Behavioural Ecology Division, Institute of Ecology and Evolution, University of Bern, Switzerland.
Centre for Ecology and Conservation, University of Exeter, Penryn Campus, UK; Institute for Data Science and Artificial Intelligence, University of Exeter, UK.
Horm Behav. 2022 Jun;142:105180. doi: 10.1016/j.yhbeh.2022.105180. Epub 2022 May 12.
Variation in stress responses has been investigated in relation to environmental factors, species ecology, life history and fitness. Moreover, mechanistic studies have unravelled molecular mechanisms of how acute and chronic stress responses cause physiological impacts ('damage'), and how this damage can be repaired. However, it is not yet understood how the fitness effects of damage and repair influence stress response evolution. Here we study the evolution of hormone levels as a function of stressor occurrence, damage and the efficiency of repair. We hypothesise that the evolution of stress responses depends on the fitness consequences of damage and the ability to repair that damage. To obtain some general insights, we model a simplified scenario in which an organism repeatedly encounters a stressor with a certain frequency and predictability (temporal autocorrelation). The organism can defend itself by mounting a stress response (elevated hormone level), but this causes damage that takes time to repair. We identify optimal strategies in this scenario and then investigate how those strategies respond to acute and chronic exposures to the stressor. We find that for higher repair rates, baseline and peak hormone levels are higher. This typically means that the organism experiences higher levels of damage, which it can afford because that damage is repaired more quickly, but for very high repair rates the damage does not build up. With increasing predictability of the stressor, stress responses are sustained for longer, because the animal expects the stressor to persist, and thus damage builds up. This can result in very high (and potentially fatal) levels of damage when organisms are exposed to chronic stressors to which they are not evolutionarily adapted. Overall, our results highlight that at least three factors need to be considered jointly to advance our understanding of how stress physiology has evolved: (i) temporal dynamics of stressor occurrence; (ii) relative mortality risk imposed by the stressor itself versus damage caused by the stress response; and (iii) the efficiency of repair mechanisms.
应激反应的变化与环境因素、物种生态学、生活史和适应性有关。此外，机制研究揭示了急性和慢性应激反应如何导致生理影响（“损伤”），以及这种损伤如何修复的分子机制。然而，目前尚不清楚损伤和修复的适应性影响如何影响应激反应的进化。在这里，我们研究了激素水平随应激源出现、损伤和修复效率的变化而进化的情况。我们假设应激反应的进化取决于损伤的适应性影响和修复损伤的能力。为了获得一些普遍的见解，我们模拟了一个简化的情景，即生物体反复遇到一个具有一定频率和可预测性（时间自相关性）的应激源。生物体可以通过发动应激反应（升高激素水平）来保护自己，但这会导致需要时间修复的损伤。我们在这种情况下确定了最佳策略，然后研究了这些策略如何应对急性和慢性应激源暴露。我们发现，对于更高的修复率，基线和峰值激素水平更高。这通常意味着生物体经历更高水平的损伤，它可以承受，因为损伤修复得更快，但对于非常高的修复率，损伤不会累积。随着应激源可预测性的增加，应激反应持续时间更长，因为动物预期应激源会持续存在，因此损伤会累积。当生物体暴露于它们没有进化适应的慢性应激源时，这可能导致非常高（甚至致命）的损伤水平。总的来说，我们的研究结果强调，至少需要考虑三个因素来共同推进我们对压力生理学是如何进化的理解：（i）应激源发生的时间动态；（ii）应激源本身造成的相对死亡率风险与应激反应引起的损伤造成的死亡率风险；（iii）修复机制的效率。
