Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, New York, 14853, USA.
Ecology. 2018 Mar;99(3):681-689. doi: 10.1002/ecy.2132. Epub 2018 Feb 20.
Predators can alter nutrient cycles simply by inducing stress in prey. This stress accelerates prey's protein catabolism, nitrogen waste production, and nitrogen cycling. Yet predators also reduce the feeding rates of their prey, inducing food deprivation that is expected to slow protein catabolism and nitrogen cycling. The physiology of prey under predation risk thus balances the influences of predation risk and food deprivation, and this balance is central to understanding the role of predators in nutrient cycles. We explored the separate and combined effects of predation risk and food deprivation on prey physiology and nutrient cycling by exposing guppies (Poecilia reticulata) to predation risk and food deprivation in a 2 × 2 design. We simulated predation risk using chemical cues from a natural predator of guppies, and we created food deprivation by rationing food availability. We measured guppy response as food consumption, growth, tissue energy density, tissue carbon:nitrogen, and nitrogen (N) excretion and assimilation. We found that N-linked physiological processes (N consumption, assimilation, excretion) were strongly affected by predation risk, independent of food consumption. Guppies excreted substantially less under predation risk than they did under food deprivation or control conditions. These results suggest that predation risk, per se, triggers physiological changes in guppies that increase N retention and decrease N excretion. We suggest that slower N metabolism under predation risk is an adaptive response that minimizes protein loss in the face of predictable, predator-induced food restriction. Notably, N metabolism shares common hormonal control with food seeking behavior, and we speculate that increased N retention is a direct and immediate result of reduced food seeking under predation risk. Contrary to predation-stress-based hypotheses for how predators affect nutrient cycling by prey, our result indicates that even short-term exposure to predators may decelerate, rather than accelerate, the speed of N cycling by suppressing N turnover by prey.
掠食者可以通过在猎物身上引起应激来改变营养循环。这种应激会加速猎物的蛋白质分解代谢、氮废物产生和氮循环。然而，掠食者也会降低猎物的进食率，导致食物匮乏，从而减缓蛋白质分解代谢和氮循环。因此，猎物在被捕食风险下的生理学平衡了捕食风险和食物匮乏的影响，这种平衡是理解掠食者在营养循环中作用的核心。我们通过在 2×2 设计中使孔雀鱼（Poecilia reticulata）暴露于捕食风险和食物匮乏来探索捕食风险和食物匮乏对猎物生理学和营养循环的单独和综合影响。我们使用来自孔雀鱼的天然捕食者的化学线索模拟捕食风险，并通过定量食物供应来制造食物匮乏。我们通过衡量鱼的食物消耗、生长、组织能量密度、组织碳氮比和氮（N）排泄和同化来测量孔雀鱼的反应。我们发现，与食物消耗无关，N 相关的生理过程（N 消耗、同化、排泄）受到捕食风险的强烈影响。与食物匮乏或对照条件相比，孔雀鱼在捕食风险下的排泄量要少得多。这些结果表明，捕食风险本身会引发孔雀鱼的生理变化，从而增加 N 保留并减少 N 排泄。我们认为，在可预测的、由捕食者引起的食物限制下，捕食风险下较慢的 N 代谢是一种适应性反应，可最大限度地减少蛋白质损失。值得注意的是，N 代谢与觅食行为具有共同的激素控制，我们推测，在捕食风险下，由于觅食减少，N 保留增加是直接和即时的结果。与捕食压力假说相反，捕食者通过猎物影响营养循环的方式表明，即使短期暴露于捕食者也可能通过抑制猎物的 N 周转率来减缓而不是加速 N 循环的速度。
