Individuals exposed to adverse childhood events (ACE) have an increased risk of developing cardiovascular disease in adulthood. In addition, low heart rate variability (HRV) is associated with an increased risk of coronary heart disease and is an independent predictor of mortality. The HRV response to acute stress, such as the cold pressor test (CPT), provides insight into autonomic function. Whether or not ACE impacts autonomic function during the CPT has yet to be determined.PURPOSETo determine whether ACE influences HRV during the CPT.METHODS12 adult participants (aged 34±5 years) volunteered for this study, half of which were classified as HI‐ACE (ACE score ≥ 4; n=6) and the other half as NO‐ACE (ACE score = 0; n=6). All participants underwent a CPT protocol which consisted of a 5 min baseline, 3 min of right hand submersion in ice water (~2°C), and a 5 min recovery period. HRV was determined using inter‐beat intervals and calculation of the root mean square of successive differences (rMSSD). In addition, hemodynamic parameters including heart rate (HR), cardiac index (CI), mean arterial pressure (MAP), and total peripheral resistance index (TPRI) were measured throughout the CPT protocol using infrared fingertip plethysmography (Finapres NOVA).RESULTSDemographics were similar between groups and no differences (all p>0.05) were observed in baseline values of HR (61±9 vs.65±5 bpm), SBP (125±9 vs. 124±15 mm Hg), or DBP (78±8 vs. 71±10 mm Hg). rMSSD was significantly lower during the CPT compared to both baseline (p=0.032) and recovery (p=0.006) in NO‐ACE. No significant changes in rMSSD in response to CPT were observed in HI‐ACE. The hemodynamic (HR, CI, MAP, and TPRI) response to CPT was similar (all p>0.05) between ACE groups.CONCLUSIONThese data indicate that autonomic function, represented by rMSSD in response to CPT, is blunted in individuals who have experienced childhood adversity compared to those who have not. Given that the HI‐ACE group presented as normotensive and otherwise apparently healthy, future studies are needed to better understand contributors to autonomic dysfunction in this cohort.Support or Funding InformationSupported in part by NIH/NHLBI P01HL069999 (DMP, JSP, RAH).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.