Wittels P, Gunga H C, Kirsch K, Kanduth B, Günther T, Vormann J, Röcker L
Spezialabteilung für Leistungsmedizin und Wehrergonomie, Heeresspital, Wien.
Wien Klin Wochenschr. 1996 Dec 27;108(24):788-94.
The aim of this study was to investigate fluidregulating mechanisms, with special regard to the role of plasma proteins in the control of plasma volume (PV), and the role of the superficial tissues as a water storage organ of the body during prolonged physical strain. 29 male subjects (mean age 22.2 +/- 2.8 years) were studied during a 5 day period of survival training with multifactorial strain including restricted water intake (11 H2O.day-1) and food intake (628 kJ.day-1) additionally to physical exercise and sleep deprivation (20 h within 5 days). Under field conditions the heart rate was monitored continuously, and body mass, body composition, thickness of the shell tissues, and blood parameters were measured at (T1), after 72 h (T2), after 120 h (T3) and in the recovery period after 48 h (T4) and 72 h (T5). The estimated energy expenditure was approximately 24,000 kJ.day-1. The mean decrease of body mass was 6.77 kg (9.5%) at T3 (p < 0.001), 0.95 kg (1.3%) at T4 (p < 0.05) and 0.68 kg (0.9%) at T5 (n.s.). A reduction of total body water of 3.8 1 was estimated at T3. Serum creatinine ([Cr]) was raised at T3 by 18.5% (p < 0.0001). No relationship was found between [Cr] and other parameters. The PV decreased by 3.7% (p < 0.0001) at T2, increased by 1.6% (p < 0.0001) at T3 and was not different to baseline at T4 (+0.2%; n.s.). Total protein concentration ([TP]) increased at T2 (11.7%; p < 0.0001) and T3 (2.6%; p < 0.01), and decreased (p < 0.0001) at T4 (8.2%) and T5 (5.7%). Plasma proteins shifted into the intravascular space at T2 and T3 and moved out of the intravascular space at T4 and T5. This gives support to the hypothesis that one of the counterregulatory mechanisms maintaining PV during prolonged exercise is provided by protein shifts from the extravascular into the intravascular space. Our data provide evidence that this mechanism assists PV homeostasis efficiently over a period of 120 h with multifactorial strain, even under conditions with a fluid loss of almost 8% of the total body water.
本研究的目的是调查液体调节机制，特别关注血浆蛋白在控制血浆容量（PV）中的作用，以及在长时间体力应激期间浅表组织作为身体储水器官的作用。29名男性受试者（平均年龄22.2±2.8岁）在为期5天的生存训练期间接受研究，训练包含多因素应激，除体育锻炼和睡眠剥夺（5天内20小时）外，还包括限制水摄入（11升/天）和食物摄入（628千焦/天）。在野外条件下持续监测心率，并在第1天（T1）、72小时后（T2）、120小时后（T3）以及48小时（T4）和72小时（T5）恢复期测量体重、身体成分、体表组织厚度和血液参数。估计能量消耗约为24000千焦/天。T3时体重平均下降6.77千克（9.5%）（p<0.001），T4时下降0.95千克（1.3%）（p<0.05），T5时下降0.68千克（0.9%）（无统计学意义）。T3时估计总体水减少3.8升。血清肌酐（[Cr]）在T3时升高18.5%（p<0.0001）。未发现[Cr]与其他参数之间存在关联。PV在T2时下降3.7%（p<0.0001），T3时升高1.6%（p<0.0001），T4时与基线无差异（+0.2%；无统计学意义）。总蛋白浓度（[TP]）在T2时升高（11.7%；p<0.0001），T3时升高（2.6%；p<0.01），T4时下降（8.2%；p<0.0001），T5时下降（5.7%；p<0.0001）。血浆蛋白在T2和T3时移入血管内空间，在T4和T5时移出血管内空间。这支持了以下假设：在长时间运动期间维持PV的一种反调节机制是由蛋白从血管外移入血管内空间提供的。我们的数据提供了证据，表明即使在总体水流失近8%的情况下，这种机制在多因素应激下120小时内有效地协助了PV的稳态。
