Magnesium Research (1990) 3, 2, 93-102
Summary: Exercise under certain conditions appears to lead to Mg depletion and may worsen a state of deficiency when Mg 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.
Key words: Sports medicine, exercise, stress, magnesium depletion, magnesium deficiency, magnesium supplementation
When metabolism is accelerated, as during exercise, the requirement for Mg may increase. It has been suggested that some athletes may have suboptimal Mg status which could adversely affect their exercise. The aim of this review is to assess whether physical exercise is a factor leading to Mg deficit, to determine the consequences of Mg deficit in the pathophysiology of sport, and to discuss the therapeutic implications.
Magnesium deficit 1 can be induced by insufficient intake (magnesium deficiency) or by a dysregulation of the metabolism of the ion (magnesium depletion). In developed countries, magnesium intake is often inadequate and a large part of the population is exposed to Mg deficiency. Magnesium depletion cannot be compensated by a simple increase in intake as in the case of magnesium deficiency. Its control requires identification and correction of the metabolic alterations that cause it 1. Exercise may condition or depend on one or other of these mechanisms inducing Mg deficit.
Animal experiments and clinical data indicate the influence of exercise on plasma and red blood cell (RBC) Mg. Since 99% of total body Mg is located in the intracellular stores or in bone, plasma Mg levels do not always reflect intracellular or total body Mg stores. Red blood cells possess several characteristics which make them different from other cells of the organism, and RBC levels of Mg depend as much on mesological as on genetic factors. It remains nonetheless true that the basic measurements of Mg status are those of plasma and erythrocyte Mg 1.
In horses and ponies, the plasma Mg falls during strenuous exercise 2. This change may be involved in the symptoms of neuromuscular excitability. An effort of physical endurance also decreases plasma Mg in racing huskies. This decrease is not totally compensated for during the recovery period 2.
Mg plays a central role within the pathogenesis of stress-related disease 3 and stress factors are implicated in the occurrence of hypomagnesaemia in ruminants. A number of environmental factors could trigger off grass tetany in dairy cows 4. The effect of feeding varying concentrations of dietary magnesium on exercise capacity and Mg status were investigated in rats 5-7. A treadmill test produces no significant modifications in RBC magnesium in rats fed normal magnesium levels in their diet, but significantly reduces erythrocyte Mg in animals fed on a diet deficient in this element 6.
Plasma and erythrocyte Mg -- Whereas short-term, high intensity exercise leads to hypermagnesaemia 8-11, prolonged submaximal exercise is accompanied by hypomagnesaemia 12-23. In the first case, hypermagnesaemia appears as the consequence of a decrease in plasma volume, a shift of cellular Mg resulting from acidosis and muscle contraction 24,25. Plasma Mg changes in this case are of the same type as those of plasma K, being both immediate and spontaneously reversible during the recovery period. Other studies have been carried out on changes in plasma during different types of prolonged submaximal exercise (marathon running, long distance cross-country skiing, cycle ergometry, swimming training, tennis, walks of long duration). There was a transient fall in plasma Mg concentrations and the decreases in plasma Mg were greater after accounting for changes in plasma volume 26. Changes in Mg are quite different from those in plasma K and Na 27. Prolonged submaximal exercise can lead to dehydration with a more or less rapid decrease in plasma volume and an increase in osmotic pressure. The increase in plasma K has been attributed to haemoconcentration and muscular activity, the increase in plasma Na to sweating.
Whereas strenuous exercise decreases plasma Mg, measurements of RBC magnesium have produced conflicting results. Inconsistencies do not seem to be the consequences of differences in experimental design, work intensity and duration, whereas the method used for RBC Mg determination, the timing of the blood sample, and variations in globular volume should be taken into account in data analysis.
