[{"issue":"2","intvolume":" 111","_id":"33400","type":"journal_article","citation":{"bibtex":"@article{Frings-Meuthen_Bühlmeier_Baecker_Stehle_Fimmers_May_Kluge_Heer_2011, title={High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses}, volume={111}, DOI={10.1152/japplphysiol.00454.2011}, number={2}, journal={Journal of Applied Physiology}, publisher={American Physiological Society}, author={Frings-Meuthen, Petra and Bühlmeier, Judith and Baecker, Natalie and Stehle, Peter and Fimmers, Rolf and May, Francisca and Kluge, Goetz and Heer, Martina}, year={2011}, pages={537–542} }","mla":"Frings-Meuthen, Petra, et al. “High Sodium Chloride Intake Exacerbates Immobilization-Induced Bone Resorption and Protein Losses.” Journal of Applied Physiology, vol. 111, no. 2, American Physiological Society, 2011, pp. 537–42, doi:10.1152/japplphysiol.00454.2011.","chicago":"Frings-Meuthen, Petra, Judith Bühlmeier, Natalie Baecker, Peter Stehle, Rolf Fimmers, Francisca May, Goetz Kluge, and Martina Heer. “High Sodium Chloride Intake Exacerbates Immobilization-Induced Bone Resorption and Protein Losses.” Journal of Applied Physiology 111, no. 2 (2011): 537–42. https://doi.org/10.1152/japplphysiol.00454.2011.","apa":"Frings-Meuthen, P., Bühlmeier, J., Baecker, N., Stehle, P., Fimmers, R., May, F., Kluge, G., & Heer, M. (2011). High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses. Journal of Applied Physiology, 111(2), 537–542. https://doi.org/10.1152/japplphysiol.00454.2011","ieee":"P. Frings-Meuthen et al., “High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses,” Journal of Applied Physiology, vol. 111, no. 2, pp. 537–542, 2011, doi: 10.1152/japplphysiol.00454.2011.","short":"P. Frings-Meuthen, J. Bühlmeier, N. Baecker, P. Stehle, R. Fimmers, F. May, G. Kluge, M. Heer, Journal of Applied Physiology 111 (2011) 537–542."},"page":"537-542","uri_base":"https://ris.uni-paderborn.de","user_id":"89838","extern":"1","abstract":[{"lang":"eng"}],"volume":111,"status":"public","date_created":"2022-09-15T09:37:29Z","author":[{"first_name":"Petra","last_name":"Frings-Meuthen"},{"last_name":"Bühlmeier","id":"89838","first_name":"Judith"},{"first_name":"Natalie","last_name":"Baecker"},{"first_name":"Peter","last_name":"Stehle"},{"last_name":"Fimmers","first_name":"Rolf"},{"last_name":"May","first_name":"Francisca"},{"first_name":"Goetz","last_name":"Kluge"},{"last_name":"Heer","first_name":"Martina"}],"keyword":[],"publication":"Journal of Applied Physiology","creator":{"id":"89838","login":"jbuehlm"},"date_updated":"2022-09-15T09:43:45Z","language":[{}],"dc":{"title":["High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses"],"identifier":["https://ris.uni-paderborn.de/record/33400"],"date":["2011"],"publisher":["American Physiological Society"],"source":["Frings-Meuthen P, Bühlmeier J, Baecker N, et al. High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses. Journal of Applied Physiology. 2011;111(2):537-542. doi:10.1152/japplphysiol.00454.2011"],"creator":["Frings-Meuthen, Petra","Bühlmeier, Judith","Baecker, Natalie","Stehle, Peter","Fimmers, Rolf","May, Francisca","Kluge, Goetz","Heer, Martina"],"description":["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+/kg body wt per day) and a low (0.7 meq Na+/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 < 0.001). High NaCl intake caused a 43–50% greater excretion of the bone resorption markers COOH- (CTX) and NH2- (NTX) terminal telopeptide of type I collagen in HDBR than low NaCl in HDBR (CTX/NTX: P < 0.001). Serum concentrations of the bone formation markers bone-specific alkaline phosphatase (bAP) and NH2-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 < 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 < 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."],"relation":["info:eu-repo/semantics/altIdentifier/doi/10.1152/japplphysiol.00454.2011","info:eu-repo/semantics/altIdentifier/issn/8750-7587","info:eu-repo/semantics/altIdentifier/issn/1522-1601"],"language":["eng"],"type":["info:eu-repo/semantics/article","doc-type:article","text","http://purl.org/coar/resource_type/c_6501"],"subject":["Physiology (medical)","Physiology"],"rights":["info:eu-repo/semantics/closedAccess"]},"publication_status":"published","dini_type":"doc-type:article","publication_identifier":{"issn":[]}}]