author><author>Dongying Li</author>
        <description><![CDATA[ObjectiveTo evaluate the effects of exercise on fall-related functional performance in postmenopausal women with osteoporosis or low bone mass and to explore whether intervention effects differed according to the reported consistency of the exercise prescription with American College of Sports Medicine (ACSM) recommendations.MethodsSix electronic databases were searched from inception to 3 May 2026. Immediate post-intervention mean differences for the Timed Up and Go (TUG) test, Berg Balance Scale (BBS), and 30-second sit-to-stand test (30STS) were pooled using inverse-variance random-effects models with restricted maximum likelihood estimation, Hartung–Knapp inference, and prediction intervals. Prespecified exercise-prescription components were classified as meeting, unclear or unreported, or not meeting the ACSM criteria.ResultsEighteen trials contributed 21 intervention arms. Exercise improved TUG performance (MD = −1.57 s, 95% CI −2.52 to −0.63; I² = 88.5%) and 30STS performance (MD = 3.88 repetitions, 95% CI 1.93 to 5.83; I² = 87.6%). The estimated effect on BBS was highly uncertain (MD = 3.37 points, 95% CI −2.68 to 9.43; I² = 83.6%). Formal tests found no evidence of a difference between the high and low/uncertain reported-consistency groups for TUG (p = 0.733), BBS (p = 0.985), or 30STS (p = 0.262). Prediction intervals crossed the null for all three outcomes. Certainty of evidence was low for TUG and 30STS and very low for BBS.ConclusionExercise may improve functional mobility and repeated sit-to-stand performance, whereas the effect on BBS remains highly uncertain. The available analyses do not demonstrate superior effects for interventions with higher reported consistency with ACSM recommendations; the subgroup findings are exploratory.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261353752, identifier CRD420261353752.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1912219</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1912219</link>
        <title><![CDATA[Toward a neuroergonomic understanding of spatial disorientation]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Jerome Carriot</author><author>Isabelle Mackrous</author><author>Pascale Brochu</author><author>Simon Corcos</author><author>Marc-Antoine Pelletier</author><author>Maurice J. Chacron</author>
        <description><![CDATA[Despite decades of research, spatial disorientation, which is the incorrect perception of one’s orientation relative to gravity, remains one of the leading causes of aviation mishaps. In this mini-review, we highlight the role of the vestibular system towards generating disorientation. Specifically, in the absence of other cues, the brain is incapable of distinguishing between the acceleration caused by a static force such as gravity from that experienced in an accelerating vehicle, which leads to an ambiguity leading to acceleration being wrongly interpreted as tilts. Finally, because vestibular signals interact with autonomic, respiratory, and vascular regulation, we propose multimodal physiological monitoring as a testable research strategy for characterizing unstable self-motion estimation, while emphasizing that percept-specific detection requires controlled labeling and prospective validation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1905092</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1905092</link>
        <title><![CDATA[Homocysteine promotes ferroptosis through NCOA4-mediated ferritinophagy in THP-1 macrophages]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yu Yang</author><author>Weiya Zhang</author><author>Dandan Huang</author>
        <description><![CDATA[IntroductionAs an independent risk factor for atherosclerosis (AS), hyperhomocysteinemia (HHcy) exerts its pathogenic effects primarily through the induction of macrophage ferroptosis. As a selective autophagic process mediated by nuclear receptor coactivator 4 (NCOA4), ferritinophagy directly influences ferroptosis via its regulation of cellular iron balance. However, whether homocysteine (Hcy) regulates macrophage ferroptosis through ferritinophagy remains unclear.MethodsHuman acute monocytic leukemia (THP-1) cells were differentiated into macrophages and subsequently treated with Hcy. Ferroptosis was assessed by measuring glutathione (GSH) levels, reactive oxygen species (ROS), Fe²⁺ content, and mitochondrial morphology. Protein expression of NCOA4, FTH1, and GPX4 was examined, and GPX4 methylation was evaluated. The involvement of ferritinophagy was further verified using the ferroptosis inhibitor ferrostatin‑1 (Fer‑1) and the inducer