Journal of applied physiology最新文献

{"title":"Sympathetic neural and cardiovascular responsiveness to involuntary stress-induced crying.","authors":"Jeremy A Bigalke, Jason R Carter","doi":"10.1152/japplphysiol.00419.2025","DOIUrl":"10.1152/japplphysiol.00419.2025","url":null,"abstract":"<p><p>Acute and chronic emotional distress are associated with an elevated risk of adverse cardiovascular events in humans. However, our understanding of how complex emotional states impact autonomic and cardiovascular regulation in humans remains limited. The purpose of the present case study was to characterize muscle sympathetic nerve activity (MSNA) and peripheral hemodynamic responses to an involuntary mental stress-related lacrimation (i.e., crying) in a healthy, young female participant (age: 22 yr; BMI: 27 kg/m²). Continuous heart rate (HR; electrocardiogram), beat-to-beat blood pressure (finger plethysmography), and MSNA (microneurography) were monitored during a 3-min resting baseline and subsequent mental arithmetic task during which an unanticipated and involuntary crying was observed after 1 min of the stress task. Sympathetic and hemodynamic reactivity during the first minute of mental arithmetic were quantified and compared with a retrospective dataset of healthy individuals in whom mental stress reactivity was similarly assessed (31 males, 30 females; age: 21 ± 3 yr; BMI: 25 ± 6 kg/m²). Changes in systolic (SBP; Δ3 mmHg) and diastolic (DBP; Δ9 mmHg) blood pressure were comparable with the comparator group (SBP: Δ4 ± 6 mmHg; DBP: Δ5 ± 5 mmHg), whereas HR reactivity appeared slightly higher (Δ32 beats/min) than the comparator group (Δ22 ± 11 beats/min). In contrast, MSNA burst frequency (BF; Δ22 bursts/min), incidence (BI; Δ20 bursts/100 heartbeats), and total area (Δ971%) reactivity were substantially elevated relative to the comparator group (BF: Δ2 ± 7 bursts/min; BI: Δ-3 ± 11 bursts/100 heartbeats; total area: Δ132 ± 285%). These findings suggest that involuntary stress-induced crying is associated with substantial sympathetic activation beyond that observed during standard laboratory mental stress, despite modest changes in hemodynamic variables.<b>NEW & NOTEWORTHY</b> The present study is the first to assess muscle sympathetic nerve activity (MSNA) during unanticipated and involuntary stress-induced lacrimation (i.e., crying) in a human. The findings demonstrate that stress-induced crying was associated with what appeared to be a substantial increase of sympathetic nervous system activity that exceeded MSNA responsiveness generally observed in young, healthy adults during acute laboratory mental stress. Exaggerated sympathetic neural reactivity to emotional distress may be one mechanism underlying stress-induced cardiovascular risk.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"334-340"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre- and postcapillary exercise contributions to pulmonary hypertension in adults > 45 yr.","authors":"Elizabeth Karvasarski, Joy Park, Simone Savaris, Anna Beale, Stephen P Wright, Robert F Bentley, John T Granton, Susanna Mak","doi":"10.1152/japplphysiol.00148.2025","DOIUrl":"10.1152/japplphysiol.00148.2025","url":null,"abstract":"<p><p>Clinical differentiation of pre- vs. postcapillary pulmonary hypertension can be challenging in older patients with risk factors for both pathophysiologies. The use of exercise pressure-flow relationships during hemodynamic assessment is now recommended when resting pulmonary artery wedge pressure is proximate to a threshold of 15 mmHg. In this study, we examined relationships between resting pulmonary artery wedge pressure and the balance of pre- and postcapillary contributions to exercise pulmonary hypertension. Patients > 45 yr suspected of precapillary pulmonary hypertension (<i>n</i> = 29, 72 ± 10 yr, 52% Female) with risk factors for left-heart disease were prospectively recruited to undergo semiupright cycle-ergometry at the time of diagnostic right-heart catheterization. Hemodynamic data, including pressure-flow slopes and contributions of transpulmonary gradient and pulmonary artery wedge pressure to mean pulmonary artery pressure, were analyzed to evaluate pre- and postcapillary contributions, respectively, at rest and during exercise. Exercise pressure-flow slopes indicated 62% with postcapillary contributions to pulmonary hypertension, and 31% with solely precapillary contributions. Of patients with pulmonary artery wedge pressure <12 mmHg, 67% had postcapillary contributions to exercise pulmonary hypertension. Conversely, 50% of patients with pulmonary artery wedge pressure >15 mmHg had precapillary contributions to exercise pulmonary hypertension. Exercise-associated increases in pulmonary artery pressures were more strongly associated with precapillary contributions, regardless of postcapillary contributions or the value of resting pulmonary artery wedge pressure. In conclusion, in this population, postcapillary contributions to exercise pulmonary hypertension were commonly disclosed over a range of resting pulmonary artery wedge pressure, including <12 mmHg. The severity of exercise pulmonary hypertension was determined by the precapillary contributions.