Stress affects core body temperature (Tc). Many kinds of stress induce transient, monophasic hyperthermia, which diminishes gradually if the stressor is terminated. Stronger stressors produce a longer-lasting effect. Repeated/chronic stress induces anticipatory hyperthermia, reduces diurnal changes in Tc, or slightly increases Tc throughout the day. Animals that are exposed to chronic stress or a cold environment exhibit an enhanced hyperthermic response to a novel stress. These changes persist for several days after cessation of stress exposure. In contrast, long-lasting inescapable stress sometimes induces hypothermia. In healthy humans, psychologic stress induces slight increases in Tc, which are within the normal range of Tc or just above it. Some individuals, however, develop extremely high Tc (up to 41°C) when they are exposed to emotional events or show persistent low-grade high Tc (37-38°C) during or after chronic stress situations. In addition to the nature of the stressor itself, such stress-induced thermal responses are modulated by sex, age, ambient temperature, cage mates, past stressful experiences and cold exposure, and coping. Stress-induced hyperthermia is driven by mechanisms distinct from infectious fever, which requires inflammatory mediators. However, both stress and infection activate the dorsomedial hypothalamus-rostral medullary raphe region-sympathetic nerve axis to increase Tc.
Keywords: brown adipose tissue; emotional fever; functional hyperthermia; hypothermia; psychogenic fever; stress; stress-induced hyperthermia.
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