Erastin. Activation of the IL‑6/STAT3 signaling pathway was also examined, along with its reciprocal regulation with ferroptosis.ResultsHcy treatment promoted ferroptosis in THP‑1 macrophages, as indicated by decreased GSH levels, increased ROS and Fe²⁺ levels, and characteristic mitochondrial morphological changes. Hcy also enhanced GPX4 methylation, resulting in reduced GPX4 expression. Mechanistically, Hcy upregulated NCOA4 and downregulated FTH1, suggesting activation of NCOA4‑mediated ferritinophagy; these effects were reversed by Fer‑1 and augmented by Erastin. In addition, Hcy activated the IL‑6/STAT3 pathway, and its crosstalk with ferroptosis was confirmed by the reciprocal modulation with Fer‑1 and Erastin.DiscussionCollectively, our study indicates that Hcy promotes ferroptosis in THP-1 macrophages through NCOA4-mediated ferritinophagy, and the IL-6/STAT3 signaling pathway plays a key role in this process. Therefore, targeting Hcy may represent a potential treatment strategy for AS.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1867073</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1867073</link>
        <title><![CDATA[Optimal exercise dose for resistance training to improve HbA1c levels in overweight and obese patients with type 2 diabetes: a systematic review of randomized controlled trials and a Bayesian network meta-analysis]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Huarui Li</author><author>Shidong Yang</author><author>Xuefeng Wang</author><author>Zhiwei Wang</author><author>Wei Zhang</author><author>Xuehai Zhang</author><author>Shouliang Huang</author>
        <description><![CDATA[BackgroundThe high prevalence of overweight or obesity in patients with type 2 diabetes (T2DM) is strongly associated with impaired quality of life and an increased risk of long-term complications. Poor glycemic control remains a fundamental clinical challenge in this population. Although resistance training (RT) is an effective intervention for improving HbA1c levels, the optimal dosing parameters​ (e.g., frequency, intensity, volume) have not been systematically established. Therefore, this meta-analysis aimed to investigate the dose-response relationships​ between various RT regimens and HbA1c reduction in overweight or obese individuals with T2DM.MethodsThis systematic review and network meta-analysis, conducted by searching PubMed, Embase, and the Cochrane Library, included randomized controlled trials on resistance training in patients with T2DM who were overweight or obese, conducted from the inception of the databases through January 19, 2026. Comprehensive data extraction covered training dose, resistance training protocols, participants’ demographic characteristics, and study duration.ResultsA total of 10 studies involving 633 participants (mean age: 60.03 ± 7.77 years; mean BMI: 30.69 ± 6.64; Male: 32.7%) were included in this study. The results of our network meta-analysis showed that resistance training variables (e.g., frequency, intensity, period, and training volume) were effective in improving HbA1c in overweight or obese patients with T2DM. Among them, the effective dose range for frequency of resistance training was 3 times/week, resistance training intensity was 30-62%, resistance training period was 17–23 weeks, resistance training time was 45 minutes per session, resistance training exercises was 10 exercises per set, resistance training repetitions was 13–18 reps, resistance training sets was 2–4 sets, resistance training volume was 1000–2100 reps per week. the analysis suggested a potential optimum around of resistance training to improve HbA1c in overweight or obese patients with T2DM is 3 times/week (MD=-0.35, 95% CrI [-0.62, -0.08]), 44% 1RM (MD=-0.41, 95% CrI [-0.74, -0.08]), 23 weeks (MD = −0.35, 95% CrI [−0.68, −0.02]), 45min (MD = −0.32, 95% CrI [−0.62, −0.01]), 10 exercises (MD = −0.32, 95% CrI [−0.63, −0.01]), 18 reps (MD=-0.38; 95% CrI [-0.74, -0.02]), 3 sets (MD=−0.36, 95% CrI [−0.63, −0.10]), 1,500 reps/week (MD = −0.51, 95% CrI [−0.86, −0.15]).ConclusionResistance training effectively improvesHbA1c in overweight or obese patients with T2DM. A recommended 23-week program includes 3 sessions per week at 44% 1RM, 45min per session, featuring 10 exercises per set, 3 sets, and 18 repetitions per exercise, totaling up to 1500 reps weekly.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420261341070.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1910107</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1910107</link>
