Experimental Physiology最新文献

{"title":"Ouabain-induced hypertension in rats: Mechanisms, variability and translational implications.","authors":"Priscilla Rodrigues O Feijó, Luis Eduardo M Quintas","doi":"10.1113/EP092956","DOIUrl":"https://doi.org/10.1113/EP092956","url":null,"abstract":"<p><p>Ouabain-induced hypertension is a multifactorial and condition-dependent phenomenon involving coordinated actions across vascular, renal and central nervous system pathways. At the vascular level, ouabain inhibits Na⁺/K⁺-ATPase, particularly the α2-isoform, leading to elevated intracellular Ca²⁺, enhanced vasoconstriction and structural remodelling of resistance arteries. These effects are exacerbated by oxidative stress, inflammation, and altered expression of Ca²⁺-mobilizing proteins such as NCX1 and TRPC channels. In the kidney, ouabain disrupts Na⁺ handling, especially in the proximal tubule, suppresses natriuretic pathways like the D1 dopamine receptor, and promotes volume expansion through renal and sympathetic mechanisms. Centrally, ouabain acts on sodium-sensitive brain regions, including the median preoptic nucleus, rostral ventrolateral medulla and paraventricular nucleus, where it increases sympathetic outflow and impairs baroreflex control. These effects are potentiated by local interactions with brain-derived angiotensin II and cerebrospinal Na⁺, independent of peripheral ouabain levels. However, the hypertensive response is not universal and may vary by strain, salt status, genetic background and experimental conditions. These insights carry important translational implications. Elevated levels of endogenous ouabain (EO) have been identified in patients with salt-sensitive, low-renin or neurogenic hypertension. Therapeutic strategies targeting ouabain-sensitive pathways include isoform-selective Na⁺/K⁺-ATPase modulators, NCX or TRPC inhibitors, and agents acting on the central renin-angiotensin system. EO-neutralizing therapies such as digoxin antibodies may also hold clinical promise. Personalized medicine approaches incorporating EO sensitivity markers and genotype-specific models may advance the management of resistant hypertension and deepen our understanding of ouabain's dual role as both physiological modulator and pathological trigger.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788626","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":"Altered peripheral CRY1 gene expression may contribute to both organic and functional gastrointestinal disease.","authors":"Sophie Fowler, Gemma M Paech, Emily C Hoedt, Jennifer C Pryor, Cheenie Nieva, Jessica K Bruce, Prema M Nair, Guy D Eslick, Simonne Sherwin, Peter Pockney, Nicholas J Talley, Grace L Burns, Simon Keely","doi":"10.1113/EP092725","DOIUrl":"https://doi.org/10.1113/EP092725","url":null,"abstract":"<p><p>Gastrointestinal conditions such as irritable bowel syndrome (IBS) and inflammatory bowel diseases (IBD) are characterized by alterations in physiological and immune functions. Given the circadian clock influences gastrointestinal physiology and immunity, we hypothesized that the peripheral circadian clock is altered in these patients and might contribute to immune activation associated with IBD and IBS. To investigate this, RNA was extracted from whole blood obtained from control subjects (n = 29), IBD (n = 40 ulcerative colitis, n = 38 Crohn's disease) and IBS (n = 38) participants to investigate peripheral clock gene expression via quantitative PCR. A linear regression model was used to assess the impact of the time of blood collection on clock gene expression. Self-reported data regarding fatigue and sleep indices were compared between patients and control subjects. Gene expression analysis revealed variations in the peripheral circadian system between IBD, IBS and control subjects. The core clock gene CRY1 had higher relative expression in IBS (p = 0.031) and ulcerative colitis patients (p = 0.042) compared with control subjects. Patients with gastrointestinal disease demonstrated poorer quality sleep (IBS p < 0.001, UC p = 0.025 and CD p = 0.007) and more troublesome sleep (IBS p < 0.001, UC p = 0.002 and CD p = 0.009) compared with control subjects. These data suggest a role for CRY1 gene expression in patients experiencing fatigue and highlight a link between circadian dysregulation and the pathophysiology of intestinal disease.