Experimental Physiology最新文献

{"title":"Integrative cardiovascular dose-response to graded lower-body negative pressure.","authors":"Richard S Whittle, Nathan Keller, Eric A Hall, Safiyya Patanam, Bonnie J Dunbar, Ana Diaz-Artiles","doi":"10.1113/EP092483","DOIUrl":"https://doi.org/10.1113/EP092483","url":null,"abstract":"<p><p>Lower-body negative pressure (LBNP) has been posited as a potential spaceflight countermeasure to counteract the physiological deconditioning related to fluid shifts in microgravity. However, open questions remain regarding the magnitude of LBNP that should be applied. We systematically characterized the cardiovascular effects of LBNP and quantified the effect size of varied LBNP doses across different parts of the cardiovascular system. Twenty-four subjects (12 male and 12 female) were exposed to graded LBNP, increasing from 0 to -50 mmHg in 10 mmHg increments, in both supine (0°) and 15° head-down tilt postures. At each pressure level, subjects first underwent a 6 min stabilization period to reach a steady-state cardiovascular response. We then assessed a wide range of variables, including those related to the systemic circulation, cardiovascular control, and haemodynamics of the eyes and neck. Building on the experimental data, dose-response curves were constructed using a Bayesian multivariate hierarchical modelling framework to quantify the effect size of every variable considered when subjected to LBNP. The methodology allows direct comparison of the variables and the underlying structural relationships between them. Furthermore, we demonstrated the potential for LBNP to reduce jugular venous flow stagnation, which is considered one of the major health risks during human spaceflight. The dose-response curves and effect sizes generated from this research effort establish the most comprehensive framework available to date that characterizes physiological responses to LBNP. These results directly inform the development of countermeasures to mitigate the negative effects of spaceflight, including cardiovascular deconditioning, spaceflight-associated neuro-ocular syndrome and venous thromboembolism events.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076528","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":"Jumping on the moon as a potential exercise countermeasure.","authors":"Patrick Swain, Filipa Santos, Luke Hughes, Dan Gordon, Nick Caplan","doi":"10.1113/EP092155","DOIUrl":"https://doi.org/10.1113/EP092155","url":null,"abstract":"<p><p>The Moon's gravitational field strength (17% Earth's gravity) may facilitate the use of bodyweight jumping as an exercise countermeasure against musculoskeletal and cardiovascular deconditioning in reduced gravity settings. The present study characterised the acute physiological and kinetic responses to bodyweight jumping in simulated Lunar gravity. Nineteen healthy adults (age: 25 ± 7 years, weight: 73 ± 11 kg; height: 1.81 ± 0.05 m, <math> <semantics> <msub><mover><mi>V</mi> <mo>̇</mo></mover> <mrow><msub><mi>O</mi> <mn>2</mn></msub> <mi>max</mi></mrow> </msub> <annotation>${dot V_{{{mathrm{O}}_2}{mathrm{max}}}}$</annotation></semantics> </math> : 50 ± 11 mL kg^-1 min^-1) performed an incremental jumping test in simulated Lunar gravity (9.5° head-up tilt suspension) comprising 4-min stages of jumping with 1-min rests, beginning at 30 cm and increasing 5 cm per stage up to 70 cm. A graded exercise test (GXT) to volitional exhaustion was subsequently performed using upright cycle ergometry. Cardiorespiratory outcomes ( <math> <semantics> <msub><mover><mi>V</mi> <mo>̇</mo></mover> <msub><mi>O</mi> <mn>2</mn></msub> </msub> <annotation>${dot V_{{{mathrm{O}}_2}}}$</annotation></semantics> </math> , <math> <semantics> <msub><mover><mi>V</mi> <mo>̇</mo></mover> <mrow><mi>C</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${dot V_{{mathrm{C}}{{mathrm{O}}_2}}}$</annotation></semantics> </math> , <math> <semantics> <msub><mover><mi>V</mi> <mo>̇</mo></mover> <mi>E</mi></msub> <annotation>${dot V_{mathrm{E}}}$</annotation></semantics> </math> , breathing frequency, respiratory exchange ratio and heart rate (HR)) and peak vertical ground reaction forces (vGRF) increased linearly (R² = 0.77-0.97) and blood lactate concentrations increased exponentially with jump height (R² = 0.98). Participants achieved HRs of 158 ± 17 beats min^-1 (88 ± 9% HR_max), metabolic rates of 35 ± 6 mL kg^-1 min^-1 (71 ± 9% <math> <semantics> <msub><mover><mi>V</mi> <mo>̇</mo></mover> <mrow><msub><mi>O</mi> <mn>2</mn></msub> <mi>max</mi></mrow> </msub> <annotation>${dot V_{{{mathrm{O}}_2}{mathrm{max}}}}$</annotation></semantics> </math> ), blood lactate concentrations of 5.8 ± 1.7 mmol L^-1 and peak vGRFs of 119 ± 17% bodyweight. Jumping at ∼20% bodyweight requires no equipment, allows for submaximal cardiovascular exercise intensities with and without blood lactate accumulation, and may have value as an exercise countermeasure in Lunar/Martian surface habitats.