Pub Date : 2025-08-01Epub Date: 2025-04-04DOI: 10.1016/j.autneu.2025.103276
Keisho Katayama , Shigehiko Ogoh
Precise cardiovascular adjustments are necessary to meet the metabolic demands of working skeletal muscle during dynamic exercise. Appropriate regulation of sympathetic vasomotor outflow is key for maintaining arterial blood pressure (ABP) and facilitating the delivery of blood flow to active skeletal muscle. Central command, the exercise pressor reflex (including mechanoreflex and metaboreflex within skeletal muscle), and the arterial baroreflex work in concert, creating complex interactions that regulate sympathetic vasomotor outflow during dynamic exercise. Although less well studied, limited evidence suggests that the cardiopulmonary baroreflex plays a significant role in modulating MSNA (muscle sympathetic nerve activity) and ABP responses during mild-intensity dynamic exercise, as well as in resetting the arterial baroreflex during dynamic exercise. This review provides an updated and comprehensive overview of the sympathetic vasomotor outflow and the ABP response during dynamic exercise via the cardiopulmonary baroreflex.
{"title":"The role of cardiopulmonary baroreflex on sympathetic vasomotor outflow and blood pressure regulation during dynamic exercise","authors":"Keisho Katayama , Shigehiko Ogoh","doi":"10.1016/j.autneu.2025.103276","DOIUrl":"10.1016/j.autneu.2025.103276","url":null,"abstract":"<div><div>Precise cardiovascular adjustments are necessary to meet the metabolic demands of working skeletal muscle during dynamic exercise. Appropriate regulation of sympathetic vasomotor outflow is key for maintaining arterial blood pressure (ABP) and facilitating the delivery of blood flow to active skeletal muscle. Central command, the exercise pressor reflex (including mechanoreflex and metaboreflex within skeletal muscle), and the arterial baroreflex work in concert, creating complex interactions that regulate sympathetic vasomotor outflow during dynamic exercise. Although less well studied, limited evidence suggests that the cardiopulmonary baroreflex plays a significant role in modulating MSNA (muscle sympathetic nerve activity) and ABP responses during mild-intensity dynamic exercise, as well as in resetting the arterial baroreflex during dynamic exercise. This review provides an updated and comprehensive overview of the sympathetic vasomotor outflow and the ABP response during dynamic exercise via the cardiopulmonary baroreflex.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103276"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143839492","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}
Pub Date : 2025-08-01Epub Date: 2025-06-19DOI: 10.1016/j.autneu.2025.103313
Gianni Sesa-Ashton , Lakshini Herat , Markus P. Schlaich
Renal nerves are critical in regulation of blood pressure and renal function. The concept of renal denervation is based on solid pathophysiologic principles and both experimental and human data. Renal denervation has consistently shown to reduce blood pressure in patients with resistant hypertension and complex to manage blood pressure. This occurs both in the clinical trial environment and in observational studies. The procedure works effectively through the disruption of the pathophysiological sympathetic drive to and from the kidney to produce its antihypertensive effect. Renal denervation is now considered a valid option for BP lowering in European and American Hypertension Guidelines.
