Role of overweight and obesity on vascular responses to the cold pressor test and hypoxia in women.

IF 3.3 3区 医学 Q1 PHYSIOLOGY
Journal of applied physiology Pub Date : 2025-07-01 Epub Date: 2025-06-26 DOI:10.1152/japplphysiol.00162.2025
Natasha G Boyes, Dain W Jacob, Brian Shariffi, Anna M Gonsalves, Jennifer L Harper, Brian P Bostick, Jacqueline K Limberg
{"title":"Role of overweight and obesity on vascular responses to the cold pressor test and hypoxia in women.","authors":"Natasha G Boyes, Dain W Jacob, Brian Shariffi, Anna M Gonsalves, Jennifer L Harper, Brian P Bostick, Jacqueline K Limberg","doi":"10.1152/japplphysiol.00162.2025","DOIUrl":null,"url":null,"abstract":"<p><p>Sympathetic-mediated vasoconstriction is attenuated during hypoxia in young women with normal weight (NW) (i.e., hypoxic sympatholysis). Obesity is associated with exaggerated sympathetic nervous system activity that may augment sympathetic vasoconstriction and impair hypoxic sympatholysis. We hypothesized that hypoxic sympatholysis would be attenuated in women with overweight (OW) and obesity compared with women with normal weight. Forearm blood flow (FBF, venous occlusion plethysmography), muscle sympathetic nerve activity (MSNA, peroneal microneurography), blood pressure (finger plethysmography), and arterial oxygen saturation ([Formula: see text], pulse oximetry) were measured in women with normal weight (NW; <i>n</i> = 15; 24 ± 7 yr; 22 ± 2 kg/m<sup>2</sup>) and women with overweight/obesity (OW; <i>n</i> = 9; 27 ± 7 yr; 33 ± 5 kg/m<sup>2</sup>). Participants completed a cold pressor test (CPT) during normoxia (98 ± 1% [Formula: see text]) and hypoxia (82 ± 2% [Formula: see text]). Hypoxia increased MSNA burst frequency in NW but not in OW (<i>P</i> = 0.030). Sympathetic vasoconstriction (<i>P</i> = 0.909) and hypoxic vasodilation (<i>P</i> = 0.295) did not differ between groups. In contrast, hypoxic sympatholysis was lower in OW than NW (<i>P</i> = 0.029). Measures of adiposity were negatively associated with hypoxic sympatholysis: percent body fat (<i>r</i> = -0.406, <i>P</i> = 0.049), android fat (<i>r</i> = -0.443, <i>P</i> = 0.030), gynoid fat (<i>r</i> = -0.447, <i>P</i> = 0.029), and waist circumference (<i>r</i> = -0.458, <i>P</i> = 0.024). Hypoxic sympatholysis is attenuated in women with increased adiposity, despite preserved sympathetic vasoconstriction and hypoxic vasodilation compared with women with normal weight. These findings have implications for vascular control of blood flow in conditions associated with obesity and hypoxia (e.g., sleep apnea).<b>NEW & NOTEWORTHY</b> Sympathetic-mediated vasoconstriction is attenuated during hypoxia in young women with normal weight, demonstrating the expected hypoxic sympatholysis. Conversely, hypoxic sympatholysis is attenuated in women with increased adiposity, despite preserved sympathetic vasoconstriction and hypoxic vasodilation compared with women with normal weight. These data advance our understanding of the impact of obesity on neurovascular control of blood flow and have implications for individuals with obesity and conditions associated with hypoxia (e.g., sleep apnea).</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"239-248"},"PeriodicalIF":3.3000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278904/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of applied physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1152/japplphysiol.00162.2025","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/26 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Sympathetic-mediated vasoconstriction is attenuated during hypoxia in young women with normal weight (NW) (i.e., hypoxic sympatholysis). Obesity is associated with exaggerated sympathetic nervous