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）或心理上的（如争吵）。两个神经生物学网络被激活以响应压力源-交感神经延髓通路（SAM-p）和下丘脑-垂体-肾上腺轴（HPA-a）-以协调管理压力源所需的生理，认知和行为反应。交叉应激适应假说认为，重复经历相同类型的应激导致随着时间的推移，对相同应激的神经生物学反应减少或习惯化，以及对性质不同的应激的习惯化或敏感化（即更明显）反应。在人类研究中，大多数研究都集中在两种异质性压力源上，即身体锻炼和心理威胁，这些研究中的大多数都在实验室中诱导威胁，以测试身体活跃和不活跃的成年人之间的差异。这些研究假设，对心理威胁的神经生物学反应的明显差异是由于身体活跃的成年人反复暴露于运动的结果。然而，为了更好地了解潜在的机制，需要研究，检查直接的神经生物学反应，一轮的运动和由此产生的影响，神经生物学反应的心理威胁引起的急性心理社会应激源。 我们的第一项研究的初步结果表明，与中度或轻度运动相比，剧烈运动时皮质醇水平较高（即HPA-a激活程度较高），可介导45分钟后皮质醇对急性心理社会应激源的反应降低。在SAM-p活化方面没有差异。 目前的发现补助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）和模式（连续，间隔;有氧，阻力）被操纵时，急性运动的复杂生物学效应，以及它们如何与神经生物学反应性相关，并从随后的急性实验室诱导的心理社会应激源中恢复。我们进一步的目的是操纵运动回合和心理社会压力之间的流逝时间，以检查流逝的时间是否会影响跨压力适应的大小。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。 这项发现补助金将使我能够实施一项研究计划，该计划将确定与交叉压力适应相关的基本机制，为未来的调查打开大门，以测试重复的运动是否会导致对心理社会压力的反应减少，正如以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了解。

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.