Myocardial blood flow and flow reserve in young and older adults exposed to hot and dry heat stress

Heat waves cause a disproportionate number of deaths in older adults relative to any other age group. Adverse cardiac events are a leading cause of death during heat waves. Older adults, having impaired heat dissipating capabilities, experience greater increases in core temperature during environmental heat exposure, and therefore may be at a greater risk for heat-related cardiac events. We tested the hypothesis that older adults, compared to young adults, would have greater increases in myocardial blood flow and would require a greater percentage of their myocardial flow reserve during environmental heat stress. We performed myocardial contrast echocardiography in 9 young adults (5 males and 4 females, 25 ± 4 years) and 11 older adults (6 males and 5 females, 72 ± 3 years) on two separate occasions: 1) before and after a coronary vasodilator stress test (intravenous regadenoson) and 2) before and after a 3 h environmental heat exposure (conditions modelled after the 2021 North American heatwave: 44°C and 20% relative humidity). To simulate activities of daily living, participants performed six 5-minute periods of light exercise (~3 METS) dispersed across the heat exposure. The primary outcomes were core temperature, estimated myocardial oxygen consumption (MVO 2 ) using a standard equation (0.00072 x heart rate x systolic blood pressure + 1.42), myocardial blood flow (calculated as the product of myocardial blood volume A and microvascular flow velocity β), and percent myocardial flow reserve (calculated as the increase myocardial blood flow during heat stress divided by the increase in myocardial blood flow during regadenoson stress). Data were analyzed using linear mixed effects models with main effects of time, age, and the time by age interaction. The increase in core temperature was greater in older (1.5 ± 0.7°C) compared to young adults (0.7 ± 0.4°C; p=.011). Following heat stress, there was a 1.2-fold increase in estimated MVO 2 in young (7.0 ± 0.8 to 8.2 ± 1.3 mL/min) and older (7.3 ± 1.3 to 9.1 ± 2.5 mL/min) adults (main effect of time: p< .001). Heat stress increased myocardial blood flow by 1.4-fold in young (76 ± 34 to 104 ± 37 AU) and 1.7-fold in older (50 ± 20 to 83 ± 46 AU) adults (main effect of time: p< .001). However, there was no difference in the increase in estimated MVO 2 (Young: Δ 1.3 ± 0.9; Older: Δ 1.8 ± 1.4 mL/min; p=.34), the increase in myocardial blood flow (Young: Δ 28 ± 20; Older: Δ 33 ± 33 AU; p=.69), or percent myocardial flow reserve (Young: 35 ± 35; Older: 49 ± 65%; p=.58) between young and older adults. These findings demonstrate that 3 h of ambient heat stress increases MVO 2 and myocardial blood flow. Importantly, in this healthy cohort, the increase in myocardial blood flow was well under the peak myocardial blood flow induced by regadenoson. Further, despite substantially higher core temperatures in older adults, these myocardial responses were not different between young and older adults. Supported by ASE EDGES (JPM), NIH F32HL168826 (ZJM), and R01AG069005 (CGC) This abstract was presented at the American Physiology Summit 2026 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.