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Dryad

Data from: Paceless life? a meta-analysis of the pace-of-life syndrome hypothesis

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Mar 05, 2019 version files 104.75 KB

Abstract

The pace-of-life syndrome hypothesis predicts that individual differences in behaviour should integrate with morphological, physiological, and life-history traits along a slow to fast pace-of-life continuum. For example, individuals with a “slow” pace-of-life are expected to exhibit a slower growth rate, delayed reproduction, longer lifespans, have stronger immune responses, and are expected to avoid risky situations relative to “fast” individuals. If supported this hypothesis would help resolve ecological and evolutionary questions regarding the origin and maintenance of phenotypic variation. Support for the pace-of-life syndrome hypothesis has, however, been mixed. Here we conducted a meta-analysis of 42 articles and 179 estimates testing the pace-of-life syndrome hypothesis as it applies to the integration of behaviours with physiological or life-history traits. We found little overall support for the pace-of-life syndrome hypothesis with the mean support estimated as r = 0.06. Support for the pace-of-life syndrome hypothesis was significantly higher in invertebrates (r = 0.23) than vertebrates (r = 0.02) and significantly higher when based on phenotypic (r = 0.10) versus genetic correlations (r = -0.09). We also found that females exhibited correlations between behaviour and life-history and physiology that were opposite the predictions of the pace-of-life syndrome hypothesis (r = -0.16) and that these correlations significantly differed from those observed in males (r = 0.01) or males and females pooled (r = 0.12). It was also the case that there was little support for the hypothesis when life-history and physiological traits were independently analysed (behaviour × life-history: r = 0.12; behaviour × physiology: r = 0.04). Exploratory post-hoc analyses revealed that correlations of behaviour with growth rate and hormone levels were more likely to show support for the predictions of the pace-of-life syndrome hypothesis. The lack of overall support found in our analyses suggests that general assertions regarding phenotypic integration due to “pace-of-life” and should be re-evaluated.