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

Pennsylvania State University, The, University Park PA

Investigators

Abstract

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.