Ogoh Shigehiko, Fisher James P, Young Colin N, Raven Peter B, Fadel Paul J
Dept. of Integrative Physiology, Univ. of North Texas Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, TX 76107, USA.
Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1416-24. doi: 10.1152/ajpheart.01223.2008. Epub 2009 Mar 13.
Previous studies have demonstrated an increase in the arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) during isolated activation of the muscle metaboreflex with postexercise muscle ischemia (PEMI). However, the increased ABR-MSNA control does not appear to manifest in an enhancement in the ABR control of arterial blood pressure (BP), suggesting alterations in the transduction of MSNA into a peripheral vascular response and a subsequent ABR-mediated change in BP. Thus we examined the operating gains of the neural and peripheral arcs of the ABR and their interactive relationship at rest and during muscle metaboreflex activation. In nine healthy subjects, graded isolation of the muscle metaboreflex was achieved by PEMI following isometric handgrip performed at 15% and 30% maximal voluntary contraction (MVC). To obtain the sensitivities of the ABR neural and peripheral arcs, the transfer function gain from BP to MSNA and MSNA to femoral vascular conductance, respectively, was analyzed. No changes from rest were observed in the ABR neural or peripheral arcs during PEMI after 15% MVC handgrip. However, PEMI following 30% MVC handgrip increased the low frequency (LF) transfer function gain between BP and MSNA (ABR neural arc; +58 +/- 28%, P = 0.036), whereas the LF gain between MSNA and femoral vascular conductance (ABR peripheral arc) was decreased from rest (-36 +/- 8%, P = 0.017). These findings suggest that during high-intensity muscle metaboreflex activation an increased ABR gain of the neural arc appears to offset an attenuation of the peripheral arc gain to help maintain the overall ABR control of systemic BP.
先前的研究表明，在运动后肌肉缺血（PEMI）诱发的肌肉代谢性反射单独激活期间，动脉压力反射（ABR）对肌肉交感神经活动（MSNA）的控制增强。然而，ABR对MSNA控制的增强似乎并未表现为ABR对动脉血压（BP）控制的增强，这表明MSNA向周围血管反应的转换以及随后ABR介导的血压变化存在改变。因此，我们研究了ABR神经和外周弧在静息状态和肌肉代谢性反射激活期间的运作增益及其相互作用关系。在9名健康受试者中，通过在15%和30%最大自主收缩（MVC）下进行等长握力运动后进行PEMI，实现了肌肉代谢性反射的分级分离。为了获得ABR神经和外周弧的敏感性，分别分析了从BP到MSNA以及从MSNA到股血管传导的传递函数增益。在15%MVC握力运动后的PEMI期间，ABR神经或外周弧与静息状态相比没有变化。然而，30%MVC握力运动后的PEMI增加了BP与MSNA之间的低频（LF）传递函数增益（ABR神经弧；+58±28%，P = 0.036），而MSNA与股血管传导之间的LF增益（ABR外周弧）与静息状态相比降低了（-36±8%，P = 0.017）。这些发现表明，在高强度肌肉代谢性反射激活期间，神经弧的ABR增益增加似乎抵消了外周弧增益的衰减，以帮助维持ABR对全身血压的整体控制。
