Abstract
ABSTRACTStress-induced hyperthermia (SIH) is commonly observed during handling in homeotherms. However, in birds, handling in cold environments typically elicits hypothermia. It is unclear whether this indicates that SIH is differently regulated in this taxon or if it is due to size, because body temperature changes during handling in low temperatures have only been measured in small birds <0.03 kg (that are more likely to suffer high heat loss when handled). We have therefore studied thermal responses to handling stress in the intermediate-sized (0.5–1.0 kg) Svalbard ptarmigan (Lagopus muta hyperborea) in 0°C and −20°C, in winter and spring. Handling caused elevated core body temperature and peripheral vasoconstriction that reduced back skin temperature. Core temperature increased less, and back skin temperature decreased more, in −20°C than in 0°C, probably because of higher heat-loss rate at the lower temperature. Responses were qualitatively consistent between seasons, despite higher body condition/insulation in winter and dramatic seasonal changes in photoperiod, both of which could possibly affect stress responsiveness. Our study supports the notion that SIH is a general thermoregulatory reaction to acute stressors in endotherms, but also suggests that body size and thermal environment should be taken into account when evaluating this response in birds.
Highlights
Stress-induced hyperthermia (SIH) is a ubiquitous feature of the body’s response to acute stressors, such as restraint or altered social context, in mammals and birds (e.g. Briese and Cabanac, 1991; Cabanac and Briese, 1992; Carere and Van Oers, 2004; Gray et al, 2008; Korhonen et al, 2000; Meyer et al, 2008)
I.e. the time taken for Tc to return to pre-handling levels for at least 30 s once the stressor had been removed, was longer in 0°C (13.4± 1.1 min) than in −20°C (5.6±1.4 min) by 7.8±1.8 min (+138%) (P
Handling of Svalbard ptarmigan was associated with increased Tc and Thead and decreased Tback that lasted, on average, 6.6 to 9.7 min after the stressor had been removed (Fig. 2)
Summary
Stress-induced hyperthermia (SIH) is a ubiquitous feature of the body’s response to acute stressors, such as restraint or altered social context, in mammals and birds (e.g. Briese and Cabanac, 1991; Cabanac and Briese, 1992; Carere and Van Oers, 2004; Gray et al, 2008; Korhonen et al, 2000; Meyer et al, 2008). It is believed that the increase in core body temperature (Tc) during SIH represents a sympathetically mediated elevation of the hypothalamic set point, i.e. an ‘active hyperthermia’ resembling pathogen-induced fevers (Briese and Cabanac, 1991; Kluger et al, 1987; Oka et al, 2001; Vinkers et al, 2009). SIH is sometimes referred to as ‘stress fever’ or. The diversion of peripheral blood flow to the core, together with stressinduced tachycardia and increased ventilation rate (Cabanac and Aizawa, 2000; Cabanac and Guillemette, 2001; Greenacre and Lusby, 2004; Mans et al, 2012) probably prepares the animal for escape or interaction (i.e. a ‘fight or flight’ response). Simultaneous centralization of the blood pool and increased blood clotting function could minimize blood loss in the event of injury (Cannon, 1915)
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