What is the clinical evidence from this study?

Study design: Observational. Population: Adverse childhood experiences (ACEs) (n=18). Intervention: High adverse childhood experiences (≥4 ACEs) vs. Low adverse childhood experiences (<4 ACEs). Primary outcome: Mean arterial pressure (MAP) during end-expiratory apnea (p=0.039).

What question did this study set out to answer?

This study aims to determine how adverse childhood experiences (ACEs) affect cardiac autonomic responses during apnea.

May 14, 2026

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

Q: What are the key findings of this study?

High adverse childhood experiences (≥4 ACEs) were associated with a lower mean arterial pressure response to end-expiratory apnea compared to low ACEs (88 vs 103 mmHg; p=0.039).

Q: What question did this study set out to answer?

This study aims to determine how adverse childhood experiences (ACEs) affect cardiac autonomic responses during apnea.

Key Result

High adverse childhood experiences (≥4 ACEs) were associated with a lower mean arterial pressure response to end-expiratory apnea compared to low ACEs (88 vs 103 mmHg; p=0.039).

Key Points

This study aims to determine how adverse childhood experiences (ACEs) affect cardiac autonomic responses during apnea.
Eighteen healthy young adults participated (12 females; mean age 22)
Participants assessed for ACEs and divided into low (<4 ACEs) and high (≥4 ACEs) groups
Cardiovascular responses measured during baseline and maximal voluntary end-expiratory apnea.
High ACEs group exhibited lower mean arterial pressure during EEA (p=0.039)
No significant differences in heart rate, stroke volume, or total peripheral resistance responses were found
A trending difference showed lower cardiac output in the high ACEs group (p=0.073).

Study Design

Type

Observational (n=18)

Structured PICO

Does high exposure to adverse childhood experiences impair the cardiac autonomic response to maximal voluntary end-expiratory apnea in healthy young adults?

Population

18 healthy young adults (12 females; mean age 22 ± 3 years).

Intervention

High exposure to adverse childhood experiences (≥4 ACEs, n=7)

Comparator

Low exposure to adverse childhood experiences (<4 ACEs, n=11)

Outcome

Autonomic control of cardiac and vascular responses (MAP, HR, SV, Q, and TPR) during the final 25% of maximal voluntary end-expiratory apnea (EEA)surrogate

High exposure to adverse childhood experiences is associated with a blunted mean arterial pressure response to maximal voluntary end-expiratory apnea, suggesting impaired cardiac autonomic function.

Main Result

Absolute Event Rate: 88% vs 103%

p-value: p=0.039

Abstract

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.

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