Does reproductive hormone status modulate the neural control of heat loss responses during heat stress in healthy female adults?

Introduction: A clearer understanding of how reproductive hormone concentrations affect temperature regulation is essential to expand our knowledge of female physiology. Resting core temperature fluctuates with changes in reproductive hormone levels. However, there is little to no evidence that these hormone fluctuations affect the output of heat loss responses during heat stress. Nonetheless, no studies have considered if variations in reproductive hormone concentrations affect the underlying neural control of heat loss responses. Objective & hypothesis: This study determined the effect of low vs. high reproductive hormone concentrations on the neural control of heat loss responses during heat stress in healthy female adults. Based on previous literature showing minimal effects of the output on heat loss responses, we hypothesized that the onset threshold for increases in skin sympathetic nerve activity (SSNA), local sweat rate (LSR), and cutaneous vascular conductance (CVC) do not differ between states of low and high reproductive hormone concentrations. Methods: Ten healthy females (20-35 years) were exposed to heat stress using a water-perfused suit (50°C) during states of low (days 1-7 post-menses [n=6], placebo phase of oral contraceptive use [n=3], or >12 weeks after intramuscular progestin injection [n=1]) and high (days 19-25 post-menses, active phase of contraceptive use, or < 12 weeks after progestin injection) reproductive hormone concentrations. Continuous measurements of SSNA (radial nerve), forearm LSR and CVC, were performed until esophageal temperature increased by 1.2°C. The mean body temperature (esophageal temperature × 0.8 + mean skin temperature × 0.2) onset threshold for SSNA, LSR, and CVC was determined using segmented linear regression. Data are presented as mean ± standard deviation or mean differences (high – low) with [95% confidence interval] and were analyzed with paired samples t-test (α of 0.05). Results: Estrogen (145 ± 55 pmol/L to 341 ± 242 pmol/L) and progesterone (1.6 ± 0.3 nmol/L to 12.0 ± 12.9 nmol/L) concentrations were greater (p< 0.05) during the high vs. low hormone phase. Baseline esophageal temperature was greater during the high (37.09 ± 0.24°C) vs. low (36.91 ± 0.30°C) hormone phase (0.18°C [0.01, 0.35], p=0.05). Baseline mean body temperature was 36.34 ± 0.31°C during the low phase and 36.54 ± 0.23°C during the high phase (0.20°C [-0.01, 0.40], p=0.06). The change in mean body temperature at the onset threshold for SSNA was 0.70 ± 0.31°C during the low phase and 0.74 ± 0.10°C during the high phase (-0.04°C [-0.23, 0.31], p=0.73). The onset threshold for forearm LSR and CVC was 0.80 ± 0.29°C and 0.81 ± 0.28°C during the low phase compared with 0.81 ± 0.12°C and 0.83 ± 0.19°C for the high phase (LSR: 0.00°C [-0.21, 0.22], p=0.98; CVC: -0.02°C [-0.19, 0.22], p=0.86). Conclusion: These results indicate that, despite resulting in a greater resting core temperature, a state of high reproductive hormone concentrations does not alter the neural control of heat loss responses during passive heat stress in healthy female adults. Funding: Natural Sciences and Engineering Research Council of Canada 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.