Magnesium is involved in numerous processes that affect muscle function including oxygen uptake, energy production and electrolyte balance. Thus, the relationship between magnesium status and exercise has received significant research attention. This research has shown that exercise induces a redistribution of magnesium in the body to accommodate metabolic needs. There is evidence that marginal magnesium deficiency impairs exercise performance and amplifies the negative consequences of strenuous exercise (e.g., oxidative stress). Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20%. Based on dietary surveys and recent human experiments, a magnesium intake less than 260 mg/day for male and 220 mg/day for female athletes may result in a magnesium-deficient status. Recent surveys also indicate that a significant number of individuals routinely have magnesium intakes that may result in a deficient status. Athletes participating in sports requiring weight control (e.g., wrestling, gymnastics) are apparently especially vulnerable to an inadequate magnesium status. Magnesium supplementation or increased dietary intake of magnesium will have beneficial effects on exercise performance in magnesium-deficient individuals. Magnesium supplementation of physically active individuals with adequate magnesium status has not been shown to enhance physical performance. An activity-linked RNI or RDA based on long-term balance data from well-controlled human experiments should be determined so that physically active individuals can ascertain whether they have a magnesium intake that may affect their performance or enhance their risk to adverse health consequences (e.g., immunosuppression, oxidative damage, arrhythmias).
Magnesium is an essential mineral that is required for optimal biological function including energy metabolism. Although national nutritional surveys indicate that usual magnesium intakes do not meet recommendations, particularly among older women, diet-induced magnesium depletion is considered rare among humans without concurrent illness. We examined the effects of dietary magnesium restriction on biochemical measures of magnesium nutriture and physiologic responses during submaximal exercise in 10 postmenopausal women, 45-71 y old, not receiving hormone replacement therapy. The women consumed diets containing conventional foods with varying magnesium content totaling 112 mg/8.4 MJ (2000 kcal) supplemented with 200 mg magnesium daily for 35d (control), then 112 mg/8.4 MJ for 93d (depletion) followed by 112 mg/8.4 MJ supplemented with 200 mg magnesium/d for 49d (repletion) in a depletion-repletion experiment. RBC magnesium concentration (P < 0.05), magnesium retention (P < 0.05) and skeletal muscle magnesium concentration (P < 0.05) decreased when dietary magnesium was restricted. Peak oxygen uptake, total and cumulative net oxygen uptake determined by using indirect calorimetry and peak heart rate increased (P < 0.05) during standardized submaximal work with restricted compared with adequate dietary magnesium. These findings indicate that dietary magnesium depletion can be induced in otherwise healthy women; it results in increased energy needs and adversely affects cardiovascular function during submaximal work. This may also explain previous observations of increased energy cost during standardized exercise in physically active men and women considered to have reduced magnesium nutriture.