INTRODUCTION MagnesiumMagnesium is the fourth most abundant mineral and the second most abundant intracellular cation in the body, contributing to over 300 metabolic reactions (1). This essential nutrient is involved in the synthesis of nucleic acids and proteins, proper bone development, maintenance of electrolyte balance and mineral homeostasis, as well as oxidative, immune, and neuromuscular functions (2). The recommended dietary allowance (RDA) for magnesium in individuals, 14 yr of age and older, is between 310 and 420 milligrams per day (mg•d −1 ); but magnesium intake is reportedly suboptimal in most populations (3). Individuals with serum magnesium concentrations greater than 0.85 mmol•L −1 are likely to have adequate magnesium status, whereas individuals with serum magnesium concentrations around or below 0.75 mmol•L −1 are most likely to have a magnesium deficiency (4). A low serum magnesium concentration is associated with various chronic diseases (e.g., hypertension, cardiovascular disease, etc.), and research has shown that adequate magnesium intake has a potential therapeutic role in improving glucose and insulin metabolism. Furthermore, magnesium has been shown to treat severe asthma and migraines and assist in alleviating muscle cramps (5,6). It is currently estimated that 45% of adults from the United States are magnesium deficient, and 22% of international athletes are also clinically deficient (7,8). Magnesium contributes to the maintenance of muscle function and blood glucose concentrations, while also promoting calcium absorption. The increased importance of these functions in athletes advances the idea that magnesium, like other minerals, may exert an ergogenic effect, specifically in individuals with low serum magnesium concentrations (1,9,10). Vitamin DVitamin D is a lipid-soluble vitamin that is essential to muscle growth, cell differentiation, and bone mineralization (11,12).
1. Five patients with chronic hypoparathyroidism were given dihydrotachysterol. 2. Calcium and phosphorus absorption and excretion were measured in three of the patients. An increased absorption of calcium from the intestine was the major source of the increased excretion of calcium after dihydrotachysterol.3. A change in the renal tubular handling of phosphorus was a major factor in the changes in the serum phosphorus after treatment with dihydrotachysterol.
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