Comparison of the changes in plasma and erythrocyte MgSeveral authors have observed an increase in erythrocyte Mg and have suggested that a major part of the loss from plasma could be accounted for by a shift of Mg into the erythrocytes 14,16,19,28,29. This shift is apparently transient, as indicated by the return to pre-exercise levels during the recovery period. Thus, intercompartmental Mg shifts in the blood, as evidenced by a decrease in plasma Mg content and an increase in erythrocyte Mg, might be the consequence of an increase in Mg requirement when metabolic activity is increased. Other studies reported no change in RBC Mg 11,22,30,31 or even a significant decrease in RBC Mg content 32. Linjen et al. 23, who studied 23 runners before and after a marathon race, reported that there was a decrease in plasma and erythrocyte Mg. This study suggest that the RBC Mg was released into the extracellular pool. The decrease in RBC Mg has been proposed as a potential mechanism for exercise-induced RBC haemolysis; however, recent experiments do not support this hypothesis 29. The decrease in RBC Mg may depend on adaptation to exercise 9. The better the subject is adapted, the smaller the variation in Mg. Decreases in RBC Mg following exercise have been reported in Mg-deficient rats, whereas no significant differences were observed in rats on a high Mg diet 6. In athletes, conflicting results concerning the effect of muscular activity on RBC Mg could be the result of differences in nutritional status and it would be of interest to test whether an improved Mg status could prevent the decrease in RBC Mg induced by exercise.
Muscle Mg -- A transient shift of Mg from the extracellular fluid to skeletal muscle tissue is another proposed mechanism for the decrease in plasma Mg during exercise. Thus, in the rat, exercise groups (6-week swimming exercise programme) demonstrated significantly higher Mg levels in skeletal muscle and a tendency towards lower levels of Mg in plasma, erythrocytes and bone compared with sedentary groups 33.
Urine Mg -- High intensity anaerobic exercise induces a transient increase in the urinary excretion of Mg. The percent increases correlates with post-exercise blood lactate concentration and oxygen consumption during exercise 31. Significant decreases in urinary excretion of Mg are observed in prolonged submaximal exercise 15,23,28. Urinary excretion of Mg increases during the recovery period to reach levels higher than those measured before exercise 23. Since these changes in urinary Mg excretion correspond to changes in plasma Mg, the following mechanism may be suggested: during high intensity anaerobic exercise, the increase in urinary Mg excretion could be the consequence of transient hypermagnesaemia and metabolic acidosis. In addition, both aldosterone and ADH, the hormone that regulated renal handling of Mg, are increased by strenuous exercise. This could result in an increased Mg excretion 31. The decline in plasma Mg concentration after prolonged submaximal exercise would lead to a decrease in urinary Mg excretion through increased tubular reabsorption 34, whereas the increase in plasma Mg concentration in the recovery period would lead to further Mg losses. Therefore, these observations do not support the hypothesis that the decrease in plasma Mg is solely due to an increase in Mg excretion.
Mg in sweat -- The measured concentrations of Mg in sweat are about 6 mg/litre 13, but may reach higher values 35-37. Hyperexcretion in sweat can acquire real importance in the case of intense activity. However in the case of excessive sweating, this Mg concentration is most often reduced homeostatically and the loss remains quantitatively moderate. In pathology, this homeostatic reaction may be maintained, for instance, in alcoholic patients 38 or may fail, especially when exercise is made in conditions of damp atmosphere and high temperatures 1. Miner's heat cramp is an illness for which compensation is awarded. The official biological criterion for this disorder is given as a decrease in urinary chloride. However, Bauman has shown that there is no correlation with Na and K chloride excretion, but rather there is a correlation with an increase in sweat Mg 39. It may be that the hyperaldosteronaemia which occurs during exercise in an attempt to correct Na depletion increases not only the losses of K by sweat, but also that of Mg 1,40,41. It is however true that in the case of marathons run in relatively low temperature conditions, the decrease in Mg content in plasma cannot be accounted for by sweat Mg losses.
Lipolysis -- Stress is accompanied by large amounts of lipolytic catecholamines which cause hypomagnesaemia 1. Blood plasma Mg has been shown to decrease when lipolysis is increased 42,43. This relationship between lipolysis and plasma Mg has been particularly studied in the case of adrenergic stress. Adrenaline infusion reduces plasma Mg. Hypomagnesaemia is increased by phentholamine (an α-adrenergic blocking agent) and inhibited by propanolol (a β-adrenergic blocking agent) or by nicotinic acid (an antilipolytic compound) 42. In the same way, fasting or exposure to low temperatures depresses plasma Mg by increasing lipolysis 43. Nicotinic acid blocks both the increase in free fatty acid levels and hypomagnesaemia. The effect of adrenaline and of lipid mobilization on plasma Mg has been confirmed in humans in various experimental conditions 2-44 and is explained by an increased uptake of Mg by adipocytes 45. A similar mechanism could probably occur during long endurance events. As fatty acids are mobilized for muscle energy, the lipolysis would cause a decrease in plasma Mg.