{"title":"Targeting renal nerves for arterial hypertension – The path to renal denervation","authors":"Gianni Sesa-Ashton , Lakshini Herat , Markus P. Schlaich","doi":"10.1016/j.autneu.2025.103313","DOIUrl":"10.1016/j.autneu.2025.103313","url":null,"abstract":"<div><div>Renal nerves are critical in regulation of blood pressure and renal function. The concept of renal denervation is based on solid pathophysiologic principles and both experimental and human data. Renal denervation has consistently shown to reduce blood pressure in patients with resistant hypertension and complex to manage blood pressure. This occurs both in the clinical trial environment and in observational studies. The procedure works effectively through the disruption of the pathophysiological sympathetic drive to and from the kidney to produce its antihypertensive effect. Renal denervation is now considered a valid option for BP lowering in European and American Hypertension Guidelines.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103313"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144338265","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}
Pub Date : 2025-08-01Epub Date: 2025-04-05DOI: 10.1016/j.autneu.2025.103277
Alec L.E. Butenas , Ashley M. Baranczuk , Raimi J. Carroll , Shannon K. Parr , Carl J. Ade , K. Sue Hageman , Timothy I. Musch , Steven W. Copp
We investigated the role played by ATP-sensitive purinergic 2 × 4 (P2X4) receptors on the sensory endings of thin fibre muscle afferents in exercise pressor reflex and mechanoreflex activation in healthy/SHAM rats and rats with heart failure with reduced ejection fraction (HF-rEF). We hypothesized that infusion of the P2X4 receptor antagonist 5-BDBD (8 μg) into the hindlimb arterial supply would reduce the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to 30s of electrically-induced hindlimb skeletal muscle contraction (model of exercise pressor reflex activation) and 30s of hindlimb skeletal muscle stretch (model of mechanoreflex activation) in decerebrate, unanesthetized HF-rEF rats but not SHAM rats. Ejection fraction was significantly lower in HF-rEF (46 ± 3 %) compared to SHAM (83 ± 2 %; P < 0.001) rats. In SHAM rats, P2X4 receptor blockade had no effect on the pressor response to hindlimb muscle contraction (n = 8) or the pressor and RSNA response to muscle stretch (n = 4). However, in SHAM rats we found that P2X4 receptor blockade significantly reduced the RSNA response to muscle contraction. In HF-rEF rats, P2X4 receptor blockade reduced the pressor and RSNA response to hindlimb muscle contraction (n = 7) as well as the pressor, but not the RNSA, response to hindlimb muscle stretch (n = 8). Collectively, the data suggest that P2X4 receptors on thin fibre muscle afferent sensory endings play a role in the evoking the exercise pressor reflex in healthy subjects that is limited to RSNA, and that in HF-rEF this expands to a significant role in mechanoreflex and exercise pressor reflex-mediated blood pressure control.
{"title":"Novel role for purinergic 2× subtype 4 (P2X4) receptors in the exercise pressor reflex and mechanoreflex: Effect of heart failure","authors":"Alec L.E. Butenas , Ashley M. Baranczuk , Raimi J. Carroll , Shannon K. Parr , Carl J. Ade , K. Sue Hageman , Timothy I. Musch , Steven W. Copp","doi":"10.1016/j.autneu.2025.103277","DOIUrl":"10.1016/j.autneu.2025.103277","url":null,"abstract":"<div><div>We investigated the role played by ATP-sensitive purinergic 2 × 4 (P2X4) receptors on the sensory endings of thin fibre muscle afferents in exercise pressor reflex and mechanoreflex activation in healthy/SHAM rats and rats with heart failure with reduced ejection fraction (HF-rEF). We hypothesized that infusion of the P2X4 receptor antagonist 5-BDBD (8 μg) into the hindlimb arterial supply would reduce the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to 30s of electrically-induced hindlimb skeletal muscle contraction (model of exercise pressor reflex activation) and 30s of hindlimb skeletal muscle stretch (model of mechanoreflex activation) in decerebrate, unanesthetized HF-rEF rats but not SHAM rats. Ejection fraction was significantly lower in HF-rEF (46 ± 3 %) compared to SHAM (83 ± 2 %; <em>P</em> < 0.001) rats. In SHAM rats, P2X4 receptor blockade had no effect on the pressor response to hindlimb muscle contraction (<em>n</em> = 8) or the pressor and RSNA response to muscle stretch (<em>n</em> = 4). However, in SHAM rats we found that P2X4 receptor blockade significantly reduced the RSNA response to muscle contraction. In HF-rEF rats, P2X4 receptor blockade reduced the pressor and RSNA response to hindlimb muscle contraction (<em>n</em> = 7) as well as the pressor, but not the RNSA, response to hindlimb muscle stretch (<em>n</em> = 8). Collectively, the data suggest that P2X4 receptors on thin fibre muscle afferent sensory endings play a role in the evoking the exercise pressor reflex in healthy subjects that is limited to RSNA, and that in HF-rEF this expands to a significant role in mechanoreflex and exercise pressor reflex-mediated blood pressure control.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103277"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143825556","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}
Pub Date : 2025-08-01Epub Date: 2025-03-30DOI: 10.1016/j.autneu.2025.103275
Jeremy A. Bigalke, Jason R. Carter
Sleep and autonomic regulation are closely related processes which incur significant influence on health and wellbeing in women across the lifespan. Aging in women is associated with increases in cardiovascular risk through greater sympathetic predominance compared to premenopausal women, as well as reductions in sleep quality and quantity. Women remain an understudied population with regards to sleep, autonomic function, and cardiovascular risk. Understanding the interplay between sleep and autonomic function across the lifespan of women is crucial to improve subsequent lifelong health outcomes. The present review integrates knowledge that has accrued regarding experimental sleep deprivation, restriction, and chronic sleep disturbance and their respective impacts on autonomic regulation at various life stages in women. The review focuses on high-fidelity measures of sympathetic regulation (i.e., microneurography), as aging in women is associated with a disproportionate increase in sympathetic activity compared to men. Evidence summarized within this review delineates a significant impact of sleep processes on autonomic function in women across the lifespan. However, there remain substantial gaps in our knowledge of this interplay between sleep processes and autonomic regulation of cardiovascular control in women. There is a need for further research efforts to disentangle the complexity associated with sleep and autonomic regulation in women at all life stages. Efforts in this area will improve our understanding of women's health and factors such as sleep and sleep disturbance which precipitate lifelong health and chronic cardiovascular risk.