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788624","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":"Redox-regulated signalling of adaptations to contractile activity in skeletal muscle: Implications for age-related muscle weakness.","authors":"Malcolm J Jackson","doi":"10.1113/EP092458","DOIUrl":"https://doi.org/10.1113/EP092458","url":null,"abstract":"<p><p>Skeletal muscle adaptation to contractile activity is modulated by redox signalling, primarily through reactive oxygen species (ROS) such as hydrogen peroxide (H₂O₂). Early research framed ROS as deleterious byproducts of exercise, but subsequent studies have established their roles as signalling molecules involved in mitochondrial biogenesis, stress responses and metabolic regulation. Central to this process appear to be peroxiredoxins (Prdxs), particularly Prdx2, which current evidence suggests mediate redox relays by sensing physiological H₂O₂ levels and initiating transcriptional programs. Our recent findings demonstrate that low levels of H₂O₂, or electrically induced contractions, rapidly oxidise Prdx1, Prdx2 and Prdx3 in mouse muscle fibres. Transcriptomic analysis of human skeletal muscle myotubes confirmed that Prdx2 is essential for upregulating mitochondrial genes in response to H₂O₂ or contraction. With ageing, skeletal muscle exhibits impaired redox signalling with elevated ROS levels. Using an ageing mouse model, we observed diminished Prdx2 oxidation during contraction, suggesting redox signalling dysfunction. This impaired response likely contributes to sarcopenia by blunting the adaptive capacity of aged muscle. Our findings emphasise the importance of redox homeostasis (not merely ROS suppression) in maintaining muscle health. Understanding the nuanced role of ROS and Prdxs in exercise adaptation and ageing could inform therapeutic strategies aimed at restoring redox-sensitive signalling to preserve muscle function across the lifespan.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788627","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":"Bioenergetic profiles and respiratory control in mitochondrial physiology: Precision analysis of oxidative phosphorylation.","authors":"Alba Timón-Gómez, Carolina Doerrier, Zuzana Sumbalová, Luiz F Garcia-Souza, Eleonora Baglivo, Luiza H D Cardoso, Erich Gnaiger","doi":"10.1113/EP092792","DOIUrl":"https://doi.org/10.1113/EP092792","url":null,"abstract":"<p><p>Oxidative phosphorylation (OXPHOS) is fundamental to mitochondrial function. Respirometry with living cells provides limited information compared to precision OXPHOS analysis with mitochondrial preparations, including isolated mitochondria, tissue homogenates, permeabilized tissues, and permeabilized cells. We studied mouse mitochondria from brain, a glucose-dependent tissue, and from heart, which relies highly on fatty acid oxidation (FAO). HEK 293T cells were analysed as a widely used experimental model. Human peripheral blood mononuclear cells (PBMCs) and platelets were obtained from non-invasive liquid biopsies, considering their potential as mitochondrial biomarkers. Twenty respiratory states were interrogated applying two substrate-uncoupler-inhibitor titration (SUIT) reference protocols in parallel. Convergent electron transfer (ET) into the coenzyme Q junction increased OXPHOS and ET capacities compared to separately stimulated pathways. In mouse heart and human PBMCs, OXPHOS capacities were identical to ET capacities in every pathway state. While this equivalence applied to the NADH-linked pathway in platelets, ET capacity exceeded OXPHOS capacity supported by NADH-linked substrates plus succinate. Surprisingly, mouse brain exhibited the highest excess ET capacity in the NADH-linked pathway. In contrast, ET capacity of different batches of HEK 293T cells varied at constant OXPHOS capacity. Precision OXPHOS analysis enables attribution of respiratory performance to nutrient-specific pathways. In studies ranging from exercise physiology to mitochondrial diseases, metabolic adjustments must be distinguished from functional defects. Bioenergetic profiles obtained by precision OXPHOS analysis gain perspective in the context of comparative mitochondrial physiology.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759488","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":"Favouring respiration over locomotion in chronic obstructive pulmonary disease.","authors":"Kiana M Schulze, David C Poole","doi":"10.1113/EP092731","DOIUrl":"https://doi.org/10.1113/EP092731","url":null,"abstract":"","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752808","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":"Imposed expiratory resistance, dynamic hyperinflation and locomotor power and fatigue.","authors":"Jonathan Cunha, Antoinette Domingo, Fred W Kolkhorst, Harry B Rossiter, Daniel T Cannon","doi":"10.1113/EP092818","DOIUrl":"https://doi.org/10.1113/EP092818","url":null,"abstract":"<p><p>Expiratory flow limitation results in dynamic hyperinflation, dyspnoea and premature exercise intolerance. We aimed to measure whether expiratory resistance reduces locomotor power via limiting maximal voluntary motor activity, exacerbating muscle fatigue, or both. Healthy volunteers (n = 14; 23 (3) years) performed a series of very heavy-domain constant power cycling exercise tests with and without an imposed expiratory flow resistance (7 cmH₂O/L/s). The decline in maximal evocable isokinetic power at intolerance during each experimental condition was apportioned to: (1) the power equivalent from a reduction in maximum voluntary muscle activation (termed 'activation fatigue'); and (2) the deficit in expected power at a given isokinetic