The effect of fasting and body reserves on cold tolerance in 2 pit-building insect predators.

Pit-building antlions and wormlions are 2 distantly-related insect species, whose larvae construct pits in loose soil to trap small arthropod prey. This convergent evolution of natural histories has led to additional similarities in their natural history and ecology, and thus, these 2 species encounter similar abiotic stress (such as periodic starvation) in their natural habitat. Here, we measured the cold tolerance of the 2 species and examined whether recent feeding or food deprivation, as well as body composition (body mass and lipid content) and condition (quantified as mass-to-size residuals) affect their cold tolerance. In contrast to other insects, in which food deprivation either enhanced or impaired cold tolerance, prolonged fasting had no effect on the cold tolerance of either species, which had similar cold tolerance. The 2 species differed, however, in how cold tolerance related to body mass and lipid content: although body mass was positively correlated with the wormlion cold tolerance, lipid content was a more reliable predictor of cold tolerance in the antlions. Cold tolerance also underwent greater change with ontogeny in wormlions than in antlions. We discuss possible reasons for this lack of effect of food deprivation on both species' cold tolerance, such as their high starvation tolerance (being sit-and-wait predators).

The negative effect of starvation and the positive effect of mild thermal stress on thermal tolerance of the red flour beetle, Tribolium castaneum.

The thermal tolerance of a terrestrial insect species can vary as a result of differences in population origin, developmental stage, age, and sex, as well as via phenotypic plasticity induced in response to changes in the abiotic environment. Here, we studied the effects of both starvation and mild cold and heat shocks on the thermal tolerance of the red flour beetle, Tribolium castaneum. Starvation led to impaired cold tolerance, measured as chill coma recovery time, and this effect, which was stronger in males than females, persisted for longer than 2 days but less than 7 days. Heat tolerance, measured as heat knockdown time, was not affected by starvation. Our results highlight the difficulty faced by insects when encountering multiple stressors simultaneously and indicate physiological trade-offs. Both mild cold and heat shocks led to improved heat tolerance in both sexes. It could be that both mild shocks lead to the expression of heat shock proteins, enhancing heat tolerance in the short run. Cold tolerance was not affected by previous mild cold shock, suggesting that such a cold shock, as a single event, causes little stress and hence elicits only weak physiological reaction. However, previous mild heat stress led to improved cold tolerance but only in males. Our results point to both hardening and cross-tolerance between cold and heat shocks.

Temperate Drosophila preserve cardiac function at low temperature.

Most insects are chill susceptible and will enter a coma if exposed to sufficiently low temperature. This chill coma has been associated with a failure of the neuromuscular system. Insect heart rate (HR) is determined by intrinsic regulation (muscle pacemaker) with extrinsic (nervous and humoral) input. By examining the continually active heart of five Drosophila species with markedly different cold tolerance, we investigated whether cardiac performance is related to the whole animal critical thermal minimum (CTmin). Further, to separate the effects of cold on extrinsic and intrinsic regulators of HR, we measured HR under similar conditions in decapitated flies as well as amputated abdomens of Drosophila montana. Cardiac performance was assessed from break points in HR-temperature relationship (Arrhenius break point, ABP) and from the HR cessation temperature. Among the five species, we found strong relationships for both the HR-ABP and HR cessation temperatures to whole animal CTmin, such that temperate Drosophila species maintained cardiac function at considerably lower temperatures than their tropical congeners. Hearts of amputated abdomens, with reduced extrinsic input, had a higher thermal sensitivity and a significantly lower break point temperature, suggesting that central neuronal input is important for stimulating HR at low temperatures.

Cold-induced depolarization of insect muscle: differing roles of extracellular K+ during acute and chronic chilling.

Insects enter chill coma, a reversible state of paralysis, at temperatures below their critical thermal minimum (CTmin), and the time required for an insect to recover after a cold exposure is termed chill coma recovery time (CCRT). The CTmin and CCRT are both important metrics of insect cold tolerance that are used interchangeably, although chill coma recovery is not necessarily permitted by a direct reversal of the mechanism causing chill coma onset. Nevertheless, onset and recovery of coma have been attributed to loss of neuromuscular function due to depolarization of muscle fibre membrane potential (Vm). Here we test the hypothesis that muscle depolarization at chill coma onset and repolarization during chill coma recovery are caused by changes in extracellular [K(+)] and/or other effects of low temperature. Using Locusta migratoria, we measured in vivo muscle resting potentials of the extensor tibialis during cooling, following prolonged exposure to -2°C and during chill coma recovery, and related changes in Vm to transmembrane [K(+)] balance and temperature. Although Vm was rapidly depolarized by cooling, hemolymph [K(+)] did not rise until locusts had spent considerable time in the cold. Nonetheless, a rise in hemolymph [K(+)] during prolonged cold exposure further depressed muscle resting potential and slowed recovery from chill coma upon rewarming. Muscle resting potentials had a bimodal distribution, and with elevation of extracellular [K(+)] (but not temperature) muscle resting potentials become unimodal. Thus, a disruption of extracellular [K(+)] does depolarize muscle resting potential and slow CCRT following prolonged cold exposure. However, onset of chill coma at the CTmin relates to an as-yet-unknown effect of temperature on neuromuscular function.