Does diurnal variation in body mass affect take-off ability in wintering willow tits?

Kullberg, Cecilia

doi:10.1006/anbe.1998.0765

Cited by 82 publications

(66 citation statements)

References 24 publications

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“…The reason for supposing an impact on predation risk is that the laws of Newtonian physics would mean that an individual bird carrying excess weight would have a slower take-off speed and aerial manoeuvrability than a leaner individual that is likely to be disadvantageous during encounters with predators (Kenward, 1978;Lima, 1986;Sullivan, 1989;McNamara and Houston, 1990;Witter and Cuthill, 1993). Empirical data on escape and flight behaviour has often supported these assumptions (Metcalfe and Ure, 1995;Kullberg et al, 1996;Lees et al, 2014;Van Den Hout et al, 2010;Nudds and Bryant, 2002;Lind et al, 1999); however, results that contradict these assumptions have also been reported (Kullberg, 1998;van der Veen and Lindström, 2000;Jones et al, 2009;Macleod, 2006;Dierschke, 2003). Empirical studies of changes in fat storage under changes in predation pressure largely support the idea that fat storage is reduced when predation pressure (or perceived predation pressure) increases (Gosler et al, 1995;Cresswell, 1998;Rogers, 2015;Pascual and Carlos Senar, 2015;Zimmer et al, 2011;MacLeod et al, 2007;Cimprich and Moore, 2006;Macleod et al, 2005a,b;Ydenberg et al, 2004;Pérez-Tris et al, 2004;Piersma et al, 2003;Gentle and Gosler, 2001;van der Veen, 1999;Carrascal and Polo, 1999;Fransson and Weber, 1997;Pravosudov and Grubb, 1998;Rogers, 1987;Witter et al, 1994; but see …”

Section: Set-point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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Human obesity has a large genetic component, yet has many serious negative consequences. How this state of affairs has evolved has generated wide debate. The thrifty gene hypothesis was the first attempt to explain obesity as a consequence of adaptive responses to an ancient environment that in modern society become disadvantageous. The idea is that genes (or more precisely, alleles) predisposing to obesity may have been selected for by repeated exposure to famines. However, this idea has many flaws: for instance, selection of the supposed magnitude over the duration of human evolution would fix any thrifty alleles (famines kill the old and young, not the obese) and there is no evidence that hunter-gatherer populations become obese between famines. An alternative idea (called thrifty late) is that selection in famines has only happened since the agricultural revolution. However, this is inconsistent with the absence of strong signatures of selection at single nucleotide polymorphisms linked to obesity. In parallel to discussions about the origin of obesity, there has been much debate regarding the regulation of body weight. There are three basic models: the setpoint, settling point and dual-intervention point models. Selection might act against low and high levels of adiposity because food unpredictability and the risk of starvation selects against low adiposity whereas the risk of predation selects against high adiposity. Although evidence for the latter is quite strong, evidence for the former is relatively weak. The release from predation ∼2-million years ago is suggested to have led to the upper intervention point drifting in evolutionary time, leading to the modern distribution of obesity: the drifty gene hypothesis. Recent critiques of the dual-intervention point/ drifty gene idea are flawed and inconsistent with known aspects of energy balance physiology. Here, I present a new formulation of the dual-intervention point model. This model includes the novel suggestion that food unpredictability and starvation are insignificant factors driving fat storage, and that the main force driving up fat storage is the risk of disease and the need to survive periods of pathogen-induced anorexia. This model shows why two independent intervention points are more likely to evolve than a single set point. The molecular basis of the lower intervention point is likely based around the leptin pathway signalling. Determining the molecular basis of the upper intervention point is a crucial key target for future obesity research. A potential definitive test to separate the different models is also described.

