Experimental Physiology最新文献

{"title":"Leg-fidgeting versus standing breaks during prolonged sitting: Impacts on blood pressure and heart rate in young women.","authors":"Saja Alghamdi, Bethany Barone Gibbs, Ghareeb Omar Alshuwaier, Jamal M Alzahrani, Abdullah Bandar Alansare","doi":"10.1113/EP093057","DOIUrl":"https://doi.org/10.1113/EP093057","url":null,"abstract":"<p><p>The objective of this work was to examine whether leg-fidgeting breaks during prolonged sitting could be a practical alternative to standing breaks in preventing blood pressure (BP) and heart rate (HR) impairments. Young women (n = 16; age = 21.9 ± 3.0 years; body mass index = 21.1 ± 4.9 kg/m²) completed three 3-h prolonged sitting conditions in a random order, including: (1) uninterrupted prolonged sitting, (2) interrupted prolonged sitting every 20 min with standing for 5 min, and (3) interrupted prolonged sitting every 4 min with leg-fidgeting for 1 min. Oscillometric brachial BP and HR were measured at baseline and after 1, 2 and 3 h of prolonged sitting. Generalized linear mixed models with random effects evaluated the effects of the three prolonged sitting conditions on BP and HR while controlling for baseline values. Effect sizes were estimated using Cohen's d. No significant differences were observed between the three prolonged sitting conditions for all BP variables (P > 0.05 for all). HR was significantly lower when prolonged sitting was interrupted with standing (β = -4.406 beats; d = 0.46; P = 0.009) or leg-fidgeting (β = -3.802 beats; d = 0.46; P = 0.023) compared to the uninterrupted prolonged sitting condition. These findings suggest that leg-fidgeting breaks during prolonged sitting may serve as a practical alternative to standing breaks in preventing some prolonged sitting-induced cardiovascular impairments, particularly HR, in young women.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haematological adaptations to high-altitude and heat acclimation training in elite male cyclists.","authors":"Claes Cubel, Magnus B Klaris, Joakim V Larsen, Raphaël Faiss, Lars Nybo, Carsten Lundby","doi":"10.1113/EP092968","DOIUrl":"https://doi.org/10.1113/EP092968","url":null,"abstract":"<p><p>High-altitude training is widely adopted by endurance athletes with the aim of increasing total haemoglobin mass (tHb_mass) and thereby endurance exercise performance. However, divergent effects on tHb_mass and exercise performance have been reported in athletes commencing altitude camps with initial high baseline levels for tHb_mass, questioning the efficacy of in-season interventions in elite athletes. Therefore, haematological adaptations and exercise performance were evaluated in 12 elite cyclists completing an in-season 'Live High-Train High' (LHTH) altitude camp (21 days at 3000 m) immediately after participating in the national championships. Additionally, for seven participants, we compared haematological and exercise performance effects with an off-season heat acclimation training (HEAT) intervention (six 1-h sessions per week for 5 weeks). The LHTH resulted in a 3.5 ± 2.0% (P < 0.001, n = 12) increase in tHb_mass, with decay to Pre levels 10 days after returning to sea-level. For participants followed for 9 months, the tHb_mass effect was comparable to that of the off-season HEAT intervention (5.4 ± 3.9% for HEAT, LHTH vs. HEAT: P = 0.801, n = 7) and baseline levels prior to the interventions were almost identical (965 g Pre-HEAT vs. 960 g Pre-LHTH). Exercise performance and maximal oxygen uptake, tested immediately (2-3 days) and 10 days after LHTH, were not improved, and individual changes were not correlated to any of the haematological parameters assessed. In conclusion, the in-season LHTH training camp effectively increased tHb_mass in elite cyclists; however, there was a rapid decay in tHb_mass upon return to sea-level and no effect on exercise performance.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of combined ginsenoside-MC1 and irisin on mitochondrial apoptosis in diabetic rats with hepatic reperfusion injury: Role of AMPK/JNK signalling.","authors":"Jie Lin, Lei Han, Zhigang Ma, Bo Yuan, Yabin Yu","doi":"10.1113/EP092982","DOIUrl":"https://doi.org/10.1113/EP092982","url":null,"abstract":"<p><p>Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury. T2DM was induced in male Sprague-Dawley rats with a high-fat diet and a low-dose streptozotocin. Following the induction of diabetes, hepatic IR injury was induced. Rats were pretreated with GMC1 and/or irisin for 28 days prior to IR injury. Liver function was evaluated by quantitation