Shoemaker J K, Mattar L, Kerbeci P, Trotter S, Arbeille P, Hughson R L
School of Kinesiology and Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada.
J Appl Physiol (1985). 2007 Jul;103(1):228-33. doi: 10.1152/japplphysiol.01334.2006. Epub 2007 Apr 5.
The mechanism of the pressor response to small muscle mass (e.g., forearm) exercise and during metaboreflex activation may include elevations in cardiac output (Q) or total peripheral resistance (TPR). Increases in Q must be supported by reductions in visceral venous volume to sustain venous return as heart rate (HR) increases. Therefore, this study tested the hypothesis that increases in Q, supported by reductions in splanchnic volume (portal vein constriction), explain the pressor response during handgrip exercise and metaboreflex activation. Seventeen healthy women performed 2 min of static ischemic handgrip exercise and 2 min of postexercise circulatory occlusion (PECO) while HR, stroke volume and superficial femoral artery flow (Doppler), blood pressure (Finometer), portal vein diameter (ultrasound imaging), and muscle sympathetic nerve activity (MSNA; microneurography) were measured followed by the calculation of Q, TPR, and leg vascular resistance (LVR). Compared with baseline, mean arterial blood pressure (MAP) (P < 0.001) and Q (P < 0.001) both increased in each minute of exercise accompanied by a approximately 5% reduction in portal vein diameter (P < 0.05). MAP remained elevated during PECO, whereas Q decreased below exercise levels. MSNA was elevated above baseline during the second minute of exercise and through the PECO period (P < 0.05). Neither TPR nor LVR was changed from baseline during exercise and PECO. The data indicate that the majority of the blood pressure response to isometric handgrip exercise in women was due to mobilization of central blood volume and elevated stroke volume and Q rather than elevations in TVR or LVR resistance.
对小肌肉群（如前臂）运动以及代谢性反射激活时的升压反应机制可能包括心输出量（Q）升高或总外周阻力（TPR）升高。随着心率（HR）增加，Q的增加必须由内脏静脉容量减少来支持，以维持静脉回流。因此，本研究检验了以下假设：在内脏容量减少（门静脉收缩）的支持下，Q的增加解释了握力运动和代谢性反射激活时的升压反应。17名健康女性进行了2分钟的静态缺血性握力运动和2分钟的运动后循环闭塞（PECO），同时测量HR、每搏输出量和股浅动脉血流（多普勒）、血压（Finometer）、门静脉直径（超声成像）以及肌肉交感神经活动（MSNA；微神经ography），随后计算Q、TPR和腿部血管阻力（LVR）。与基线相比，运动的每分钟平均动脉血压（MAP）（P<0.001）和Q（P<0.001）均升高，同时门静脉直径大约降低5%（P<0.05）。在PECO期间MAP仍保持升高，而Q降至运动水平以下。在运动的第二分钟以及整个PECO期间，MSNA高于基线水平（P<0.05）。在运动和PECO期间，TPR和LVR均未相对于基线发生变化。数据表明，女性对等长握力运动的血压反应主要是由于中心血容量的动员、每搏输出量和Q升高，而非TVR或LVR阻力升高。