muscle activity (muscle fatigue). Imposed expiratory resistance reduced exercise tolerance (487 (145) vs. 575 (137) s; 95% confidence interval of the difference (CI_diff) 52, 125 s; P = 0.0002). At isotime-control, imposed expiratory resistance resulted in a greater decline in inspiratory reserve volume (CI_diff 0.20, 0.94 L; P = 0.007), and increased dyspnoea (Borg CR-10; CI_diff 0.7, 3.0; P = 0.006) than without. Muscle fatigue was unaffected (CI_diff -20, 17 W; P = 0.873), but activation fatigue was greater with expiratory resistance (CI_diff 1, 49 W; P = 0.044) and related to the reduction in inspiratory reserve volume (r²= 0.53; P = 0.028). As a result, locomotor power reserve was reduced with expiratory resistance (253 (83) vs. 201 (92) W; CI_diff -10, 113; P = 0.09). Imposed expiratory resistive loading initiated a cascade of abnormal lung mechanics and symptoms. These abnormalities conflate to reduce exercise tolerance through limiting maximal voluntary motor activity.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752809","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":"Vascular, inflammatory and perceptual responses to hot water immersion: Impacts of water depth and temperature in young healthy adults.","authors":"Campbell Menzies, Neil D Clarke, Charles J Steward, Charles Douglas Thake, Christopher J A Pugh, Tom Cullen","doi":"10.1113/EP092761","DOIUrl":"https://doi.org/10.1113/EP092761","url":null,"abstract":"<p><p>Repeated hot water immersion can improve cardiovascular health; however, the respective effects of distinct immersion protocols remain unclear. Twenty-two healthy adults completed three 30-min hot water immersion bouts of different water temperatures and immersion depths (40°C shoulder-deep immersion, 40-Shoulder; 42°C waist-deep immersion, 42-Waist; and 40°C waist-deep immersion, 40-Waist) in a randomised crossover design. Vascular, inflammatory and perceptual responses were collected via brachial and superficial femoral artery ultrasound, venous blood sampling and perceptual scales. Rectal temperature increased less in the 40-Waist (Δ0.5 ± 0.1°C) condition than the other conditions (40-Shoulder: Δ0.9 ± 0.3°C, 42-Waist: Δ0.9 ± 0.3°C, P < 0.001). Arm skin temperature increased more in the 40-Shoulder (Δ5.2 ± 1.9°C) condition than the other conditions (40-Waist: Δ2.6 ± 1.0°C, 42-Waist: Δ3.6 ± 1.1°C, P < 0.001), whilst thigh temperature had a greater increase in the 42-Waist (8.6 ± 1.3°C) condition than either the 40-Waist (7.8 ± 0.2°C) or 40-Shoulder (Δ7.8 ± 1.0°C) conditions (P < 0.001). Brachial artery shear rate was greatest post-immersion following the 40-Shoulder condition (40-Shoulder: Δ121 ± 94/s, 42-Waist: Δ47 ± 73/s, 40-Waist: Δ-21 ± 41/s, P < 0.001) whereas superficial femoral artery shear rate was largest following the 42-Waist condition (40-Shoulder: Δ143 ± 61/s, 42-Waist: 196 ± 85/s, 40-Waist: 131 ± 93/s, P < 0.001). IL-6 (P = 0.16) and cortisol (P = 0.83) responses did not differ between conditions. Perceptual responses were more favourable in the 40-Waist condition. Taken together, these data demonstrate that the distinct region-specific arterial responses align with increases in local skin temperature to alterations in hot water immersion protocols, whilst showing that beneficial physiological responses may be accompanied with less favourable perceptual responses.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741679","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":"Muscle oxygen saturation plateau: Definition and verification in different oxygen availability conditions in locomotor and non-locomotor muscles.","authors":"Tomasz Kowalski, Kinga Rębiś, Adrian Wilk, Dominika Granda, Andrzej Białecki, Tadej Debevec, Raphael Faiss","doi":"10.1113/EP092862","DOIUrl":"https://doi.org/10.1113/EP092862","url":null,"abstract":"<p><p>Novel wearable near-infrared spectroscopy devices allow for a better understanding of muscle oxygenation kinetics during exercise. A muscle oxygen saturation (SmO₂) plateau is often applied in the scientific literature, but clear criteria for its definition remain unestablished to date. The aim of this study was to develop criteria allowing for definition of SmO₂ plateaus. Multiple variables associated with physiological plateaus during exercise were assessed to develop a framework for an SmO₂ plateau. Subsequently, the existence of an SmO₂ plateau during 3 min all-out cycling trials (critical oxygenation plateau) was tested in different conditions of oxygen availability (i.e., normoxia and hypoxia) in vastus lateralis and triceps brachii among 30 endurance athletes. Plateau determination methods based on a threshold of change of ±5 arbitrary units (a.u.) of SmO₂ and expert visual assessment showed almost perfect agreement. However, a threshold of 10 a.u. yielded high SmO₂ variability associated with a large number of possibly false-positive detections. Conversely, relative changes (thresholds of 5% and 10%) did not align with other methods, corresponding to low absolute changes, limiting their applicability. The inter-rater agreement between individual visual assessments exhibited a higher reliability among expert versus non-expert raters. The determination of an SmO₂ plateau depends on the applied methodology. Overall, a critical oxygenation plateau was observed in the vastus lateralis in both normoxia and hypoxia in >90% of cases. The results of this study allow recommendation either for the use of a threshold of change corresponding to 5 a.u. of SmO₂ or expert visual assessment, using 30 s segments.