{"title":"The influence of sleep on autonomic nervous system regulation in women across the lifespan","authors":"Jeremy A. Bigalke, Jason R. Carter","doi":"10.1016/j.autneu.2025.103275","DOIUrl":"10.1016/j.autneu.2025.103275","url":null,"abstract":"<div><div>Sleep and autonomic regulation are closely related processes which incur significant influence on health and wellbeing in women across the lifespan. Aging in women is associated with increases in cardiovascular risk through greater sympathetic predominance compared to premenopausal women, as well as reductions in sleep quality and quantity. Women remain an understudied population with regards to sleep, autonomic function, and cardiovascular risk. Understanding the interplay between sleep and autonomic function across the lifespan of women is crucial to improve subsequent lifelong health outcomes. The present review integrates knowledge that has accrued regarding experimental sleep deprivation, restriction, and chronic sleep disturbance and their respective impacts on autonomic regulation at various life stages in women. The review focuses on high-fidelity measures of sympathetic regulation (i.e., microneurography), as aging in women is associated with a disproportionate increase in sympathetic activity compared to men. Evidence summarized within this review delineates a significant impact of sleep processes on autonomic function in women across the lifespan. However, there remain substantial gaps in our knowledge of this interplay between sleep processes and autonomic regulation of cardiovascular control in women. There is a need for further research efforts to disentangle the complexity associated with sleep and autonomic regulation in women at all life stages. Efforts in this area will improve our understanding of women's health and factors such as sleep and sleep disturbance which precipitate lifelong health and chronic cardiovascular risk.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103275"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776448","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}
Pub Date : 2025-08-01Epub Date: 2025-04-05DOI: 10.1016/j.autneu.2025.103278
Sophie É. Collins , Devin B. Phillips , Michael K. Stickland
Rationale
Chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD) are characterized by exaggerated carotid chemoreceptor (CC) sensitivity and exercise intolerance. We tested the hypothesis that participants with elevated CC sensitivity would have the greatest improvement in exercise tolerance with CC inhibition, secondary to increased vascular conductance, and lower ventilatory requirements, dyspnea and leg discomfort.
Methods
Data from healthy controls, and patients with CHF or COPD were included in this secondary analysis of results from 2 randomized placebo-controlled double-blind crossover trials. Assessments included pulmonary function, incremental cardiopulmonary exercise test, and basal CC sensitivity assessment. High CC sensitivity was defined as either a stepwise hypoxic ventilatory response (HVR) or transient HVR greater than one SD above the mean in healthy controls. Participants received 2 μg/kg/min dopamine or placebo infusions (randomized) during 2 separate constant work-rate exercise tests to examine exercise endurance time (EET) and cardiopulmonary responses.
Results
Among 33 adults, 17 were categorized to normal HVR (11 controls/3 COPD/3 CHF), and 16 to high HVR (1 control/7 COPD/8 CHF). Participants with high HVR experienced significant dopamine-induced improvements in EET (pinteraction = 0.011), and reduced leg discomfort at the 4-min isotime (pinteraction = 0.024). Those with improved vascular conductance and leg discomfort had the greatest improvements in EET (p = 0.042 and p = 0.021, respectively).
