scholarly journals A Diet High in Meat Protein and Potential Renal Acid Load Increases Fractional Calcium Absorption and Urinary Calcium Excretion without Affecting Markers of Bone Resorption or Formation in Postmenopausal Women

2010 ◽  
Vol 141 (3) ◽  
pp. 391-397 ◽  
Author(s):  
Jay J. Cao ◽  
LuAnn K. Johnson ◽  
Janet R. Hunt
1991 ◽  
Vol 12 (2) ◽  
pp. 171
Author(s):  
Steven A. Abrams ◽  
Tomas J. Silber ◽  
Nora V. Esteban ◽  
Nancy E. Vieira ◽  
Mansoud Majd ◽  
...  

1997 ◽  
Vol 83 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
Noriko Ashizawa ◽  
Rei Fujimura ◽  
Kumpei Tokuyama ◽  
Masashige Suzuki

Ashizawa, Noriko, Rei Fujimura, Kumpei Tokuyama, and Masashige Suzuki. A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men. J. Appl. Physiol. 83(4): 1159–1163, 1997.—Metabolic acidosis increases urinary calcium excretion in humans as a result of administration of ammonium chloride, an increase in dietary protein intake, and fasting-induced ketoacidosis. An intense bout of exercise, exceeding aerobic capacity, also causes significant decrease in blood pH as a result of increase in blood lactate concentration. In this study we investigated changes in renal calcium handling, plasma parathyroid hormone concentration, and osteoclastic bone resorption after a single bout of resistance exercise. Ten male subjects completed a bout of resistance exercise with an intensity of 60% of one repetition maximum for the first set and 80% of one repetition maximum for the second and third sets. After exercise, blood and urine pH shifted toward acidity and urinary calcium excretion increased. Hypercalciuria was observed in the presence of an increased fractional calcium excretion and an unchanged filtered load of calcium. Therefore, the observed increase in urinary calcium excretion was due primarily to decrease in renal tubular reabsorption of calcium. Likely causes of the increase in renal excretion of calcium are metabolic acidosis itself and decreased parathyroid hormone. When urinary calcium excretion increased, urinary deoxypyridinoline, a marker of osteoclastic bone resorption, decreased. These results suggest that 1) strenuous resistance exercise increased urinary calcium excretion by decreasing renal tubular calcium reabsorption, 2) urinary calcium excretion increased independently of osteoclast activation, and 3) the mechanism resulting in postexercise hypercalciuria might involve non-cell-mediated physicochemical bone dissolution.


1989 ◽  
Vol 50 (5) ◽  
pp. 1088-1094 ◽  
Author(s):  
M Zarkadas ◽  
R Gougeon-Reyburn ◽  
E B Marliss ◽  
E Block ◽  
M Alton-Mackey

1972 ◽  
Vol 71 (2) ◽  
pp. 313-320 ◽  
Author(s):  
O. Helmer Sørensen ◽  
Inge Hindberg ◽  
S. Nistrup Madsen

ABSTRACT Bone resorption, intestinal absorption of calcium, and urinary calcium excretion were studied in young rats given prolonged calcitonin treatment. The animals soon developed a resistance to the hypocalcaemic effect of calcitonin, probably due to a secondary hyperparathyroidism. In one of the experiments the rats were given 45Ca 2 weeks before the start of the calcitonin treatment in order to label the deep parts of bone. The release of isotope from bone was inhibited after the first injections of the hormone, but even after a few days of calcitonin treatment no differences could be detected between the treated animals and their corresponding controls. An increased release of isotope from bone was registered as soon as the treatment was interrupted, indicating the presence of a secondary hyperparathyroidism. No conclusive changes could be detected in the intestinal absorption of calcium. A transitory reduction in the excretion of calcium in the urine was followed by a considerable loss of calcium.


2009 ◽  
Vol 104 (10) ◽  
pp. 1512-1516 ◽  
Author(s):  
Kristina L. Penniston ◽  
Andrea N. Jones ◽  
Stephen Y. Nakada ◽  
Karen E. Hansen

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