Magnesium deficiencies have been demonstrated even on relatively brief space missions, secondary to partial loss of storage sites in skeletal muscle and bone, as a result of hypokinesia, despite regular exercise. Furthermore, microgravity. leading to fluid shifts to the upper body, leads to invariable dehydration, secondary to impairment in thirst and excessive water excretion compounding hypokinesia-related reduction of muscle storage sites of water. This dehydration triggers angiotension and aldosterone elevations leading in turn to elevated catecholamines and vicious cycles with Mg ion deficiency conducive to ischemia. Elevated catecholamines and Mg deficiency, as well as a water deficiency, would contribute to oxidative stress; high free radicals (superoxide anions), inactivate nitric oxide, conducive to endothelial injuries. Insulin resistance demonstrated in astronauts, in conjunction with space flights, can develop from Mg deficiency and overactivity of the renin-angiotensin system with impairment in microvascular endothelial function. Since insulin is an important factor in the regulation of muscle protein synthesis, insulin resistance is likely to be closely associated with muscle protein loss.

Human space flight has been shown to lead to loss of body protein, which is necessary to sequester iron. Excess "free" iron can lead to lipid peroxidation, and injury to cell membranes, leading to early atherosclerosis. Since Mg is a "calcium blocker," coronary vasospasm and myocardial cell injury would be more likely in the presence of a Mg deficit. In addition, it has recently been shown in experimental animals that Mg deficiency enhances tissue iron accumulation and may impair the homeostatic control of transport iron.

Presented at the 9th International Magnesium Symposium, September 10-15, 2000 at Vichy, France