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973545","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":"TRPV1 blockade restores the baroreflex control of renal sympathetic nerve activity in cisplatin-induced renal injury in rats.","authors":"Mohammed H Abdulla, Ella Murphy, Lauren Mulcahy, Edward J Johns","doi":"10.1113/EP092618","DOIUrl":"https://doi.org/10.1113/EP092618","url":null,"abstract":"<p><p>Renal injury is associated with inflammatory responses within the kidney which could involve activation of transient receptor potential vanilloid 1 (TRPV1) channels. This study investigated whether TRPV1 channels modulate baroreflex regulation of renal sympathetic nerve activity (RSNA) in a rat model of cisplatin-mediated renal injury. Rats were anaesthetised and prepared for measurement of mean arterial pressure (MAP), heart rate (HR) and RSNA 4 days after a single i.p. dose of cisplatin (5 mg kg^-1). RSNA and HR baroreflex gain curves (BRC) were generated and the decrease in RSNA to volume expansion was determined during intrarenal capsazepine (CPZ, 15 µg kg^-1 h^-1) infusion. In the cisplatin group (MAP: 85 ± 13 mmHg; HR: 328 ± 17 bpm; RSNA: 0.83 ± 0.41 µV s), the slope and maximum gain of the BRC were approximately 50% lower (P = 0.015-0.033) than the control group (MAP: 78 ± 12 mmHg; HR: 352 ± 27 bpm; RSNA: 0.57 ± 0.36 µV s). Intrarenal CPZ infusion in the cisplatin group restored the slope (0.15 ± 0.04 vs. 0.09 ± 0.02, P = 0.014) of the RSNA BRC to near normal values. The RSNA response to volume expansion in the cisplatin group was enhanced following CPZ compared to vehicle infusion (-24 ± 14% vs. 1.7 ± 39%, P = 0.015). Intrarenal tumour necrosis factor α (TNF-α) infusion ( 2 µg kg^-1 h^-1) in normal rats decreased the slope of the BRC by 40% (P = 0.035) compared to vehicle infusion, which was slightly enhanced following intrarenal CPZ infusion. These findings demonstrate that TRPV1 channels contribute to the depressed baroreceptor control of RSNA in renal injury. Furthermore, the action of TNF-α in disrupting the baroreflex control mechanism partially involves TRPV1 channels.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143991375","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":"Combined effects of normobaric hypoxia and cold on respiratory system responses to high-intensity exercise.","authors":"Alexa Callovini, Alessandro Fornasiero, Aldo Savoldelli, Gianluigi Dorelli, Marco Decet, Lorenzo Bortolan, Barbara Pellegrini, Federico Schena","doi":"10.1113/EP092468","DOIUrl":"https://doi.org/10.1113/EP092468","url":null,"abstract":"<p><p>Cold temperatures (<-15°C) increase exercise-induced bronchoconstriction (EIB), while hypoxic-induced hyperventilation exacerbates respiratory muscle fatigue for a given exercising task. This study aimed to determine the individual and combined effects of cold and normobaric hypoxia on the respiratory system responses to high-intensity exercise. Fourteen trained male runners ( <math> <semantics> <msub><mover><mi>V</mi> <mo>̇</mo></mover> <mrow><msub><mi>O</mi> <mn>2</mn></msub> <mi>max</mi></mrow> </msub> <annotation>${{dot{V}}_{{{{mathrm{O}}}_2}{mathrm{max}}}}$</annotation></semantics> </math> : 64 ± 5 mL/kg/min) randomly performed an incremental cardiopulmonary exercise test (CPET) to volitional exhaustion under four environmental conditions: normothermic (18°C) normoxia ( <math> <semantics><msub><mi>F</mi> <mrow><mi>I</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${{F}_{{mathrm{I}}{{{mathrm{O}}}_2}}}$</annotation></semantics> </math> : 20.9%) and hypoxia ( <math> <semantics><msub><mi>F</mi> <mrow><mi>I</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${{F}_{{mathrm{I}}{{{mathrm{O}}}_2}}}$</annotation></semantics> </math> : 13.5%), and cold (-20°C) normoxia and hypoxia. Ventilatory responses during exercise and lung function (LF), maximal inspiratory (MIP) and expiratory (MEP) pressure measurements before and after exercise were evaluated. Volume of air forcefully exhaled in 1 s (FEV1), FEV1/forced vital capacity (FVC), peak expiratory flow, forced expiratory flow during the mid (25-75%) portion of the FVC, and maximal expiratory flow at 50% of FVC were affected by cold exposure. No significant pre- to post-exercise change in MIP and MEP was found, independent