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Cause of Exercise Associated Muscle Cramps (EAMC) - Altered neuromuscular control, dehydration or electrolyte depletion?

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Abstract

Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the "electrolyte depletion" and "dehydration" hypotheses and (2) the "altered neuromuscular control" hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the "electrolyte depletion" and "dehydration" hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the "electrolyte depletion" and "dehydration" hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the "altered neuromuscular control" hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the "altered neuromuscular control" hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC.
doi:10.1136/bjsm.2008.050401
2009;43;401-408; originally published online 3 Nov 2008; Br. J. Sports Med.
M P Schwellnus
dehydration or electrolyte depletion?
(EAMC)  altered neuromuscular control,
Cause of Exercise Associated Muscle Cramps
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Cause of Exercise Associated Muscle Cramps
(EAMC) — altered neuromuscular control,
dehydration or electrolyte depletion?
M P Schwellnus
Correspondence to:
Martin P Schwellnus, UCT/MRC
Research Unit for Exercise
Science and Sports Medicine,
Department of Human Biology,
Faculty of Health Sciences,
University of Cape Town, South
Africa, 3rd Floor, Sports Science
Institute of South Africa,
Boundary Road, Newlands, Cape
Town, 7700, South Africa;
martin.schwellnus@uct.ac.za
Accepted 18 October 2008
Published Online First
3 November 2008
ABSTRACT
Exercise Associated Muscle Cramps (EAMC) is one of the
most common conditions that require medical attention
during or immediately after sports events. Despite the
high prevalence of this condition the aetiology of EAMC in
athletes is still not well understood. The purpose of this
review is to examine current scientific evidence in support
of (1) the ‘‘electrolyte depletion’’ and ‘‘dehydration’’
hypotheses and (2) the ‘‘altered neuromuscular control’’
hypothesis in the aetiology of EAMC. In this review,
scientific evidence will, as far as possible, be presented
using evidence-based medicine criteria. This is particularly
relevant in this field, as the quality of experimental
methodology varies considerably among studies that are
commonly cited in support of hypotheses to explain the
aetiology of EAMC. Scientific evidence in support of the
‘‘electrolyte depletion’’ and ‘‘dehydration’’ hypotheses for
the aetiology of EAMC comes mainly from anecdotal
clinical observations, case series totalling 18 cases, and
one small (n = 10) case–control study. Results from four
prospective cohort studies do not support these
hypotheses. In addition, the ‘‘electrolyte depletion’’ and
‘‘dehydration’’ hypotheses do not offer plausible patho-
physiological mechanisms with supporting scientific
evidence that could adequately explain the clinical
presentation and management of EAMC. Scientific
evidence for the ‘‘altered neuromuscular control’’
hypothesis is based on evidence from research studies in
human models of muscle cramping, epidemiological
studies in cramping athletes, and animal experimental
data. Whilst it is clear that further evidence to support the
‘‘altered neuromuscular control’’ hypothesis is also
required, research data are accumulating that support this
as the principal pathophysiological mechanism for the
aetiology of EAMC.
Exercise Associated Muscle Cramps (EAMC) is one
of the most common conditions that require
medical attention during or immediately after
sports events. EAMC is particularly common in
endurance events such as ultra-marathon running
and triathlon.
1–4
Despite the high prevalence of this
condition the aetiology of EAMC in athletes is still
not well understood.
Muscle cramping in athletes may occur as a
result of many underlying medical conditions,
5
and
therefore not all athletes with muscle cramping
suffer from EAMC. However, in the sports
medicine literature, cramping during or immedi-
ately after exercise is more commonly referred to as
Exercise Associated Muscle Cramping (EAMC),
6–9
which has been defined as a ‘‘painful, spasmodic
and involuntary contraction of skeletal muscle that
occurs during or immediately after exercise’’.
10
This
term will be used in this review.
The first reports of muscle cramping related to
physical activity were from labourers working on
steamships and in mines in hot, humid conditions
more than 100 years ago.
11 12
In these early reports
it was noted not only that muscle cramping
occurred in the heat but also that cramps were
accompanied by profuse sweating.
12
These early
anecdotal observations led to the development of
the traditional ‘‘electrolyte depletion’’ and ‘‘dehy-
dration’’ hypotheses for the aetiology of EAMC.
These case reports often related the development
of cramping to physical activity performed in hot
and humid environmental conditions, and this has
led to the terminology ‘‘heat cramps’’ or ‘‘exer-
tional heat cramps’’. This terminology is still used
today,
561314
often synonymously with EAMC.
This is despite the fact that EAMC is known to
occur in individuals exercising in moderate to cool
temperatures,
615
and exposure to extreme cold has
also been associated with EAMC in swimmers.
2
It
has also been reported that the development of
EAMC is not directly related to an increased core
temperature.
16
Furthermore, passive heating alone
(at rest) does not result in EAMC and cooling does
not relieve muscle cramps.
10
It would therefore
appear that heat alone is not a direct cause of
muscle cramping during exercise, and therefore the
term ‘‘heat cramps’’ is a misnomer, and its use
should be discouraged.
