Dept. of Physiology, Wayne State Univ. School of Medicine, Detroit MI 48201, USA.
J Appl Physiol (1985). 2011 Dec;111(6):1854-62. doi: 10.1152/japplphysiol.00961.2011. Epub 2011 Oct 6.
The negative effects of sympathetic overactivity on long-term cardiovascular health are becoming increasingly clear. Moreover, recent work done in animal models of cardiovascular disease suggests that sympathetic tone to the splanchnic vasculature may play an important role in the development and maintenance of these disease states. Work from our laboratory and others led us to hypothesize that a lack of chronic physical activity increases resting and reflex-mediated splanchnic sympathetic nerve activity, possibly through changes occurring in a key brain stem center involved in sympathetic regulation, the rostral ventrolateral medulla (RVLM). To address this hypothesis, we recorded mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (SSNA) in a group of active and sedentary animals that had been housed for 10-13 wk with or without running wheels, respectively. In experiments performed under Inactin anesthesia, we tested responses to RVLM microinjections of glutamate, responses to baroreceptor unloading, and vascular reactivity, the latter of which was performed under conditions of autonomic blockade. Sedentary animals exhibited enhanced resting SSNA and MAP, augmented increases in SSNA to RVLM activation and baroreceptor unloading, and enhanced vascular reactivity to α(1)-receptor mediated vasoconstriction. Our results suggest that a sedentary lifestyle increases the risk of cardiovascular disease by augmenting resting and reflex-mediated sympathetic output to the splanchnic circulation and also by increasing vascular sensitivity to adrenergic stimulation. We speculate that regular physical exercise offsets or reverses the progression of these disease processes via similar or disparate mechanisms and warrant further examination into physical (in)activity-induced sympathetic nervous system plasticity.
交感神经过度活跃对长期心血管健康的负面影响越来越明显。此外，最近在心血管疾病的动物模型中进行的研究工作表明，内脏血管的交感神经张力可能在这些疾病状态的发展和维持中发挥重要作用。我们实验室和其他实验室的工作使我们假设，缺乏慢性体力活动会增加静息和反射介导的内脏交感神经活动，这可能是通过涉及交感神经调节的关键脑干中枢（延髓头端腹外侧区，RVLM）发生的变化。为了验证这一假设，我们在一组活跃和久坐的动物中记录了平均动脉压（MAP）和内脏交感神经活动（SSNA），这些动物分别在有或没有跑步轮的情况下被饲养了 10-13 周。在氯醛酮麻醉下进行的实验中，我们测试了 RVLM 内注射谷氨酸的反应、对压力感受器卸载的反应以及血管反应性，后者是在自主神经阻断的情况下进行的。久坐的动物表现出静息 SSNA 和 MAP 增加，RVLM 激活和压力感受器卸载时 SSNA 增加增强，以及对α（1）-受体介导的血管收缩的血管反应性增强。我们的结果表明，久坐的生活方式通过增加内脏循环的静息和反射介导的交感神经输出，以及增加血管对肾上腺素能刺激的敏感性，增加了患心血管疾病的风险。我们推测，有规律的体育锻炼通过类似或不同的机制抵消或逆转这些疾病过程的进展，值得进一步研究身体（不）活动引起的交感神经系统可塑性。