        <title><![CDATA[Prostaglandin E2 modulates contractility of mouse bladder smooth muscle cells]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Rok Šumak</author><author>Igor But</author><author>Andraž Stožer</author><author>Jurij Dolenšek</author><author>Tamara Serdinšek</author>
        <description><![CDATA[BackgroundProstaglandin E2 (PGE2) is an important local mediator in the urinary bladder, where it contributes to the regulation of detrusor excitability and is implicated in pathological conditions such as overactive bladder. Although previous studies have shown that exogenous PGE enhances bladder contractile activity, its effects on calcium signaling in individual detrusor smooth muscle cells (SMCs) and its interaction with cholinergic stimulation remain incompletely understood.MethodsAcute detrusor tissue slices were prepared from adult female NMRI mice and loaded with the calcium indicator Calbryte 520 AM. Confocal calcium imaging was used to quantify spontaneous and stimulated intracellular Ca2+ activity in individual SMCs. The effects of PGE2 alone and in combination with increasing concentrations of carbachol (CCh) were assessed by measuring oscillation active time, frequency, and duration of Ca²+ events. Tissue contractions were evaluated by visual inspection of image sequences.ResultsPGE2 increased spontaneous Ca2+ activity in detrusor SMCs, as reflected by a significant increase in active time due to increases in oscillation frequency, while oscillation duration remained unchanged. PGE2 also recruited additional SMCs into an active state and induced localized tissue contractions. In the presence of PGE2, lower concentrations of CCh evoked greater Ca²+ activity than under control conditions, suggesting that PGE2 increased baseline detrusor excitability and reduced the additional cholinergic input required to evoke detectable Ca²+ activity. This effect was again mediated predominantly by an increase in oscillation frequency rather than duration. At the tissue level, PGE2 enhanced CCh-induced contractility and shifted generalized contractions to lower CCh concentrations.ConclusionsPGE2 acts as a local excitatory modulator of mouse detrusor smooth muscle, increasing spontaneous Ca2+ activity and sensitizing the tissue to cholinergic stimulation. These effects are associated primarily with frequency-based modulation of Ca2+ oscillations and may represent a cellular mechanism contributing to detrusor overactivity under conditions of increased prostaglandin signaling.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1833828</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1833828</link>
        <title><![CDATA[MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Virginie Joris</author><author>Dorothée Marchand</author><author>Thomas Metzinger</author><author>Laurent Dumas</author><author>Hrag Esfahani</author><author>Olivier Feron</author><author>Sandrine Horman</author><author>Chantal Dessy</author>
        <description><![CDATA[Among potential molecular mechanisms supporting cardiovascular homeostasis, miRNAs (miRs) represent interesting candidates. We recently highlighted that miR-199a controls the Nitric oxide synthase/nitric oxide (NOS/NO) pathway in the endothelium and showed that both mature strands of miR-199a are overexpressed in heart and vessels from a mouse model of hypertension. Here we investigated the fate of miR-199a in heart and vessels from mice developing physiological or pathological cardiac hypertrophy. Our working hypothesis is that alterations in cell phenotypes driven by changes in miR-199a abundance account for cardiac and/or vascular adaptation to increased workload in patho-physiological contexts. C57BL/6J mice were given access to voluntary dynamic wheel training during 22 weeks or underwent transverse aortic constriction (TAC) surgery. As a result, those mice respectively developed physiological and pathological cardiac hypertrophy. An opposite modulation of miR-199a-3p and miR-199a-5p expression was observed in vessels and heart from running vs TAC mice which correlated with opposite regulation of Retinobastoma1 (RB1) in cardiac tissue. We show that miR-199a-3p upregulation, by indirectly modulating CCAAT/enhancer binding protein (C/EBP)β, promotes cardiomyocyte hypertrophy in the pathological settings, while its repression by exercise drives metabolic adaptations associated with physiological remodeling. Interestingly, miR-199a-5p repression also directly target Sirtuin 1 (Sirt-1) and Peroxisome proliferator-activated receptor coactivator (PGC1)α Taken together, our findings indicate that both mature arms of miR-199a act in tandem to drive morphologic and metabolic adaptations encountered in physiological and pathological cardiac hypertrophy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1946734</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1946734</link>
