German Aerospace Center (DLR), Institute of Aerospace Medicine, Cologne, Germany.
J Appl Physiol (1985). 2011 Aug;111(2):537-42. doi: 10.1152/japplphysiol.00454.2011. Epub 2011 May 19.
We examined, in immobilization, the effect of a diet high in sodium chloride (NaCl) on bone markers, nitrogen balance, and acid-base status. Eight healthy male test subjects participated in a 14-day head-down-tilt bed rest (HDBR) study. During the bed rest period they received, in a randomized crossover design, a high (7.7 meq Na(+)/kg body wt per day) and a low (0.7 meq Na(+)/kg body wt per day) NaCl diet. As expected, 24-h excretion of urinary calcium was significantly greater in the high-NaCl-intake HDBR phase than in the low-NaCl-intake HDBR phase (P < 0.001). High NaCl intake caused a 43-50% greater excretion of the bone resorption markers COOH- (CTX) and NH(2)- (NTX) terminal telopeptide of type I collagen in HDBR than low NaCl in HDBR (CTX/NTX: P < 0.001). Serum concentrations of the bone formation markers bone-specific alkaline phosphatase (bAP) and NH(2)-terminal propeptide of type I procollagen (PINP) were identical in both NaCl intake phases. High NaCl intake led to a more negative nitrogen balance in HDBR (P < 0.001). Changes were accompanied by increased serum chloride concentration (P = 0.008), reduced blood bicarbonate (P = 0.017), and base excess (P = 0.009) whereas net acid excretion was lower during high than during low NaCl intake in immobilization (P < 0.001). High NaCl intake during immobilization exacerbates disuse-induced bone and muscle loss by causing further protein wasting and an increase in bone resorption. Changes in the acid-base status, mainly caused by disturbances in electrolyte metabolism, seem to determine NaCl-induced degradation processes.
我们在固定状态下研究了高盐饮食（NaCl）对骨标志物、氮平衡和酸碱状态的影响。8 名健康男性受试者参加了为期 14 天的头低位卧床休息（HDBR）研究。在卧床休息期间，他们按照随机交叉设计接受了高（7.7 meq Na(+)/kg 体重/天）和低（0.7 meq Na(+)/kg 体重/天）NaCl 饮食。正如预期的那样，高盐摄入 HDBR 期的 24 小时尿钙排泄量明显高于低盐摄入 HDBR 期（P < 0.001）。高 NaCl 摄入导致 HDBR 中 COOH-（CTX）和 NH(2)-（NTX）末端胶原 I 型肽骨吸收标志物的排泄增加了 43-50%，而在 HDBR 中 NaCl 摄入则较低（CTX/NTX：P < 0.001）。两种 NaCl 摄入阶段的血清骨形成标志物骨特异性碱性磷酸酶（bAP）和 NH(2)-末端 I 型原胶原前肽（PINP）浓度相同。高 NaCl 摄入导致 HDBR 中的氮平衡更为负值（P < 0.001）。变化伴随着血清氯浓度增加（P = 0.008）、血碳酸氢盐减少（P = 0.017）和碱剩余减少（P = 0.009），而在固定状态下高 NaCl 摄入时的净酸排泄低于低 NaCl 摄入时（P < 0.001）。固定状态下高 NaCl 摄入通过导致进一步的蛋白质丢失和骨吸收增加，加剧了废用性骨和肌肉丢失。酸碱状态的变化主要是由电解质代谢紊乱引起的，似乎决定了 NaCl 诱导的降解过程。