<b>NEW & NOTEWORTHY</b> Exercise is recommended in patients with pulmonary artery wedge pressure (PAWP) between 12 and 15 mmHg and risk factors for left-heart disease to differentiate pre- versus postcapillary contributions to pulmonary hypertension (PH). However, our prospective experience shows resting PAWP does not reliably predict exercise postcapillary PH, which remains common even at lower PAWP ranges (<12 mmHg). Our findings suggest that exercise may retain utility to elicit postcapillary PH across a broad range of resting PAWP.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"517-528"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physiological impact of controlled emergency swimming ascents training in professional divers: evidence of subclinical lung stress.","authors":"Olivier Castagna, Vianney Hamar, Bruno Schmid, Arnaud Druelle","doi":"10.1152/japplphysiol.00462.2025","DOIUrl":"10.1152/japplphysiol.00462.2025","url":null,"abstract":"<p><p>Controlled emergency swimming ascent (CESA) training is a standard safety procedure in diving, which is designed to simulate ascent in the event of gas supply failure. However, the potential pulmonary risks associated with this exercise remain poorly documented. This study aimed to evaluate whether CESA training induces subclinical pulmonary alterations and assess the effectiveness of expiratory control during ascent. In Step 1, seven experienced military divers each performed two dives to 10 meters of seawater (msw): one control dive with normal breathing through a regulator and one CESA dive involving continuous expiration without a mouthpiece during ascent. Lung ultrasound was conducted before and after immersion to quantify extravascular lung water (EVLW) using ultrasound lung comets (ULCs). In Step 2, four divers performed CESA from 5 and 10 msw, although ventilatory kinetics were recorded using a custom underwater pneumotachograph. All divers remained asymptomatic throughout. However, ULCs increased significantly after CESA dives (0 vs. 7.3 ± 4.6, <i>P</i> < 0.01), but not after control dives [0 vs. 0.7 ± 0.7, not significant (NS)], suggesting subclinical pulmonary stress. Ventilatory analysis revealed marked interindividual variability: preascent expirations ranged from 15% to 45% of slow vital capacity (SVC), and residual volumes at the surface were between 5% and 12% of SVC. These findings indicate that even trained divers do not consistently match expiratory effort to gas expansion, potentially increasing mechanical stress on the lungs. CESA training may, therefore, expose healthy individuals to silent alveolar stress, highlighting the need for improved monitoring tools and individualized ventilatory assessment during ascent training.<b>NEW & NOTEWORTHY</b> This is the first study to objectively quantify pulmonary stress and expiratory dynamics during controlled emergency swimming ascent (CESA) in healthy and trained divers. Using lung ultrasound and underwater spirometry, we demonstrate that CESA induces subclinical alveolar alterations and reveals wide variability in expiratory strategies. These findings challenge current assumptions about the safety and reproducibility of CESA training and suggest the need for individualized ventilatory monitoring in diving instruction.