Sodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest

There is disagreement regarding the impact of dietary sodium on alterations in extracellular volume during head-down bed rest (HDBR). The primary purpose of this study was to assess the effects of salt intake on extracellular volume (ECV) during HDBR.

We performed whole-body bioimpedance spectroscopy with controlled sodium intake during 4 d of ambulation and 8 d of -6 degrees HDBR in 10 normotensive men. Each subject performed an initial 12-d familiarization run with moderate sodium (246 +/- 12 mmol x L(-1) x d(-1) excreted) during which no measurements were made. They then participated in treatment runs involving low sodium (LS: 143 +/- 10 mmol x L(-1) x d(-1) Na+ excreted) and high sodium (HS: 434 +/- 17 mmol x L(-1) x d(-1) Na+ excreted). The different treatments were separated by > or =1 mo and the order of LS and HS was balanced among the subjects. These treatments were based on controlled food and drink supplies as prepared by a dietitian. We monitored sodium output and measured aldosterone, plasma renin activity (PRA), and vasopressin. Bioimpedance was measured every second day in supine position using tetrapolar electrodes.

Based on exponential data fitting, we calculated an ECV decrease of 0.79 +/- 0.32 L (-5.8%; p = 0.018) in LS, and 1.21 +/- 0.31 L (-4.0%; p = 0.002) in HS during HDBR. LS and HS were not different (p > 0.1); 4 d pre-HDBR sodium adjustment produced a fall in ECV in the LS group only (-3.7%, p = 0.023). Hormone levels were not changed by HDBR. Plasma aldosterone was lower in HS (69 +/- 7 pg x ml(-1)) than in LS (180 +/- 24 pg x ml(-1)).

Our bioimpedance data confirm that low sodium intake decreases ECV in ambulatory conditions and indicate that 8 d of HDBR produce a loss of ECV of about 5% (p < 0.05). The loss did not seem to be influenced by sodium intake between approximately 3 and approximately 10 g x d(-1).