Sex Differences in Hemodynamic Response to Acute Passive Heat Exposure

A single bout of passive heat stress elicits an increase in cardiac output, a redistribution of blood flow, and a subsequent increase in conduit vessel shear stress. This increased shear stress acutely improves vascular function in a dose‐dependent manner and potentiates many of the beneficial vascular adaptations that accompany chronic heat therapy. However, physical and physiologic differences exist between sexes and influence the thermoregulatory response to passive heat stress. It is unknown if these sex‐related thermoregulatory differences alter the adaptive shear stimulus accompanying passive heat stress. Purpose To compare the hemodynamic response to acute passive heat exposure (APHE) between sexes. Methods 10 women (W) and 11 men (M) between the ages of 18–31 years completed a one‐hour APHE session immersed to the level of the sternum in 40°C water. W were studied under low hormone conditions. Rectal temperature (T re ), mean arterial pressure (MAP), and brachial and carotid artery hemodynamics (ultrasound) were measured at baseline (seated rest before APHE) and every 15 min throughout APHE. Automated wall‐tracking software was used to determine brachial and carotid diameter, velocity, flow, and total shear rate. Data are reported as mean ± SEM. Subject characteristics, reported as mean ± SD, were compared using unpaired t‐tests. A 2 X 5 mixed model ANOVA was used to compare T re , MAP, and brachial and carotid hemodynamics across time and between sexes. Results Both body mass (W: 62.9 ± 8.1 kg, M: 74.2 ± 5.1 kg, P < 0.01) and body surface area (W: 1.71 ± 0.14 m 2 , M: 1.93 ± 0.10 m 2 , P < 0.001) were lower in W compared to M. W had a higher T re than M ( P < 0.05) at baseline (W: 37.5 ± 0.1°C, M: 37.2 ± 0.1°C) and after 60 min APHE (W: 38.7 ± 0.03°C, M: 38.5 ± 0.1°C). W had a lower MAP than M ( P < 0.05) at baseline (W: 85 ± 2 mmHg, M: 88 ± 2 mmHg) and throughout APHE (W: 74 ± 2 mmHg, M: 82 ± 3 mmHg at 60 min APHE). W and M had a similar baseline brachial total shear rate (W: 170 ± 30 1/s, M: 105 ± 19 1/s). Brachial total shear rate was elevated to a greater extent in W than M during APHE ( P < 0.01), reaching 651 ± 49 1/s and 396 ± 24 1/s at 60 min APHE, respectively. The sex difference in brachial shear response to APHE was the result of a greater increase in brachial velocity seen in W (+47 ± 6 cm/s) compared to M (+35 ± 4 cm/s) with APHE ( P < 0.1). This elevated brachial velocity allowed for a similar increase in brachial blood flow between sexes with APHE (W: +339 ± 53 mL/min, M: +369 ± 37 mL/min) despite the smaller brachial diameter in W compared to M ( P < 0.0001) at baseline (W: 0.31 ± 0.01 cm, M: 0.41 ± 0.01 cm) and throughout APHE (W: 0.37 ± 0.01 cm, M: 0.46 ± 0.01cm at 60 min APHE). In contrast, no differences were seen between sexes in carotid total shear rate, flow, velocity, or diameter at baseline or throughout APHE. Conclusion These data indicate the presence of an artery‐specific sex difference in the hemodynamic response to a single bout of passive heat stress. Although a “threshold” or “dose‐response” relationship between shear stress and vascular adaptation has not been determined, these findings may have implications for sex‐specific vascular adaption accompanying chronic heat therapy. Support or Funding Information APS Porter Pre‐Doctoral Fellowship