Human experimental anxiety: actual public speaking induces more intense physiological responses than simulated public speaking

Objectives: a) To perform a systematic and meta-analytic review to verify whether the Simulated Public Speaking Task (SPST) leads to a greater increase in self-rated anxiety than in physiological correlates of anxiety; and b) to compare the results obtained with the SPST with an actual public speaking task involving healthy volunteers. Methods: a) The PubMed and ISI Web of Knowledge databases were searched for studies involving the SPST prior to 2012. Eleven publications were eligible and provided data from 143 healthy volunteers for meta-analysis; b) 48 university students without somatic or psychiatric disorders were divided into three experimental groups of 16 subjects to undergo one of the following: SPST, real-world public speaking task (real-world), and control situation (control). Results: The meta-analysis showed that the SPST induced a significant increase in the Visual Analogue Mood Scale (VAMS) anxiety factor, but no significant increases in systolic blood pressure or heart rate. The empirical study showed that the real-world public speaking task increased heart rate, systolic blood pressure and diastolic blood pressure significantly more than the control and SPST conditions. Conclusions: These results suggest that real public speaking might be better than SPST in inducing experimental anxiety. .

Defense-related emotions in humans

The study of the role of serotonin in anxiety has led to the view that this neurotransmitter enhances anxiety, but inhibits panic. Validation of this hypothesis has been made using two experimental procedures that increase anxiety in human volunteers. One is classical conditioning of the skin electrical conductance response, which is assumed to represent anxiety. The other is simulated public speaking, which is believed to mobilize the same neural networks that are operative in panic and social anxiety disorders. In general, the results of these studies have fulfilled the predictions derived from the above hypothesis. The same procedures have been applied to panic disorder patients, and the obtained results have shown that these patients had a blunted anxiety response to public speaking. This speaking stress also did not activate the hypothalamic-pituitary-adrenal axis, which, in contrast, was activated by anticipatory anxiety. It may be concluded that anxiety and panic are qualitatively different emotional states, respectively related to the animal defense reactions to potential and proximal threat. In agreement, reported results of recent neuroimaging studies have shown that anxiety activates prefrontal cortical areas, whereas panic activates midbrain regions, particularly the periaqueductal gray matter. As a general conclusion, it may be said that anxiety, fear and panic do not belong to the same continuum of increasing intensity; instead, they are qualitatively different emotional states.