Although sport and physical activity are generally considered as positive factors for bone metabolism some endurance trainings such as running and bicycling have few or no beneficial or even deleterious effects on bone mineral density. The present study was designed to investigate the acute effect of an intensive endurance cycling exercise on biochemical bone markers. Furthermore, the effect of the oral intake of 1 g calcium load, by drinking high-calcium mineral water, just prior to and during the exercise was checked. Twelve well-trained elite male triathletes aged 23-37 years were explored. The serum concentrations of calcium, phosphate, PTH, bone alkaline phosphatase (BALP) and C-terminal cross-linking telopeptide of type 1 collagen (CTX) were measured before, during and after a 60 min 80% VO2max cycle ergometer exercise. Since cycling exercise was accompanied by a reduction in plasma volume the total amount of biochemical bone markers was calculated. When the exercise was performed without calcium load both serum concentrations and total amount of CTX began to increase progressively 30 min after the start of the exercise and were still significantly elevated, by 45-50%, 2h after the end of the exercise. Ingestion of high-calcium mineral water completely suppressed the CTX response. By contrast serum concentrations and total amount of BALP fluctuated and showed no significant difference with or without calcium load. The present study demonstrates that the burst of osteoclastic activity acutely induced by an endurance cycling exercise can be suppressed by the previous intake of a calcium load afforded by drinking high-calcium mineral water.

The first part of this study consisted of an 18 month follow-up of the vitamin D status and parathyroid function in a group of 54 French male adolescents, aged from 13 to 16 years old and all pupils of a jockey training school. During the 18 month period four samplings were made, one every 6 months. The first was during September of the first year, the second and third during March and October of the second year, and the last in March of the third year. Therefore we had two main periods: summer and winter. The summer 25-hydroxyvitamin D (25(OH)D) concentrations were higher (71.6 +/- 19.9 and 52.4 +/- 16.5 nmol/l) than the winter ones (20.4 +/- 6.9 and 21.4 +/- 6.1 nmol/l). Conversely, the winter intact parathyroid hormone (iPTH) serum levels (4.18 +/- 1.18 and 4.11 +/- 1.35 pmol/l) were higher than the summer ones (2.44 +/- 0.82 and 2.71 +/- 0.71 pmol/l). At the two winter time points the 25(OH)D concentrations were lower than 25 nmol/l (10 ng/ml) in 72% (2nd year) and 68% (3rd year) of the adolescents. In the second part of the study we tried a vitamin D3 supplementation procedure designed to maintain the 25(OH)D and iPTH postsummer serum levels throughout the winter. Pairs of male adolescents matched for height, weight and Tanner pubertal stage were randomly assigned to either vitamin D3 supplementation (2.5 mg, i.e., 100,000 IU) administered orally at three specific periods (end of September, November and January) or no vitamin D3 treatment (control subjects). Blood was collected just before the first intake of vitamin D3 and 2 months after the last intake (March). The control subjects had blood drawn at the same time points. In the vitamin D3-treated subjects, the concentrations of 25 (OH)D (55.3 +/- 11.5 nmol/l) and of iPTH (3.09 +/- 1.16 pmol/l) in March and September (53.8 +/- 12.3 nmol/l and 2.75 +/- 1.26 pmol/l) were not significantly different. In the control subjects, March 25(OH)D levels (21.0 +/- nmol/l were low, with values below 25 nmol/l in 78% of subjects, and iPTH concentrations (3.97 +/- 1.08 pmol/l) were significantly (p<0.001) higher than in September (2.91 +/- 0.81 pmol/l). The constant vitamin D wintertime deficiency and wintertime rise in iPTH in adolescent French males throughout puberty has been demonstrated. In adolescents with low dairy calcium intakes, the vitamin D3 treatment was sufficient to maintain 25(OH)D concentrations at their summer levels throughout winter and to prevent an excessive wintertime rise in iPTH levels.

The vitamin D status was determined on one to four occasions either after summer (September-October) or after winter (March-April) in 175 male adolescents (13-17 years), resulting in 394 measurements of serum 25-hydroxyvitamin D (25(OH)D) and intact parathyroid hormone (iPTH). The subjects lived in a rural area to the north of Paris (49 degrees N). After summer the 25(OH)D concentration was 58.5 +/- 18.0 nmol/l (mean +/- SD), while after winter it had fallen to 20.6 +/-6.0 nmol/l (p = 0.0001). Meanwhile the iPTH concentration was 2.76 +/- 0.97 pmol/l (mean +/- SD) after summer and increased to 4.20 +/- 1.21 pmol/l after winter (p = 0. 0001). All the results were pooled and a nonlinear population model with random parameters was used to describe the relationship between serum iPTH and 25(OH)D. When the concentration of 25(OH)D was higher than 83 nmol/l, an iPTH mean 'plateau' level at 2.48 pmol/l was reached. When 25(OH)D concentrations fell below 83 nmol/l, the increase in iPTH concentration accelerates, and when the mean 25(OH)D concentration was equal to or lower than 10 nmol/l the mean iPTH level (4.97 pmol/l) was twice as high as the 'plateau' value.

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