Magnesium: The Multi-Purpose Mineral
Magnesium is a versatile mineral that has some major implications with regards to athletes. It has been studied quite extensively in the research. This article tries to answer the question "Why is magnesium so important to athletes and what are its functions?" By exploring some general information on magnesium and then examining the research, it may be clear to see why this mineral is so important for proper metabolic function.
Magnesium in the human body ranks fourth in overall abundance, but intracellularly (within cells) it is second only to potassium. Between 60-65% of magnesium in the human body is found in bone. Magnesium that does not exist as part of bone, is mainly found within muscle intracellularly. About 1% of magnesium is found in the extracellular fluid. Inside cells, magnesium may be found bound to phospholipids. In animal studies, it has been shown that bone magnesium is used to maintain levels throughout the body and muscle magnesium is maintained, when magnesium intake is restricted. Magnesium absorption when ingested is carrier-mediated and is influenced by transit time through the gut, dietary intake of magnesium, and the amounts of phosphorous and calcium in the diet. These minerals compete for absorption sites in the intestinal mucosa. Excess magnesium that is not deposited in bone or retained in tissue is excreted through the urine.
This mineral is involved in over 300 enzymatic reactions in the body including glycolysis, the krebs cycle, creatine phosphate formation, nucleic acid synthesis, amino acid activation, cardiac and smooth muscle contractability, cyclic AMP formation, and most importantly for strength athletes, protein synthesis. Some of the functions of this important macromineral are relevant to endurance and strength athletes. To fully understand the implications this mineral has on athletes, we must explore the roles of magnesium further.
ATP (adenosine triphosphate or energy) is always present as magnesium: ATP complex. Magnesium basically provides stability to ATP. Magnesium binds to phosphate groups in ATP, thus making a complex that aids in the transfer of ATP phosphate. Since working muscles generally contain more ADP (adenosine diphosphate), allowing ATP to release a phosphate group is important to exercising individuals.
Magnesium is also a cofactor to the enzyme creatine kinase which converts creatine into creatine phosphate or phosphocreatine (which is the storage form of creatine). Since creatine monohydrate supplements are extremely popular and proven to be effective, magnesium may be an important mineral in helping to optimize creatine function. In active muscle, creatine kinase also helps phosphocreatine combine with ADP to resynthesize ATP in contractile activity. This process, which involves magnesium, basically increases anaerobic endurance. By the way, phosphocreatine possesses a higher phosphate group transfer potential than ATP so it may be able to form ATP quickly and provide energy for muscular activity.
Magnesium also plays an important role in protein biosynthesis which is certainly applicable to athletes. It is necessary for the activation of amino acids and the attachment of mRNA to the ribosome. This process helps "make" proteins. In other words, protein synthesis depends on optimal magnesium concentrations. It is hypothesized that low magnesium levels may negatively affect protein metabolism, and may result in diminished strength gains in a structured workout regimen. It is important to note that increasing dietary protein intake may increase magnesium requirements because high protein intake may decrease magnesium retention.
To completely understand magnesium function, it is necessary to explore magnesium's relationship with calcium and potassium. Magnesium is needed for PTH (parathyroid hormone) secretion. PTH helps maintain calcium homeostasis. High magnesium or calcium levels actually inhibit PTH secretion. Magnesium may actually compete with calcium for nonspecific binding sites on myosin. Magnesium may also cause an alteration in calcium distribution by changing the flux of calcium across the cell membrane. It may also decrease intracellular calcium concentrations by inhibiting the release of calcium from the sarcoplasmic reticulum. In the process of blood coagulation, magnesium and calcium are actually antagonistic. Calcium basically promotes this process while magnesium inhibits it. If you take high amounts of calcium daily, you may have a magnesium deficiency. Most experts suggest that your calcium: magnesium ration should be 2:1. In other words, if you take 1500 mg of calcium daily through diet and supplementation, you should try to consume at least 750 mg of magnesium daily as well. this may help prevent an imbalance from occurring. Calcium and magnesium supplements should be taken at different times to allow for better absorption of each of these minerals.
