Forty-three subjects were stimulated in the laboratory to "fear" and "anger," during which the following physiological reactions were recorded: (1) heart rate, (2) ballistocardiogram, (3) respiration rate, (4) face temperature, (5) hand temperature, (6) skin conductance, and (7) integrated muscle potential. The scores used were the maximum rise and maximum fall from the preceding resting level and the number of responses of a critical value per unit time. Of the 14 scores thus obtained, 7 showed significant discrimination between anger and fear. Diastolic blood pressure rises, heart rate falls, number of rises in skin conductance, and muscle potential increases, were greater for anger than for fear, whereas skin conductance increases, number of muscle potential increases, and respiration rate increases were greater for fear than for anger. Profile difference scores, computed from appropriate combinations of these differences, were found to be greater than zero in 42 of the 43 cases and to have a mean which deviated very significantly from zero, which rejects the null hypothesis that there is no difference in physiological reaction between anger and fear.
The patterns obtained for anger and fear argue against the Arnold proposal that anger is a strong reaction of both the sympathetic and parasympathetic branches of the autonomic nervous systems, whereas fear is but a sympathetic reaction.
Another finding was the very low correlations among the physiological reactions and the significantly higher intercorrelations for anger than for fear, which was interpreted as indicating greater physiological integration during anger.
Between-subject variance was significantly greater than within-subject variance, which supports the findings of Lacey and Malmo that there is considerable specificity in physiological response patterns.
The physiological response patterns of anger were suggested as being similar to those produced by injections of epinephrine and nor-epinephrine combined, and those of fear as being similar to injections of epinephrine.
Support for this study was provided by the Laboratory of Social Relations at Harvard University; the Boston Psychopathic Hospital; and the Department of Psychiatry, University of Washington School of Medicine. Dr. and Mrs. Joseph Schachter and Andrew Jensen cooperated in this research.
Received July 29, 1952
Copyright © 1953 by American Psychosomatic Society