Department of Marine Ecosystems and Society, Rosenstiel School of Marine and Atmospheric Sciences, University of Miami, Miami, Florida 33149, USA.
Leonard and Jayne Abess Center for Ecosystem Science and Policy, University of Miami, Coral Gables, Florida 33146, USA.
Ecology. 2017 Dec;98(12):3199-3210. doi: 10.1002/ecy.2049.
Predators can impact ecosystems through consumptive or risk effects on prey. Physiologically, risk effects can be mediated by energetic mechanisms or stress responses. The predation-stress hypothesis predicts that risk induces stress in prey, which can affect survival and reproduction. However, empirical support for this hypothesis is both mixed and limited, and the conditions that cause predation risk to induce stress responses in some cases, but not others, remain unclear. Unusually clear-cut variation in exposure of Cape fur seals (Arctocephalus pusillus pusillus) to predation risk from white sharks (Carcharodon carcharias) in the waters of Southwestern Africa provides an opportunity to test the predation-stress hypothesis in the wild. Here, we measured fecal glucocorticoid concentrations (fGCM) from Cape fur seals at six discrete islands colonies exposed to spatiotemporal variation in predation risk from white sharks over a period of three years. We found highly elevated fGCM concentrations in seals at colonies exposed to high levels of unpredictable and relatively uncontrollable risk of shark attack, but not at colonies where seals were either not exposed to shark predation or could proactively mitigate their risk through antipredatory behavior. Differences in measured fGCM levels were consistent with patterns of risk at the site and seasonal level, for both seal adults and juveniles. Seal fGCM levels were not correlated with colony population size, density, and geographic location. Investigation at a high risk site (False Bay) also revealed strong correlations between fGCM levels and temporal variation in shark attack rates, but not with shark relative abundance. Our results suggest that predation risk will induce a stress response when risk cannot be predicted and/or proactively mitigated by behavioral responses.
捕食者可以通过对猎物的消耗或风险效应来影响生态系统。从生理学上讲,风险效应可以通过能量机制或应激反应来介导。捕食压力假说预测,风险会给猎物带来压力,从而影响其生存和繁殖。然而,该假说的经验支持既混杂又有限,并且导致捕食风险在某些情况下而非其他情况下引起应激反应的条件仍不清楚。南非西南部水域的海角海豹(Arctocephalus pusillus pusillus)暴露于大白鲨(Carcharodon carcharias)捕食风险的程度异常明显,为在野外检验捕食压力假说提供了机会。在这里,我们在三年的时间里,从暴露于大白鲨捕食风险时空变化的六个离散岛屿的海角海豹身上测量了粪便皮质醇浓度(fGCM)。我们发现,在暴露于高水平不可预测且相对不可控制的鲨鱼攻击风险的海豹身上,fGCM 浓度非常高,但在未暴露于鲨鱼捕食或可以通过反捕食行为主动减轻其风险的海豹身上则不然。在测量的 fGCM 水平上的差异与该地点和季节性水平的风险模式一致,无论是海豹成体还是幼体。海豹的 fGCM 水平与种群大小、密度和地理位置无关。在高风险地点(False Bay)的调查还揭示了 fGCM 水平与鲨鱼攻击率的时间变化之间的强烈相关性,但与鲨鱼相对丰度无关。我们的研究结果表明,当风险无法预测且/或无法通过行为反应主动减轻时,捕食风险会引发应激反应。