of environmental conditions. Greater LF impairments in cold-normoxia and coldhypoxia were associated with the lowest peak ventilatory responses during exercise. Cold exposure was found to negatively impact peak ventilatory responses and post-exercise LF, further highlighting a relationship between EIB presence and the blunted ventilatory response in the cold. Respiratory muscle strength remained unchanged after exercise regardless of the environmental condition, suggesting no detrimental effect of hypoxia on this parameter when intermittent short-duration high-intensity exercises are performed. Future studies should investigate the combined cold-hypoxic effect on longer exercise durations at a sustained high intensity, accounting for differences between normobaric and hypobaric hypoxia exposures.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981446","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":"Exercise oximetry in clinical practice: A single-centre perspective on procedure and techniques.","authors":"Simon Lecoq, Jeanne Hersant, Mathieu Feuilloy, Nafi Ouedraogo, Mariève Houle, Pierre Abraham","doi":"10.1113/EP092711","DOIUrl":"https://doi.org/10.1113/EP092711","url":null,"abstract":"<p><p>In moderate lower extremity artery disease (LEAD), when tissue ischaemia due to impaired inflow occurs at exercise but not during rest, exercise oximetry may be evaluated as a part of the diagnosis process. Initially used when assessing critical limb ischaemia at rest, transcutaneous oximetry (TcpO₂) has also been used in the last two decades during exercise assessment as a non-invasive method to measure oxygen pressure at the skin's surface, offering insights into loco-regional oxygen delivery-requirement mismatch. The introduction of decrease from rest of oxygen pressure (DROP) analysis in the TcpO₂ technique, which corresponds to the difference between limb oxygen pressure changes and chest oxygen pressure changes from rest, provides new information about the severity of the local ischaemia during exercise. In this paper, we elucidate the utilization of TcpO₂ during exercises (Ex-TcpO₂) over the years and provide information about how the technique has evolved and how the changes in the testing procedures have provided the opportunity for detecting abnormalities in both vascular and non-vascular clinical practice. We discuss the importance of Ex-TcpO₂ in the diagnosis of peripheral artery disease and its valuable contribution as a differential diagnostic tool for patients with co-morbid conditions such as lumbar spinal stenosis. We also provide recommendations about the utilization of Ex-TcpO₂ and contribute to a better understanding of the techniques in terms of efficacy, limitations and clinical applications. However, clarifications about its role in the diagnostic algorithm are needed, to ensure a better integration of the technique in clinical practice.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004794","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":"The multifaceted roles of ketones in physiology.","authors":"Seyed Amirhossein Tabatabaei Dakhili, Kunyan Yang, Magnus J Stenlund, John R Ussher","doi":"10.1113/EP092243","DOIUrl":"https://doi.org/10.1113/EP092243","url":null,"abstract":"<p><p>The production of ketones, referred to as ketogenesis, plays an essential role in maintaining energy homeostasis during prolonged fasting/starvation, which primarily stems from its ability to serve as a fuel source to support neuronal ATP production, thereby limiting muscle wasting. Over the years, the field has come to appreciate that ketones are much more than just a fuel source supporting neuronal metabolism, as many other oxidative organs, such as the heart and skeletal muscle, are capable of metabolizing ketones. Furthermore, ketones appear to be an important fuel source for exercising muscle. Beyond supporting ATP production, it is also becoming widely recognized that ketones are powerful signalling molecules, as they serve as ligands for G-protein coupled receptors and can even modify gene expression via regulating DNA post-translational modifications. As they play a key role in supporting whole-body physiology, it is not surprising that perturbations in ketone metabolism can contribute to various pathologies, particularly in relation to cardiometabolic diseases. Some of the strongest evidence supporting the aforementioned statement is seen for both heart failure and type 2 diabetes. Accordingly, we will review herein the multifaceted roles of ketones in supporting whole-body physiology, while interrogating the evidence to suggest whether modifying ketone metabolism may have a therapeutic role in the management of heart failure and type 2 diabetes.