Self-enhancement and cardiovascular reactivity: Limitations of the hemodynamic profile–compensation deficit (HP–CD) model of blood pressure regulation

• Published in: Biological psychology Vol. 92; no. 2; pp. 205 - 211
• Main Authors: Why, Yong Peng, Chen, Maximillian Ruyang
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.02.2013; Elsevier
• Subjects: Adolescent; Adult; Analysis of Variance; Behavioral psychophysiology; Biological and medical sciences; Blood Pressure - physiology; Cardiac Output - physiology; Cardiovascular; Cardiovascular System; Defense Mechanisms; Fundamental and applied biological sciences. Psychology; Heart Rate - physiology; Hemodynamic processes; Hemodynamics - physiology; Humans; Male; Models, Biological; Motivation - physiology; Psychological Tests; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Reactivity; Self-enhancement; Stress; Vascular Resistance - physiology; Young Adult; Self-enhancement; Reactivity; Hemodynamic processes; Cardiovascular; Stress; Compensation; Self image; Models; Blood pressure; Hemodynamics
• ISSN: 0301-0511; 1873-6246
• DOI: 10.1016/j.biopsycho.2012.08.010

► Self-enhancers developed a passive cardiovascular profile gradually. ► Significant effects for self-enhancement were absent when HP scores were used. ► Repeated acute stress resulted in an increase in resting cardiovascular baselines. ► HP–CD model does not discriminate between baseline and task cardiovascular changes. ► Analysing raw cardiovascular data is still superior to the HP–CD model. We examined the consistency of results obtained when examining the relationship between self-enhancement and cardiovascular reactivity via analysing raw cardiovascular data and compared this with the hemodynamic profile–compensation deficit (HP–CD) model of blood pressure regulation (James et al., 2012) method. A sample of 112 male participants underwent a computer-based task three times in three weeks. Our results indicate that significant results for self-enhancement and hemodynamic cardiovascular reactivity found using raw cardiovascular data were non-significant when HP–CD model was used. Furthermore, the HP–CD model also obfuscates significant baseline changes with reactivity. We also found that the correlations between blood pressure reactivity and hemodynamic processes obtained in the laboratory setting was reduced rather than enhanced with the use of the HP–CD model. Our results suggest that the HP–CD model should be used cautiously and could contribute to inconsistent results when examining the role of psychological factors in biological outcomes.