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"594-603"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of short-term high-altitude acclimatization on the relationship between cerebral blood flow and symptoms of mild acute mountain sickness in males.","authors":"Kazunobu Okazaki, Katsumi Asano, Masahiro Horiuchi","doi":"10.1152/japplphysiol.00434.2024","DOIUrl":"10.1152/japplphysiol.00434.2024","url":null,"abstract":"<p><p>People who climb high altitudes frequently experience headaches, which are the primary symptoms of acute mountain sickness (AMS). Although headaches and AMS are primarily caused by hypoxia, they remain poorly understood, specifically, the effects of regional cerebral blood flow on headache and AMS. In this high-altitude laboratory study, we investigated the hypothesis that regional cerebrovascular responses to high-altitude (3,776 m) sojourns are associated with AMS symptoms. The internal carotid artery (ICA), vertebral artery (VA), cardiorespiratory and vascular responses, and symptoms of AMS were assessed in eight healthy male lowlanders (mean age, 34 yr) at sea level (SL, 450 m) and on three consecutive days at the summit of Mount Fuji (3,776 m). Compared with sea level, ICA flow increased on <i>day 3</i> (<i>P</i> = 0.009) and ICA diameter increased on <i>days 1</i>-<i>3</i> (<i>P</i> < 0.001). In contrast, VA flow increased on <i>days 1</i> and <i>2</i> (<i>P</i> = 0.008 and <i>P</i> = 0.018, respectively) and VA velocity increased on <i>day 1</i> (<i>P</i> = 0.044). Headaches increased over the 3 days (<i>P</i> = 0.011 to <i>P</i> = 0.048), but AMS increased on <i>day 3</i> (<i>P</i> = 0.001). Repeated-measures correlation analysis revealed that changes in headaches from the previous day were correlated with percent changes in ICA diameter (<i>r</i>_rm = 0.596, <i>P</i> = 0.012), VA flow, and velocity (<i>r</i>_rm = 0.537, <i>P</i> = 0.026 and <i>r</i>_rm = 0.619, <i>P</i> = 0.008, respectively). Thus, a high-altitude-induced increase in cerebrovascular perfusion may contribute to the worsening of headaches, which is a typical AMS pathogenesis.<b>NEW & NOTEWORTHY</b> Acute mountain sickness (AMS) symptoms for 3 days at 3,776 m were assessed using volumetric cerebral blood flow. Internal carotid arterial (ICA) flow increased gradually, whereas vertebral arterial (VA) flow acutely increased on <i>day 1</i> but decreased thereafter. Headaches increased over 3 days, but AMS did not until <i>day 3</i>. Changes in headaches were correlated with those in ICA diameter and VA flow/velocity. Thus, a high-altitude-induced increase in cerebrovascular perfusion may contribute to worsening headaches.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"571-581"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal measurements of NO-mediated vasodilation and physical activity over 1 yr following endometriosis excision surgery: a passive experiment.","authors":"Auni C Williams, Virginia G Content, Raegan E Atha, Arpit Davé, Kristin Riley, Lacy M Alexander","doi":"10.1152/japplphysiol.00297.2025","DOIUrl":"10.1152/japplphysiol.00297.2025","url":null,"abstract":"<p><p>Women with endometriosis are at increased risk of cardiovascular disease and demonstrate endothelial dysfunction. The gold standard for diagnosis of endometriosis is through operative laparoscopy with surgical excision and histopathologic identification of endometrial-type glands and stroma. Symptoms of endometriosis are often immediately improved or resolved following excision surgery, but the cardiovascular impact of excision surgery is underappreciated. This passive experiment reports the longitudinal adaptations of the macrovascular and cutaneous microvascular endothelium in a single patient following surgical excision of endometriosis. The patient participated in multiple vascular research studies targeting nitric oxide-mediated vasodilation over the course of the succeeding 13 mo postsurgery. We show no nitric oxide (NO)-mediated vasodilation in the microvascular endothelium [-34 arbitrary units (AU)] and no flow-mediated dilation (FMD) in the brachial conduit artery (-0.06%) 1-mo postsurgery, with a recovery seeming to occur ∼8 mo postsurgery (178 AU, 3.69% FMD) that does not remain ∼13 mo postsurgery (3 AU, 0.43%). These values occur in tandem with reported exercise before testing [1,746 to 3,759 to 1,954 metabolic equivalent (MET) min/wk, respectively]. The results of these studies, placebo and baseline visits, are presented here. These findings suggest that microvascular endothelial function in an otherwise healthy young woman with endometriosis is not necessarily recovered following excision surgery, but may be dramatically improved with resistance exercise. Our data may lend insight into the progression of vascular dysfunction in this disease and the role of surgical versus lifestyle intervention in this realm.<b>NEW & NOTEWORTHY</b> This passive experiment demonstrates that vascular endothelial function is not recovered following endometriosis surgery but may be improved with resistance exercise.