High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses

<jats:p>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<jats:sup>+</jats:sup>/kg body wt per day) and a low (0.7 meq Na<jats:sup>+</jats:sup>/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 &lt; 0.001). High NaCl intake caused a 43–50% greater excretion of the bone resorption markers COOH- (CTX) and NH<jats:sub>2</jats:sub>- (NTX) terminal telopeptide of type I collagen in HDBR than low NaCl in HDBR (CTX/NTX: P &lt; 0.001). Serum concentrations of the bone formation markers bone-specific alkaline phosphatase (bAP) and NH<jats:sub>2</jats:sub>-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 &lt; 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 &lt; 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.</jats:p>