Frontiers in Physiology最新文献

Resistance training plays a crucial role in cardiovascular health by promoting epigenetic adaptations that beneficially modulate gene expression. These modifications include DNA methylation, histone alterations, and regulation by non-coding RNAs, which directly affect cardiac muscle and the vascular system. Such epigenetic changes lead to improved cardiac function, reduced inflammation, optimized metabolism, and protection against cardiovascular diseases. Resistance training induces the release of signaling molecules that mediate favorable systemic adaptations. Studies demonstrate that resistance training, especially when combined with aerobic training, improves cardiovascular risk factors such as blood pressure and lipid profile. Epigenetic regulation is fundamental to the plasticity of the cardiovascular system and the reversibility of exercise-induced adaptations. Although extreme exercise may pose risks, regular and moderate resistance training is safe and effective in the prevention and management of cardiovascular diseases through these molecular mechanisms. Further investigation into these epigenetic modifications may unveil novel exercise-based therapeutic strategies to enhance cardiovascular health.

Perivascular adipose tissue (PVAT) has emerged as an active paracrine and metabolic organ that modulates vascular function in both humans and rodents, rather than serving merely as structural support. Vascular inflammation is a central mechanism driving cardiovascular diseases such as atherosclerosis, representing a maladaptive response to vascular injury. Recent evidence indicates that PVAT actively participates in this process through dynamic phenotypic changes, including adipose tissue browning or beiging. Furthermore, advances in imaging have enabled the noninvasive evaluation of vascular inflammation using computed tomography-derived indices that reflect PVAT characteristics. This review summarizes current understanding of the interplay between PVAT and vascular inflammation, highlights the biological and clinical implications of PVAT remodeling, and discusses emerging diagnostic approaches and future research directions.

Purpose: To investigate the effects of different dosages of exercise on anxiety symptoms in children and adolescents.

Methods: The present study screened randomized controlled trials (RCTs) from PubMed, Embase, Web of Science and Cochrane Library databases. According to the suggestions of American College of Sports Medicine (ACSM), all included studies were categorised into a high and a low/uncertain adherence group. The random-effects model was adopted in the meta-analysis. Subgroup analyses were also conducted to explore the differences in outcomes.

Results: A total of 27 RCTs including 2022 participants were extracted and included for analysis. The results indicated that exercise interventions may have an anxiolytic effect in youth (SMD = -0.36, 95% CI: -0.58 to -0.15, p = 0.0009). According to the ACSM, 13 studies were classified into high adherence group, and 14 studies were classified into low/uncertain adherence group. Subgroup analysis showed that the anxiety reduction was significantly larger in high ACSM adherence group (SMD = -0.67, 95% CI: -1.10 to -0.23, p = 0.002) than in low/uncertain ACSM adherence group (SMD = -0.13, 95% CI: -0.33 to 0.07, p = 0.21). Furthermore, exercise interventions longer than 11 weeks showed significantly greater effects than those shorter than 11 weeks. Only interventions delivered at least three times per week and incorporating combined exercise modalities exerted anxiolytic effects. Moreover, exercise interventions significantly reduced anxiety symptoms in populations with physical illnesses.

Conclusion: The meta-analysis demonstrated that exercise interventions showed significant anxiolytic effects in children and adolescents. Moreover, the anxiety reduction in the high ACSM adherence group was significantly larger than that in the low/uncertain ACSM adherence group.

Exercise remains one of the most effective non-pharmacological strategies for improving non-alcoholic and metabolic-associated fatty liver disease (NAFLD/MASLD). Beyond its systemic effects, regular physical activity rewires hepatic energy metabolism and enhances mitochondrial efficiency. Within this adaptive process, members of the Sirtuin family-particularly SIRT1, SIRT3 and SIRT6-have received considerable attention. These proteins operate at distinct regulatory layers: SIRT1 modulates transcriptional programs, SIRT3 shapes mitochondrial metabolic fluxes, and SIRT6 influences chromatin architecture and epigenetic repression. Together, they are widely regarded as the principal molecular mediators linking exercise to improved hepatic metabolic function. However, the Sirtuin family consists of seven members, and accumulating evidence indicates that the remaining isoforms-SIRT2, SIRT4, SIRT5 and SIRT7-also participate in the hepatic response to exercise. Their potential roles include buffering metabolic stress, supporting protein quality control, and modulating inflammatory signaling, suggesting a broader regulatory network than currently emphasized. This Perspective revisits the exercise-Sirtuin axis from a mechanistic physiology standpoint. It examines why research focus has historically converged on SIRT1, SIRT3 and SIRT6, and considers emerging data implicating the full Sirtuin repertoire in exercise-induced metabolic remodeling. The argument put forward is that future work may benefit from a more integrated framework that views exercise not as a trigger for a few dominant pathways, but as a stimulus capable of reorganizing an interdependent Sirtuin network governing hepatic metabolic resilience. Collectively, these considerations prompt a shift from a single-axis understanding toward a distributed regulatory model of hepatic adaptation to exercise.

