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都在增加。在 与此同时，全球老年人口正在增加。衰老与体温调节受损有关 在严重的环境高温事件中，会增加发病和死亡的风险。 伴随着衰老过程的是多种并存的发展，这可能会进一步损害 体温调节功能。据报道，在40岁的成年人中，超过40%的人患有肥胖症。 或者更老。脂肪组织的热性质(即，比热和导热系数相对于 瘦体重)，以及与非肥胖者相比，肥胖者的身体表面积与质量的比率较低， 可能会导致更多的热量储存和核心温度(TC)的上升，在那些肥胖的人在物理上 在高温下的活动。因此，肥胖者较大的热应激可能会增加与热应激相关的风险。 发病率和死亡率。65岁以上的成年人是发病率和死亡率的最高风险人群 与严重的环境热事件有关；然而，与肥胖相关的体温调节障碍可能 缩小与风险升高相关的年龄范围。大多数体温调节研究都是在 年轻人(18-30岁)和/或老年人(65岁以上)，对40-65岁或 中年和肥胖的复合效应。 人类体温调节反应是通过交感胆碱能系统介导的，该系统支配 皮肤，血管周围神经末梢释放乙酰胆碱和其他共递质(S)诱导 出汗和皮肤血管扩张。因此，减少出汗和反射性皮肤血管扩张 热应激可能是由于交感神经外流减少和/或终末器官反应性受损(例如，释放 血管扩张剂一氧化氮(NO))。据报道，人类肥胖的交感神经活动增加，典型的 测量肌肉交感神经活动或器官特异性去甲肾上腺素释放。然而，没有一项研究 检测了肥胖者在热应激期间的皮肤交感神经活动(SSNA)。因此，很少有 已知肥胖对热应激反应的交感神经控制的影响。 目前的建议旨在从机械上表征反射性出汗和交感神经控制 被动全身加热时的皮肤血管扩张反应(特定目标1)。那些机械的数据 将通过确定关键环境条件(环境温度和 湿度)，其中体温调节功能的改变可能危及在光物理期间的健康和安全 40-65岁肥胖和非肥胖成年人的活动(特定目标2)。这些研究的结果将是 可直接转化为开发基于证据的警报通信、策略决策、分类 即将发生的高温事件，以及实施药物干预和/或其他安全干预 在肥胖和非肥胖的成年人中。