(In)activity-related neuroplasticity in brainstem control of sympathetic outflow: unraveling underlying molecular, cellular, and anatomical mechanisms.
(In)activity-related neuroplasticity in brainstem control of sympathetic outflow: unraveling underlying molecular, cellular, and anatomical mechanisms.
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DOI：
10.1152/ajpheart.00929.2014
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发表时间：
2015-07
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影响因子：
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通讯作者：
N. Mischel;M. Subramanian;M. Dombrowski;I. Llewellyn-Smith;P. Mueller
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作者：
N. Mischel;M. Subramanian;M. Dombrowski;I. Llewellyn-Smith;P. Mueller
更多的人死于身体活动不足，而不是任何其他可预防的风险因素，包括吸烟，高胆固醇和肥胖。心血管疾病是美国的头号死因，也是与不活动有关的疾病之首。然而，绝大多数美国人继续选择生活方式，这给美国医疗保健系统造成了迅速增长的流行病规模和影响负担。我们必须提高对身体不活动增加心血管疾病发病率的机制以及运动如何预防或挽救不活动表型的理解。目前的审查总结了大脑的变化，有助于不活动相关的心血管疾病的研究。具体来说，我们专注于延髓头端腹外侧（RVLM），一个关键的基础和交感神经活动的反射控制的大脑区域的变化。RVLM与包括高血压和心力衰竭在内的几种心血管疾病相关的交感神经流出增加有关。我们假设RVLM的变化有助于与缺乏体力活动相关的慢性心血管疾病。从我们的翻译啮齿类动物模型的慢性，自愿运动和不活动的数据表明，功能，解剖和分子神经可塑性增强的RVLM的久坐动物的mammatergic神经传递。总的来说，这里提供的证据表明，久坐条件下引起的RVLM变化是有害的，并有助于心血管疾病，在久坐的个人中患病率增加。这些变化随时间发生的机制及其影响是未来研究的重要领域。
More people die as a result of physical inactivity than any other preventable risk factor including smoking, high cholesterol, and obesity. Cardiovascular disease, the number one cause of death in the United States, tops the list of inactivity-related diseases. Nevertheless, the vast majority of Americans continue to make lifestyle choices that are creating a rapidly growing burden of epidemic size and impact on the United States healthcare system. It is imperative that we improve our understanding of the mechanisms by which physical inactivity increases the incidence of cardiovascular disease and how exercise can prevent or rescue the inactivity phenotype. The current review summarizes research on changes in the brain that contribute to inactivity-related cardiovascular disease. Specifically, we focus on changes in the rostral ventrolateral medulla (RVLM), a critical brain region for basal and reflex control of sympathetic activity. The RVLM is implicated in elevated sympathetic outflow associated with several cardiovascular diseases including hypertension and heart failure. We hypothesize that changes in the RVLM contribute to chronic cardiovascular disease related to physical inactivity. Data obtained from our translational rodent models of chronic, voluntary exercise and inactivity suggest that functional, anatomical, and molecular neuroplasticity enhances glutamatergic neurotransmission in the RVLM of sedentary animals. Collectively, the evidence presented here suggests that changes in the RVLM resulting from sedentary conditions are deleterious and contribute to cardiovascular diseases that have an increased prevalence in sedentary individuals. The mechanisms by which these changes occur over time and their impact are important areas for future study.