Exercise effects on neural circuits for CVD risk

运动对心血管疾病风险神经回路的影响

• 批准号: 10181012
• 负责人: Kirk I Erickson
• 金额: $ 52.82万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-04-01 至 2023-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10181012
• 关键词: Address; Adult; Aerobic; Aerobic Exercise; Affect; Affective; Amygdaloid structure; Anterior; Area; Baroreflex; Behavioral; Biological; Biological Markers; Blood Vessels; Blood flow; Brain; Cardiac; Cardiovascular Diseases; Cardiovascular system; Cerebrum; Clinical; Control Groups; Data; Ecological momentary assessment; Emotions; Endothelium; Epidemiology; Equation; Event; Exercise; Experimental Designs; Functional Magnetic Resonance Imaging; Glucocorticoids; Guidelines; Health Status; Health education; Hippocampus (Brain); Immune; Individual; Insula of Reil; Insulin Resistance; Intervention; Life; Life Stress; Light; Measures; Medial; Mediating; Mediator of activation protein; Methods; Modeling; Moderate Exercise; Monitor; Morbidity - disease rate; Morphology; Neurobiology; Neurosecretory Systems; Oxidative Stress; Pathway interactions; Patient Self-Report; Perfusion; Peripheral; Physical activity; Physiologic pulse; Physiological; Physiology; Prefrontal Cortex; Process; Public Health; Randomized; Regulation; Risk Factors; Risk Marker; Social Interaction; Specific qualifier value; Stress; Stretching; Structure; Temporal Lobe; Testing; Time; Tissues; Visceral; Walking; Work; arterial stiffness; biobehavior; brain health; cardiorespiratory fitness; cardiovascular disorder risk; cingulate cortex; cohort; design; exercise intensity; exercise intervention; gray matter; heart rate variability; innovation; instrument; middle age; negative affect; neural circuit; neuroimaging; neuroregulation; novel; physical inactivity; psychological stressor; relating to nervous system; stress reactivity; synergism; treatment group; white matter

ABSTRACT Project 3 (Kirk Erickson, PL) Exercise effects on neural circuits for CVD risk The mechanisms by which physical activity (PA) may reduce CVD risk remain unclear. Multiple lines of evidence, however, show that PA – particularly aerobic exercise – exerts beneficial effects on brain health and brain plasticity. Critically, the brain areas reliably affected by exercise are visceral control areas under study in Projects (Ps) 1 and 2. These areas regulate aspects of peripheral autonomic, neuroendocrine, and immune physiology that are involved in conferring CVD risk and favorably affected by exercise. Accordingly, we propose to integrate historically separate lines of work on (1) exercise and CVD risk, (2) exercise and brain plasticity, and (3) exercise and stress, affect, and physiological control. To this end, we propose a 12-month intervention in which 150 midlife and inactive adults will be randomized to (1) 150 min/wk of moderate exercise (e.g., brisk walking; N=75) or (2) a light stretching control group with similar health instruction and social interaction as the treatment group (N=75). We will collect neuroimaging measures integral to Ps 1-2: behaviorally-evoked neural activity, cerebral perfusion and functional connectivity, white matter integrity, and gray matter morphology at 3 waves (baseline, 6-months, 12-months). Moreover, we use ambulatory CV monitoring and ecological momentary assessment (EMA) methods for the first time to test whether exercise impacts daily life stress physiology and affect, and whether these effects are partly explained by changes to visceral control areas. Our design allows us to test several hypotheses by the following Aims: Aim 1: To determine the neurobiology of exercise and biological CVD risk factors: (1A) Body-to-Brain hypothesis: Exercise-induced changes in peripheral markers of CVD risk (e.g., insulin resistance, cardiorespiratory fitness, peripheral vascular function) will precede and partly explain (statistically mediate) some of the exercise-induced changes in functional and structural features of areas defining visceral control circuits. (1B) Brain-to-Body hypothesis: Exercise-induced changes in functional and structural features of areas defining visceral control circuits precede and partly explain (statistically mediate) consequent changes in autonomic and neuroendocrine mediators of CVD risk that are under neural regulation, including baroreflex sensitivity, heart rate variability, and glucocorticoid control. Aim 2: To determine the neurobiology of exercise and stress- and affect-related CVD risk factors: (2A) Stress-related parameters of CVD risk: Exercise will induce changes in visceral control areas engaged by an fMRI stress battery, and these changes will partly explain exercise-induced reductions in cardiovascular stress reactivity in daily life (synergy with P's 1 & 2). (2B) Affect-related parameters of CVD risk: Exercise will induce changes in visceral control areas engaged by an fMRI emotion processing and regulation paradigm in synergy with P1, and these changes will partly explain exercise-induced improvements in affect measured in daily life by EMA and by conventional self-report instruments in synergy with P2. The public health significance of this Project is that it is designed to more precisely define and refine neurobiological targets to reduce CVD risk.

抽象的 项目 3（Kirk Erickson，PL） 运动对心血管疾病风险神经回路的影响 体力活动 (PA) 降低 CVD 风险的机制仍不清楚。 然而，有证据表明，体能活动（尤其是有氧运动）对大脑健康和健康产生有益影响。 至关重要的是，受运动影响的大脑区域是正在研究的内脏控制区域。 项目 (Ps) 1 和 2。这些区域调节外周自主神经、神经内分泌和免疫的各个方面 生理学与心血管疾病风险有关，并且受运动的有利影响。 整合历史上独立的工作线：(1) 运动和 CVD 风险，(2) 运动和大脑可塑性， (3) 运动与压力、情感和生理控制 为此，我们建议进行为期 12 个月的干预。 其中 150 名中年和不活跃的成年人将被随机分配到 (1) 每周 150 分钟的适度运动（例如轻快的运动） 步行；N=75) 或 (2) 轻度伸展对照组，其健康指导和社交互动与 我们将收集 Ps 1-2 中不可或缺的神经影像学测量：行为诱发。 神经活动、脑灌注和功能连接、白质完整性和灰质 3 波形态（基线、6 个月、12 个月）此外，我们使用动态 CV 监测和 首次采用生态瞬时评估（EMA）方法测试运动是否影响日常生活 压力生理和影响，以及这些影响是否部分由内脏控制区域的变化解释。 我们的设计使我们能够通过以下目标来测试几个假设： 目标 1：确定神经生物学 运动和生物性 CVD 危险因素的关系：(1A) 身体到大脑假说：运动引起的变化 CVD 风险的外周标志物（例如胰岛素抵抗、心肺健康、外周血管功能） 将先于并部分解释（统计介导）一些运动引起的功能和功能变化 定义内脏控制回路的区域的结构特征 (1B) 大脑到身体假说：运动引起的。 定义内脏控制电路的区域的功能和结构特征的变化先于并部分发生 解释（统计介导）CVD 风险的自主神经和神经内分泌介质的后续变化 受神经调节，包括压力反射敏感性、心率变异性和糖皮质激素 目标 2：确定运动和压力及情绪相关 CVD 危险因素的神经生物学：(2A) 心血管疾病风险的压力相关参数：运动会引起内脏控制区域的变化 fMRI 压力电池，这些变化将部分解释运动引起的心血管压力降低 日常生活中的反应性（与 P's 1 和 2 协同作用）（2B）影响 CVD 风险的相关参数：运动会诱发。 功能磁共振成像情绪处理和调节范式协同作用引起的内脏控制区域的变化 与 P1 相同，这些变化将部分解释运动引起的日常生活中测量的情感改善 EMA 和传统自我报告工具与 P2 的协同作用。 该项目旨在更精确地定义和完善神经生物学目标，以降低 CVD 风险。