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144729012","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":"Sex differences in loop gain measured via superimposed end-expiratory breath holds and inspired steady-state hypoxia.","authors":"Benjamin W L MacKenzie, Nicole A Johnson, Nicholas D J Strzalkowski, Trevor A Day","doi":"10.1113/EP092285","DOIUrl":"https://doi.org/10.1113/EP092285","url":null,"abstract":"<p><p>Acute low oxygen exposure (hypoxia) elicits a hypoxic ventilatory response (HVR), which increases ventilation and mitigates hypoxaemia. During sustained exposure to hypoxia, ventilatory acclimatization increases peripheral chemoreflex (HVR) sensitivity or chemoreflex loop gain (LG). Although increased ventilation protects oxygenation, increased LG contributes to ventilatory instability during sleep (central sleep apnoea; CSA). The HVR is highly variable between individuals, and the impact of sex on HVR variability and LG is unclear. At low altitude (1100 m), we aimed to characterize a novel breath hold method to quantify LG using a standardized series of short (∼10 s), voluntary, end-expiratory breath holds (EEBH), using a background of steady-state normobaric inspired hyperoxia (fraction of inspired oxygen; <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>  = 1.0), normoxia (i.e., ambient air; <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>  = 0.21) 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>  = 0.14; equivalent to ∼4300 m altitude). Further, we investigated sex differences in LG during differential oxygen exposure using this novel EEBH protocol to quantify LG. We hypothesized that (a) LG magnitude would follow an inverse oxygen-dependent pattern with each inspired gas condition, and (b) that males would have higher LG than females. We recruited 36 healthy participants (18 females; 18 males). We found (a) a graded, inverse oxygen-dependent effect on LG magnitude (P < 0.0001), and (b) a sex-specific effect, whereby males had significantly larger LG magnitudes than females, but only in steady-state inspired hypoxia (P < 0.032). Our EEBH protocol illustrates an intrinsic sex difference in chemoreflex LG in hypoxia, which may underlie known sex differences in CSA at high altitude and in heart failure populations.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144729013","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":"Sweat evaporation in humans: A molecular and thermodynamic perspective.","authors":"Edward T Ashworth","doi":"10.1113/EP093011","DOIUrl":"https://doi.org/10.1113/EP093011","url":null,"abstract":"<p><p>Evaporative heat loss through sweating is essential for maintaining thermal balance in humans, particularly during exercise or in hot environments. Although the physiological mechanisms regulating sweat production and skin blood flow are well documented, the molecular processes underpinning sweat evaporation are less often considered. This review explores the physics of sweat evaporation from first principles, examining how energy is transferred, how water molecules escape the liquid phase and how this process is shaped by local and systemic factors. At the molecular level, evaporation occurs when surface water molecules attain sufficient kinetic energy to overcome hydrogen bonding. The energy required for this phase change, the latent heat of vaporisation, is supplied via conduction from the skin and, ultimately, from core body heat. The molecular energy within the sweat layer follows a Boltzmann distribution, meaning that only a subset of molecules have sufficient energy to evaporate at any time. As these high-energy molecules escape, the remaining sweat cools, helping to lower body temperature. This process continues as long as heat is resupplied via skin blood flow. Environmental conditions, such as humidity, airflow and clothing, affect the likelihood that evaporated molecules will remain in the vapour phase, while electrolytes in sweat can slightly reduce vapour pressure by locally altering the bonding structure of water. These factors determine how effectively sweat can evaporate by influencing surface area and liquid retention. By linking classical thermodynamics to human physiology, this review presents a unified framework for understanding how molecular interactions, statistical physics and environmental conditions converge to influence heat loss.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144729014","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}