Other mechanisms -- Stress caused by physical exercise is capable of inducing Mg deficit by other mechanisms. It renders different processes of Mg homeostasis ineffective and it brings into play neurohormonal secretions that increase Mg losses 1. Although explanations have been offered for the compartmental shifts of Mg, the precise mechanism remains to be established. It is important to evaluate whether there is only a transient fall in plasma Mg concentration or whether participation in sustained physical activity may induce alterations in the Mg balance and necessitate Mg supplementation.
Several studies indicate that there is a sustained fall in plasma Mg concentration after strenuous exercise and that hypomagnesaemia either persists or worsens during a season of training 21,46,47,48, a sound reason for looking more carefully at the Mg intake of athletes. A recent longitudinal study of a group of medium-distance runners carried out over a training season also demonstrated plasma Mg reductions during the competition period, although there were no variations in erythrocyte Mg. Since both their energy intake and their work load remained more or less constant during the study, a relationship can be established between plasma Mg changes and the stress of the competition period 48. In conclusion, exercise under certain conditions appears to lead to magnesium depletion both in humans and in animals and may worsen a state of deficiency when Mg intake is inadequate.
In developed countries, magnesium intake is often marginal (4 mg/kg. d) and much lower than the recommended intake (6 mg/kg. d) 2,49. Since an athlete is an adolescent or adult who eats the same diet as the population to which he belongs, this also applies to him 50. It has been reported that an intake of between 100% and 150% of the levels recommended for subjects with moderate physical activity should be supplied to athletes, an assertion which remains to be established 25,41. However the risk of deficiency may be particularly worrying in athletes 51,52. A recent study shows the food intake of both athletes and sedentary subjects to be very similar, apart from significantly higher energy values in the intake of athletes. Since a positive correlation exists between Mg intake and the energy value of the diet, Mg intake is higher in the athletes than in the control group, though the prevalence of an intake of less than 400 mg/day remains very high 52.
Athletes are therefore a group at risk from magnesium deficit owing to metabolic depletion linked to physical exercise, which itself can aggravate the consequences of marginal intake of this element. This notion is of particular importance in the prevention of possible long-term detriment to health and when choosing subjects in order to establish the norms for magnesium indices 53.
Severe deficiency and performance -- The effects of feeding varying concentrations of dietary Mg on exercise capacity were investigated in rats. Based on treadmill or swimming tests, the Mg-deficient rats showed a markedly lower exercise endurance capacity than rats fed the higher levels of dietary Mg 5-7,54.
In a recent experiment 6 weanling male rats were pair-fed diets containing 960 or 35 mg/kg Mg for 8 days. Rats were trained on a treadmill with electrical stimulation for 2 days before the test. The speed was fixed at 20 m/min. In the first experiment, rats were placed on the treadmill for 2 hours or removed because of exhaustion. Mg-deficient rats had a lower capacity for exercise (87 ± 10 min) than control rats (120 min). This difference in exhaustion time would have been more pronounced if the test had not been stopped for control rats after 120 min. In the second experiment, blood indices were studied in control and deficient rats at rest or after 1 h of running. In the non-running animals, the results confirmed earlier findings from Mg-deficient states: the Mg-deficient rats had a lower plasma concentration of Mg; RBC concentrations of Mg and K decreased and Na increased; Mg deficiency produced modifications in plasma lipids 55, but there were no significant changes in the blood levels of glucose, lactate, alanine and β-OH butyrate. In the control rats, after the test, as compared to the resting condition, no significant differences were observed in these variables. As compared to the resting condition, Mg-deficient rats showed a significant decrease in RBC Mg concentration, and a significant increase in plasma free fatty acid and lactate concentrations. These studies, which clearly show that dietary deficiency may influence exercise performance, also indicate that exercise adversely affects RBC Mg concentration when Mg intake is inadequate. An improved magnesium nutritional state can prevent the decrease in RBC Mg induced by increased physical activity.