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"438-443"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12368910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of adipose tissue in critical illness-induced skeletal muscle wasting-new considerations for treatment approaches.","authors":"Casey L Sexton, Selene Meza-Perez, Konstantinos Papanikolaou, Tomasz M Kaminski, Marta Nowacka-Chmielewska, Piotr Rodak, Yi Lin, Thomas W Buford, Peter E Morris, Davis A Englund, Robert T Mankowski","doi":"10.1152/japplphysiol.00203.2025","DOIUrl":"10.1152/japplphysiol.00203.2025","url":null,"abstract":"<p><p>Critical illness-induced muscle wasting is associated with poor in-hospital and long-term outcomes, but prevention strategies are lacking. Critical illness elicits muscle wasting through upregulation of protein degradation and downregulation of protein synthesis via primary (i.e., modulation of ubiquitin-proteasome, autophagy-lysosome, calpain, and caspase-3 pathways) and secondary (i.e., bed rest/disuse, nutritional modulation, and accumulation of cellular damage) mechanisms. However, therapeutic targeting of these skeletal muscle mechanisms has not advanced the prevention of critical illness-induced muscle wasting, which may require exploring the roles of other peripheral organs. For example, recent research has demonstrated positive associations between whole-body adipose tissue mass, maintenance of muscle mass, and lower mortality rates in critically ill patients. However, having excess adiposity is often associated with impaired skeletal muscle remodeling due to blunted anabolic signaling, which has been tied to insulin resistance, lipid accumulation, and inflammation. Thus, the positive association between adiposity and beneficial outcomes in critical illness is paradoxical. This may be explained, at least partially, by an incomplete understanding of the processes by which adipose tissue influences skeletal muscle health and function in the context of critical illness. This review highlights the current evidence and key questions that warrant further investigations to improve understanding of the relationship between adipose tissue and skeletal muscle health. This knowledge may then be leveraged to facilitate new therapeutic approaches aimed at improving skeletal muscle health and functional outcomes in patients with critical illness.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"414-437"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultrasound detection of lymphatic bubbles in a porcine dive model.","authors":"Joshua B Currens, Richard E Moon, Matthew S Makowski, Michael J Natoli, Jayne Leypoldt, Jean Woolard, David Brown, Arian Azarang, Robert Brown, Eric Schinazi, Zach Ransom, Virginie Papadopoulou, Rachel M Lance","doi":"10.1152/japplphysiol.00171.2025","DOIUrl":"10.1152/japplphysiol.00171.2025","url":null,"abstract":"<p><p>Ultrasound is currently the optimal imaging modality in the decompression research field for assessing intracorporeal gas. Decompression sickness (DCS) is triggered by excess gas bubble presence in the body; however, the relationship is not well understood. Presently, the decompression physiology field does not have a strong predictive DCS biomarker. In this study, we explore the presence of lymph node decompression bubbles in a porcine model after a provocative hyperbaric exposure. Porcine test subjects (<i>n</i> = 37 subjects) underwent an aggressive decompression profile as part of a larger study, and a subsequent investigation of the left inguinal lymph node was conducted with ultrasound. Ultrasound images were assessed by three trained sonographers for lymph node bubbles. Regional brightness was analyzed after post hoc phantom-calibrated standardization of ultrasound depth and gain settings. Out of the 37 animals that we examined for lymph node bubbles, 17 were diagnosed with severe DCS and 14 identified to have lymph node bubbles. A postmortem dissection was conducted for a few animals, and bubbles could be found streaming from the lymph node corresponding to a severe DCS subject. The brightness assessment of the standardized ultrasound images indicated that DCS cases typically had a decrease in the region intensity after the dive with a potential peak sensitivity of 94.1% and specificity of 55% based on receiver-operating curve analysis. This study is the first noninvasive detection of lymph node decompression bubbles with confirmation of bubbles by postmortem dissection. A positive correlation between lymph node bubbles and DCS severity was found.