ANALYSIS OF HEART RATE VARIABILITY

已经证实，无论是正常体重还是正常体重的变化 肥胖受试者伴有自主神经活动的变化 神经系统。这可能很重要，因为自主神经功能可能 能量代谢变化的效应臂，这种变化往往会恢复 诱发体重变化后的体重恢复到“正常”体重 体重减轻或体重增加。我们用药理学研究的方法 心脏功能的自主控制作为一般自主神经的估计 活动。具体地说，以前测量过患者的心脏周期 在心脏选择性β-1肾上腺素能阻滞剂和毒扁豆碱 胆碱能阻断以获得交感神经控制和 副交感神经控制。同时，心率的频谱分析 可变性是对这些参数的进一步估计，也是为了 确定封锁的充分性。 已经有可能表明，不仅是自主神经的变化 正常体重变化时的功能，但肥胖的人在平时 肥胖者的体重与非肥胖者不同。肥胖者往往有 较低的副交感控制和较高的交感控制。我们相信 这使得自主神经的主要缺陷不太可能 系统对肥胖负有责任。更有可能的是，自主神经的变化 发现的只是当脂肪质量增加或减少时出现的那些 通过实验手段。 我们建议利用这些评估自主神经功能的技术 不仅由热量变化引起的体重反应的研究，而且 同样是通过药物的管理，这些药物反过来也会影响能量 新陈代谢。肥胖者自主神经功能改变的程度 通常权重的状态也将作为一种衡量标准进行评估，可能会有所不同 不同的遗传因素在肥胖的发病机制中起重要作用。 随着人们对人类肥胖的分子遗传学有了更好的理解，每一种 将对出现的亚型进行自主神经功能评估。

It has been established that alterations in body weight both in normal and in obese subjects are accompanied by changes in activity of the autonomic nervous system. This may be important since autonomic function may be an effector arm of alterations in energy metabolism which tend to restore body weight to the "usual" weight after alterations in weight by induced weight loss or weight gain. We employ pharmacological studies of the autonomic control of cardiac function as an estimate of general autonomic activity. Specifically, patients' heart periodicity was measured before and after cardio-selective beta-1 adrenergic blockade and muscarinic cholinergic blockade to obtain estimates of sympathetic control and parasympathetic control. Simultaneously, spectral analysis of heart rate variability is done as a further estimate of these parameters and also to determine the adequacy of blockade. It has been possible to show that there are not only changes in autonomic function when usual weight is varied, but obese individuals at their usual obese weight are different from the non-obese. The obese tend to have lower parasympathetic control and higher sympathetic control. We believe that this makes it unlikely that a primary defect in the autonomic nervous system is responsible for obesity. More likely, the autonomic changes found are simply those that occur when fat mass is increased or decreased by experimental means. We propose to utilize these techniques of evaluating autonomic function in studies of weight response induced not only by caloric alterations but also by the administration of drugs which, in turn, affect energy also metabolism. The degree of alteration in autonomic function in the obese state at usual weight will also be evaluated as a measure which may vary with different genetic factors important in the pathogenesis of obesity. As the molecular genetics of human obesity is better understood, each of the subtypes that emerge will be evaluated for autonomic function.