Hypertension stands as one of the most significant preventable risk factors for cardiovascular disease, which is the leading cause of mortality worldwide. There is a disturbing gap, in preclinical research, between simplified cell culture and complex in vivo models. To contribute to bridge this gap, we have developed a simplified but realistic in vitro dynamic model of hypertension allowing the discrimination between mechanical pressure effects and Angiotensin II's pharmacological action. We utilized an advanced bioreactor system capable of producing adjustable flow rates to culture human umbilical vein endothelial cells (HUVEC). This system allows for the investigation of the possible effects of Angiotensin II and/or an increase in intraluminal pressure (via the Live-Pa pressure-actuation device) exerted directly upon the HUVEC monolayer without simulating transmural pressure. Key hypertension-associated inflammatory markers, such as NF-kB, p38MAPK, Interleukins (IL)-6/8, and Endothelin-1 (ET-1), were subsequently assessed. Angiotensin II induced HUVEC NF-kB and p38MAPK phosphorylation, and elevated IL-6 and ET-1 secretion, with a trend in IL-8 increase. Live-Pa alone enhanced NF-kB and p38MAPK and influenced cytokine/chemokine secretion. Combined stimuli significantly augmented the inflammatory parameters as compared to unstimulated cells, suggesting a synergistic effect between chemical and mechanical stimuli. Overall, these in vitro results demonstrate both key consistencies (e.g., NF-kB and p38MAPK activation) and specific distinctions (e.g., no significant IL-6 increase in Live-Pa-exposed versus control HUVEC) when compared to published data from hypertensive versus normotensive animal models. The proposed advanced in vitro model may successfully reproduce some features of vascular function in hypertension and simulate hemodynamic conditions by controlled flow with adjustable pressure parameters. Crucially, this system allows discrimination between mechanical blood pressure effects and Angiotensin II's pharmacological action on the endothelium, paving the way for understanding pathophysiological mechanisms and developing new therapies. Established methods make it possible that studies on cultured endothelial cells will be better comparable to the results of in vivo studies, thus directly supporting the 3Rs framework-Replacement, Reduction, and Refinement-which is essential for high-standard and ethical research.

Introduction: The long-term effect of training with Whole-Body Vibration (WBV) has been documented to have benefits on health, but its acute role in performance remains unclear. This study evaluated whether a 5-minute WBV warm-up could serve as an effective warm-up to optimize sport performance.

Methods: Ninety-three participants healthy, active but not professional athletes, (23.6 ± 5.7 years) were randomized into three groups: control (CG), sham vibration group (SVG), and vibration group (VG). All participants completed tests at two time points (T0 and T1): countermovement jump (CMJ) the primary outcome, reaction time (RT), reactive strength index (RSI), and sit-and-reach (SRT). During assessments, superficial electromyography (sEMG) was recorded to explore potential neuromuscular changes associated with the interventions. Between T0 and T1, the VG performed a 5-minute WBV warm-up, the SVG completed the same warm-up without vibration, and the CG remained at rest.

Results: VG improved in the primary outcome, CMJ (p < 0.01), SRT (p < 0.01), and RT (p < 0.01), while RSI remained unchanged (p > 0.05). SVG showed similar improvements (CMJ (p < 0.01), SRT (p < 0.01), and RT (p < 0.01), RSI (p > 0.05), whereas CG experienced a decline in RSI (p < 0.05). Between-group contrasts at the post-test endpoint for the primary outcome (CMJ) showed no statistical significance (all p > 0.05), a finding consistent across all other variables.

Conclusion: The proposed 5-minute warm-up protocol, whether performed with or without whole-body vibration, effectively enhanced performance in sport-related tests without inducing a performance decrease. However, WBV did not provide additional benefits over the same warm-up performed without vibration.

