Perturbations in growth trajectory due to early diet affect age‐related deterioration in performance

Lee, Who‐Seung; Monaghan, Pat; Metcalfe, Neil B.

doi:10.1111/1365-2435.12538

Cited by 25 publications

(24 citation statements)

References 60 publications

(101 reference statements)

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“…Several studies did demonstrate a reduced longevity in animals showing accelerated growth after dietary restrictions (e.g. Inness & Metcalfe, ; Lee, Monaghan, & Metcalfe, ), yet disentangling the effects of the life‐history acceleration from the nutritional effects is challenging in such design (Lee et al., ). By manipulating development time using different photoperiods, hence levels of perceived time stress, we avoided this problem.…”

Section: Discussionmentioning

confidence: 99%

Rapid larval development under time stress reduces adult life span through increasing oxidative damage

Janssens

Stoks

2018

Functional Ecology

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While a trade‐off between larval development and adult life span is key to understand why not all animals develop at their maximum rate and why life histories align along a fast‐slow continuum, it has been rarely studied. More general, the physiological mechanisms underlying life‐history trade‐offs are poorly understood and there is ongoing debate about the mediatory role of oxidative stress. We explicitly investigated the role of oxidative stress in mediating the trade‐off between larval development and adult life span in the damselfly Lestes viridis. We exposed larvae to time stress (by manipulating photoperiods) and manipulated oxidative stress levels using the mitochondrial uncoupler 2,4‐dinitrophenol (DNP) that causes a reduced production of reactive oxygen species. In addition, we considered other costs of an accelerated development in terms of reductions in immune function (the activity of phenoloxidase [PO]) and energy storage (fat content). Larvae accelerated their development but not growth under time stress, allowing to identify costs of rapid development without confounding effects of rapid growth. Rapid development came at the cost of a much shorter life span, which was associated with an increase in oxidative damage to lipids, proteins and DNA. Other costs in the adult stage of a rapid larval development included a lower body mass and reduced immune function, while the fat and protein contents were not reduced. Time‐stressed animals exposed to DNP developed even faster and did not show the increase in oxidative damage. Notably, they did not suffer the costs of rapid development: they had no shorter life span, lower body mass or reduced PO activity. Our results provide strong experimental support for a trade‐off between rapid development and life span and for the mediatory role of oxidative stress in shaping this life‐history trade‐off. Our study highlights that manipulation of mitochondrial uncoupling may be a powerful method to study the mechanistic underpinnings of life‐history trade‐offs. A http://onlinelibrary.wiley.com/doi/10.1111/1365-2435.13068/suppinfo is available for this article.

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Section: Discussionmentioning

confidence: 99%

Rapid larval development under time stress reduces adult life span through increasing oxidative damage

Janssens

Stoks

2018

Functional Ecology

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“…Depending on whether accelerated growth affects energy allocation, individuals that accelerate their growth rate through increased foraging may pay an immediate cost in the form of delays in structural development (Arendt and Wilson, 2000), individual performance (e.g. swimming sprinting speed; Killen et al, 2014)reduced investment in tissue maintenance (Morgan et al, 2000) or reproduction (Auer et al, 2010;Lee et al, 2012Lee et al, , 2016, increased risk of predation while foraging (Gotthard, 2000). Rapid growth may lead to longer-term costs when it results in damage at the physiological or cellular level (Jennings et al, 1999;andreviewed in Metcalfe andMonaghan, 2001, 2003) and on a decreased lifespan (Lee et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Can individual variation in phenotypic plasticity enhance population viability?

Maldonado-Chaparro

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Blumstein

2017

Ecological Modelling

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a b s t r a c tIn response to climatic and other sources of environmental variation, individuals within a population may adjust their behavioral, morphological or physiological responses to varying environmental conditions through phenotypic plasticity. In seasonal environments, time constraints related to seasonality, as well as variation in climatic factors, may affect body mass growth rates. To cope with the consequences of a harsh period, individuals may, for example, compensate for lost body mass by accelerating their growth rate in the following period. Phenotypically plastic responses like this can, therefore, directly affect body mass, which may affect individual fitness and, ultimately, population dynamics. Here, we use a well-studied population of yellow-bellied marmots, Marmota flaviventris, in Colorado to parametrize and develop an individual-based model (IBM) to investigate how phenotypically plastic responses in body mass growth rate may compensate for an individual's bad start after a harsh period (compensatory growth), and to explore whether individual variation in compensatory growth favors population persistence under less favorable climatic scenarios. A simulation model that allowed marmots with a body mass less than the population's average body mass to compensate their growth provided the best match with observed population sizes, suggesting the importance of trade-offs in population dynamics. We also found that compensatory growth plays an important role in decreasing the probability of extinction under both less favorable colder and random climate scenarios. Our results lead to a deeper understanding of the mechanisms that govern population fluctuations and highlight the importance of quantifying the fitness cost of phenotypically plastic responses.

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“…Both theoretical models and empirical studies have associated costs of compensatory growth with other fitness components (Metcalfe and Monaghan 2001, Yearsley et al 2004, Mangel and Munch 2005. For example, individuals that undergo compensatory responses during earlier life stages may have decreased ability to cope with starvation and oxidative stress (De Block and Stoks 2008a, Dmitriew and Rowe 2011, Gomez-Mestre et al 2013, reduced locomotion performance (Alonso-Alvarez et al 2006, Criscuolo et al 2011, life span (Lee et al 2013) or reproduction (Lee et al 2012(Lee et al , 2016. However, it is far from clear what the costs of the tradeoff between accelerated growth and fitness are, and on which fitness components these costs are reflected (Monaghan et al 2009, Auld et al 2010, as also conflicting results (i.e.…”

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confidence: 99%

Compensating for delayed hatching reduces offspring immune response and increases life‐history costs

Murillo-Rincón

Laurila

Orizaola

2016

Oikos

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Organisms are exposed to multiple sources of stress in nature. When confronted with a stressful period affecting growth and development, compensatory responses allow the restoration of individual fitness, providing an important buffering mechanism against climatic and other environmental variability. However, tradeoffs between increased growth/development and other physiological traits are predicted to prevent these high growth and development rates from becoming constitutive. Here, we investigated how compensatory responses in growth and development affect immune responses. By using low temperature to stop embryonic development, we exposed moor frog Rana arvalis tadpoles to two levels of time‐constraints: non‐delayed hatching and 12‐day delayed hatching. In a common garden experiment, we recorded larval growth and development, as well as their immune response, measured as the inflammatory reaction after the injection of phytohaemagglutinin (PHA). Tadpoles originating from delayed hatching treatments had a lower immune response to PHA challenge than those from the non‐delayed hatching treatment. In general, tadpoles from the delayed hatching treatment reached metamorphosis faster and at a smaller size than control tadpoles. However, immune‐challenged tadpoles were not able to accelerate their development in response to delayed hatching. Our results indicate that 1) the innate immune response can be reduced in organisms undergoing compensatory developmental responses in growth and development and 2) compensatory capacity can be reduced when organisms are immunologically challenged. These dual findings reveal the complexity of handling multiple stressors and highlight the importance of examining the costs and limits of mounting an immune response in the context of increasing phenological instability ascribed to climate change.

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Perturbations in growth trajectory due to early diet affect age‐related deterioration in performance

Cited by 25 publications

References 60 publications

Rapid larval development under time stress reduces adult life span through increasing oxidative damage

Rapid larval development under time stress reduces adult life span through increasing oxidative damage

Can individual variation in phenotypic plasticity enhance population viability?

Compensating for delayed hatching reduces offspring immune response and increases life‐history costs

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