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063032","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":"Heat to hypoxia cross-adaptation: Effects of 6-week post-exercise hot-water immersion on exercise performance in acute hypoxia.","authors":"Patrick Rodrigues, Lydia L Simpson, Justin S Lawley, Heru S Lesmana, Anne Hecksteden","doi":"10.1113/EP092726","DOIUrl":"https://doi.org/10.1113/EP092726","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Cross-adaptation occurs when exposure to one environmental stressor (e.g., heat) induces protective responses to another (e.g., hypoxia). Although post-exercise hot-water immersion (HWI) induces heat acclimation, its potential to elicit cross-adaptation remains unclear. This study evaluated the effectiveness of a 6-week post-exercise HWI intervention on exercise performance in hypoxia (O&lt;sub&gt;2 &lt;/sub&gt;= 13%). Twenty healthy volunteers (28 ± 5 years; &lt;math&gt; &lt;semantics&gt; &lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt; &lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt; &lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt; &lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt; &lt;mi&gt;peak&lt;/mi&gt;&lt;/mrow&gt; &lt;/msub&gt; &lt;annotation&gt;${dot V_{{{mathrm{O}}_2}{mathrm{peak}}}}$&lt;/annotation&gt;&lt;/semantics&gt; &lt;/math&gt; 47.4 ± 8.9 mL kg&lt;sup&gt;-1&lt;/sup&gt; min&lt;sup&gt;-1&lt;/sup&gt;; 12 males, 8 females) completed interval cycling (4×4 min at 90 ± 5% maximal heart rate, 3×/week) followed by water immersion at either 34.5°C (control) or 42°C (HWI) for 40-50 min, five times per week. Following the 6-week intervention, the post-exercise HWI group exhibited lower resting heart rate (P &lt; 0.01, q = 0.02; d = -1.32) and core temperature (P &lt; 0.01, q = 0.001; d = -1.88) and elevated haemoglobin concentration (P &lt; 0.01, q = 0.02; d = 1.38). Compared to the control group, the HWI group also showed greater improvements in time-to-exhaustion (TTE) trial (P and q &lt; 0.01; d = 1.2) under hypoxia, but not in aerobic peak power (P = 0.03, q = 0.08; d = 0.86) or peak oxygen consumption ( &lt;math&gt; &lt;semantics&gt; &lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt; &lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt; &lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt; &lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt; &lt;mi&gt;peak&lt;/mi&gt;&lt;/mrow&gt; &lt;/msub&gt; &lt;annotation&gt;${dot V_{{{mathrm{O}}_2}{mathrm{peak}}}}$&lt;/annotation&gt;&lt;/semantics&gt; &lt;/math&gt; ) (P = 0.04, q = 0.10; d = 0.82). Throughout the TTE, lower core temperature and tidal volume, with increased oxygen saturation and &lt;math&gt; &lt;semantics&gt; &lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt; &lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt; &lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt; &lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt; &lt;/msub&gt; &lt;annotation&gt;${dot V_{{{mathrm{O}}_2}}}$&lt;/annotation&gt;&lt;/semantics&gt; &lt;/math&gt; were observed (P and q &lt; 0.05). During hypoxic steady-state exercise at 60% of &lt;math&gt; &lt;semantics&gt; &lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt; &lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt; &lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt; &lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt; &lt;mi&gt;peak&lt;/mi&gt;&lt;/mrow&gt; &lt;/msub&gt; &lt;annotation&gt;${dot V_{{{mathrm{O}}_2}{mathrm{peak}}}}$&lt;/annotation&gt;&lt;/semantics&gt; &lt;/math&gt; , the HWI group exhibited lower core temperature and higher peripheral oxygen saturation in hypoxia. No between-group differences were observed in mean &lt;math&gt; &lt;semantics&gt; &lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt; &lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt; &lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt; &lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt; &lt;/msub&gt; &lt;annotation&gt;${dot V_{{{mathrm{O}}_2}}}$&lt;/annotation&gt;&lt;/semantics&gt; &lt;/math&gt; , respiratory exchange ratio, heart rate or rate of perceived exertion, nor in &lt;math&gt; &lt;semantics&gt; &lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt; &lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt; &lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt; &lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt; &lt;mi&gt;peak&lt;/mi&gt;&lt;/mrow&gt; &lt;/msub&gt; &lt;annotation&gt;${dot