Center of Human Performance (CIPER), Faculty of Human Kinetics, Technical University of Lisbon, Estrada da Costa, Cruz Quebrada, 1495-688, Cruz Quebrada Dafundo, Lisbon, Portugal.
Eur J Appl Physiol. 2012 Jul;112(7):2495-501. doi: 10.1007/s00421-011-2223-6. Epub 2011 Nov 10.
Water drinking activates sympathetic vasoconstriction in healthy young adults; however, this is not accompanied by a concomitant increase in resting blood pressure. It is not known whether the water pressor effect is unmasked by a physiological condition such as exercise. Therefore, we examined the effect of water ingestion (50 vs. 500 mL) on the cardiovascular and autonomic responses to isometric handgrip in 17 healthy participants (9 men, 8 women, aged 28.4 ± 9.7 years). Beat-to-beat blood pressure and R-R intervals were recorded in both conditions at rest (pre- and post-ingestion) and during handgrip at 30% of maximal voluntary contraction. R-R series were spectrally decomposed using an autoregressive approach. Water ingestion did not interact with the increase in mean arterial pressure (MAP) from rest to exercise, which was similar between conditions. In contrast, there was an overall bradycardic effect of water and this was accompanied by increased high frequency power (condition main effect, p < 0.05). When the differences in high frequency power between conditions were controlled for, MAP was significantly higher after drinking 500 mL of water (condition main effect, p < 0.05). In addition, water ingestion attenuated the increase in the low to high frequency power ratio from rest to handgrip (interaction effect, p < 0.05). In conclusion, the rise in blood pressure post-water ingestion is prevented both at rest and during isometric handgrip. Interestingly, this is not sustained after controlling for the enhanced vagal drive caused by water ingestion. Therefore, the mechanisms underlying this response most likely depend on reflex bradycardia of vagal origin.
饮水会激活健康年轻成年人的交感血管收缩;然而,这并不会伴随静息血压的相应升高。目前尚不清楚水升压效应是否会被运动等生理状况所掩盖。因此,我们研究了在 17 名健康参与者(9 名男性,8 名女性,年龄 28.4±9.7 岁)中,饮水(50 毫升与 500 毫升)对等长握力时心血管和自主神经反应的影响。在两种情况下,参与者在休息时(摄入前后)和在握力达到最大自主收缩 30%时,记录逐拍血压和 R-R 间期。使用自回归方法对 R-R 序列进行频谱分解。饮水与从休息到运动时平均动脉压(MAP)的增加没有相互作用,两种情况下的 MAP 增加相似。相比之下,饮水会引起整体心率减慢,同时高频功率增加(条件主效应,p<0.05)。当控制条件之间高频功率的差异时,饮用 500 毫升水后 MAP 显著升高(条件主效应,p<0.05)。此外,饮水摄入会减弱从休息到握力时低频到高频功率比的增加(交互效应,p<0.05)。总之,在休息和等长握力时,饮水后血压升高都会受到抑制。有趣的是,在控制饮水引起的增强的迷走神经驱动后,这种抑制作用就不再持续了。因此,这种反应的机制很可能依赖于迷走神经起源的反射性心动过缓。