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Section: Set-point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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“…The performance chamber consisted of a wooden frame 2.5!1!1 m covered with fine plastic netting (top and left end), black plastic sheeting (bottom), clear Plexiglas (front) and a white plastic back with a 10!10 cm grid. Given the important difference between alarmed and non-alarmed (also called routine or spontaneous) flight (Kullberg et al 1996;Kullberg 1998;Veasey et al 1998;Nudds & Bryant 2002), we initially modelled our chamber on that of Kullberg et al (2002a,b), with the bird being released at the bottom of the vertical chamber and vertical take-off ability being measured during the simulated escape flight. However, while this method was effective for adult birds, fledglings proved incapable of sustained vertical take-off.…”

Section: Methodsmentioning

confidence: 99%

Juveniles exposed to embryonic corticosterone have enhanced flight performance

et al. 2008

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Exposure to maternally derived glucocorticoids during embryonic development impacts offspring phenotype. Although many of these effects appear to be transiently 'negative', embryonic exposure to maternally derived stress hormones is hypothesized to induce preparative responses that increase survival prospects for offspring in low-quality environments; however, little is known about how maternal stress influences longer-term survival-related performance traits in free-living individuals. Using an experimental elevation of yolk corticosterone (embryonic signal of low maternal quality), we examined potential impacts of embryonic exposure to maternally derived stress on flight performance, wing loading, muscle morphology and muscle physiology in juvenile European starlings (Sturnus vulgaris). Here we report that fledglings exposed to experimentally increased corticosterone in ovo performed better during flight performance trials than control fledglings. Consistent with differences in performance, individuals exposed to elevated embryonic corticosterone fledged with lower wing loading and had heavier and more functionally mature flight muscles compared with control fledglings. Our results indicate that the positive effects on a survivalrelated trait in response to embryonic exposure to maternally derived stress hormones may balance some of the associated negative developmental costs that have recently been reported. Moreover, if embryonic experience is a good predictor of the quality or risk of future environments, a preparative phenotype associated with exposure to apparently negative stimuli during development may be adaptive.

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“…Models predicting daily foraging patterns of birds often assume a balance between the risk of starvation and the risk of predation because of the opposite effects that these two risks have in defining optimal energy reserves [2 -5]. Carrying large energy reserves in the form of fat reduces the risk of starvation if food supplies are interrupted, but this strategy may be maladaptive if too much fat were deposited because increasing weight decreases flight speeds and manoeuvrability, and exposes a bird to an increased risk of predation [2,6]; but also see [7].…”

Section: Introductionmentioning

confidence: 99%

Daily foraging patterns in free-living birds: exploring the predation–starvation trade-off

et al. 2013

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Daily patterns in the foraging behaviour of birds are assumed to balance the counteracting risks of predation and starvation. Predation risks are a function of the influence of weight on flight performance and foraging behaviours that may expose individuals to predators. Although recent research sheds light on daily patterns in weight gain, little data exist on daily foraging routines in free-living birds. In order to test the predictions of various hypotheses about daily patterns of foraging, we quantified the activity of four species of passerines in winter using radio-frequency identification receivers built into supplemental feeding stations. From records of 472 368 feeder visits by tagged birds, we found that birds generally started to feed before sunrise and continued to forage at a steady to increasing rate throughout the day. Foraging in most species terminated well before sunset, suggesting their required level of energy reserves was being reached before the end of the day. These results support the risk-spreading theorem over a long-standing hypothesis predicting bimodality in foraging behaviour purportedly driven by a trade-off between the risks of starvation and predation. Given the increased energetic demands experienced by birds during colder weather, our results suggest that birds' perceptions of risk are biased towards starvation avoidance in winter.

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Does diurnal variation in body mass affect take-off ability in wintering willow tits?

Cited by 82 publications

References 24 publications

The evolution of body fatness: trading off disease and predation risk

The evolution of body fatness: trading off disease and predation risk

Juveniles exposed to embryonic corticosterone have enhanced flight performance

Daily foraging patterns in free-living birds: exploring the predation–starvation trade-off

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