V_{{{mathrm{O}}_2}{mathrm{peak}}}}$&lt;/annotation&gt;&lt;/semantics&gt; &lt;/math&gt; and aerobic peak power under normoxia (P and q &gt; 0.05). In conclusion, post-exercise HWI enhances maximal exercise perfo","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998967","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 shaking experience: My exposure to hypothermia.","authors":"Ryan P Sixtus","doi":"10.1113/EP092839","DOIUrl":"https://doi.org/10.1113/EP092839","url":null,"abstract":"","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143991553","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":"Increases in cardiac vagal modulation following muscle mechanoreflex activation via passive calf stretch: Impact of interindividual differences.","authors":"Georgia C S Lehnen, Marcela S Araujo, Igor S Rocha, Jeann L Sabino-Carvalho, Rosa V D Guerrero, Gabriel S Trajano, Lauro C Vianna","doi":"10.1113/EP092498","DOIUrl":"https://doi.org/10.1113/EP092498","url":null,"abstract":"<p><p>Muscle mechanoreflex is crucial to cardiac vagal modulation during exercise and can be activated during passive calf stretch. Herein, we aimed to determine whether cardiac vagal modulation following a single session of passive stretch is linked to interindividual cardiac vagal responses at the onset of passive calf muscle stretching in healthy young adults. Twenty-four volunteers (10 women) completed the experimental conditions in a randomised order over different days: a time-control condition and five sets of 1 min of unilateral passive stretching of the calf, with 15 s of rest between each stretching trial. Heart rate and systolic and diastolic blood pressure were continuously measured on a beat-to-beat basis before, immediately following, and at 15 and 30 min after the passive stretching intervention. Interindividual variations in cardiac vagal inhibition during the passive stretching session were identified, classifying volunteers into responder (n = 16) and non-responder (n = 8) groups. The onset of passive muscle stretching elicited an immediate reduction in cardiac vagal modulation (P = 0.026) and an increase in heart rate (P = 0.009) for the responders only. Cardiac vagal modulation significantly increased following 30 min of passive stretching (P = 0.010 vs. rest) for the responders only. During time control, all cardiac vagal variables were unchanged for both groups. In summary, our findings demonstrate that a single session of passive calf muscle stretching can enhance cardiac vagal modulation, but this effect is dependent on interindividual responses at the onset of stretching. These results highlight the role of muscle mechanoreflex activation in cardiac autonomic regulation and suggest that passive stretching may have potential cardiovascular benefits, particularly for individuals who exhibit a mechanoreflex-mediated response.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005170","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":"Environmental modulators of vascular physiology and inflammation.","authors":"Anusha N Seneviratne, Anne Majumdar, Kalpana Surendranath, Mark R Miller","doi":"10.1113/EP092309","DOIUrl":"https://doi.org/10.1113/EP092309","url":null,"abstract":"<p><p>Environmental factors play a crucial role in modulating vascular inflammation, contributing significantly to the development of atherosclerosis and cardiovascular disease. This review synthesizes current evidence on how various environmental exposures influence vascular function and inflammation, with a focus on pollutants such as particulate matter and chemical toxins like bisphenols and per- and polyfluoroalkyl substances. These environmental stressors can trigger oxidative stress, chronic inflammation and vascular dysfunction, potentially accelerating the progression of atherosclerosis. We also explore the protective effects of natural compounds and exposure to green spaces in dampening inflammation and reducing cardiovascular risk. By examining the complex interplay between traditional risk factors and environmental exposures, this work highlights the need for comprehensive public health strategies that address both individual lifestyle factors and broader environmental determinants of cardiovascular health. We underscore the importance of further research to elucidate the precise cellular and molecular mechanisms by which environmental factors influence vascular function, with the aim of developing targeted interventions to mitigate their harmful effects and promote cardiovascular well-being.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986294","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}