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健康受试者的体脂与交感神经活动

Body fat and sympathetic nerve activity in healthy subjects.

作者信息

Scherrer U, Randin D, Tappy L, Vollenweider P, Jéquier E, Nicod P

机构信息

Department of Internal Medicine B, CHUV, Lausanne, Switzerland.

出版信息

Circulation. 1994 Jun;89(6):2634-40. doi: 10.1161/01.cir.89.6.2634.

Abstract

BACKGROUND

Obesity is associated with an increased incidence of cardiovascular complications, but the underlying mechanism is unknown. In experimental animals, overfeeding is associated with sympathetic activation, and there is evidence that adrenergic mechanisms contribute to cardiovascular complications.

METHODS AND RESULTS

We recorded resting postganglionic sympathetic nerve discharge (using intraneural microelectrodes) to skeletal muscle blood vessels in 37 healthy subjects covering a broad spectrum of percent body fat. To assess potential functional consequences of sympathetic nerve discharge, we simultaneously measured calf vascular resistance and energy expenditure. The resting rate of sympathetic nerve discharge to skeletal muscle was directly correlated with body mass index (r = .67, P < .0001) and percent body fat (r = .64, P < .0001). In addition to body fat, muscle sympathetic nerve activity was correlated with age (r = .40, P < .02), plasma insulin concentration (r = .34, P < .04), and plasma lactate concentration (r = .35, P < .04). Together, these four covariates accounted for 58% of the variance of muscle sympathetic nerve activity (P < .0001). The rate of sympathetic nerve discharge to calf blood vessels was directly correlated with calf vascular resistance (r = .40, P < .02) but did not predict energy expenditure (r = .22, P = .19).

CONCLUSIONS

In healthy humans, body fat is a major determinant of the resting rate of muscle sympathetic nerve discharge. Overweight-associated sympathetic activation could represent one potential mechanism contributing to the increased incidence of cardiovascular complications in overweight subjects.

摘要

背景

肥胖与心血管并发症发生率增加相关,但潜在机制尚不清楚。在实验动物中,过度喂养与交感神经激活有关,且有证据表明肾上腺素能机制促成心血管并发症。

方法与结果

我们使用神经内微电极记录了37名健康受试者骨骼肌血管的静息节后交感神经放电,这些受试者涵盖了广泛的体脂百分比范围。为评估交感神经放电的潜在功能后果,我们同时测量了小腿血管阻力和能量消耗。骨骼肌交感神经放电的静息率与体重指数直接相关(r = 0.67,P < 0.0001)和体脂百分比直接相关(r = 0.64,P < 0.0001)。除了体脂外,肌肉交感神经活动还与年龄相关(r = 0.40,P < 0.02)、血浆胰岛素浓度相关(r = 0.34,P < 0.04)以及血浆乳酸浓度相关(r = 0.35,P < 0.04)。这四个协变量共同解释了肌肉交感神经活动方差的58%(P < 0.0001)。小腿血管交感神经放电率与小腿血管阻力直接相关(r = 0.40,P < 0.02),但不能预测能量消耗(r =

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