Obesity, not age, drives increased cardiovascular strain during passive heat stress in middle-aged compared with young women

As heat waves occur at higher frequency and severity due to global warming, so do the prevalence of heat-related cardiovascular events. Epidemiological and experimental data suggest that middle-aged and older women may be at greater heat-related risk compared to age-matched men. Likewise, obesity - a factor for over 40% of adults over 40 years of age - may increase cardiac strain during passive whole-body heating. The purpose of this study was to determine whether aging and obesity may synergistically cause an increase in cardiovascular strain during passive whole-body heat stress in middle-aged (MA) women. Three young healthy women (19 ± 2 yr; BMI: 24.2 ± 4.8), and four MA obese (54 ± 11 yr; BMI: 33.1 ± 2.8) and four MA non-obese (55 ± 5 yr; BMI: 23.6 ± 0.8) women were screened and included based on BMI. In the middle-aged women only, body fat percentage (MA obese: 45.83 ± 2.34%; MA non-obese: 35.95 ± 4.74%; p < 0.01) was measured using dual x-ray absorptiometry. Red blood cell flux was measured on the left forearm 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 (∆T gi ), 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 (%CVC max ) at baseline and at ∆T gi = 0.5°C and 1°C. Heart rate (HR) was measured continuously and blood pressure (BP) was measured at each ∆T gi = 0.1°C. Rate pressure product (RPP; HR x systolic BP) was calculated as an index of cardiac strain at ∆T gi = 0.5°C and 1°C. There were no differences among groups in baseline RPP (Young: 7694.5 ± 1296.6 mmHg·min -1 ; MA obese: 8840.8 ± 1159.6 mmHg·min -1 ; MA non-obese: 7491.8 ± 1081 mmHg·min -1 ; p ≥ 0.14) or %CVC max (Young: 25.6 ± 31.3%; MA obese: 6.7 ± 1.7%; MA non-obese: 8.9 ± 4.9%; p ≥ 0.43), nor were there differences in maximal CVC (p ≥ 0.12). There were no differences in %CVC max among groups at ∆T gi = 0.5°C (p ≥ 0.34). The %CVC max at ∆T gi = 1°C was lower in MA obese women compared to young women (Young: 70.2 ± 4.7%; MA obese: 61.3 ± 9.4%; p =.02), but was not different in MA non-obese women (52.7 ± 14.3%) compared to young (p = 0.052) or MA obese women (p = 0.54). RPP was significantly higher in MA obese women compared to young women at ∆T gi = 0.5°C (Young: 9384.3 ± 933.7 mmHg·min -1 ; MA obese: 11650.3 ± 1015.1 mmHg·min -1 ; p =.01) and at ∆T gi = 1°C (Young: 10191.7 ± 2335.9 mmHg·min -1 ; MA obese: 14162 ± 1910.3 mmHg·min -1 ; p =.006), and to MA non-obese women at 0.5°C rise (MA Non-obese: 9403 ± 1349.5 mmHg·min -1 ; p = 0.04). There were otherwise no differences in RPP among groups (p ≥ 0.16). Similarly, ∆RPP at ∆T gi = 1°C was higher in MA obese women compared to young women (Young: 2497.3 ± 2335.9 mmHg·min -1 ; MA obese: 5321.3 ± 1447.9 mmHg·min -1 ; p =.03), but there were otherwise no differences among groups (p ≥ 0.27). These data suggest that obesity, but not age, increases cardiovascular strain during passive whole-body heat stress in middle-aged women. This work was supported by NIH F32 AG079581 and a seed grant from the University of Georgia Obesity Research Initiative. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.