Magnesium and potassium also have a close relationship. Magnesium is necessary for the function of the sodium/potassium pump. If a magnesium deficiency occurs, then pumping sodium out of the cell and pumping potassium into the cell may be impaired. Prescription diuretics tend to deplete magnesium and potassium. In this situation, magnesium intake can normalize both magnesium and potassium levels in the muscle.
Magnesium has also been implicated in the prevention of muscle cramps and muscle spasms. In a clinical study, 500 mg of magnesium gluconate relieved muscle spasms (within a few days) in an adult female tennis player who was complaining about having muscle spasms associated with prolonged outdoor exercise. This may be due to the fact that mineral losses through sweat and urine are increased during prolonged exercise. In specific, sweat losses of magnesium may increase during exercise. Increased loss of magnesium from the body have been seen during and after exercise. A shift in magnesium from the plasma into the erythrocytes was found . Basically , the more anaerobic the exercise (i.e. glycolytic), the greater the movement of magnesium from the plasma into the erythrocytes. This is why athletes may have a greater magnesium requirement.
New experimental and clinical data on the relationship between magnesium and sport
Exercise under certain conditions appears to lead to Mg depletion and may worsen a state of deficiency when magnesium intake is inadequate. Whereas hypermagnesaemia occurs following short term high intensity exercise as the consequence of a decrease in plasma volume and a shift of cellular magnesium resulting from acidosis, prolonged submaximal exercise is accompanied by hypomagnesaemia. Discordant findings on the effect of physical exercise on erythrocyte concentrations have been reported. A mechanism for the observed decrease in plasma magnesium concentration after long term physical exercise could be a shift of Mg into the erythrocyte. However, in several studies the decrease in plasma Mg was not accompanied by an increase in RBC Mg, but a decrease in cellular Mg was observed. Urinary Mg losses during an endurance event could play a role in this depletion but are often reduced, reflecting renal compensation. Loss of Mg by sweating takes place only when there is a failure in sweat homeostasis, a situation which arises when exercise is made in conditions of damp atmosphere and high temperature. Stress caused by physical exercise is capable of inducing Mg deficit by various mechanisms. A possible explanation for decreased plasma Mg concentration during long endurance events is the effect of lipolysis. Since fatty acids are mobilized for muscle energy, lipolysis would cause a decrease in plasma Mg. In developed countries Mg intake is often marginal and sport is a factor which is particularly likely to expose athletes to Mg deficit through metabolic depletion linked to exercise itself, which can only aggravate the consequences of a frequent marginal deficiency. Mg depletion and deficiency therefore play a role in the pathophysiology of physical exercise.
Experiments on animals have shown that severe Mg deficiency reduces physical performance and in particular the efficiency of energy metabolism. These data, however, do not correspond to those of marginal deficiency most commonly observed in humans. Clinical symptomatology, both in athletes and in other patients, is dominated by the symptomatology of neuromuscular hyperexcitability. Medical authorities in sport have enforced obligatory tests for latent tetany in athletes, with ionic assessment. The effects of the correction of magnesium deficiency are judged from clinical signs, Chvosteck sign, electromyogram and echocardiogram findings and plasma Mg, erythrocyte and urine analysis. These may also be complemented by cardiac and respiratory investigations after exercise. The positive effects (analysis after a minimum period of one month) of a simple oral supplement administered in physiological doses (5 mg/kg body weight/day) provides evidence for the existence of a deficiency. The evidence of depletion is much more difficult to evaluate because of the limited number of anti-depletive treatments available. It is easy to understand what favourable effects on performance would result from the correction of magnesium deficiency. However, similar effects in a subject with no magnesium deficit remain hypothetical, since the possibility of a marginal magnesium deficiency would have to be eliminated before proof could be established.