Osmotically inactive sodium retention: How might this affect bone loss in immobilization?

Paper number

IAC-06-A1.2.05

Author

Dr. Martina Heer, German Aerospace Center (DLR), Germany

Coauthor

Mrs. Petra Frings, German Aerospace Center (DLR), Germany

Coauthor

Dr. Natalie Baecker, German Aerospace Center (DLR), Germany

Year

2006

Abstract

High salt intake led to osmotically inactive sodium retention in space as well as in metabolic balance studies on Earth (Drummer et al., EJCI 2000;Heer et al. AJP 2000). Concurrently, it is well known that high salt intake is also considered as a risk factor for osteoporosis. Now, astronauts in space experience lowered mechanical loading of their bones during their stay in microgravity. As a physiological adaptation to the reduced mechanical loading bone resorption increases which leads to disuse induced bone loss. On the other hand, astronauts do have high salt intake because of lowered smell and taste sensations.
Since high salt intake independently from mechanical loading increases bone resorption as well, the question is whether high salt intake in immobilization may exacerbate bone resorption. If this holds true the next question is, which the underlying mechanism is.
We examined the effect of increased dietary sodium on bone metabolism in ambulatory conditions in our metabolic ward. They received a standardized, exactly controlled nutrient intake. Only sodium intake was altered by variations in the NaCl- amount of the diet. 24 h urinary excretion of calcium and bone resorption markers (C- and N- terminal telopeptide of type I collagen (CTX, NTX) were measured. Bone formation markers, bone specific alkaline phosphatase (bAP), C-and N-terminal of propeptide of type I prokollagen (PICP, PINP), pH and bicarbonate (HCO3-) were analyzed in blood samples. Calcium excretion rose significantly from phase 1 and 2 to phase 3 (both: p < 0.001). CTX and NTX increased significantly from phase 1 to 2 (CTX: p = 0,03; NTX: p = 0,005), from phase 1 to 3 (CTX: p = 0.009; NTX: p = 0.005) and from phase 2 to 3 (CTX: p = 0.05; NTX: p = 0.005), but bAP, PICP and PINP remained unchanged. Between high and low salt intake there was a significant fall in pH level (p = 0.01) and HCO3-. Nearly all bone resorption markers and acid-base parameters reached their phase 1 level in phase 4. We conclude that high salt intake induces low-grade metabolic acidosis and thereby causes calcium loss via a physicochemical process and by activating osteoclasts. As a result, bone mass is lost due to high salt intake and might exacerbate the disuse induced bone loss in space.

Abstract document

IAC-06-A1.2.05.pdf

Manuscript document

IAC-06-A1.2.05.pdf (🔒 authorized access only).

To get the manuscript, please contact IAF Secretariat.