German Aerospace Center (DLR), Institute of Aerospace Medicine, 51147, Cologne, Germany.
Novartis AG, Basel, Switzerland.
Osteoporos Int. 2019 Feb;30(2):431-439. doi: 10.1007/s00198-018-4703-6. Epub 2018 Sep 25.
Potassium bicarbonate was administrated to an already alkaline diet in seven male subjects during a 21-day bed rest study and was able to decrease bed rest induced increased calcium excretion but failed to prevent bed rest-induced bone resorption.
Supplementation with alkali salts appears to positively influence calcium and bone metabolism and, thus, could be a countermeasure for population groups with an increased risk for bone loss. However, the extent to which alkalization counteracts acid-induced bone resorption or whether it merely has a calcium and bone maintenance effect is still not completely understood. In the present study, we hypothesized that additional alkalization to an already alkaline diet can further counteract bed rest-induced bone loss.
Seven healthy male subjects completed two parts of a crossover designed 21-day bed rest study: bed rest only (control) and bed rest supplemented with 90 mmol potassium bicarbonate (KHCO) daily.
KHCOsupplementation during bed rest resulted in a more alkaline status compared to the control intervention, demonstrated by the increase in pH and buffer capacity level (pH p = 0.023, HCOp = 0.02, ABE p = 0.03). Urinary calcium excretion was decreased during KHCO supplementation (control 6.05 ± 2.74 mmol/24 h; KHCO 4.87 ± 2.21 mmol/24 h, p = 0.03); whereas, bone formation was not affected by additional alkalization (bAP p = 0.58; PINP p = 0.60). Bone resorption marker UCTX tended to be lower during alkaline supplementation (UCTX p = 0.16).
The more alkaline acid-base status, achieved by KHCO supplementation, reduced renal calcium excretion during bed rest, but was not able to prevent immobilization-induced bone resorption. However, advantages of alkaline salts on bone metabolism may occur under acidic metabolic conditions or with respect to the positive effect of reduced calcium excretion within a longer time frame.
Trial number: NCT01509456.
在一项为期 21 天卧床休息的研究中，向已经处于碱性饮食的 7 名男性受试者给予碳酸氢钾，并观察其能否降低卧床休息引起的钙排泄增加，但未能预防卧床休息引起的骨吸收。
补充碱盐似乎对钙和骨代谢有积极影响，因此，它可能是骨质疏松风险增加人群的一种对策。然而，碱化作用在多大程度上能抵消酸引起的骨吸收，或者它是否仅仅具有钙和骨维持作用，仍不完全清楚。在本研究中，我们假设在已经处于碱性的饮食中再添加碱可以进一步对抗卧床休息引起的骨丢失。
7 名健康男性受试者完成了一项交叉设计的 21 天卧床休息研究的两部分：仅卧床休息（对照组）和卧床休息时每天补充 90mmol 碳酸氢钾（KHCO3）。
与对照组相比，卧床休息时补充 KHCO3 导致更碱性的状态，这表现为 pH 和缓冲能力水平的增加（pHp=0.023，HCO3p=0.02，ABEp=0.03）。尿钙排泄在 KHCO3 补充时减少（对照组 6.05±2.74mmol/24h；KHCO3 4.87±2.21mmol/24h，p=0.03）；然而，骨形成不受额外碱化的影响（bAPp=0.58；PINPp=0.60）。骨吸收标志物 UCTX 在碱性补充时趋于较低（UCTXp=0.16）。
通过 KHCO3 补充达到更碱性的酸碱状态，可减少卧床休息期间的肾脏钙排泄，但不能预防固定引起的骨吸收。然而，在酸性代谢条件下或在更长时间内减少钙排泄的积极作用下，碱盐对骨代谢的优势可能会显现出来。
试验编号：NCT01509456。
