Adverse childhood experiences (ACEs) affect the cardiac autonomic response to apnea

Adverse childhood experiences (ACEs)—e.g., physical and emotional abuse—are associated with autonomic dysfunction and increased risk for cardiovascular disease. Previous literature has demonstrated blunted cardiac autonomic responses to orthostatic stress (e.g., head-up tilt) in those with high exposure to ACEs. However, whether ACEs affect cardiac autonomic responses to other forms of physiological stress remains uncertain. This study tested the hypothesis that those with high ACEs will have a blunted cardiac autonomic response to maximal voluntary end-expiratory apnea (EEA) compared to those with low ACEs. Eighteen healthy young adults [12 females; 22 ± 3 (mean ± SD)] participated in this study. ACEs were assessed (Childhood Trust Event Survey 2.0), and participants were dichotomized into low [(< 4 ACEs) n=11] and high [(≥4 ACEs) n=7] exposure groups. Beat-by-beat mean arterial pressure (MAP; Finometer) and heart rate (HR; ECG) were measured during a 5-minute baseline and an EEA. Stroke volume (SV) and cardiac output (Q) were calculated with ModelFlow algorithm. Total peripheral resistance (TPR) was calculated as the quotient of MAP and Q. Autonomic control of cardiac and vascular responses to EEA (e.g., MAP, HR, SV, Q, and TPR) were analyzed during the final 25% of apnea. Independent t-tests were conducted. Across ACEs groups, there were no significant differences in age (Low ACEs: 22 ± 3, High ACEs: 21 ± 3 years; p = 0.455) or body mass index (Low ACEs: 25 ± 5 vs. High ACEs: 24 ± 5 kg/m 2 ; p = 0.925). At baseline, there were no differences in MAP (Low ACEs: 86 ± 9 vs. High ACEs: 79 ± 10 mmHg; p = 0.832), HR (Low ACEs: 69 ± 10 vs. High ACEs: 64 ± 11 bpm; p = 0.579), SV (Low ACEs: 90 ± 22 vs. High ACEs: 81 ± 14 mL; p = 0.322), Q (Low ACEs: 6 ± 1 vs. High ACEs: 5 ± 1 L/min; p = 0.147), or TPR (Low ACEs: 14 ± 3 vs. High ACEs: 16 ± 2 mmHg/L/min; p = 0.261). EEA duration did not differ between groups (Low ACEs: 33 ± 12 vs. High ACEs: 27 ± 6 s; p = 0.235). Compared to the low ACEs group, the high ACEs group MAP was lower during EEA (Low ACEs: 103 ± 14 vs. High ACEs: 88 ± 7 mmHg; p= 0.039). However, between groups there were no significant differences in HR (Low ACEs: 74 ± 13 vs. High ACEs: 70 ± 15 bpm; p = 0.530), SV (Low ACEs: 84 ± 18 vs. High ACEs: 72 ± 20 mL; p = 0.202), or TPR (Low ACEs: 18 ± 5.7 vs. High ACEs: 19 ± 5.1 mmHg/L/min; p = 0.581) responses to EEA. There was a trending difference in Q with the high ACEs group exhibiting a lower Q response (Low ACEs: 6 ± 2 vs. High ACEs: 5 ± 1 L/min; p = 0.073), suggesting HR and SV may be contributing to the lower MAP response. As evidenced by the blunted MAP response and a trending Q response, these data suggest that high ACEs exposure may impair the cardiac autonomic response to maximal EEAs. Further research is required to elucidate the underlying physiological mechanisms governing the blunted MAP response to EEA in individuals with high ACEs exposure. This study was supported by funding from the Brock University Advancement – Fund Explore Program. 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.