The results of these tests, showing a reduction in performance in the case of Mg deficiency, could be compared to those of studies made on the response of deficient animals to cold. From the metabolic point of view, exercise and cold stress have been found to produce similar changes 56. Rats with a marginal Mg deficiency were shown to be less tolerant to cold as evaluated by the fall in their body temperature after severe cold stress. There was more damage to the heart and longevity was reduced 57.
Decreased endurance capacity may be the result of various consequences of Mg deficiency 1,25. Mg, the second most abundant intracellular cation, serves essential roles in metabolism and deficiency is likely to affect the energy substrates of effort at muscular and extramuscular levels.
Many investigations have indicated that Mg plays an important role in the synthesis and use of compounds rich in energy and in the maintenance of the membrane properties. Several investigations indicate mitochondrial disorders during Mg deficiency 58,59. Histological studies have reported a reduction in the number of mitochondria or mitochondrial swelling, and metabolic studies have revealed a partial uncoupling of oxidative phosphorylation. Cellular phosphagen levels (ATP, creatineosphate) appear to become rapidly depleted 60. Mg deficiency is accompanied by a subsequent loss of K and gain in Ca and Na.
Fluorescence polarization was used to compare the fluidity of membrane preparation from Mg-deficient and control rats 61,62. Erythrocyte membranes and hepatocyte plasma membranes from Mg-deficient animals were more fluid than those of control rats, and Mg deficiency induced a significant decrease in the anisotropy both of intact hepatic mitochondria and of inner mitochondrial membrane 63. Several functional alterations in the membrane occurred in parallel to the physical changes measured by the increase in its fluidity. The results support the hypothesis that defective membrane function could be the primary lesion underlying the cellular disturbances that occur in Mg deficiency.
The increased fluidity of RBC membranes is accompanied by morphological changes: increased permeability to cations, premature destruction of the cells, and the development of anaemia. Changes in membrane fluidity affect red cell deformability and clinical experiments indicate that blood rheological parameters influence performance. However, decreased tissue oxygenation and enhanced cardiac work are associated with a decrease in red cell deformability 64.
Changes in skeletal muscles induced by Mg deficiency have repeatedly been reported 65-67. Chronic Mg deficiency leads to a complex array of biochemical, electrophysiological and morphologic abnormalities in skeletal muscle. Several reports suggest that development of of cellular phosphorus deficiency may play a role in the myopathy of magnesium deficiency. Rhabdomyolysis, which is the physiological destruction of a certain percentage of cells depending on the type and length of exercise, is one of the limiting factors in prolonged exercise, being reflected in a substantial rise in muscle CPK enzymes and myoglobin. This phenomenon is in part linked to membrane function disorder during physical exercise. The role of marginal Mg deficiency in this pathogenesis has been suggested 65-67. Mag plays an important role in muscle excitation-contraction coupling and the activity of the Ca transport system in the sarcoplasmic reticulum membranes depends on the presence of Mg ions 68. Neuromuscular abnormalities and irritability (weakness, paraesthesiae, muscle fasciculations, tetany) are prominent findings in animals fed Mg-deficient diets, but the origin of neuromuscular hyperexcitability remains unclear 1. The central and peripheral nervous system and the neuromuscular junctions are other areas in which Mg deficiency may exert its effects 1,69.
Additional factors which may contribute to decreased endurance capacity are the cardiovascular consequences of Mg deficiency, which have been associated with changes in blood pressure, vascular reactivity, and cardiac rhythm disorders 70. These changes could result in altered blood flow to the muscle. While is is likely that the diminished endurance capacity of Mg-deficient animals is multifactorial, these data should be treated with care when used in human application, since the effects of Mg deficiency on endurance capacity have been observed in markedly deficient animals.
When analysing the role of Mg deficit in athletes, the same approach should be used as that used for any patient suspected of Mg deficit 1, accompanied by the tests normally carried out in sports medicine.
First, an investigation should be made for nonspecific signs of neuromuscular hyperexcitability (anxious hyperemotivity, paraesthesiae, asthenia, headaches, insomnia, muscular fasciculations, cramps, contractures, myoclonia, exaggerated tiredness with muscular effort, tetany after hyperventilation). The patient should be tested for clinical and paraclinical signs of neuromuscular hyperexcitability. The most significant is Chvostek's sign, more frequently positive in athletes than in sedentary subjects 71. Careful auscultation of the heart must be done looking for a systolic click and a mitral valve murmur. Paraclinical examination involves electromyogram (EMG), electroencephalogram (EEG), and echocardiogram (ECC), mitral valve prolapse often being identified after ECC examination. It also includes plasma and RBC Mg, plasma CA, and urinary Mg. If indicated the measurements may be much more numerous whether on the ionic level or with regard to evaluating the neuroendocrine factors of regulation or dysregulation.