Conclusions
CC inhibition with dopamine in participants with high HVR was associated with improvement in EET. These findings suggest that high HVR is related to exercise limitation, and that improvement in EET is associated with a CC-mediated increase in vascular conductance and leg discomfort.
{"title":"Carotid chemoreceptor inhibition improves exercise tolerance in participants with elevated carotid chemosensitivity: A secondary analysis","authors":"Sophie É. Collins , Devin B. Phillips , Michael K. Stickland","doi":"10.1016/j.autneu.2025.103278","DOIUrl":"10.1016/j.autneu.2025.103278","url":null,"abstract":"<div><h3>Rationale</h3><div>Chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD) are characterized by exaggerated carotid chemoreceptor (CC) sensitivity and exercise intolerance. We tested the hypothesis that participants with elevated CC sensitivity would have the greatest improvement in exercise tolerance with CC inhibition, secondary to increased vascular conductance, and lower ventilatory requirements, dyspnea and leg discomfort.</div></div><div><h3>Methods</h3><div>Data from healthy controls, and patients with CHF or COPD were included in this secondary analysis of results from 2 randomized placebo-controlled double-blind crossover trials. Assessments included pulmonary function, incremental cardiopulmonary exercise test, and basal CC sensitivity assessment. High CC sensitivity was defined as either a stepwise hypoxic ventilatory response (HVR) or transient HVR greater than one SD above the mean in healthy controls. Participants received 2 μg/kg/min dopamine or placebo infusions (randomized) during 2 separate constant work-rate exercise tests to examine exercise endurance time (EET) and cardiopulmonary responses.</div></div><div><h3>Results</h3><div>Among 33 adults, 17 were categorized to normal HVR (11 controls/3 COPD/3 CHF), and 16 to high HVR (1 control/7 COPD/8 CHF). Participants with high HVR experienced significant dopamine-induced improvements in EET (p<sub>interaction</sub> = 0.011), and reduced leg discomfort at the 4-min isotime (p<sub>interaction</sub> = 0.024). Those with improved vascular conductance and leg discomfort had the greatest improvements in EET (<em>p</em> = 0.042 and <em>p</em> = 0.021, respectively).</div></div><div><h3>Conclusions</h3><div>CC inhibition with dopamine in participants with high HVR was associated with improvement in EET. These findings suggest that high HVR is related to exercise limitation, and that improvement in EET is associated with a CC-mediated increase in vascular conductance and leg discomfort.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103278"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143820525","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}
Pub Date : 2025-08-01Epub Date: 2025-05-30DOI: 10.1016/j.autneu.2025.103307
Feliberto De La Cruz , Nikos Makris , Andy Schumann , Jon Haitz Legarreta , Yuqian Chen , Katrin Rieger , Monica Di Giuliano , Ryan Zurrin , Tashrif Billah , Nicholas Kim , Owen Borders , Yogesh Rathi , Marek Kubicki , Lauren O'Donnell , Karl-Jürgen Bär , Zora Kikinis
Anorexia nervosa (AN) is linked to changes in autonomic function, but the specific neuroanatomical substrates of these changes are not well understood. In this study, we used diffusion-weighted imaging to examine white matter structure in the ventromedial prefrontal cortex–dorsal vagal complex (vmPFC-DVC) pathway, which is essential for autonomic regulation. Compared to healthy controls, individuals with AN showed significantly higher fractional anisotropy and axial diffusivity, as well as more streamlines connecting the vmPFC and DVC—indicating altered structural organization. However, radial diffusivity, which relates to myelin integrity, did not differ between groups, suggesting that changes are not due to higher myelination in AN individuals. Region-specific analysis located the differences in white matter metrics to the region of fiber decussation at the ponto-midbrain junction. Fractional anisotropy and radial diffusivity of vmPFC-DVC were associated with autonomic function in healthy controls but not in individuals with AN, pointing to a disruption in brain-body communication in AN. No differences were found in tensor metrics in other white matter tracts in the brainstem, indicating these alterations are specific to autonomic pathways rather than reflecting widespread brainstem abnormalities. This study provides the first evidence of structural disruptions in a key autonomic circuit in AN and highlights a potential decoupling between white matter integrity and autonomic regulation.
