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

Introduction: 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. Methods: We performed whole-body bioimpedance spectroscopy with controlled sodium intake during 4 d of ambulation and 8 d of -6° HDBR in 10 normotensive men. Each subject performed an initial 12-d familiarization run with moderate sodium (246 ′ 12 mmol . L - 1 . d - 1 excreted) during which no measurements were made. They then participated in treatment runs involving low sodium (LS: 143 ′ 10 mmol . L - 1 . d - 1 Na + excreted) and high sodium (HS: 434 ′ 17 mmol . L - 1 . d - 1 Na + excreted). The different treatments were separated by ≥ 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. Results: 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 . ml - 1 ) than in LS (180 ′ 24 pg ml - 1 ). Discussion: 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 3 and 10 g d - 1 .