Obesity increases cardiovascular strain during passive heat stress in middle-aged women

Abstract

Heat waves are becoming more frequent and severe, and cardiovascular events are a contributing cause in most heat-related deaths. Obesity is reported in over 40% of adults over the age of 40 yrs, and is associated with greater heat-related mortality, although the precise mechanisms are not well-understood. To determine whether obesity increases heat-related cardiovascular vulnerability in middle-aged women, this study examined cardiovascular responses to passive whole-body heat stress in four obese (54 ± 11 yr; BMI: 33.1 ± 2.8) and four non-obese (55 ± 5 yr; BMI: 23.6 ± 0.8) middle-aged women. Red cell flux was measured at each site by laser-Doppler flowmetry (LDF) while reflex vasodilation was induced via whole-body heating using a water-perfused suit. After a 1.0°C rise in gastrointestinal temperature (ΔTgi), local skin temperature was increased to 43°C to elicit a maximal vasodilation response. Cutaneous vascular conductance was calculated (CVC = LDF/mean arterial pressure) and expressed as a percentage of maximum (%CVCmax) for each ΔTgi of 0.1°C. Heart rate (HR) was measured continuously and blood pressure (BP) was measured at each ΔTgi of 0.1°C, and rate pressure product (RPP; HR x systolic BP) was calculated as an index of cardiac strain. Percent body fat was measured with dual x-ray absorptiometry (DXA). Time to reach a ΔTgi of 1.0°C was not different between groups (Obese: 65 ± 16 min; Non-obese: 63 ± 13 min; p = 0.85). There was no group difference in CVCmax (Obese: 2.5 ± 0.6; Non-obese: 2.01 ± 0.3; p = 0.19). Likewise, there were no group differences in %CVCmax at baseline or any point throughout local heating (all p ≥ 0.47). RPP was not different between groups at baseline (Obese: 8840 ± 1160; Non-obese: 7492 ± 1081; p > 0.99), but increased to a greater degree in obese women such that there was a significant difference at ΔTgi of 1.0°C (Obese: 14162 ± 1910; Non-obese: 11393 ± 3448; p = 0.05). Further, %BF was directly related to peak RPP (p = 0.03; r = 0.75), but not resting RPP (p = 0.16). Obese women demonstrated an exaggerated RPP response for a given rise in %CVC (p < 0.0001, r = 0.82) relative to non-obese women (p = 0.21, r = 0.19; difference between slopes = 0.002). These data suggest that although thermoregulatory responses are preserved in obese middle-aged women relative to their non-obese counterparts, cardiovascular strain may be exaggerated in obese women for a given magnitude of thermoregulatory response, potentially contributing to increased heat-related mortality. This work was supported by NIH F32 AG079581 (STW) and a seed grant from the University of Georgia Obesity Research Initiative (STW). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.