Since Coirault 72, the diagnosis of latent tetany has often been supported by the presence of the 'the magnesium hook' on the time-intensity curve of galvanic muscle stimulation.
This measurement, made with an electronic rheothome, has met with much criticism, the strongest of which is based on the extreme variability of cutaneous resistivity. This method is still in use but is currently being replaced by EMG 2 73. A repetitive EMG constitutes the principal neurophysiological mark of tetany. The more recent use of EMG spectral analysis during muscular contraction has allowed the identification of an electric response characteristic of fatigue. Its correlation with Mg deficit has not yet however been correctly defined. In France, FFESSM now insists that all new members undergo tests for latent tetany before diving. The examination of athletes includes cardiorespiratory function and aerobic metabolism of skeletal muscles, with maximum working capacity, O2 consumption, blood pressure, and heart rate.
The effect of Mg on exercise has been reported in several studies. There may be an inverse correlation between the maximal voluntary contraction force of the quadriceps femoris muscle and serum Mg levels 74. Plasma Mg was significantly correlated with maximal oxygen consumption among athletes but only a weak association was found in untrained men 75,76. No correlation was found in a recent study 77. When a relationship between maximal oxygen consumption, which is dependent on oxygen delivery to the working muscle, and plasma Mg is observed in athletes, it may represent a cellular adaptation of Mg metabolism to physical training. Mg may contribute to the facilitation of oxygen delivery to the working muscle by the production of 2,3-diphosphoglycerate in the erythrocyte 75.
Therapy by oral physiological doses of Mg represents a major step in treating Mg deficit. The normal treatment consists of oral intake of 5 mg/kg.day of Mg for the adult in a Mg salt that is well absorbed and well tolerated. It represents the exclusive treatment for Mg deficiency. In Mg depletion, where the deficit depends on dysregulation of Mg metabolism, the goal is to identify the nature of the depletion and correct it specifically 1. Whatever the treatment used, the parallel correction of Mg deficit and its symptomatology forms the best argument for the role of Mg in the genesis of non-specific disorders 91. The therapeutic implications are to be found in a healthy lifestyle and treatments adapted to physical activity.
Several studies have been performed to test the effect of using oral Mg supplementation on muscular work performance. A 4-week administration of Mg to athletes increased their physical performance. This amelioration was shown by registering the maximum oxygen consumption as well as the PWC170, using both a running board and bicycle ergometry 78. Mg supplementation resulted in a significant decrease in protein release from the muscle cells during a marathon run and total creatine kinase (CCK) in serum increased less 79-80. Mg supplementation has a significant effect on respiration indices and improves lactate elimination in competitive rowers during exhaustive simulated rowing. In moderately trained subjects, the effects of magnesium supplementation were tested on some cardiorespiratory variables monitored during a 30 min submaximal effort test 81. In the Mg group, a significant decrease was found in blood pressure, heart rate and oxygen consumption. The results indicate that magnesium supplementation induces an overall improvement in cardiorespiratory performance.
In these studies however the possibility of a subclinical deficiency cannot be excluded and it is thus not improbable that the improvement in physical performance was the result of the correction of the deficiency. While it is easy to explain the favourable effects of Mg supplementation in athletes with Mg deficiency, what result Mg supplementation has on the physical performance on healthy subjects needs further investigation 82,83. Moreover, attention should be drawn to the risks attached to ovversupplementation of Mg, something which is at present carried out systematically in top level athletes. Couzy et al. 84 have provided data on hypozincaemia found in the French national skiing team and which may be associated with Mg overload.
To conclude, sport is a factor which is particularly likely to expose athletes to magnesium deficit through metabolic depletion linked to exercise itself, which can only aggravate the consequences of a frequent marginal deficiency. Experimental and clinical data show that magnesium deficiency is one of the nutritional factors influencing the pathophysiology of sport. However, the use of oral supplemental Mg and antidepletive magnesium treatments to aid muscular work performance remains to be defined satisfactorily by further studies.
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