REVIEW ARTICLE
Magnesium Research (1990) 3, 2, 93-102
New experimental and clinical data on the relationship
between magnesium and sport
Y. Rayssiguier1, C. Y. Guezennec2, and
J. Durlach3
1INRA, Laboratoire des Maladies
Métaboliques, Theix 63122 Ceyrat, France;
2CERMA, Bretigny, France; 3SDRM, 64 rue de
Longchamp, Neuilly, France
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
Introduction
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.
Physical exercise as a factor leading to magnesium
deficit
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.
Animal experiments
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.
Clinical data
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.
Mechanisms
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.
Physical exercise and Mg deficiency: dietary intake
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.
The consequences of magnesium deficit in the pathophysiology
of sport
Experiments on animals
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.
Mechanisms
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.
Clinical data
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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