Cardiovascular regulation during water immersion.

K S Park, J K Choi, Y S Park
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引用次数: 157

Abstract

Head-out water immersion at thermoneutral temperature (34-35 degrees C) increases cardiac output for a given O2 consumption, leading to a relative hyperperfusion of peripheral tissues. To determine if subjects immersed in water at a colder temperature show similar responses and to explore the significance of the hyperperfusion, cardiovascular functions were investigated (impedance cardiography) on 10 men at rest and while performing exercise on a leg cycle ergometer (delta M = approximately 95 W.m-2) in air and in water at 34.5 degrees C and 30 degrees C, respectively. In subjects resting in water, the cardiac output increased by approximately 50% compared to that in air, mainly due to a rise in stroke volume. The stroke volume change tended to be greater in 30 degrees C water than in 34.5 degrees C water, and this was due to a greater increase in cardiac preload, as indicated by a significantly greater left ventricular end-diastolic volume. Arterial systolic pressure rose slightly during water immersion. Arterial diastolic pressure remained unchanged in 34.5 degrees C water, but it rose in 30 degrees C water. The total peripheral resistance fell 37% in 34.5 degrees C water and 32% in 30 degrees C water. Both in air and in water, mild exercise increased the cardiac output, and this was mainly due to an increase in heart rate. Since, however, the stroke volume increased with water immersion, cardiac output at a given work load appeared to be significantly higher in water than in air. The arterial pressures did not decrease with water immersion, despite a marked reduction in total peripheral resistance. These results suggest that 1) during cold water immersion, peripheral vasoconstriction provides an additional increase in cardiac preload, leading to a further increase in the stroke volume compared to that of the thermoneutral water immersion, 2) the mechanism of cardiovascular adjustment during dynamic exercise is not changed by the persistent increase in cardiac preload in water immersion, and 3) a relatively high cardiac output during water immersion is to maintain a proper arterial pressure in the face of reduced vascular resistance.

水浸泡时心血管的调节。
在热中性温度(34-35℃)下,头出水浸泡可增加给定耗氧量下的心输出量,导致周围组织相对高灌注。为了确定浸泡在温度较低的水中的受试者是否会表现出类似的反应,并探讨过度灌注的重要性,研究人员对10名男性进行了心血管功能(阻抗心动图)研究,他们分别在34.5摄氏度的空气和30摄氏度的水中,在静止状态下和在腿部循环测力仪(δ M =约95 w - M -2)上进行运动。受试者在水中休息时,心输出量比在空气中休息时增加了约50%,这主要是由于中风量的增加。卒中容量变化在30℃的水中比在34.5℃的水中更大,这是由于心脏预负荷的增加更大,左心室舒张末期容积显著增加。浸水期间动脉收缩压略有升高。动脉舒张压在摄氏34.5度的水中保持不变,但在摄氏30度的水中上升。总外围电阻在34.5℃的水中下降37%,在30℃的水中下降32%。无论是在空气中还是在水中,轻度运动都增加了心输出量,这主要是由于心率的增加。然而,由于中风量随着浸泡在水中而增加,在给定的工作负荷下,心脏输出量在水中明显高于在空气中。动脉压没有随着水的浸泡而降低,尽管总外周阻力明显降低。结果表明:1)与热中性水浸泡相比,冷水浸泡时外周血管收缩增加了心脏预负荷,导致脑卒中量进一步增加;2)动态运动时心血管调节的机制不因水浸泡时心脏预负荷的持续增加而改变。3)浸泡时较高的心输出量是为了在血管阻力降低的情况下维持适当的动脉压。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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