Effect of high salt intake on acid base and nitrogen balance during 14 days of head-down-tilt bed rest (HDBR)

Abstract

Human spaceflight is associated with a loss of body protein most likely caused by muscle degradation. Additionally astronauts tend towards a high dietary intake of sodium chloride (NaCl), which has recently been shown to induce low grade metabolic acidosis (Frings-Meuthen et al. JBMR, Epub 2007). In several patterns, e.g. chronical renal failure, metabolic acidosis is associated with protein catabolism. We therefore hypothesized that high dietary intake of NaCl enforces protein losses in HDBR, a model for physiological changes in microgravity (µG). Eight healthy male subjects (mean age 26.25 ± 3.5; mean body weight: 78.5 ± 4.1 kg) participated in a 14-day bed rest study in the metabolic ward of the DLR – Institute of Aerospace Medicine, Cologne, Germany. The study was carried out in a cross over design, consisting of two phases, each lasting 22 days (5 days adaptation, 14 days 6° HDBR and 3 days recovery). Both study phases were identical with respect to environmental conditions and study protocol. Subjects received an individually tailored, weight-maintaining diet containing 1.3 g protein/kg/day. The diet was identical in both study phases with the exception of NaCl-intake: Every subject received a low NaCl diet (0.7 mmol/kg/day) in one phase and a high NaCl diet (7.7 mmol/kg/day) in another one. Blood gas for analysis of acid-base balance was implemented at days 4 and 5 of adaptation, days 2, 5, 7, 10, 12, 14 of HDBR and days 2, 3 of recovery. Continuous urine collection started on the first day in the metabolic ward to analyze nitrogen excretion. Nitrogen balance was calculated from the difference between protein intake and urinary nitrogen excretion, determined by use of chemiluminescence. Plasma pH did not change significantly (p=0.285), but plasma bicarbonate and base excess decreased with high NaCl intake in HDBR compared to the low NaCl diet (bicarbonate high salt 25,2 ± 0,16 mmol/l, low salt 26,4 ± 0,39 mmol/l (p=0.0175); base excess high salt 0,88 ± 0,20, low salt 2,0 ± 0,44 mmol/l (p=0.0093)) Nitrogen balance in HDBR was negative, as expected in immobilization with low NaCl diet ( 0.34 ± 1.2 g/d). However, high NaCl intake in HDBR exacerbated the negative nitrogen balance to 1.34 ± 1.0 g/d (p<0.001) compared to low NaCl. We conclude that high dietary NaCl intake induces low grade metabolic acidosis during HDBR. Low grade metabolic acidosis may be a reason for an increased protein turnover reflected by an exaggerated negative nitrogen balance in HDBR. Accordingly, a high dietary NaCl intake may exacerbate loss of body protein in µG via low grade metabolic acidosis.