of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH). Histopathological changes were observed with haematoxylin-eosin staining. Apoptotic markers (Bax, Bcl-2, cleaved caspase-3) and signalling proteins (AMP-activated protein kinase (AMPK), c-Jun N-terminal kinase (JNK)) were examined by western blotting. Mitochondrial function was evaluated by measuring reactive oxygen species, membrane potential and ATP content. Oxidative stress markers, such as malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx), were also measured. Combined therapy lowered AST, ALT and LDH levels, and histopathological injury (P < 0.05). It restored mitochondrial function; upregulated Bcl-2 and phosphorylated AMPK expression; downregulated Bax, cleaved caspase-3 and phosphorylated JNK expression; and reduced MDA levels, while elevating SOD and GPx activity (P < 0.05). AMPK inhibition by compound C reversed these protective effects. GMC1-irisin combination therapy safeguarded diabetic rats against IR-caused liver damage through suppressing mitochondrial apoptosis by AMPK/JNK signalling, a hopeful therapeutic approach in diabetic patients.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of metabolism-related molecules in rat model of autism spectrum disorders.","authors":"Süeda Tunçak, Ayşen Çakır, Bülent Gören, Nevzat Kahveci","doi":"10.1113/EP092734","DOIUrl":"https://doi.org/10.1113/EP092734","url":null,"abstract":"<p><p>Autism spectrum disorders (ASD) are neurodevelopmental pathologies. Investigating both sexes is crucial for understanding sex-specific manifestations of ASD. This study aims to examine ASD-like behaviours and metabolic alterations in male and female rats prenatally exposed to valproic acid (VPA). Pregnant Wistar albino rats were administered 400 mg/kg VPA or saline on embryonic day 12. Pups were subjected to various behavioural tests, including olfactory discrimination, sociability, locomotion, anxiety and exploratory behaviour assessments. On postnatal day 35, pups were sacrificed, and blood glucose levels were measured. Serum and brain leptin, orexin-A, nesfatin-1 and ghrelin levels were assessed by the ELISA method. VPA-exposed pups exhibited increased latency to reach maternal bedding, reduced sociability, decreased locomotion and increased immobility in both sexes. In the elevated plus maze, VPA-exposed females showed an increase in open-arm entries, while males showed a reduction compared to control groups. Blood glucose levels were significantly elevated in VPA-exposed males but not females. Significant sex-independent changes were observed in serum and brain levels of leptin and nesfatin-1 in the VPA groups. Brain orexin-A and serum ghrelin levels were altered in the VPA group in a sex-dependent manner. Prenatal VPA exposure induces ASD-like symptoms in both sexes, with notable sex-specific differences in behaviour and metabolic regulation. These findings highlight the importance of including both sexes in ASD research to better understand sex-dependent characteristics of the disorder, particularly concerning metabolic dysregulation.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of premature ventricular complexes with the PDE5 inhibitor sildenafil: First clinical experience.","authors":"David C Hutchings, Christopher P Denton, Luigi Venetucci, Andrew W Trafford","doi":"10.1113/EP092932","DOIUrl":"https://doi.org/10.1113/EP092932","url":null,"abstract":"<p><p>The phosphodiesterase-5 inhibitor sildenafil suppresses ventricular arrhythmias in a sheep model of drug-induced long QT. In that study, ventricular arrhythmias were abolished by reducing premature ventricular complexes (PVCs) and delaying PVC onset, thus preventing 'R-on-T' ventricular tachycardia. Evidence for effects in humans with arrhythmias is lacking. In this case study, a 50-year-old female with a history of PVCs and systemic sclerosis was started on sildenafil for Raynaud's phenomenon in line with current treatment recommendations. During initiation, the patient wore a 7-day cardiac monitor. Two subtypes of PVCs were observed: one distinct morphology arising <400 ms from the preceding sinus beat ('early') and a separate morphology >400 ms from the preceding sinus beat ('late'). Sildenafil abolished late PVCs and substantially reduced the frequency of early PVCs. Of those early PVCs remaining during sildenafil treatment, PVCs arose later in the cardiac cycle, 21 ms further from the preceding T wave apex. During washout, PVCs returned in frequency and timing towards baseline values. We report the first case suggesting an anti-arrhythmic property of sildenafil in a human.