        <title><![CDATA[Editorial: Insights in vascular physiology: 2025]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Luis A. Martinez-Lemus</author><author>Christopher Garland</author><author>Andrew P. Braun</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1892106</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1892106</link>
        <title><![CDATA[Metabolic and skeletal muscle dysfunctions correlate with fatigue behavior in an animal model of multiple sclerosis]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kody M. Moore</author><author>Marcella Whetsell</author><author>Lei Wang</author><author>Ethan M. Meadows</author><author>Amanda Stewart</author><author>Alan D. Mizener</author><author>Stuart A. Clayton</author><author>Lauren E. Rentz</author><author>Christa Lilly</author><author>John M. Hollander</author><author>Gangqing Hu</author><author>Emidio E. Pistilli</author><author>Edwin C.K. Wan</author>
        <description><![CDATA[Multiple sclerosis associated fatigue (MS fatigue) is one of the most common and troubling symptoms experienced by people with MS, but the cause of MS fatigue remains unknown. The nature of cognitive and physical exhaustion suggests that MS fatigue can be a metabolic disease that impacts energy demanding processes such as neuronal activity and skeletal muscle contraction. In this study, we investigated how autoimmune-mediated inflammation causes skeletal muscle atrophy and metabolic dysfunctions, which may contribute to MS fatigue. Using a relapsing-remitting model of experimental autoimmune encephalomyelitis (EAE), we found that disease manifestations substantially altered the metabolic activities of the mice over time. EAE decreased muscle mass and force production in both fast extensor digitorum longus (EDL) and slow soleus muscles but only increased the rate of fatigue in the EDL muscle. Gene expression analysis of the EDL muscle shows that genes related to cellular respiration and mitochondrial functions were significantly downregulated when EAE manifestations were the most severe, but the phenotype was reversed during disease remission. In addition, EAE-induced mice showed fatigue behavior during a maximal treadmill test. Surprisingly, this fatigue behavior was also observed with mice immunized with a CNS non-specific antigen, suggesting there are contributions from central nervous system-independent immune activation. To our knowledge, this is the first report to characterize skeletal muscle properties and fatigue behavior in mice following EAE induction.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1900140</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1900140</link>
        <title><![CDATA[Body mass index–related heterogeneity in diaphragm thickening fraction response to exercise training in stable chronic obstructive pulmonary disease]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yide Wang</author><author>Yidie Bao</author><author>Xinliao Deng</author><author>Hongxia Duan</author><author>Hui Li</author><author>Jiachi Zhang</author><author>Jian Li</author><author>Peijun Li</author><author>Xiaodan Liu</author>
        <description><![CDATA[BackgroundDiaphragmatic dysfunction contributes to exercise intolerance in COPD, but whether BMI shapes baseline function and response to exercise remains unclear. This secondary analysis characterized BMI-related diaphragmatic phenotypes and whether diaphragm thickening fraction (TFdi) links exercise training to functional improvement.MethodsData were analyzed from 103 patients with stable COPD in a completed 2×2 factorial randomized trial. Because no exercise-by-acupuncture interaction was detected for 4-week TFdi, participants were regrouped as exercise-exposed or non-exercise. Associations between BMI and baseline TFdi were assessed using restricted cubic splines and threshold models. Regression models estimated exercise effects on 4-week TFdi and 6-minute walk distance (6MWD), with BMI-stratified interaction and exploratory mediation analyses.ResultsBMI showed a nonlinear association with baseline TFdi, with an adjusted turning point at 23.7 kg/m². Below this threshold, BMI was positively associated with TFdi (β=0.05, 95% CI 0.03–0.08); above it, the association was negative (β=−0.05, 95% CI −0.07 to −0.03). Exercise was associated with higher 4-week TFdi (β=0.15, 95% CI 0.01–0.29) and longer 6MWD (β=59.61 m, 95% CI 10.65–108.57). The TFdi response was most pronounced at BMI ≥25.0 kg/m², with borderline interaction evidence. Exploratory mediation suggested TFdi partially mediated exercise-related 6MWD gains, particularly in this BMI group.ConclusionsThis study integrates BMI phenotyping, diaphragm ultrasound, and mediation analysis to show that diaphragmatic function and exercise-induced diaphragmatic adaptation in COPD are BMI dependent. BMI may help identify patients most likely to derive diaphragmatic benefit from rehabilitation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1908766</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1908766</link>
