The mechanisms underlying the pronounced transient fall in arterial blood pressure evoked by a 3 s bout of bicycle exercise were investigated in twenty healthy young adults and four patients with hypoadrenergic orthostatic hypotension. 2. In healthy subjects a 3 s bout of upright cycling induced a 28 +/- 3 mmHg fall in mean arterial pressure at 12 s. The fall in mean arterial pressure was preceded by a 12 +/- 2 mmHg rise in right atrial pressure at 3 s and accompanied by a 54 +/- 7% increase in left ventricle stroke volume at 6 s. Systemic vascular resistance dropped 48 +/- 2% at 7 s after the start of the manoeuvre to remain at that level for approximately 5 s. The total response lasted about 20 s. During sustained upright cycling the initial fall in mean arterial pressure was also present, but less pronounced (17 +/- 2 vs. 26 +/- 3 mmHg). A 3 s bout of supine cycling in four patients with hypoadrenergic orthostatic hypotension also elicited a pronounced fall in mean arterial pressure (22 +/- 4 mmHg) and in systemic vascular resistance (38 +/- 4%). 3. A bout of exercise with a large muscle mass induces two main effects. First, it mechanically increases filling of the heart due to activation of the muscle pump, resulting in an increase in cardiac output. Second, it induces a drop in systemic vascular resistance. The increase in cardiac output is not sufficient to compensate fully for the pronounced fall in systemic vascular resistance and the result is a transient fall in arterial pressure at the onset of whole-body exercise. The rise in right atrial pressure evoked by 3 s cycling is abrupt and large, but the almost immediate onset and rapid fall of the systemic vascular resistance is too fast for sympathetically mediated reflex effects due to stimulation of the cardiopulmonary afferents. An important factor involved in the drop in systemic vascular resistance appears to be local, non-autonomically mediated vasodilatation in exercising muscles, since it also occurs in patients with autonomic failure.
摘要
在20名健康年轻成年人和4名低肾上腺素能直立性低血压患者中,研究了3秒自行车运动诱发动脉血压显著短暂下降的潜在机制。2. 在健康受试者中,3秒的直立骑行在12秒时导致平均动脉压下降28±3 mmHg。平均动脉压下降之前,右心房压力在3秒时升高12±2 mmHg,并伴有左心室每搏输出量在6秒时增加54±7%。在动作开始后7秒,全身血管阻力下降48±2%,并在该水平维持约5秒。总反应持续约20秒。在持续直立骑行过程中,平均动脉压的初始下降也存在,但不太明显(17±2 vs. 26±3 mmHg)。在4名低肾上腺素能直立性低血压患者中进行3秒的仰卧骑行,也引起了平均动脉压(22±4 mmHg)和全身血管阻力(38±4%)的显著下降。3. 一次涉及大量肌肉群的运动产生两种主要影响。首先,由于肌肉泵的激活,它机械性地增加了心脏的充盈,导致心输出量增加。其次,它引起全身血管阻力下降。心输出量的增加不足以完全补偿全身血管阻力的显著下降,结果是全身运动开始时动脉压短暂下降。3秒骑行引起的右心房压力升高突然且幅度大,但全身血管阻力几乎立即开始并迅速下降,对于心肺传入神经刺激引起的交感神经介导的反射效应来说太快了。全身血管阻力下降所涉及的一个重要因素似乎是运动肌肉中局部的、非自主神经介导的血管舒张,因为在自主神经功能衰竭的患者中也会出现这种情况。