Acute effects of an oral calcium load on markers of bone metabolism during endurance cycling exercise in male athletes.

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.

Mineral water as a source of dietary calcium: acute effects on parathyroid function and bone resorption in young men.

BACKGROUND: Calcium is a major component of mineralized tissues and is required for normal growth and maintenance of bone. Epidemiologic studies showed that a large percentage of the population fails to meet the currently recommended guidelines for optimal calcium intake. OBJECTIVE: The present study was designed to determine whether high-calcium mineral water is an efficient additional source of dietary calcium. DESIGN: Twelve healthy young men (mean +/- SD age: 21.1 +/- 1.2 y) ingested in a randomized order either 0.5 L of a mineral water containing 344 mg Ca/L or 0.5 L of a mineral water with a very low concentration of calcium (<10 mg/L) as a control. Blood samples were drawn before and 1, 2, 3, and 4 h after intake of the water. Urine was collected for 2 h before and every 2 h for 4 h after ingestion of the water. Serum concentrations of intact parathyroid hormone (iPTH) and serum concentrations and urinary excretion of a recently developed biochemical marker of bone resorption, type 1 collagen cross-linked C-telopeptide (CTx), were measured. RESULTS: Serum iPTH was significantly (P < 0.002) lower after ingestion of high-calcium water than after ingestion of the control. There was a significant (P = 0.01) progressive decrease in urinary CTx after ingestion of the high-calcium water, whereas after ingestion of low-calcium water the changes were modest and not significant. The fall in serum CTx concentrations was 34.7% 3 h after ingestion of high-calcium water, compared with 17.6% with the control. The decreases in serum CTx concentrations were significantly (P < 0.05) lower 1, 2, 3, and 4 h after ingestion of high-calcium water than after ingestion of the control. CONCLUSION: The present study showed that one oral intake of water containing a very moderate dose of calcium (172 mg) acutely inhibited iPTH secretion and bone resorption.

Action of different nucleotides on the last step of aldosterone synthesis.

The effect of various nucleotides on the last step of aldosterone biosynthesis, the so-called "18 oxidation" (transformation of 18-hydroxycorticosterone to aldosterone), was studied by incubation of tritiated 18-hydroxycorticosterone with untreated duck adrenal mitochondria in vitro. The study was carried out in the absence or in the presence of antimycin A which blocks the respiratory chain. Results show that, when oxidative phosphorylation chain functions normally, GTP and CTP had no effect, UTP stimulated this reaction but ADP and ATP inhibited the transformation of 18-hydroxycorticosterone into aldosterone to the same extent. For this reason ATP is included in all controls for experiments studying the effect of ATP when "18 oxidation" is inhibited by antimycin A. When oxidative phosphorylation chain is inhibited by antimycin A, ATP is able to reverse the inhibition of "18 oxidation" induced by antimycin A, in the presence of succinate. Under these conditions UTP is not able to reverse the inhibition induced by antimycin A; GTP and CTP had no effect. Effects of ATP and UTP on the last step of aldosterone biosynthesis are related to different mechanisms. ATP clearly acts as an energy source for "18 oxidation" in the presence of succinate. The role of UTP must still be determined.

The final step of aldosterone biosynthesis requires reducing power. It is not a dehydrogenation.

A mitochondrial preparation from adult duck adrenal gland was used to study the mechanism (dehydrogenation or other) of the last step of aldosterone biosynthesis (18-oxidation) by incubation of tritiated 18-hydroxycorticosterone. Results show that the role of citric acid cycle metabolites is to provide reducing power. When reducing power is provided by malate, which yields NADH or NADPH directly, the reoxidation of reduced coenzymes in the oxidative phosphorylation chain is not necessary. In the presence of succinate, the oxidative phosphorylation chain is required, but only to provide ATP. Stimulation of the reaction by low concentrations of KCN in the presence of malate shows that the reducing power is not used in the oxidative phosphorylation chain. These data suggest that the reaction is not a dehydrogenation and that the reducing power is used in a pathway competing with the respiratory chain, most probably a hydroxylating pathway, in mitochondria.