{"title":"White matter correlates of autonomic cardiac dysfunction in anorexia nervosa","authors":"Feliberto De La Cruz , Nikos Makris , Andy Schumann , Jon Haitz Legarreta , Yuqian Chen , Katrin Rieger , Monica Di Giuliano , Ryan Zurrin , Tashrif Billah , Nicholas Kim , Owen Borders , Yogesh Rathi , Marek Kubicki , Lauren O'Donnell , Karl-Jürgen Bär , Zora Kikinis","doi":"10.1016/j.autneu.2025.103307","DOIUrl":"10.1016/j.autneu.2025.103307","url":null,"abstract":"<div><div>Anorexia nervosa (AN) is linked to changes in autonomic function, but the specific neuroanatomical substrates of these changes are not well understood. In this study, we used diffusion-weighted imaging to examine white matter structure in the ventromedial prefrontal cortex–dorsal vagal complex (vmPFC-DVC) pathway, which is essential for autonomic regulation. Compared to healthy controls, individuals with AN showed significantly higher fractional anisotropy and axial diffusivity, as well as more streamlines connecting the vmPFC and DVC—indicating altered structural organization. However, radial diffusivity, which relates to myelin integrity, did not differ between groups, suggesting that changes are not due to higher myelination in AN individuals. Region-specific analysis located the differences in white matter metrics to the region of fiber decussation at the ponto-midbrain junction. Fractional anisotropy and radial diffusivity of vmPFC-DVC were associated with autonomic function in healthy controls but not in individuals with AN, pointing to a disruption in brain-body communication in AN. No differences were found in tensor metrics in other white matter tracts in the brainstem, indicating these alterations are specific to autonomic pathways rather than reflecting widespread brainstem abnormalities. This study provides the first evidence of structural disruptions in a key autonomic circuit in AN and highlights a potential decoupling between white matter integrity and autonomic regulation.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103307"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144194758","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}
Pub Date : 2025-08-01Epub Date: 2025-05-27DOI: 10.1016/j.autneu.2025.103294
Amélie Debray , Soha Sardar , Thomas A. Deshayes , Adèle Mornas , Katia Oubouchou , Yousra Ouazaa , Daniel Gagnon
Epidemiological studies have observed that female sex is associated with a greater risk of adverse health outcomes during heat extremes. It remains unclear if sex-related differences in autonomic temperature regulation contribute to these observations. This narrative review article provides an overview of studies that compared autonomic temperature regulation during heat stress between males and females across the lifespan. Our literature search focused on studies that investigated components of heat loss thermoeffector loops and/or that accounted for confounding differences in body morphology and metabolic heat production between males and females. Guided by this framework, we present studies that compared autonomic temperature regulation between males and females during childhood to adolescence, adulthood, middle-age, and older age. The review highlights that few studies have specifically studied sex-related differences in autonomic temperature regulation during heat stress. Most studies have focused on thermoeffector output and core temperature. In contrast, little is known regarding thermoafferent signalling, central integration of thermoafferent feedback, thermoefferent signalling and thermoeffector organ structure and function. Additional research is needed to understand how biological sex modulates autonomic temperature regulation during heat stress and how any sex-related difference may contribute to the greater health risks observed in females during heat extremes.