<b>NEW & NOTEWORTHY</b> This is the first ever study to noninvasively detect lymphatic decompression bubbles and examine their correspondence with severe decompression sickness (DCS) outcome. The image brightness analysis found that subjects with severe DCS were likely to have darker lymph node images postdive indicating potential gas presence, after variable ultrasound system settings were unified post hoc. These findings may provide an early framework for a wearable ultrasound device to monitor real-time decompression stress.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"365-375"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol restores indices of neurovascular coupling following acute sleep restriction in young men and women.","authors":"Matthew J McDonald, Sharon D Fears, Samuel A Martin, Brian Shariffi, Todd L Lancaster, Jill A Kanaley, Jacqueline K Limberg","doi":"10.1152/japplphysiol.00402.2025","DOIUrl":"10.1152/japplphysiol.00402.2025","url":null,"abstract":"<p><p>Acute sleep restriction (4 h time in bed) impairs the link between neural activity and cerebral blood flow (i.e., neurovascular coupling, NVC). Nitric oxide (NO) is an important mechanism in the NVC response. Insufficient sleep increases reactive oxygen species (ROS) and reduces NO bioavailability. Resveratrol, a polyphenol with antioxidant properties, reduces ROS and improves vascular function. We hypothesized that NVC following acute sleep restriction would be improved with acute oral resveratrol supplementation. Sixteen adults (8 M/8 F, age: 28 ± 7 yr, 25 ± 3 kg/m²) completed two morning visits following a night of normal (NS; 449 ± 46 min) or restricted (RS; 243 ± 12 min) sleep. During each visit, middle (MCAv) and posterior (PCAv) cerebral artery velocity (transcranial Doppler ultrasound) were measured before and 45 min following oral resveratrol (250 mg) during: <i>1</i>) a validated visual search paradigm (Where's Waldo) and <i>2</i>) 5-min carbogen (95% O₂, 5% CO₂) air breathing. The peak cerebral blood velocity response to visual stimulation was reduced following sleep restriction (MCAV: NS 16 ± 7%, RS 11 ± 7%, <i>P</i> = 0.017; PCAv: NS 43 ± 13%, RS 32 ± 14%, <i>P</i> = 0.017) and restored with resveratrol in the PCA (RS + resveratrol: 40 ± 17%; <i>P</i> = 0.028), but not the MCA (RS + resveratrol: 9 ± 5%; <i>P</i> = 0.391). There was no effect of oral resveratrol on the peak response to visual stimulation following normal sleep. There was no effect of sleep restriction nor oral resveratrol on cerebrovascular response to carbogen air breathing. One night of RS (4 h time in bed) impairs NVC and resveratrol mitigates this impairment, particularly in the PCA. These results enhance our mechanistic understanding of sleep-associated impairments in NVC.<b>NEW & NOTEWORTHY</b> Herein, we demonstrate that one night of restricted sleep (4 h time in bed) impairs the link between neural activity and cerebral blood flow (i.e., neurovascular coupling, NVC) of both middle and posterior cerebral arteries, and oral resveratrol supplementation may mitigate these impairments, particularly in the posterior cerebral artery. These results enhance our mechanistic understanding of sleep-associated impairments in NVC and advance our knowledge of neurovascular dysfunction occurring after restricted sleep.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"376-383"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of physical activity, sedentary time, and sleep with maternal vascular function in women with a history of preeclampsia.","authors":"Virginia R Nuckols, Kristen G Davis, Meaghan Smith, Mariah L Carey, Blair Bell, Mark K Santillan, Donna A Santillan, Gary L Pierce","doi":"10.1152/japplphysiol.00928.2024","DOIUrl":"10.1152/japplphysiol.00928.2024","url":null,"abstract":"<p><p>A history of preeclampsia (hxPE) is associated with persistent vascular dysfunction and elevated risk of chronic hypertension. Twenty-four-hour activity behaviors, including physical activity, sedentary time (SED), and sleep, are modifiable factors that may promote favorable vascular function and blood pressure in women with a hxPE. The primary objective of this study was to investigate the cross-sectional relations between habitual physical activity, SED, and sleep with aortic stiffness and 24-h blood pressure patterns in young women with a hxPE and healthy pregnancy controls. Participants (<i>n</i> = 68; aged 21-42 yr, 1-5 yr after delivery) wore a thigh-mounted activity monitor (activPAL) for 7 days and maintained a sleep log to assess habitual physical activity, SED, and sleep duration. Participants underwent measures of aortic stiffness (measured by carotid-femoral pulse wave velocity, CFPWV) and 24-h ambulatory blood pressure monitoring (ABPM). Women with a