ABSTRACT
Stress reactivity refers to a stable individual difference in response to stressors. This article addresses three questions about reactivity: (1) Are cardiovascular, endocrine, and immune responses to acute laboratory stressors stable over time and across stressor tasks? (2) Are cardiovascular, endocrine, and immune reactors the same people? and (3) Are reactive people more vulnerable to stressor-induced effects on susceptibility to infectious disease? We conclude that for many individual indicators of physiological responsiveness to stressors there is moderate stability over time and across stressor tasks indicating the possible existence of underlying dispositional characteristics; the commonality of immune and cardiovascular and hormonal responses to stress depend on the nature of regulation of the immune response being assessed; reactivity appears to have implications for vulnerability to stressor-associated disease risk (stress-by-reactivity interaction) in the natural environment, but the exact nature of this vulnerability is not as yet entirely clear.
Subject(s)
Cardiovascular System/physiopathology , Endocrine System/physiopathology , Stress, Physiological/immunology , Adaptation, Physiological/immunology , Humans , Hypothalamo-Hypophyseal System/physiology , Individuality , Reproducibility of Results , Sympathetic Nervous System/physiologyABSTRACT
One hundred fifteen college students were exposed to an evaluative speech task twice, separated by 2 weeks. At both sessions, we assessed cardiovascular, endocrine, immune, and psychological response at baseline and during the task. We found stability across sessions for stress-induced increases in anxiety and task engagement, heart rate, blood pressure, norepinephrine (but not epinephrine), cortisol, natural killer cell cytotoxicity, and numbers of circulating CD3+, CD8+, and CD56+ (but not CD4+ or CD19+) lymphocytes. The stable cardiovascular, immune, and endocrine reactivities were intercorrelated, providing evidence of a unified physiological stress response across these outcomes. Although stable stress-induced increases in task engagement were associated with the physiological stress responses, stress-induced anxiety was not.
