Characterization of passive and active whole-body heat stress responses in obese and non-obese adults

肥胖和非肥胖成人被动和主动全身热应激反应的特征

• 批准号: 10675123
• 负责人: Stephen Anthony Wolf
• 金额: $ 1.46万
• 依托单位: PENNSYLVANIA STATE UNIVERSITY, THE
• 依托单位国家: 美国
• 财政年份: 2023
• 资助国家: 美国
• 起止时间: 2023-06-08 至 2023-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10675123
• 关键词: Acetylcholine; Adipose tissue; Adult; Age; Aging; Attenuated; Blood Vessels; Blood flow; Body Surface Area; Cardiac Output; Circulation; Climate; Communication; Cutaneous; Data; Data Collection; Delaware; Development; Equilibrium; Equipment; Event; Exertion; Fatty acid glycerol esters; Frequencies; Funding; Health; Heat Stress Disorders; Heat Waves; Heating; Human; Humidity; Impairment; Individual; Infrastructure; Intervention; Laboratories; Light; Measures; Mediating; Metabolic; Morbidity - disease rate; Muscle; Nerve; Nitric Oxide; Non obese; Norepinephrine; Obesity; Organ; Participant; Pennsylvania; Physical activity; Physiologic Thermoregulation; Planet Earth; Policies; Population; Populations at Risk; Predisposition; Prevalence; Process; Property; Reflex action; Reflex control; Reporting; Reproducibility; Research; Resources; Risk; Risk Reduction; Safety; Sampling; Series; Severities; Skin; Sweating; System; Temperature; Thermal Conductivity; Thermogenesis; Thinness; Time; Training; Translating; Triage; Universities; Vasodilation; Vasodilator Agents; Weather; adult obesity; age related; aged; aging population; biological adaptation to stress; cholinergic; comorbidity; evidence base; human old age (65+); improved; innovation; middle age; mortality; obese person; parent grant; pharmacologic; response; thermal stress

Project Summary The global climate is warming, and the frequency, duration, and severity of heat waves are increasing. At the same time, the global population of aged adults is increasing. Aging is associated with impaired thermoregulatory function, resulting in increased risk of morbidity and mortality during severe environmental heat events. Accompanying the aging process is the development of multiple comorbidities that may further compromise thermoregulatory function. Obesity is one such comorbidity that is reported in over 40% of adults aged 40 years or older. The thermal properties of adipose tissue (i.e., lower specific heat and thermal conductivity relative to lean mass), as well as a lower body surface area-to-mass ratio in obese compared to non-obese individuals, may result in greater heat storage and rises in core temperature (Tc) in those who are obese during physical activity in the heat. Thus, greater heat strain in obese individuals may increase the risk of heat stress-related morbidity and mortality. Adults over the age of 65 are the most at-risk population for morbidity and mortality due to severe environmental heat events; however, thermoregulatory impairments associated with obesity may reduce the age range associated with elevated risk. Most thermoregulation research has been conducted on young (18-30 yrs) and/or older (65+ yrs) adults, with far less known about those in the 40-65 yr age range or the compounding effects of middle age and obesity. Human thermoregulatory responses are mediated through a sympathetic cholinergic system that innervates the skin, in which the release of acetylcholine and other cotransmitter(s) from the perivascular nerve terminal induces sweating and cutaneous vasodilation. As such, reductions in sweating and reflex cutaneous vasodilation during heat stress may be due to reduced sympathetic outflow and/or impaired end-organ responsiveness (e.g., release of the vasodilator, nitric oxide (NO)). Increased sympathetic activity has been reported in human obesity, typically measured as muscle sympathetic nerve activity or organ-specific norepinephrine release. However, no study has examined skin sympathetic nerve activity (SSNA) in obese individuals during heat stress. Therefore, little is known about the impact of obesity on the sympathetic control of thermoeffector responses to heat stress. The current proposal aims to mechanistically characterize the sympathetic control of reflex sweating and cutaneous vasodilation responses during passive whole-body heating (Specific Aim 1). Those mechanistic data will be translated by identifying critical environmental conditions (combinations of ambient temperature and humidity) in which altered thermoregulatory function may compromise health and safety during light physical activity (Specific Aim 2) in obese and non-obese adults aged 40-65 yrs. The findings from these studies will be directly translatable toward developing evidence-based alert communication, policy decisions, triage for impending heat events, and implementation of pharmacological interventions and/or other safety interventions in obese and non-obese adults.

项目摘要 全球气候正在变暖，热浪的频率，持续时间和严重程度正在增加。在 同时，全球老年成年人人口正在增加。衰老与温度调节受损有关 功能，导致在严重的环境热事件中增加发病率和死亡率的风险。 伴随衰老过程是多种合并症的发展，可能会进一步妥协 温度调节功能。肥胖就是一种合并症，在40％以上的40岁成年人中报道了一种合并症 或年龄较大。脂肪组织的热特性（即，相对于较低的特异性热和导热率相对于 与非肥胖个体相比 可能会导致更大的热量储存，并在身体中肥胖的人的核心温度（TC）上升 热量活动。因此，肥胖个体的更大热应变可能会增加与热应力有关的风险 发病率和死亡率。 65岁以上的成年人是发病率和死亡率最高的人口 发生严重的环境热事件；但是，与肥胖相关的温度调节障碍可能 减少与风险升高有关的年龄范围。大多数温度调节研究已在 年轻（18-30岁）和/或年龄较大（65岁以上）成年人，对40-65岁年龄范围或 中年和肥胖的复合作用。 人体温度调节反应是通过交感神经胆碱能系统介导的，该系统神经支配 皮肤，其中乙酰胆碱和其他共透明剂从血管周神经末端诱导 出汗和皮肤血管舒张。因此，减少出汗和反射皮肤血管舒张 热应力可能是由于交感神经流出减少和/或最终器官反应性受损所致（例如，释放 血管扩张剂，一氧化氮（NO）。人类肥胖症已经报道了同情活动的增加，通常是 以肌肉交感神经活性或器官特异性去甲肾上腺素的释放来衡量。但是，没有研究 在热应激期间，已经检查了肥胖个体的皮肤交感神经活动（SSNA）。因此，几乎没有 知道肥胖对热应激反应的交感神经控制的影响。 当前的建议旨在机械地表征反射出汗和的同情控制 被动全身加热期间皮肤血管舒张反应（特定目标1）。这些机械数据 通过识别关键环境条件（环境温度和 湿度）在轻度物理时，改变温度调节功能可能会损害健康和安全性 肥胖和非肥胖成年人40 - 65岁的活性（特定目标2）。这些研究的发现将是 直接转化为开发基于证据的警报沟通，政策决策，分类 即将进行的热量事件，并实施药理学干预措施和/或其他安全干预措施 在肥胖和非肥胖成年人中。