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

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.生命速率综合征假说（pace-of-life syndrome hypothesis）预测，个体的行为差异应与形态、生理及生活史特征沿慢至快的生命速率连续体实现整合。例如，相较于“快节奏”个体，“慢节奏”个体预计会表现出更缓慢的生长速率、延迟的繁殖时机、更长的寿命以及更强的免疫应答，且更倾向于规避风险情境。若该假说得到实证支持，将有助于解决有关表型变异起源与维持的生态学和进化学问题。然而，当前针对生命速率综合征假说的支持证据存在分歧。本研究针对42篇文献、共179项检验生命速率综合征假说的效应量开展元分析，该检验聚焦行为与生理或生活史特征的整合关联。整体而言，本研究未发现对该假说的显著支持，平均效应量r值为0.06。无脊椎动物类群中的支持度（r=0.23）显著高于脊椎动物类群（r=0.02）；基于表型相关（r=0.10）的研究支持度也显著高于基于遗传相关（r=-0.09）的研究。研究还发现，雌性个体的行为与生活史、生理特征间的相关方向与生命速率综合征假说的预测相反（r=-0.16），且该相关模式与雄性个体（r=0.01）或雌雄混合样本（r=0.12）观测到的结果存在显著差异。此外，当单独分析生活史与生理特征时，也未发现对该假说的足够支持：行为与生活史的相关系数为r=0.12，行为与生理的相关系数为r=0.04。探索性事后分析显示，行为与生长速率、激素水平的相关更易符合生命速率综合征假说的预测。本研究整体未发现对该假说的有效支持，表明基于“生命速率”的表型整合一般性论断有待重新评估。