hxPE (<i>n</i> = 33) did not differ in physical activity, SED, or sleep compared with healthy pregnancy controls (<i>n</i> = 35). SED (β = 0.214, 95CI [0.004, 0.416]) and light-intensity physical activity (β = -0.204, 95CI [-0.397, -0.004]) were independently related to CFPWV. Frequency of sleep disturbances, but not shorter sleep duration, was associated with higher 24-h diastolic blood pressure (β = 0.258, 95CI [0.009, 0.525]). Select perceived benefits and barriers to exercise were more pronounced among women with hxPE, and benefits were associated with higher moderate-vigorous physical activity (ρ = 0.43, <i>P</i> = 0.003). Our findings link habitual activity, pregnancy history, and perceived exercise benefits with aortic stiffness and identify population and behavioral targets to improve cardiovascular health in young parous women.<b>NEW & NOTEWORTHY</b> Preeclampsia is associated with persistent vascular dysfunction and incident hypertension, but the contributing behavioral factors are unclear. We demonstrate that greater light-intensity physical activity and lower sedentary time are associated with lower aortic stiffness, and link sleep disturbances to 24-h blood pressure among women with a recent history of preeclampsia and healthy pregnancy controls. Time spent in light intensity activity and sedentary behavior may represent interventional targets to mitigate elevated cardiovascular risk in postpartum women.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"384-393"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12335295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Central command activation during exercise is an essential mechanism to sustain diving bradycardia.","authors":"Marcela S Araújo, Adamor S Lima, Rosa V D Guerrero, Lauro C Vianna","doi":"10.1152/japplphysiol.00274.2025","DOIUrl":"10.1152/japplphysiol.00274.2025","url":null,"abstract":"<p><p>Previous studies have shown that the bradycardic response to diving is maintained or enhanced during exercise. However, the integrative mechanism by which diving-induced bradycardia supersedes exercise-induced tachycardia remains unclear. This study aimed to elucidate the contributions of central and peripheral afferent mechanisms to the diving response in humans under controlled laboratory conditions. Thirty-two healthy participants [17 males, 15 females; mean age: 22 ± 3 yr; body mass index (BMI): 24 ± 4 kg/m²] were exposed to simulated diving via trigeminal nerve stimulation (TGS) under three experimental conditions: <i>1</i>) voluntary light (LEx) and moderate (MEx) leg cycling exercise, <i>2</i>) passive exercise and the cold pressor test (CPT), and <i>3</i>) a combination of voluntary exercise and CPT. Continuous beat-to-beat heart rate (HR) and arterial blood pressure were measured, with surface electromyography confirming the absence of voluntary muscle contractions during passive cycling. TGS elicited significant bradycardia at rest, and this response was increased during voluntary LEx, and preserved during voluntary MEx when compared with rest. In contrast, compared with rest, the HR response to TGS during passive exercise was significantly attenuated, whereas CPT completely abolished the bradycardic response to TGS. However, during LEx combined with CPT, TGS elicited a significant bradycardic response when compared with CPT alone. Overall, these findings suggest that <i>1</i>) central command activation is an essential mechanism for sustaining the diving bradycardia; <i>2</i>) isolated peripheral afferent reflexes exert inhibitory feedback to regulate diving-induced bradycardia; and <i>3</i>) central and peripheral afferent feedback are important mechanisms by which volitional skeletal muscle contractions modulate the cardiovascular adjustments to \"diving.\"<b>NEW & NOTEWORTHY</b> Diving triggers conflicting heart rate control pathways: the diving response induces bradycardia, whereas muscular contraction engages neural signals that can cause tachycardia. Although bradycardia persists during exercise, the mechanisms by which diving-induced bradycardia overrides exercise-induced tachycardia are unclear. Our findings show that central command activation is essential for sustaining diving bradycardia, whereas peripheral afferent reflexes provide inhibitory feedback. These results advance our understanding of cardiovascular adaptations to diving, with implications for marine biology and exercise physiology.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"355-364"},"PeriodicalIF":3.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}