{"title":"Sex-related differences in temperature regulation during heat stress from childhood to older age","authors":"Amélie Debray , Soha Sardar , Thomas A. Deshayes , Adèle Mornas , Katia Oubouchou , Yousra Ouazaa , Daniel Gagnon","doi":"10.1016/j.autneu.2025.103294","DOIUrl":"10.1016/j.autneu.2025.103294","url":null,"abstract":"<div><div>Epidemiological studies have observed that female sex is associated with a greater risk of adverse health outcomes during heat extremes. It remains unclear if sex-related differences in autonomic temperature regulation contribute to these observations. This narrative review article provides an overview of studies that compared autonomic temperature regulation during heat stress between males and females across the lifespan. Our literature search focused on studies that investigated components of heat loss thermoeffector loops and/or that accounted for confounding differences in body morphology and metabolic heat production between males and females. Guided by this framework, we present studies that compared autonomic temperature regulation between males and females during childhood to adolescence, adulthood, middle-age, and older age. The review highlights that few studies have specifically studied sex-related differences in autonomic temperature regulation during heat stress. Most studies have focused on thermoeffector output and core temperature. In contrast, little is known regarding thermoafferent signalling, central integration of thermoafferent feedback, thermoefferent signalling and thermoeffector organ structure and function. Additional research is needed to understand how biological sex modulates autonomic temperature regulation during heat stress and how any sex-related difference may contribute to the greater health risks observed in females during heat extremes.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103294"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144190431","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}
Pub Date : 2025-08-01Epub Date: 2025-06-10DOI: 10.1016/j.autneu.2025.103309
Claire E. Kissell , Rachel J. Skow , Denis J. Wakeham , Takuro Washio , Giorgio Manferdelli , Mitchel Samels , Qi Fu , Mark J. Haykowsky , Tiffany L. Brazile , James P. MacNamara , Satyam Sarma , Benjamin D. Levine , Paul J. Fadel , Christopher M. Hearon Jr
Impaired exercise hyperemia and blunted vasoconstrictor responsiveness have been reported in patients with heart failure with preserved ejection fraction (HFpEF). However, there is considerable heterogeneity in the degree to which vasodilatory capacity and sympathetic vasoconstrictor reserve are diminished. Given the integration of both vasodilation and vasoconstriction to appropriately regulate blood flow during exercise, we hypothesized that patients with HFpEF who are unable to vasoconstrict to sympatho-excitation (i.e., a cold pressor test; CPT; non-constrictors) have blunted leg blood flow (LBF) responses to single leg knee extensor (SLKE) exercise compared to patients with HFpEF who are able to vasoconstrict in response to sympatho-excitation (constrictors). Forty-three patients diagnosed with HFpEF underwent a CPT and performed submaximal and peak SLKE exercise while heart rate, blood pressure and common femoral artery blood flow were measured. The percent change in leg vascular conductance (LVC) during the CPT was used to categorize participants as non-constrictors (+26 ± 24%Δ LVC; n = 22, 16 female) or constrictors (−15 ± 14%Δ LVC; n = 21, 13 female). During submaximal SLKE exercise (7.5 watts) non-constrictors had a smaller increase in LBF (non-constrictors: Δ 1139 ± 425 ml/min; constrictors: Δ 1497 ± 454 ml/min; P = 0.011) and LVC (non-constrictors: Δ 9.8 ± 3.4 ml/min/mmHg; constrictors: Δ 13.3 ± 4.5 ml/min/mmHg; P = 0.007). LBF at peak SLKE exercise was also less in non-constrictors compared to constrictors (P = 0.033). In summary, patients with HFpEF without a sympathetic vasoconstrictor reserve present with impaired hemodynamic responses to exercise.
