Journal of Nutrition

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Journal of Nutrition Vol. 110 No. 6 June 1980, pp. 1161-1168
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Long-Term Effects of Calcium, Phosphorus and Forced Exercise on the Bones of Mature Mice

R. Raines Bell1, D. Y. Tzeng2 and H. H. Draper3

School of Human Resources and Family Studies and Department of Food Science, University of Illinois, Urbana, IL 61801

The long-term effects of dietary calcium and phosphorus level and of forced exercise on bone were evaluated in mature female mice. The animals were fed either a control diet providing adequate Ca (0.6%) and P (0.3%) or a high level of P (1.2%) with increasing levels of Ca (0.6, 1.2 or 2.4%). Half of the mice in each group were subjected to 1 hour of forced exercise 5 days per week for 50 weeks. The non-exercised mice fed the 1.2% P diet with 0.6% Ca had significantly lower femur and tibia weights, bone mineral content and femoral cortical thickness than the controls fed the same level of Ca with 0.3% P. Femur fat-free dry weight was reduced from 44.6±1.9 mg (mean ± .D) to 33.2±2.3 mg. Femur Ca averaged 10.57±0.86 mg in the 0.6% Ca, 0.3% P group and 6.17±0.80 mg in the 0.6% Ca, 1.2% P group. Increasing dietary Ca partially overcame the adverse effects of high dietary P. Increasing Ca from 0.6 to 2.4% in the presence of 1.2% P increased femur weight from 33.2±2.3 to 41.8±2.5 mg and femur calcium from 6.17±0.80 to 9.85±0.84 mg. These values were still significantly lower than those of the control mice (0.6% Ca, 0.3% P) even though the Ca:P ratio was 2:1 in both cases, indicating that the absolute intake of calcium and phosphorus as well as the ratio of these minerals is important in determining their effect on bone. Forced exercise tended to increase bone weight and mineral content of the mice in all groups, but the improvements were generally small and were significant only for tibia weight, femoral cortical thickness, cortical area and percent cortical area.


KEY WORDS: • calcium • phosphorus • exercise • bone composition

1 Present address: Department of Community Health Science, Western Australian Institute of Technology, South Bentley, 6102, Western Australia.

2 Present address: Laboratory for Experimental Oncology, School of Medicine, Indiana University, Indianapolis, IN 46223.

3 To whom reprint requests should be sent at present address: Department of Nutrition, College of Biological Science, University of Guelph, Guelph, Ontario, N1G 2W1.

Manuscript received 8 June 1979.





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