Characterization of Cardiovascular Responses to Passive Whole-Body Heat Stress in Obese and Non-Obese Middle-Aged Adults

• Sponsor
  American Heart Association
  $230,247

• Principal investigator
  S. Tony Wolf
  Assistant professor, Department of Kinesiology
  

• Active since
  April 2025

Abstract

The global climate is warming, and the frequency, duration, and severity of heat waves are increasing. Aging is associated with impairments in thermoregulatory and cardiovascular (CV) function, resulting in a greater risk of morbidity and mortality during severe environmental heat events in those who are over the age of 65 relative to their younger counterparts.

Importantly, CV events are a contributing cause in most heat-related deaths. Obesity is reported in over 40% of adults aged 40 years and may exacerbate age-related decrements in thermoregulatory and CV function, thereby reducing the age range for increased risk of heat-related vulnerability. Rates of heat-related morbidity and mortality are greater in obese compared to non-obese adults. However, little is known about the impact of obesity on CV responses to heat stress. Obesity is associated with alterations of the metabolome that may increase CV health risk. Altered metabolomic profiles are associated with changes in cardiac autonomic modulation and blood pressure control.

The human response to heat stress includes CV adjustments that are mediated by the sympathetic arm of the autonomic nervous system. Thus, exaggerated CV strain during heat stress in obese adults may be due to increases in sympathetic nervous system activity that are related to metabolomic alterations. Racial identity is likewise associated with heat-related morbidity and mortality in the U.S.A., with rates in the non-Hispanic Black (NHB) population among the highest. The causes of this disparity are multifactorial, including socioeconomic (e.g., neighborhood characteristics, air conditioning availability, etc.) and health-related (e.g., cardiometabolic diseases and medication use) factors.

The NHB population experiences a disproportionate CV disease burden compared to all other groups in the US, and even young NHB adults have reduced microvascular function relative to their non-Hispanic White (NHW) counterparts. Thus, by middle age, NHB adults may experience increased CV strain during extreme heat exposures, although this has yet to be examined. We will investigate heat-related CV strain in middle-aged NHB and NHW adults with and without obesity, allowing us to separately and intersectionally characterize CV vulnerability of these two sub-populations in a warming climate. Further, we will examine whether metabolomic alterations are associated with exaggerated CV strain during heat stress in middle-aged adults with obesity.