Abstract：
The physiological, perceptual, and functional effects of dehydration may depend on how it is incurred (e.g., intense exercise releases endogenous water via glycogenolysis) but this basic notion has rarely been examined. We investigated the effects of active (exercise) heat- vs. passive heat-induced dehydration, and the kinetics of ad libitum rehydration following each method. Twelve fit participants (five females and seven males) completed four trials in randomised order: DEHydration to -3% change in body mass (∆BM) under passive or active heat stress, and EUHydration to prevent ∆BM under passive or active heat stress. In all trials, participants then sat in a temperate-controlled environment, ate a standard snack and had free access to water and sports drink during their two-hour recovery. During mild dehydration (≤2% ∆BM), active and passive heating caused comparable increases in plasma osmolality (Posm: ~4 mOsmol/kg, interaction: p = 0.138) and reductions in plasma volume (PV: ~10%, interaction: p = 0.718), but heat stress per se was the main driver of hypovolaemia. Thirst in DEHydration was comparably stimulated by active than passive heat stress (p < 0.161) and shared the same relation to Posm (r ≥ 0.744) and ∆BM (r ≥ 0.882). Following heat exposures, at 3% gross ∆BM, PV reduction was approximately twice as large from passive versus active heating (p = 0.003), whereas Posm perturbations were approximately twice as large from EUHydration versus DEHydration (p < 0.001). Rehydrating ad libitum resulted in a similar net fluid balance between passive versus active heat stress and restored PV despite the incomplete replacement of ∆BM. In conclusion, dehydrating by 2% ∆BM via passive heat stress generally did not cause larger changes to PV or Posm than via active heat stress. The heat stressors themselves caused a greater reduction in PV than dehydration did, whereas ingesting water to maintain euhydration produced large reductions in Posm in recovery and therefore appears to be of more physiological significance.
摘要：
生理，感性的，脱水的功能影响可能取决于它是如何发生的(例如，剧烈运动通过糖原分解释放内源性水），但很少研究这一基本概念。我们调查了活跃（运动）热量与被动热诱导脱水，以及每种方法后任意再水化的动力学。12名参与者（5名女性和7名男性）按随机顺序完成了4项试验：在被动或主动热应激下，脱水至-3％的体重变化（ΔBM），和EUHydration，以防止在被动或主动热应激下ΔBM。在所有的试验中,然后参与者坐在温带控制的环境中，在他们两个小时的康复过程中，他们吃了标准的小吃，并免费获得了水和运动饮料。轻度脱水期间(≤2%ΔBM)，主动和被动加热导致血浆渗透压相当的增加(Posm:~4mOsmol/kg，相互作用：p=0.138)和血浆体积减少(PV：~10%，相互作用：p=0.718)，但热应激本身是低血容量的主要驱动因素。主动热应激比被动热应激刺激脱水口渴（p<0.161），与Posm（r≥0.744）和ΔBM（r≥0.882）具有相同的关系。在热暴露之后，在3%的总ΔBM，被动加热与主动加热的PV减少大约是主动加热的两倍（p=0.003），而EURHydration与脱水的Posm扰动约为两倍(p<0.001)。尽管ΔBM的替换不完全，但任意再水化导致被动与主动热应力与恢复的PV之间的净流体平衡相似。总之,通过被动热应力脱水2％ΔBM通常不会引起比主动热应力更大的PV或Posm变化。与脱水相比，热应激源本身引起的PV减少更大，而摄取水以维持水合状态会大大降低Posm的回收率，因此似乎具有更多的生理意义。
