Short-term high dietary calcium intake during bedrest has no effect on markers of bone turnover in healthy men

ObjectiveImmobilization and space flight are causes of disuse osteoporosis. Increasing calcium intake may counteract this disuse-induced bone loss.MethodsWe conducted two bedrest experiments (crossover design: bedrest versus ambulatory control) in a metabolic ward, studying the effect of 1000 mg/d of calcium intake (study A, length of intervention 14 d) compared with that of a high calcium intake of 2000 mg/d (study B, 6 d) on markers of bone turnover. Both studies were randomized, controlled studies with the subjects staying under well-controlled environmental conditions (study A, 9 male subjects, age 23.6 ± 3.0 y; study B, 8 male subjects, age 25.5 ± 2.9 y). Blood was drawn to analyze serum calcium, parathyroid hormone, procollagen type I C-terminal propeptide, and bone alkaline phosphatase. Urine (24-h) was collected for analysis of calcium, C-terminal telopeptide of collagen type I, and N-terminal telopeptide of collagen type I.ResultsIn both studies, serum calcium levels remained unchanged. Procollagen type I C-terminal propeptide was lower (P = 0.03) in the bedrest phase than in the ambulatory phase in study A and tended to be lower (P = 0.08) in bedrest in study B, whereas bone alkaline phosphatase was not affected in either study. Urinary calcium excretion was greater during bedrest than during the ambulatory phase (study A, P = 0.005; study B, P = 0.002). C-terminal telopeptide of collagen type I excretion was also greater during bedrest in both studies (study A, P < 0.001; study B, P < 0.001).ConclusionDoubling calcium intake to 2000 mg/d does not prevent increased bone resorption induced by bedrest.