A novel hypothesis for the aetiology of EAMC
was first proposed about 10 years ago.
10
This
hypothesis explored evidence that altered neuro-
muscular control as a result of the development of
muscle fatigue may be the primary factor that is
associated with the development of EAMC.
10
This
‘‘altered neuromuscular control’’ hypothesis has
only recently gained some acceptance and ‘‘muscle
fatigue’’ has, in a recent review, been acknowl-
edged as a predisposing factor in the development
of EAMC.
6
The purpose of this review is to examine current
scientific evidence in support of (1) the ‘‘electrolyte
depletion’’ and ‘‘dehydration’’ hypotheses’’ and
(2) the ‘‘altered neuromuscular control’’ hypo-
thesis in the aetiology of EAMC. In this review,
scientific evidence will, as far as possible, be
presented using evidence-based medicine (EBM)
criteria.
17
This is particularly relevant in this field,
as the quality of experimental methodology varies
considerably among studies that are commonly
cited in support of hypotheses to explain the
aetiology of EAMC.
Review
Br J Sports Med 2009;43:401–408. doi:10.1136/bjsm.2008.050401 401
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SCIENTIFIC EVIDENCE SUPPORTING THE ‘‘ELECTROLYTE
DEPLETION’’ AND ‘‘DEHYDRATION’’ HYPOTHESES FOR THE
AETIOLOGY OF EAMC
Scientific evidence in support of the electrolyte depletion
hypothesis for the aetiology of EAMC
More than a century ago, it was first reported that individuals
who were exposed to physical exercise in hot and humid
environments could develop muscle cramps that were appar-
ently associated with disturbances in serum electrolyte con-
centrations, notably hypochloraemia.
11 18
Following these early
reports, it has been suggested that other serum electrolyte
abnormalities, including hyperkalaemia, hypomagnesaemia and
hypocalcaemia, can also be associated with EAMC.
12 19–21
The
scientific methodology in all these studies was in the form of
case reports or case series, with no control groups. There is not a
single published study that has shown that serum electrolyte
concentrations are abnormal in athletes at the time of acute
EAMC, when compared with non-cramping control athletes.
In contrast, there are now four prospective cohort studies,
from two laboratories, in two different endurance sports that
have shown no relationship between serum electrolyte abnorm-
alities and EAMC in marathon runners or triathletes
8916
(Drew
N, MPhil Sports Medicine dissertation, University of Cape
Town, 2006). In all these studies a cohort of endurance athletes
(runners or triathletes) with normal pre-exercise serum electro-
lyte concentrations was followed and those with EAMC that
occurred during the race (cramp group) were compared with a
control group of athletes who did not develop EAMC. In a very
consistent fashion, the results of these four prospective cohort
studies have shown that in the cramp group serum electrolyte
concentrations were not significantly different from those in
the control (non-cramping) group at the time of the acute
EAMC. Furthermore, as cramping subsided, and athletes
became asymptomatic, no changes were observed in serum
electrolyte concentrations (immediately post-race to recovery),
indicating that recovery from EAMC was not associated with
any normalisation of serum electrolyte concentration.
Therefore, there is a dissociation between EAMC and serum
electrolyte concentrations.
89
Small decreases in pre–post serum
sodium concentrations in the cramp group reported in these
studies were within the normal range and were not of any
clinical significance.
89
These reductions in serum sodium
concentrations in the cramp group were likely as a result of
increased fluid intake, because the pre–post percentage change
in body weight was consistently less in the cramp group.
89
The
findings in these studies are consistent and do not support any
association between EAMC and abnormalities in serum
electrolyte concentrations.
This finding of a dissociation between EAMC and serum
electrolyte concentrations has more recently prompted the
proponents of the ‘‘electrolyte depletion’’ hypothesis to suggest
that, rather than changes in serum electrolyte concentrations,
the mechanism for EAMC is increased sweat sodium concen-
tration or ‘‘salty sweating’’, resulting in sodium depletion,
which then causes EAMC.
22 23
However, the pathophysiological
basis for this hypothesis is not clear, and has never been
formally outlined. In this review, an attempt was made, using
the explanation offered by Bergeron,
23
to formulate the possible
progression of physiological events that may take place and
how, through ‘‘salty sweating’’ as a result of exercise, this can
lead to the development of EAMC (fig 1).
In this hypothesis (fig 1) it has been suggested that excessive
sodium loss in sweat results in the development of EAMC
22–25
without altering serum sodium or chloride concentrations.
23
Because sweat sodium concentration is always hypotonic,
26–29
a
significant loss of sodium through sweat can therefore only
occur if there is an accompanying large loss of fluid. This would
mean that dehydration would accompany any significant
sodium loss in athletes presenting with EAMC. The proponents
of this hypothesis cannot, however, offer a plausible pathophy-
siological mechanism by which ‘‘salty sweating’’ alone can
cause cramping,
22
and therefore include dehydration and, more
recently, muscle fatigue as additional predisposing factors in the
development of EAMC
6
— the so-called ‘‘triad’’.
