Hew-Butler Tamara, Hummel Jed, Rider Brian C, Verbalis Joseph G
Exercise Science Program, Oakland University, Rochester, Michigan; and
Exercise Science Program, Oakland University, Rochester, Michigan; and.
Am J Physiol Regul Integr Comp Physiol. 2014 Aug 15;307(4):R366-75. doi: 10.1152/ajpregu.00120.2014. Epub 2014 Jun 18.
A regulatory effect of arginine vasopressin (AVP) on sweat water conservation has been hypothesized but not definitively evaluated. AVP-mediated insertion of sweat and salivary gland aquaporin-5 (AQP5) water channels through activation of the vasopressin type 2 receptor (V2R) remains an attractive, yet unexplored, mechanism that could result in a more concentrated sweat with resultant decreased water loss. Ten runners participated in a double-blind randomized control treadmill trial under three separate pharmacological conditions: a placebo, V2R agonist (0.2 mg desmopressin), or V2R antagonist (30 mg tolvaptan). After a familiarization trial, runners ran for 60 min at 60% of peak speed followed by a performance trial to volitional exhaustion. Outcome variables were collected at three exercise time points: baseline, after the steady-state run, and after the performance run. Body weight losses were <2% across all three trials. Significant pharmacological condition effects were noted for urine osmolality [F = 84.98; P < 0.0001] and urine sodium concentration ([Na(+)]) [F = 38.9; P < 0.0001], which verified both pharmacological activation and inhibition of the V2R at the kidney collecting duct. Plasma osmolality and [Na(+)] demonstrated significant exercise (F = 26.0 and F = 11.1; P < 0.0001) and condition (F = 5.1 and F = 3.8; P < 0.05) effects (osmolality and [Na(+)], respectively). No significant exercise or condition effects were noted for either sweat or salivary [Na(+)]. Significant exercise effects were noted for plasma [AVP] (F = 22.3; P < 0.0001), peak core temperature (F = 103.3; P < 0.0001), percent body weight change (F = 6.3; P = 0.02), plasma volume change (F = 21.8; P < 0.0001), and thirst rating (F = 78.2; P < 0.0001). Performance time was not altered between conditions (P = 0.80). In summary, AVP acting at V2R does not appear to regulate water losses from body fluids other than renal excretion during exercise.
精氨酸加压素（AVP）对汗液水分保存具有调节作用，这一观点已被提出，但尚未得到确切评估。AVP通过激活2型血管加压素受体（V2R）介导汗液和唾液腺水通道蛋白5（AQP5）水通道的插入，这一机制颇具吸引力，但尚未得到探索，该机制可能导致汗液更加浓缩，从而减少水分流失。10名跑步者在三种不同的药理学条件下参加了一项双盲随机对照跑步机试验：安慰剂、V2R激动剂（0.2mg去氨加压素）或V2R拮抗剂（30mg托伐普坦）。在熟悉试验后，跑步者以峰值速度的60%跑60分钟，随后进行力竭性的性能试验。在三个运动时间点收集结果变量：基线、稳态跑步后和性能跑步后。在所有三项试验中体重减轻均<2%。观察到尿液渗透压[F = 84.98；P < 0.0001]和尿钠浓度（[Na(+)]）[F = 38.9；P < 0.0001]存在显著的药理学条件效应，这证实了在肾集合管对V2R的药理学激活和抑制。血浆渗透压和[Na(+)]表现出显著的运动（F = 26.0和F = 11.1；P < 0.0001）和条件（F = 5.1和F = 3.8；P < 0.05）效应（分别为渗透压和[Na(+)]）。汗液或唾液中的[Na(+)]未观察到显著的运动或条件效应。血浆[AVP]（F = 22.3；P < 0.0001）、峰值核心温度（F = 103.3；P < 0.0001）、体重变化百分比（F = 6.3；P = 0.02）、血浆容量变化（F = 21.8；P < 0.0001）和口渴评分（F = 78.2；P < 0.0001）存在显著的运动效应。不同条件下的运动表现时间没有改变（P = 0.80）。总之，在运动过程中，作用于V2R的AVP似乎不会调节除肾脏排泄外的体液水分流失。
