(757.4) Effect of Acute Heat Exposure on the Pressor Response to a Voluntary Hypoxic Apnea: A Cross-Tolerance Study

Poster Board Number: E453

Heidi Cope (University of North Texas Health Science Center), Holden Hemingway (University of North Texas Health Science Center), Benjamin Saul (University of North Texas Health Science Center), Rauchelle Richey (University of North Texas Health Science Center), Amy Moore (University of North Texas Health Science Center), Austin Shokraeifard (University of North Texas Health Science Center), Albert Olivencia-Yurvati (University of North Texas Health Science Center), Michael Smith (University of North Texas Health Science Center), Steven Romero (University of North Texas Health Science Center)

The pressor response induced by a voluntary hypoxic apnea is exaggerated in individuals with obstructive sleep apnea and is strongly correlated to sympathetic overactivity. Acute heat exposure alters neural control of blood pressure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Therefore, we tested the hypothesis that acute heat exposure would attenuate the pressor response to a voluntary hypoxic apnea, and thereby manifest as a form of physiological cross-tolerance. Six young adults (2 females, 25 ± 1 yrs) were exposed to passive heat stress (water-perfused suit) sufficient to increase body core temperature by 1.2 °C. Voluntary hypoxic apneas were performed in duplicate before acute heat exposure (pre-heat) and in recovery when body core temperature returned to ≤ 0.3 °C of baseline. Participants breathed gas mixtures of varying FiO2 (21%, 16%, and 12%; randomized) for 1 min followed immediately by a 15 s end-expiratory apnea. Beat-by-beat arterial blood pressure (Finometer) and arterial oxygen saturation (finger pulse oximetry) were measured throughout. The pressor response was calculated as the difference between baseline mean arterial pressure and the peak response following each apnea. The change in arterial oxygen saturation during each apnea did not differ from pre-heat to recovery (FiO2 21%: pre-heat, Δ0 ± 1 % vs. recovery, Δ1 ± 2 %; FiO2 16%: pre-heat, Δ-4 ± 1 % vs. recovery, Δ-3 ± 1 %; FiO2 12%: pre-heat, Δ-9 ± 3 % vs. recovery, Δ-10 ± 4 %; P = 0.6 for interaction). The pressor response to a voluntary apnea was attenuated in recovery from acute heat exposure across all gas mixtures (FiO2 21%: pre-heat, Δ14 ± 11 mmHg vs. recovery, Δ10 ± 7 mmHg; FiO2 16%: pre-heat, Δ22 ± 15 mmHg vs. recovery, Δ15 ± 11 mmHg; FiO2 12%: pre-heat, Δ28 ± 15 mmHg vs. recovery, Δ21 ± 16 mmHg; P lt; 0.01 for main effect of time). These data suggest that acute heat exposure induces a cross-tolerance effect such that the pressor response to a voluntary hypoxic apnea is reduced. Acute heat exposure could improve hypertension in adults with obstructive sleep apnea, secondary to altered chemoreflex function and sympathetic neural control, and provide additional therapeutic options for this population to improve cardiovascular health.

UNTHSC Seed Grant