Caitlin P. Jarrard

We present novel data on between-visit cerebrovascular and cardiovascular reactivity reproducibility during the CPT. Relative agreement was stronger for BP and mean MCAv reactivity during the second minute of the CPT, suggesting that future work should use protocols >1 min. Cerebrovascular and cardiovascular variables had similar reproducibility; changes in [Formula: see text] and perceived pain significantly predicted CVCi reactivity. Controlling [Formula: see text] could improve reproducibility; future work could consider pain perception while assessing cerebrovascular reactivity to the CPT.

Comparing healthy young and older adults, we assessed left ventricular cardiac function (using echocardiography) during two separate 3-h extreme heat exposures in a very hot and dry or hot humid climate type. Although the augmentation of diastolic function and cardiac output were similar between age groups, older adults showed a greater increase in mitral annular systolic velocity with heat exposure, indicating a stronger reliance on systolic mechanisms to maintain stroke volume.

Addressing two unique aims, we observed that sublingual sufentanil administration does not impair tolerance or cardiovascular responses to lower-body negative pressure (LBNP)-induced progressive central hypovolemia. Second, despite pain perception being reduced, sublingual sufentanil did not attenuate mean blood pressure responses to a cold pressor test (CPT).

Herein we present plasma epinephrine and norepinephrine concentrations to 3 h of very hot and dry, as well as hot and humid, heat exposures with accompanying activities of daily living in young and older participants. We found 1) increased plasma concentrations of epinephrine in young and older adults following the hot and humid, but not the very hot and dry exposures and 2) decreased concentrations of norepinephrine in both groups following exposure to both conditions.

Profound heat stress can damage the gastrointestinal barrier, leading to microbial translocation from the gut and subsequent systemic inflammation. Despite the greater vulnerability of older people to heat wave-related morbidity and mortality, it is unknown if age modulates gastrointestinal barrier damage and inflammation during heat stress. Therefore, the aim of this study was to determine if aging impacted enterocyte damage and systemic inflammatory responses to a 3-h exposure to very hot and dry (47 °C, 15% humidity) heat with accompanying activities of daily living (intermittent activity at 3 METS). Data from 16 young (age 21 to 39 years) and 16 older (age 65 to 76 years) humans were used to address this aim. In each group, log-transformed plasma concentrations of intestinal fatty acid binding protein (I-FABP_log), interleukin-8 (IL-8_log), and tissue factor (TF_log) were assessed as indices of enterocyte damage, systemic inflammation, and blood coagulation, respectively, before and after the 3-h heat exposure. In the younger cohort, I-FABP_log concentration did not increase from pre to post heat exposure (p = 0.264, d = 0.20), although it was elevated in the older group (p = 0.014, d = 0.67). The magnitude of the increase in I-FABP_log was greater in the older participants (p = 0.084, d = 0.55). Across all participants, there was no correlation between the change in core temperature and the change in IFABP_log. There was no change in IL-8_log in the younger group (p = 0.193, d = 0.23) following heat exposure, but we observed a decrease in IL-8_log in the older group (p = 0.047, d = 0.48). TF_log decreased in the younger group (p = 0.071, d = 0.41), but did not change in the older group (p = 0.193, d = 0.15). Our data indicate that I-FABP_log concentration (an index of enterocyte damage) is increased in older humans during a 3-h extreme heat exposure. Future studies should determine whether this marker reflects increased gastrointestinal barrier permeability in older individuals during heat exposure.

Using an experimental model of extreme heat exposure that incorporates brief periods of light physical activity to simulate activities of daily living, the extent of thermal strain reported herein more accurately represents what would occur during actual heatwave conditions. Despite matching metabolic heat generation and environmental conditions, we show that older adults have augmented core temperature responses, likely due to age-related reductions in heat dissipating mechanisms.