With the advancement of minimally invasive techniques and the reevaluation of surgical indications, gallbladder-preserving cholecystolithotomy is anticipated to serve as an alternative to cholecystectomy in specific cases. The choice of surgical incision is critical for optimizing gallbladder function preservation, which is a pivotal factor influencing the prognosis of gallbladder-preserving cholecystolithotomy. Consequently, a comprehensive understanding of the distribution of microstructures, including gallbladder blood vessels and nerves, is of substantial significance. For this study, we selected the gallbladders of healthy four-year-old children as our subjects. Gallbladder specimens were dehydrated, paraffin-embedded, and serially sectioned into hundreds of 4-μm-thick slices. Sections were selectively stained with distinct protocols-hematoxylin and eosin (H&E) and anti-tyrosine hydroxylase immunohistochemical staining-followed by sequential numbering. Digitized sections were reconstructed into three-dimensional models (3D) using computational software. The resultant 3D gallbladder models achieved a resolution threshold of <20 μm, enabling visualization of microvascular and neural structures. Independent and integrated analyses of the modeled cystic arteries, veins, and sympathetic neural networks revealed two superficial arterial trunks and one deep branch originating from the superficial division of the cystic artery, with their interactive patterns defining nutrient-supplying territories. Further mapping of microvascular and neural trajectories within the digital models identified a minimally function-disruptive surgical incision site, diverging from conventional fundal incision approaches for gallstone extraction. This approach offers a 3D visualization framework to enhance pathological slice interpretation-thereby facilitating histopathological diagnosis-and is proposed as a novel surgical route for gallbladder-preserving cholelithotomy.

Introduction: Serum-based hormone analysis is considered essential for determining menstrual cycle phases in sport and exercise science. However, its reliance on venous blood sampling limits applicability in field-based or operational contexts. This study evaluated the validity of larger-volume capillary samples obtained from the earlobe for the quantification of progesterone (P4) and 17ß-estradiol (E2) in comparison to venous blood sampling.

Materials and method: Twelve eumenorrheic female soldiers (mean age: 24.4 ± 2.9 years; BMI: 24.4 ± 2.2 kg/m²) participated in a longitudinal protocol involving paired capillary and venous blood sampling twice weekly across one complete individual menstrual cycle. Blood was drawn from the earlobe (capillary, 100-250 µL) and antecubital vein (venous, 4 mL) and analyzed via ELISA for P4 and E2 concentrations.

Results: All participants completed six or more sampling timepoints and had ovulatory cycles, with a mean cycle length of 28.3 ± 3.6 days and ovulation occurring on day 16.6 ± 4.7. On average, P4 concentrations were 1.6 ng/mL higher in venous compared to capillary samples, while E2 values were 0.34 pg/mL lower. The concordance correlation coefficients were 0.911 for P4 and 0.919 for E2, indicating good to very good agreement between the sampling methods. Repeated measures Bland-Altman analysis with mixed effects revealed minimal mean bias for both hormones, with acceptable limits of agreement. Repeated measures correlation coefficients were 0.915 and 0.982 for E2 and P4, respectively.

Discussion and conclusion: The results demonstrate that earlobe-derived capillary sampling is a valid and practical alternative to venous sampling for hormonal assessment across the menstrual cycle. The method yielded robust results for both P4 and E2, with sufficient accuracy to support cycle phase classification and the detection of anovulatory or luteal-phase deficient cycles. The logistical advantages include minimal invasiveness, no need for medical personnel, and the ability to analyze the frozen samples at a later date. This makes capillary sampling particularly well suited for use with athletes and tactical populations. Future studies should explore its application in elite athletes and incorporate participant-reported burden to optimize feasibility in high-frequency sampling protocols.

Background: Vascular dysfunction has been described as worsening in Chronic Obstructive Pulmonary Disease (COPD), but there is a lack of knowledge regarding severe patients. This retrospective cross-sectional study aimed to investigate it in COPD with Chronic Respiratory Failure (CRF) versus COPD and controls.

Methods: A baseline screening was performed, including a health history, a physical examination, and an anthropometric assessment. All subjects underwent an arterial blood gas analysis, spirometry, a 6-min walking test, and a thigh muscle volume assessment. The vascular function was determined via single Passive Leg Movement (sPLM) on the dominant leg.

Results: Fifteen patients with moderate COPD (FEV₁ 53.3% ± 11.4%), 15 patients with severe COPD (CRF; FEV₁ 30.6% ± 10.3%), and 15 age-matched healthy controls (CTRL) were recruited. Reactive hyperemia following sPLM was decreased in CRF [peak LBF (Leg Blood Flow) 70 ± 38 mL/min)] compared to COPD (peak LBF 162 ± 115 mL/min) and CTRL (peak LBF 268 ± 134 mL/min), p < 0.05. Interestingly, when the vascular function was normalized to the thigh muscle volume, the difference in the hyperaemic response among the CRF, COPD, and CTRL groups was mitigated but not eliminated. Moreover, the peak LBF was associated with the 6-min walking test (r = 0.7027, p < 0,0001), FEV₁ (r = 0.5432, p = 0.0001), disease duration (r = 0.5062, p = 0.0004), oxygen saturation (SpO₂) (r = 0.4343, p = 0.0029), and prescribed oxygen flow (r = -0.5413, p < 0.0001).

Conclusion: These data provide evidence of an intrinsic vascular dysfunction during the progression of COPD, which depends only partially on locomotor muscle volume loss observed in this clinical population.