Effects of Different Features of a Single Bout of Exercise on Neurobiological Activation and Recovery Following Induction of Psychological Threat

压力源可以是身体上的（如锻炼、寒冷暴露）或心理上的（如争吵）。面对压力源，两个神经生物学网络被激活——交感神经髓通路（SAM-p）和下丘脑-垂体-肾上腺轴（HPA-a）——协调生理、认知和行为反应，以应对压力源。交叉压力源适应假说认为，对同一类型压力源的重复经历会导致对同一压力源的神经生物学反应随着时间的推移而减少或习惯化，并且对性质不同的压力源的反应要么习惯化，要么敏感化（即更明显）。在人类研究中，大多数研究集中在两种异型压力源上，即体育锻炼和心理威胁，这些研究大多在实验室中诱导威胁，以测试运动和不运动的成年人之间的差异。这些研究假设，活跃的成年人对心理威胁的神经生物学反应的明显差异是由于反复接触运动造成的。然而，为了更好地理解潜在的机制，需要进行研究，检查对一次运动的即时神经生物学反应，以及它们对急性社会心理压力源引起的心理威胁的神经生物学反应的影响。我们针对这个问题的第一项研究的初步结果表明，与中度或轻度运动相比，剧烈运动后皮质醇水平更高（即更大的HPA-a激活），会在45分钟后介导对急性社会心理压力源的皮质醇反应降低。在SAM-p激活方面无差异。当前发现基金的目的是概述和实施一系列严格的实验，以了解当强度（中等，剧烈，高强度）和模式（连续，间歇；有氧，抵抗）被控制时急性运动的复杂生物学效应，以及它们如何与随后急性实验室诱导的社会心理压力源的神经生物学反应和恢复有关。我们进一步的目的是操纵运动和社会心理压力源之间的时间，以检验时间是否影响交叉压力源适应的大小。最后，我们将测试在性别，年龄或心肺健康的交叉点是否存在差异。这项发现基金将允许我实施一个研究项目，以确定与交叉压力源适应相关的基本机制，为未来的研究打开大门，测试反复锻炼是否会导致对心理社会压力源的反应减少，正如之前的准实验研究所证明的那样。这项研究将加深我们对与人类生命科学和行为神经科学相关的基本机制的认识。

Stressors can be physical (e.g. exercise, cold exposure) or psychological in (e.g. arguments). Two neurobiological networks are activated in response to stressors - the sympathomedullary pathway (SAM-p) and hypothalamus-pituitary-adrenal axis (HPA-a) - to coordinate physiological, cognitive, and behavioural responses necessary to manage the stressor. The cross-stressor adaptation hypothesis suggests that repeated experiences with the same type of stressor lead to a reduced, or habituated, neurobiological response over time to that same stressor, and either habituated or sensitized (i.e. more pronounced) responses to stressors dissimilar in nature. In human research, the majority of studies have focused on two heterotypic stressors, namely physical exercise and psychological threat, and the majority of these studies induced threat in the lab to test differences between physically active and inactive adults. These studies make the assumption that apparent differences in neurobiological responses to psychological threat result from the repeated exposure to bouts of exercise in physically active adults. To better understand the underlying mechanisms, however, research is required that examines the immediate neurobiological responses to a single bout of exercise and their resulting effects on neurobiological responses to psychological threat induced by an acute psychosocial stressor. Our preliminary results from our first study tackling this question demonstrate that higher levels of cortisol (i.e. greater HPA-a activation) in response to vigorous exercise, as compared to moderate or light, mediates the reduced cortisol response to an acute psychosocial stressor that follows 45 minutes later. No differences were evidenced in SAM-p activation. The purpose of the current Discovery Grant is to outline and implement a series of rigorous experiments to understand the complex biological effects of an acute bout of exercise when intensity (moderate, vigorous, high) and mode (continuous, interval; aerobic, resistance) are manipulated and how they may relate to the neurobiological reactivity to and recovery from a subsequent acute laboratory-induced psychosocial stressor. We further aim to manipulate the elapsed time between the exercise bout and psychosocial stressor to examine whether elapsed time impacts the magnitude of the cross-stressor adaptation. Finally, we will test if there are differences at the intersection of sex, age, or cardiorespiratory fitness. This Discovery Grant will allow me to implement a program of research that will identify fundamental mechanisms associated with cross-stressor adaptation, opening the door to future investigations that test whether repeated bouts of exercise lead to reduced responses to psychosocial stressors, as evidenced in previous quasi-experimental studies. This research will deepen our knowledge of fundamental mechanisms relevant to human life sciences and behavioural neuroscience.