Heatwaves cause disproportionately high mortality rates in those aged ≥ 65 years. While age differences in the cardiovascular responses to heat stress have been investigated, previous studies used a water-perfused suit to elicit heat stress. Therefore, how aging affects the cardiovascular responses to prolonged environmental heat stress is not fully understood. Purpose: We tested the hypothesis that 3 hours of exposure to a very hot and dry heat wave condition would increase core temperature and left ventricular systolic contractility (s’) to a greater extent in older, compared with younger adults. Methods: Healthy young (n = 13, 6F/7M, 29±4 years, 1.82±0.13 m-2) and older (n = 19, 10F/9M, 70±4 years, 1.85±0.18 m-2) adults were exposed to 47°C, 15% humidity) for 3-hours, interspersed with seven 5-minute bouts of physical activity at 3 METS to replicate heat generation associated with activities of daily living. Core temperature, brachial blood pressure and heart rate were monitored continuously during heating. Echocardiograms were obtained at baseline (in a thermoneutral environment) and at three hours into heat stress (i.e., post-heat wave) to assess s’. Drinking water was provided throughout the protocol to minimize dehydration. The magnitude of the change in each variable from baseline to post-heatwave between age groups was compared using independent samples t-tests. The association between the change in core temperature and the change in s’ was assessed with linear regression. Results: From baseline to 3-hour heatwave exposure, there was a greater increase in core temperature (Δ1.36±0.28 vs Δ0.74±0.28 °C, p < 0.0001) and s’ (Δ3.3±2.2 vs Δ1.6±1.8 cm/s, p = 0.011) in older, compared with younger subjects, respectively. However, the magnitude of the change in core temperature was not associated with the increase in s’ in older of young subjects (R2 = 0.065 and 0.120, respectively). The older subjects showed a greater decrease in mean arterial pressure compared with younger subjects (-14±10 vs -4±7 mmHg, p = 0.004). Heart rate increased similarly in older and young subjects (27±13 vs 27±12 b/min, p = 0.412). Conclusions: Our findings suggest that an index of left ventricular systolic contractility (s’) increases to a greater extent in older, compared with younger subjects. The change in s’ was not associated with the change in core temperature in either age group. Supported by NIH R01AG069005 (CGC), F32HL154559 & K01HL160772 (JCW), and F32HL154565 (LNB). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this Physiology was not involved in the peer review process.

The frequency, intensity, and duration of heat waves are projected to increase in the coming decades. Older adults have impaired heat-dissipating capabilities and are at a greater risk for heat-related morbidity and mortality. Many hospitalizations and deaths in this population during heat waves are due to renal complications. Indeed, age-related reductions in kidney function, altered fluid regulation, and impaired thermoregulation, may place the elderly at an increased risk for heat-related renal complications. Purpose: Therefore, we tested the hypothesis that aging augments heatwave-induced renal stress. Methods: We assessed core temperature, mean skin temperature, whole-body sweat loss, and estimated glomerular filtration rate (eGFR) via serum creatinine in healthy older (8 Female/7 Male; 70±4 years) and younger (6 Female/7 Male; 29±4 years) adults exposed to three hours of 1) very hot and dry (DRY: 47ºC, 10% relative humidity) and 2) hot and humid (HUMID: 41ºC, 40% relative humidity) heatwave conditions on different days (random order). To simulate activities of daily living, participants performed seven 5-minute periods of light exercise (~3 METS; metabolic heat production: Old: 2.98±0.42; Young: 2.96±0.34 W/kg) dispersed across the heat exposure. Additionally, participants consumed 3 mL/kg/hr of tap-temperature water to maintain euhydration. We analyzed data from each heatwave condition independently using linear mixed effect models with main effects of time (pre and post) and group (Older and Younger) or unpaired t-tests, as appropriate. Repeated measures correlation was used to determine any relation between the change (Δ) in core temperature and Δ eGFR across both heatwave conditions. Results: Following exposure to DRY, older adults had greater increases in core temperature (Older: Δ 1.46±0.42, Younger: Δ 0.74±0.28ºC, interaction p<0.01), but no difference in mean skin temperature increases (Older: Δ 2.09±1.31, Younger: Δ 1.73±0.48ºC, interaction p=0.404) or whole body sweat loss (Older: 1479±391, Younger: 1556±542 mL, p=0.661). In addition, following DRY, eGFR decreased in older but increased in younger adults (Older: Δ -4.3±5.9; Younger: Δ 4.12±4.75 mL/min/1.73 m2, interaction p<0.01). Following exposure to HUMID, older adults had greater increases in core temperature (Older: Δ 1.09±0.29, Younger: Δ 0.55±0.28ºC, interaction p<0.01) and mean skin temperature (Older: Δ 2.43±1.05, Younger: Δ1.37±1.13ºC, interaction p=0.018), but no difference in whole body sweat loss (Older: 979±304, Younger: 1011 ± 269 mL, p=0.774). eGFR increased in younger, but not older, adults (Older: Δ 0.30±4.01, Younger: Δ 6.16±3.37 mL/min/1.73 m2, interaction p<0.01) following HUMID. There was a significant negative relation between Δ core temperature and Δ eGFR (r=-0.48, p<0.01). Conclusion: These preliminary data suggest that older individuals exhibit greater increases in core temperature during heatwave exposures that may contribute to reducedrenal function. Supported by NIH R01AG069005 (CGC), F32HL154559 & K01HL160772 (JCW), and F32HL154565 (LNB). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this Physiology was not involved in the peer review process.