Exercise Science Program, School of Health Sciences, Oakland University, Rochester, Michigan 48309, USA.
Sports Med. 2010 Jun 1;40(6):459-79. doi: 10.2165/11532070-000000000-00000.
The ability of the human body to regulate plasma osmolality (POsm) within a very narrow and well defined physiological range underscores the vital importance of preserving water and sodium balance at rest and during exercise. The principle endocrine regulator of whole body fluid homeostasis is the posterior pituitary hormone, arginine vasopressin (AVP). Inappropriate AVP secretion may perpetuate either slow or rapid violation of these biological boundaries, thereby promoting pathophysiology, morbidity and occasional mortality. In the resting state, AVP secretion is primarily regulated by changes in POsm (osmotic regulation). The osmotic regulation of AVP secretion during exercise, however, may possibly be enhanced or overridden by many potential non-osmotic factors concurrently stimulated during physical activity, particularly during competition. The prevalence of these highly volatile non-osmotic AVP stimuli during strenuous or prolonged physical activity may reflect a teleological mechanism to promote water conservation during exercise. However, non-osmotic AVP secretion, combined with high fluid availability plus sustained fluid intake (exceeding fluid output), has been hypothesized to lead to an increase in both the incidence and related deaths from exercise-associated hyponatraemia (EAH) in lay and military populations. Inappropriately, high plasma AVP concentrations (AVP) associated with low blood sodium concentrations facilitate fluid retention and sodium loss, thereby possibly reconciling both the water intoxication and sodium loss theories of hyponatraemia that are currently under debate. Therefore, given the potential for a variety of exercise-induced non-osmotic stimuli for AVP secretion, hydration strategies must be flexible, individualized and open to change during competitive events to prevent the occurrence of rare, but life-threatening, EAH. This review focuses on the potential osmotic and non-osmotic stimuli to AVP secretion that may affect fluid homeostasis during physical activity. Recent laboratory and field data support: (i) stimulatory effects of exercise intensity and duration on AVP; (ii) possible relationships between changes in POsm with changes in both sweat and urinary osmolality; (iii) alterations in the AVP osmoregulatory set-point by sex steroid hormones; (iv) differences in AVP in trained versus untrained athletes; and (v) potential inter-relationships between AVP and classical (aldosterone, atrial natriuretic peptide) and non-classical (oxytocin, interleukin-6) endocrine mediators. The review concludes with a hypothesis on how sustained fluid intakes beyond the capacity for fluid loss might possibly facilitate the development of hyponatraemia if exercise-induced non-osmotic stimuli override 'normal' osmotic suppression of AVP when hypo-osmolality exists.
人体调节血浆渗透压（POsm）的能力在非常狭窄和明确的生理范围内，强调了在休息和运动时保持水和钠平衡的至关重要性。全身液体动态平衡的主要内分泌调节剂是垂体后叶激素，精氨酸加压素（AVP）。不合适的 AVP 分泌可能会持续违反这些生理边界，从而促进病理生理学、发病率和偶尔的死亡率。在休息状态下，AVP 的分泌主要受 POsm（渗透压调节）变化的调节。然而，在运动期间，AVP 分泌的渗透压调节可能会被许多同时在体力活动中被刺激的潜在非渗透压因素增强或取代，尤其是在竞争期间。在剧烈或长时间的体力活动中，这些高度易变的非渗透压 AVP 刺激物的出现可能反映了一种促进运动中水分保存的目的论机制。然而，非渗透压 AVP 分泌与高液体供应加上持续液体摄入（超过液体输出）相结合，已被假设导致运动相关低钠血症（EAH）的发病率和相关死亡增加，无论是在普通人群还是军事人群中。不合适的是，与低血钠浓度相关的高血浆 AVP 浓度（AVP）促进了液体潴留和钠丢失，从而可能调和目前正在争论的低钠血症的水中毒和钠丢失理论。因此，鉴于运动诱导的 AVP 分泌的各种非渗透压刺激的可能性，水合策略必须在竞争事件期间灵活、个体化和开放，以防止罕见但危及生命的 EAH 的发生。本综述重点介绍了可能影响体力活动期间液体动态平衡的 AVP 分泌的渗透压和非渗透压刺激。最近的实验室和现场数据支持：（i）运动强度和持续时间对AVP的刺激作用；（ii）POsm 变化与汗液和尿液渗透压变化之间可能存在的关系；（iii）性激素对 AVP 渗透压调节基准点的改变；（iv）训练有素和未训练运动员之间AVP的差异；和（v）AVP 与经典（醛固酮、心钠肽）和非经典（催产素、白细胞介素-6）内分泌介质之间的潜在相互关系。该综述以一个假设结束，即如果运动诱导的非渗透压刺激物在存在低渗透压时覆盖“正常”渗透压对 AVP 的抑制，那么持续超过液体丢失能力的液体摄入可能会促进低钠血症的发展。