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rising from the ashes: the return of The Climatic Physiology Group meeting.","authors":"Josh Foster, Mike Tipton","doi":"10.1113/EP092641","DOIUrl":"https://doi.org/10.1113/EP092641","url":null,"abstract":"","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alveolar deadspace and intrapulmonary shunt in healthy individuals and in individuals who have recovered from COVID-19 infection.","authors":"Dominic Sandhu, Snapper R M Magor-Elliott, Nayia Petousi, Nick P Talbot, Alexander N Bennett, David A Holdsworth, Grant A D Ritchie, Peter A Robbins","doi":"10.1113/EP092971","DOIUrl":"https://doi.org/10.1113/EP092971","url":null,"abstract":"<p><p>Following acute COVID-19 infection, unvaccinated patients have been reported to exhibit elevated alveolar deadspace (̇V_D,alv/̇V_T) and intrapulmonary shunt (̇Q_s/̇Q_T) fractions. However, as there is uncertainty surrounding the upper limits of normal for ̇V_D,alv/̇V_T and ̇Q_s/̇Q_T, we sought to replicate the findings from a separate, previously reported cohort of COVID-19 patients that also included a healthy control group never infected with COVID-19. Data from 81 participants, classified into four different groups based on the severity of prior COVID-19 infection, were used. All participants had arterial blood-gas samples drawn while highly precise measurements of their respiratory gas exchange were made. The gas exchange data were used to estimate alveolar <math> <semantics><msub><mi>P</mi> <mrow><mi>C</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${P_{{mathrm{C}}{{mathrm{O}}_2}}}$</annotation></semantics> </math> and <math> <semantics><msub><mi>P</mi> <msub><mi>O</mi> <mn>2</mn></msub> </msub> <annotation>${P_{{{mathrm{O}}_2}}}$</annotation></semantics> </math> , and the differences between these values and the corresponding arterial blood-gas values provided the alveolar-arterial gradients from which ̇V_D,alv/̇V_T and ̇Q_s/̇Q_T were calculated. Mean ̇V_D,alv/̇V_T was 0.115 ± 0.062 and mean ̇Q_s/̇Q_T was 0.014 ± 0.011. No significant differences between the groups, including the uninfected control group, were detected for either ̇V_D,alv/̇V_T or ̇Q_s/̇Q_T, although if severity was instead treated as an interval measure, then a small increase in ̇Q_s/̇Q_T with severity (P = 0.00934) could be detected. Many participants, including controls, exceeded the originally proposed upper limit of normal for ̇V_D,alv/̇V_T, whereas no participant exceeded the originally proposed upper limit for ̇Q_s/̇Q_T. We conclude that prior infection with COVID-19 had no effect on ̇V_D,alv/̇V_T and little effect on ̇Q_s/̇Q_T, and that the supposedly high values of ̇V_D,alv/̇V_T are within the normal range.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144992011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antenatal betamethasone impairs markers of cardiac development and function in near-term lambs.","authors":"Reza Amanollahi, Ashley S Meakin, Stacey L Holman, Vicki L Clifton, Kent L Thornburg, Michael D Wiese, Kathryn L Gatford, Mitchell C Lock, Janna L Morrison","doi":"10.1113/EP093025","DOIUrl":"https://doi.org/10.1113/EP093025","url":null,"abstract":"<p><p>Antenatal corticosteroids are commonly administered to promote fetal lung maturation; however, their impact on heart development is not well understood. This study therefore investigated the effects of antenatal betamethasone on cardiac development in near-term lambs, using tissues collected from a cohort of ewes with mild experimentally induced asthma. Pregnant ewes received two doses of either saline (Saline) or betamethasone (Betamethasone, intramuscular, 11.4 mg) given 24 h apart, before delivery at 140 days of gestation (term = 150days of gestation). Cardiac protein expression and hormone concentrations in the left ventricle were analysed using western blot and LC-MS/MS, respectively. Fetal and neonatal heart rate and blood pressure were higher in Betamethasone compared to Saline lambs. Betamethasone lambs had lower cardiac concentrations of cortisol, corticosterone, oestradiol, progesterone and thyroxine but a higher triiodothyronine. The protein ratio of glucocorticoid receptor GRβ:GRα-A was higher in the hearts of Betamethasone compared to Saline. Additionally, the expression of insulin-like growth factor 1 receptor (a marker of cardiac proliferative capacity), proliferating cell nuclear antigen (a marker of DNA replication) and the fatty acid transporter CD36 were lower in Betamethasone lambs. These findings suggest that antenatal betamethasone may disrupt normal heart development by altering glucocorticoid receptor isoform expression and reducing cardiac exposure to glucocorticoid and sex hormones. Consequently, this leads to decreased expression of markers associated with cardiac growth and fatty acid uptake. These alterations in heart development caused by antenatal corticosteroids exposure may increase the risk of cardiovascular disease later in life if these changes persist into adulthood.