Adverse childhood family environment is associated with altered cardiovascular regulation during exercise among young adults in the Coronary Artery Risk Development in Young Adults (CARDIA) Study.

UNLABELLED: The purposes of this study were to determine 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 in a large, population-based cohort. We hypothesized that ACFE exposure would be associated with an exaggerated exercise pressor response in young adulthood, independent of resting BP. We further hypothesized that the association between ACFE and the hemodynamic response to exercise would be stronger in females than males, and in Black versus White participants.

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 that included participant-specific random intercepts and random 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), heart rate (HR), and rate pressure product (RPP). All models were adjusted for resting values of the hemodynamic outcome, as well as age, sex, race, study center, body mass index, current hypertension medication use, smoking status, and alcohol consumption.

RESULTS

Graded exercise hemodynamic responses were analyzed in 3,346-3,417 participants in the final models, providing 15,372-17,481 observations. 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). These findings were robust to additional adjustment for central adiposity, exercise capacity, and maximal heart rate and heart rate recovery.

CONCLUSION

Our findings add nuanced evidence revealing that 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.