        <title><![CDATA[Reactive oxygen species regulation of ferroptosis, autophagy, apoptosis, and immunogenic cell death in cancer]]></title>
        <pubdate>2026-08-10T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Seema Kumari</author><author>Sudhir Kumar Rai</author>
        <description><![CDATA[Reactive oxygen species (ROS) are produced during metabolism through mitochondrial oxidative phosphorylation and NADPH oxidase activity. In cancer, ROS exhibit a paradoxical, concentration-dependent dual role. At low to moderate levels, ROS promote tumor cell survival, EMT, and metastasis, and at high levels, ROS overwhelm antioxidant defenses and induce regulated cell death (RCD); ferroptosis, autophagy, apoptosis, and immunogenic cell death (ICD) have emerged as significant ROS-dependent targets in cancer therapy. This review summarizes recent advances in ROS-controlled ferroptosis, autophagy, apoptosis, and ICD, emphasizing the roles of the GPX4/SLC7A11, AMPK/mTORC1/Beclin-1, Bcl-2/Bax/cytochrome c, and damage-associated molecular pattern (DAMP)-mediated signal cascade, their crosstalk, and therapeutic potential for targeting tumor redox vulnerabilities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1876988</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1876988</link>
        <title><![CDATA[Propofol for depression: mechanisms and therapeutic potential]]></title>
        <pubdate>2026-08-10T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Dan Yu</author><author>Ye Liao</author><author>Jie Li</author><author>Aiqiu Zheng</author><author>Xin Meng</author><author>Shumin Gong</author><author>Can Li</author><author>Kunwei Wu</author>
        <description><![CDATA[Propofol, one of the most widely used intravenous anesthetics, is undergoing a transformative identity shift from a purely surgical agent to a potential therapeutic tool for neuropsychiatric disorders. This review synthesizes current evidence on the emerging field of propofol therapeutics, with a focus on its rapid antidepressant, anti-anhedonia, and anxiolytic effects. We first examine preliminary clinical evidence from open-label studies suggesting that propofol may produce dose-dependent mood-elevating effects in treatment-resistant depression; however, this evidence remains limited by small sample sizes and lack of large controlled trials. Next, we explore putative mechanisms, including GABAA receptor modulation, dopamine transporter inhibition, BDNF/TrkB signaling, and network-level reorganization of the default mode network and sleep architecture. We then compare propofol with other anesthetic agents possessing antidepressant properties, particularly ketamine, highlighting their distinct receptor targets, efficacy profiles, and safety considerations. Finally, we discuss major challenges including optimal dosing strategies, tolerance with repeated administration, long-term safety concerns, and implementation barriers. Despite these challenges, propofol represents a promising candidate for anesthetic repurposing in psychiatry, offering a mechanistically distinct alternative to ketamine that targets both GABAergic and dopaminergic systems with a well-established clinical safety profile for surgical anesthesia.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1830128</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1830128</link>
        <title><![CDATA[Spatial disorientation and countermeasure training for next-generation aircraft: a review and recommendations]]></title>
        <pubdate>2026-08-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>John Jong-Jin Kim</author><author>Ramy Kirollos</author>
