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

Helmut G. Hinghofer-Szalkay, Z. László, Helfried Passath, Karl Pilz, Andreas Rössler, Daniela Jezova, Hermann Scharfetter

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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-1d-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.

Original languageEnglish
Pages (from-to)1036-1041
Number of pages6
JournalAviation Space and Environmental Medicine
Volume75
Issue number12
Publication statusPublished - Dec 2004

Fingerprint

Bed Rest
Sodium
Head
Aldosterone
Dietary Sodium
Nutritionists
Plasmas
Food Supply
Supine Position
Vasopressins
Hormones
Renin
Walking
Spectrum Analysis
Electrodes
Therapeutics
Salts
Spectroscopy

Keywords

  • Aldosterone
  • Bioelectrical impedance spectroscopy
  • Plasma renin activity
  • Renal function
  • Vasopressin

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Pollution
  • Medicine(all)

Cite this

Hinghofer-Szalkay, H. G., László, Z., Passath, H., Pilz, K., Rössler, A., Jezova, D., & Scharfetter, H. (2004). Sodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest. Aviation Space and Environmental Medicine, 75(12), 1036-1041.

Sodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest. / Hinghofer-Szalkay, Helmut G.; László, Z.; Passath, Helfried; Pilz, Karl; Rössler, Andreas; Jezova, Daniela; Scharfetter, Hermann.

In: Aviation Space and Environmental Medicine, Vol. 75, No. 12, 12.2004, p. 1036-1041.

Research output: Contribution to journalArticle

Hinghofer-Szalkay, HG, László, Z, Passath, H, Pilz, K, Rössler, A, Jezova, D & Scharfetter, H 2004, 'Sodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest', Aviation Space and Environmental Medicine, vol. 75, no. 12, pp. 1036-1041.
Hinghofer-Szalkay, Helmut G. ; László, Z. ; Passath, Helfried ; Pilz, Karl ; Rössler, Andreas ; Jezova, Daniela ; Scharfetter, Hermann. / Sodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest. In: Aviation Space and Environmental Medicine. 2004 ; Vol. 75, No. 12. pp. 1036-1041.
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abstract = "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-1d-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.",
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AU - Rössler, Andreas

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N2 - 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-1d-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.

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