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new method for non-invasive determination of effective pulmonary blood flow and cardiac output in spontaneously breathing subjects.","authors":"Andras Gedeon, Jakob Jansson, David Patrickson, Mats Wallin","doi":"10.1113/EP093079","DOIUrl":"https://doi.org/10.1113/EP093079","url":null,"abstract":"<p><p>The differential Fick method is well established for measuring effective pulmonary blood flow (EPBF) and cardiac output (CO) but until now it has only been used for patients on mechanical ventilation. Here we present and evaluate a new approach adapted to spontaneous breathing situations. Ten healthy subjects with diverse anthropometric and respiratory parameters were studied in the sitting position. Rebreathing through a dead space of precisely known volume and recording the resulting rise in the end-tidal CO₂ value allowed the determination of EPBF. The shunted blood flow fraction was estimated from the arterial oxygen saturation to obtain cardiac output (FickCO). Two measurements were made on each subject 15 min apart. Reference values for cardiac output (RefCO), were calculated as the product of stroke volume and heart rate where the stroke volume was measured with established echocardiography techniques. Heart rate and arterial oxygen saturation were measured with an ordinary pulse oximeter. Comparing FickCO to RefCO using a Bland-Altman analysis, we obtained a mean bias of 0.03 L/min, limits of agreement (LoA) of +1.43 to -1.37 (95% CI) L/min and a percentage error (PE) of 0.25. For the mean of two FickCO observations, we obtained a mean bias of -0.04 L/min, LoA +0.94 to -1.01 (95% CI) and PE of 0.17. The differential Fick method can be adapted to spontaneously breathing situations with good absolute accuracy using simple equipment. Short data collection times make it possible to use the mean of repeated observations and thereby get adequate precision. The new method could therefore be of value both in the pre-operative and the post-operative setting.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fmr1 knockout disrupts multiple intrinsic properties via reduced HCN channel activity in mediodorsal thalamocortical neurons.","authors":"Gregory J Ordemann, Polina Lyuboslavsky, Alena Kizimenko, Audrey C Brumback","doi":"10.1113/EP092894","DOIUrl":"10.1113/EP092894","url":null,"abstract":"<p><p>The neurodevelopmental disorder fragile X syndrome (FXS) results from hypermethylation of the FMR1 gene, which prevents production of the FMRP protein. FMRP modulates the expression and function of a variety of proteins, including voltage-gated ion channels, such as hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels, which are integral to rhythmic activity in thalamic structures. Thalamocortical pathology, particularly involving the mediodorsal thalamus (MD), has been implicated in neurodevelopmental disorders such as FXS. MD connectivity with the medial prefrontal cortex (mPFC) is integral to executive functions such as working memory and social behaviours that are disrupted in FXS. We used a combination of retrograde labelling and ex vivo brain slice whole-cell electrophysiology in 40 wild-type and 42 Fmr1 knockout male mice to investigate how a lack of Fmr1 affects intrinsic cellular properties in lateral (MD-L) and medial (MD-M) MD neurons that project to the mPFC (MD→mPFC neurons). In MD-L neurons, Fmr1 knockout decreased the HCN-mediated membrane properties voltage sag and membrane after-hyperpolarization. We also identified a delay in rebound spike timing in both complex bursts and low-threshold spikes. In Fmr1 knockout mice, reduced HCN channel activity in MD-L→mPFC neurons impaired both the timing and the magnitude of HCN-mediated membrane potential regulation. Changes in response timing might adversely affect rhythm propagation in Fmr1 KO thalamocortical circuitry. MD thalamic neurons are crucial for maintaining rhythmic activity involved in cognitive and affective functions. Understanding specific mechanisms of thalamocortical circuit activity might lead to therapeutic interventions for individuals with FXS and other conditions characterized by thalamic dysrhythmia.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}