Adverse childhood family environment is associated with altered cardiovascular regulation during exercise: the CARDIA...

We determined whether adverse childhood family environment (ACFE) exposure is associated with altered hemodynamic responses to graded exercise in young adulthood, and whether this association was modified by sex and race. Methods: Exercising blood pressure (BP) and heart rate (HR) responses were recorded during graded exercise testing and ACFE exposure was assessed among 3,417 young adults (mean age = 25±4 y; 44% female; 46% Black). Linear mixed-effects models with exercising workload (METs) modeled as a within-subject, intensity-varying predictor and participant-specific random intercepts and slopes were used to assess the relation between ACFE exposure and exercising systolic (SBP), diastolic, and mean BP, pulse pressure (PP), pulse pressure index (PPI), HR, and rate pressure product (RPP), adjusted for resting hemodynamic values, age, sex, race, study center, BMI, antihypertensive medication, smoking, and alcohol. Results: Higher ACFE exposure was associated with lower SBP (β=-0.304 mmHg/ACFE, p=0.033), HR (β=-0.485 bpm/ACFE, p<0.001), and RPP (β=-83.404 bpm·mmHg/ACFE, p=0.002) at the lowest workload, but steeper workload-related increases in SBP (interaction β=0.044 mmHg·MET^-1·ACFE^-1, p=0.029), HR (β=0.061 bpm·MET^-1·ACFE^-1, p<0.001), RPP (β=10.16 bpm·mmHg·MET^-1·ACFE^-1, p=0.025), and PP (β=0.052 mmHg·MET^-1·ACFE^-1, p=0.038) and PPI (β=0.000232 units·MET^-1·ACFE^-1, p=0.018). Predicted hemodynamic responses converged across ACFE levels at moderate-to-vigorous intensities for SBP (11.0 METs), HR (12.0 METs), and RPP (12.3 METs), beyond which higher ACFE exposure was associated with progressively greater pulsatile and myocardial load responses. Sex and race generally did not moderate ACFE-hemodynamic associations. Conclusions: Early adversity is associated with a demand-dependent shift in cardiovascular regulation, with attenuated responses at low demand, but more dramatic increases in pulsatile and myocardial load responses during progressive physiological stress.