        <description><![CDATA[Spatial disorientation (SD) is the most common cause of human error in military aircraft incident reports over the last few decades. Vestibular SD typically occurs when the vestibular (balance) system cannot distinguish between acceleration from gravity and from the aircraft. Current and next-generation fighter aircraft (e.g., F-35) expose pilots to unprecedented acceleration forces, possibly amplifying SD frequency and severity. Therefore, research investigating SD and countermeasures in modern fighter aircraft is becoming increasingly important. The main objective of this review paper was to assess modern technologies that can be used in counter-SD training and provide directions for future research on SD training. To accomplish this objective, we reviewed a total of 118 books, technical reports, and scientific papers to examine the current state of knowledge in SD and countermeasures used in military aviation. Past literature mostly focused on the subjective pilot experience without considering the human sensory system as the root cause. In addition, studies investigating modern technologies (e.g., virtual reality head-mounted display) in SD countermeasure training were limited. In this review, we define and evaluate the common SD illusions and their causes based on the available scientific literature. Then, we examine successful contemporary SD countermeasure training methods and tools currently used. Finally, we provide recommendations for future SD research focusing on vestibular SD countermeasure training given recent technological advancements covered. Our recommendations include the exploration of various combinations of artificial vestibular stimulation, virtual reality, and centrifuge as viable SD training methods. We also provide potential solutions to evaluate SD countermeasures effectively and objectively.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1886678</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1886678</link>
        <title><![CDATA[Association between imbalanced lower extremity muscle quality and the development of knee osteoarthritis: a Systematic Review and meta-analysis]]></title>
        <pubdate>2026-08-10T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Zhi Liang</author><author>Guozhi Yang</author><author>Jiawen Zhang</author><author>Biao Tan</author><author>Yawei Dong</author><author>Yan Yan</author>
        <description><![CDATA[BackgroundKnee osteoarthritis (KOA) is the most prevalent musculoskeletal degenerative disease worldwide. Periarticular muscle abnormalities are considered closely associated with its pathogenesis, yet the relationships between various muscle parameters and KOA remain controversial.ObjectiveTo clarify the correlations of thigh muscle quantity, muscle quality, and muscle strength with KOA through a systematic review and meta-analysis, and to provide evidence-based support for the risk screening and early intervention of KOA in high-risk populations.MethodsRelevant cross-sectional, cohort, and case-control studies published up to March 2026 were searched in PubMed, Embase, and MEDLINE (accessed via the Ovid). Methodological quality was assessed using the AHRQ scale for cross-sectional studies and the Newcastle-Ottawa Scale for cohort and case-control studies. Meta-analyses were performed using RevMan 5.3 software, and subgroup analyses stratified by study design were conducted to explore sources of heterogeneity.ResultsA total of 24 studies involving 10,300 participants were included. Patients with KOA showed significantly increased cross-sectional areas of sartorius muscle (SMD = 0.09, P = 0.002) and flexor muscles (SMD = 0.09, P = 0.0008), and markedly reduced thickness of vastus lateralis muscle (SMD=-0.61, P = 0.03). Intermuscular adipose tissue content was significantly higher in KOA patients than in healthy controls (SMD = 0.35, P = 0.001). For muscle strength, KOA patients exhibited significant reductions in knee extensor torque (SMD=-1.09, P = 0.0001), extensor strength (SMD=-0.16, P = 0.0002), knee extensor relative strength (SMD=-0.15, P = 0.04), flexor torque (SMD=-0.95, P = 0.04), and flexor strength (SMD=-0.12, P = 0.004). Substantial heterogeneity was observed in key outcomes including knee extensor torque (I²=97%), knee flexor torque (I²=99%) and intermuscular adipose tissue (I²=72%). Low knee extensor strength was associated with a 1.45-fold increased odds of KOA (OR = 1.45, P = 0.01), and this association was more prominent in women (OR = 1.54, P = 0.0006).ConclusionAlterations in thigh muscle quantity, quality and strength are significantly associated with KOA, particularly increased intermuscular adipose tissue infiltration and decreased knee extensor strength. Current evidence is predominantly derived from cross-sectional and case-control studies, and causal inferences cannot be established. These muscle parameters may serve as potential indicators for KOA risk stratification, and their predictive value and clinical utility require further verification in large-scale prospective cohort studies.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261350323, identifier CRD420261350323.]]></description>
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