{"title":"Impaired exercise hemodynamic responses in patients with HFpEF without a sympathetic vasoconstrictor reserve","authors":"Claire E. Kissell , Rachel J. Skow , Denis J. Wakeham , Takuro Washio , Giorgio Manferdelli , Mitchel Samels , Qi Fu , Mark J. Haykowsky , Tiffany L. Brazile , James P. MacNamara , Satyam Sarma , Benjamin D. Levine , Paul J. Fadel , Christopher M. Hearon Jr","doi":"10.1016/j.autneu.2025.103309","DOIUrl":"10.1016/j.autneu.2025.103309","url":null,"abstract":"<div><div>Impaired exercise hyperemia and blunted vasoconstrictor responsiveness have been reported in patients with heart failure with preserved ejection fraction (HFpEF). However, there is considerable heterogeneity in the degree to which vasodilatory capacity and sympathetic vasoconstrictor reserve are diminished. Given the integration of both vasodilation and vasoconstriction to appropriately regulate blood flow during exercise, we hypothesized that patients with HFpEF who are unable to vasoconstrict to sympatho-excitation (i.e., a cold pressor test; CPT; non-constrictors) have blunted leg blood flow (LBF) responses to single leg knee extensor (SLKE) exercise compared to patients with HFpEF who are able to vasoconstrict in response to sympatho-excitation (constrictors). Forty-three patients diagnosed with HFpEF underwent a CPT and performed submaximal and peak SLKE exercise while heart rate, blood pressure and common femoral artery blood flow were measured. The percent change in leg vascular conductance (LVC) during the CPT was used to categorize participants as non-constrictors (+26 ± 24%Δ LVC; <em>n = 22</em>, 16 female) or constrictors (−15 ± 14%Δ LVC; <em>n = 21</em>, 13 female). During submaximal SLKE exercise (7.5 watts) non-constrictors had a smaller increase in LBF (non-constrictors: Δ 1139 ± 425 ml/min; constrictors: Δ 1497 ± 454 ml/min; <em>P</em> = 0.011) and LVC (non-constrictors: Δ 9.8 ± 3.4 ml/min/mmHg; constrictors: Δ 13.3 ± 4.5 ml/min/mmHg; <em>P</em> = 0.007). LBF at peak SLKE exercise was also less in non-constrictors compared to constrictors (<em>P</em> = 0.033). In summary, patients with HFpEF without a sympathetic vasoconstrictor reserve present with impaired hemodynamic responses to exercise.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"260 ","pages":"Article 103309"},"PeriodicalIF":3.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366947","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}
Pub Date : 2025-07-01DOI: 10.1016/j.autneu.2025.103319
Julian F.R. Paton , Peter Hunter , David Nickerson
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Pub Date : 2025-06-01Epub Date: 2025-03-06DOI: 10.1016/j.autneu.2025.103256
Riki Edo Saputro , Chun-Chung Chou , Yi-Yuan Lin , Takashi Tarumi , Yi-Hung Liao
Sleep deprivation is a growing concern in cardiovascular risk, causing physiological disruptions like autonomic dysregulation and inflammation. Recent research indicates that sleep deprivation increases sympathetic nervous activity while decreasing parasympathetic activity, leading to increased blood pressure, impaired endothelial function, and heightened inflammation. Exercise has emerged as a non-pharmacological approach to increase cardiovascular health. However, the impact of exercise on sleep deprivation-induced changes in autonomic activity and inflammation remains unclear. To explore this, we reviewed studies investigating the effects of acute exercise on autonomic regulation and inflammatory markers following sleep deprivation. We conducted a narrative review of the literature. PubMed/MEDLINE, Google Scholar, and Web of Science (WOS) searched the articles between May 2022 and April 2023. The papers had to: [1] focus on recent studies between 2000 and 2023; [2] consist of sleep deprivation participants; [3] be published in English. Acute moderate- to high-intensity exercise after sleep deprivation may reduce parasympathetic activity, trigger pro-inflammatory cytokines, and delay recovery to normal levels. In contrast, regular exercise routines may mitigate the adverse effects of sleep deprivation on autonomic regulation and reduce systemic inflammation. Sleep deprivation can lead to autonomic imbalance, increased blood pressure, and increased inflammatory responses, which are further amplified by acute exercise, increasing the cardiovascular burden. When sleep deprivation occurs, exercise intensity and timing should be carefully chosen to avoid adverse cardiovascular health risks.
人们越来越担心睡眠不足会导致心血管疾病，导致自主神经失调和炎症等生理紊乱。最近的研究表明，睡眠剥夺会增加交感神经活动，同时降低副交感神经活动，导致血压升高、内皮功能受损和炎症加剧。运动已经成为一种非药物的方法来增加心血管健康。然而，运动对睡眠剥夺引起的自主神经活动和炎症变化的影响尚不清楚。为了探讨这一点，我们回顾了关于睡眠剥夺后急性运动对自主神经调节和炎症标志物影响的研究。我们对文献进行了叙述性回顾。PubMed/MEDLINE、b谷歌Scholar和Web of Science （WOS）检索了2022年5月至2023年4月之间的文章。论文必须关注2000年至2023年之间的最新研究；[2]由睡眠剥夺参与者组成；b[3]将以英文出版。睡眠剥夺后的急性中高强度运动可降低副交感神经活动，触发促炎细胞因子，并延迟恢复到正常水平。相反，有规律的锻炼可以减轻睡眠剥夺对自主神经调节的不利影响，减少全身炎症。睡眠不足会导致自主神经失衡、血压升高和炎症反应加剧，这些会在急性运动中进一步放大，从而增加心血管负担。当发生睡眠剥夺时，应仔细选择运动强度和时间，以避免不利的心血管健康风险。
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