system activity that may augment sympathetic vasoconstriction and impair hypoxic sympatholysis. We hypothesized that hypoxic sympatholysis would be attenuated in women with overweight (OW) and obesity compared with women with normal weight. Forearm blood flow (FBF, venous occlusion plethysmography), muscle sympathetic nerve activity (MSNA, peroneal microneurography), blood pressure (finger plethysmography), and arterial oxygen saturation ([Formula: see text], pulse oximetry) were measured in women with normal weight (NW; n = 15; 24 ± 7 yr; 22 ± 2 kg/m2) and women with overweight/obesity (OW; n = 9; 27 ± 7 yr; 33 ± 5 kg/m2). Participants completed a cold pressor test (CPT) during normoxia (98 ± 1% [Formula: see text]) and hypoxia (82 ± 2% [Formula: see text]). Hypoxia increased MSNA burst frequency in NW but not in OW (P = 0.030). Sympathetic vasoconstriction (P = 0.909) and hypoxic vasodilation (P = 0.295) did not differ between groups. In contrast, hypoxic sympatholysis was lower in OW than NW (P = 0.029). Measures of adiposity were negatively associated with hypoxic sympatholysis: percent body fat (r = -0.406, P = 0.049), android fat (r = -0.443, P = 0.030), gynoid fat (r = -0.447, P = 0.029), and waist circumference (r = -0.458, P = 0.024). Hypoxic sympatholysis is attenuated in women with increased adiposity, despite preserved sympathetic vasoconstriction and hypoxic vasodilation compared with women with normal weight. These findings have implications for vascular control of blood flow in conditions associated with obesity and hypoxia (e.g., sleep apnea).NEW & NOTEWORTHY Sympathetic-mediated vasoconstriction is attenuated during hypoxia in young women with normal weight, demonstrating the expected hypoxic sympatholysis. Conversely, hypoxic sympatholysis is attenuated in women with increased adiposity, despite preserved sympathetic vasoconstriction and hypoxic vasodilation compared with women with normal weight. These data advance our understanding of the impact of obesity on neurovascular control of blood flow and have implications for individuals with obesity and conditions associated with hypoxia (e.g., sleep apnea).

超重和肥胖对女性冷压试验和缺氧血管反应的作用
在体重正常的年轻女性中,交感神经介导的血管收缩在缺氧时减弱(即,缺氧交感神经溶解)。肥胖与过度的交感神经系统活动有关,可增强交感血管收缩并损害缺氧交感神经溶解。我们假设,与正常体重的女性相比,超重和肥胖女性的缺氧交感神经溶解会减弱。方法:测量正常体重女性(NW;n = 15;24±7年;22±2 kg/m2)和超重/肥胖女性(OW;n = 9;27±7年;33±5 kg / m2)。参与者在常氧(98±1% SpO2)和低氧(82±2% SpO2)条件下完成冷压试验(CPT)。结果:缺氧增加了西北地区的MSNA爆发频率,而无明显差异(p=0.030)。交感血管收缩(p=0.909)和缺氧血管舒张(p=0.295)两组间无差异。相比之下,低氧交感神经溶解较低(p=0.029)。肥胖的测量与低氧交感神经溶解呈负相关:体脂百分比(r=-0.406, p=0.049)、android脂肪(r=-0.443, p=0.030)、gynoid脂肪(r=-0.447, p=0.029)和腰围(r=-0.458, p=0.024)。结论:与体重正常的女性相比,尽管交感血管收缩和低氧血管舒张得以保留,但肥胖女性的低氧交感神经溶解减弱。这些发现对与肥胖和缺氧(如睡眠呼吸暂停)相关的血管血流控制具有启示意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
6.00
自引率
9.10%
发文量
296
审稿时长
2-4 weeks
期刊介绍: The Journal of Applied Physiology publishes the highest quality original research and reviews that examine novel adaptive and integrative physiological mechanisms in humans and animals that advance the field. The journal encourages the submission of manuscripts that examine the acute and adaptive responses of various organs, tissues, cells and/or molecular pathways to environmental, physiological and/or pathophysiological stressors. As an applied physiology journal, topics of interest are not limited to a particular organ system. The journal, therefore, considers a wide array of integrative and translational research topics examining the mechanisms involved in disease processes and mitigation strategies, as well as the promotion of health and well-being throughout the lifespan. Priority is given to manuscripts that provide mechanistic insight deemed to exert an impact on the field.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信