622
The only
pathophysiological mechanism that has been suggested is that
‘‘salty sweating’’ coupled with significant dehydration causes
contraction of the extracellular fluid compartment.
23
It is then
suggested, with no evidence to support this, that the resultant
‘‘loss of interstitial volume causes a mechanical deformation of
nerve endings and increasing the surrounding ionic and
neurotransmitter concentrations’’, which then cause selected
motor nerve terminals to become hyperexcitable and sponta-
neously discharge.
23
It is important to point out that scientific evidence for this
hypothesis is based on reports in which sweat sodium
concentrations were measured (1) during exercise in athletes
with a self-reported past history of EAMC, and (2) never at the
time of an acute EAMC, or during an exercise bout where
EAMC occurred.
23–25
There are no published studies in which
increased sweat sodium concentrations above those of suitable
matched non-cramping controls were measured in athletes
presenting with an acute episode of EAMC. It is also important
to note that sweat sodium concentrations during exercise,
which were measured in athletes with a self-reported past
history of EAMC, are only available in 23 subjects from three
studies: (1) a single case of one tennis player with EAMC,
24
(2) a
case series of 17 tennis players with a past history of cramping,
23
and (3) a small observational study in 10 American football
players (five players with a past history of cramping, and five
players with no history of cramping).
25
These 23 cases with a
past history of EAMC are the only cases where a reportedly
‘‘high’’ sweat sodium concentration is linked to EAMC.
Important methodological considerations in these three
studies
23–25
are that (i) no suitable control groups were included
in the studies on tennis players,
23 24
(ii) the sample sizes of cases
and control groups in the American football study were very
small,
25
(iii) sweat sodium concentrations were not measured at
the time when athletes experienced EAMC, and (iv) other
factors that could determine sweat sodium concentrations, such
as dietary intake of sodium, state of acclimatisation, anatomical
variability in sweat collection site, variability of sweat electro-
lyte concentrations within an exercise bout, and seasonal
variation were either not documented or not taken into
account. Furthermore, in two of these studies, it was suggested
that sweat sodium losses could result in ‘‘deficits of total
exchangeable sodium’’, a claim that is not substantiated by any
direct measurement.
The definition of what constitutes a ‘‘salty sweater’’ also
requires some discussion. At present, there are no data available
to define an ‘‘abnormally high’’ sweat sodium concentration
during exercise. However, it is important to note that sweat
sodium concentrations have been measured during exercise in
normal (non-cramping) athletes) of varying ages,
26
different
genders,
27
in varying states of acclimatisation
28
or fitness,
26
in
different body regions,
26 26 27
in different exercise durations,
27
in
different environmental conditions
27
and using different tech-
niques to collect sweat and then measure the sweat sodium
concentration.
28 29
The findings of these studies show that the
Review
402 Br J Sports Med 2009;43:401–408. doi:10.1136/bjsm.2008.050401
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mean sweat sodium concentration of these normal athletes
(with no past history of cramping) is consistently higher than or
the same as those mean sweat sodium concentrations reported
in the ‘‘salty sweaters’’ listed in the three case series previously
mentioned. Therefore, in the 23 cases that form the basis of the
‘‘salty sweating’’ in the ‘‘electrolyte depletion’’ hypothesis,
sweat sodium concentrations during exercise were in fact
normal to low.
Experimentally induced hyponatraemia, if accompanied by
sodium loss, has been associated with generalised skeletal
muscle cramping at rest.
30 31
In another clinical setting general-
ised muscle cramping has been reported in 5–20% of patients
undergoing haemodialysis.
32
Although the mechanisms of
cramping during haemodialysis are also not well understood,
this form of cramping has been linked to changes in plasma
osmolality and altered serum sodium concentrations.
33
Recently, it has been shown that this form of cramping can
be reduced if serum osmolality and serum sodium concentra-
tions are normalised using a technique known as ‘‘sodium
profiling’’.
32
Altered serum electrolyte concentrations caused by
systemic abnormalities can therefore result in generalised
skeletal muscle cramping at rest.
34
However, it is important to
note that, in the majority of athletes presenting with EAMC,
cramping occurs in the localised muscle groups that are involved
in the repetitive contractions associated with exercise,
23 25 35
and
that these contractions occur in spasms lasting 1–3 minutes.
6
This clinical presentation of localised EAMC has been well
described, even by proponents of the ‘‘electrolyte depletion’’
hypothesis.
623
In the ‘‘electrolyte depletion’’ hypothesis there is
no suitable physiological explanation of how a systemic
abnormality such as electrolyte depletion could result in
localised symptoms that are episodic. Furthermore, the propo-
nents of the ‘‘electrolyte depletion’’ hypothesis indicated that
the immediate treatment of acute EAMC is rest, prolonged
passive stretching, and oral sodium chloride.
6
The ‘‘electrolyte
depletion’’ hypothesis does not explain why interventions such
as rest and passive stretching are effective and why these are
supported.
6
In summary, there is evidence that altered serum osmolality
and altered serum electrolyte concentrations (notably hypo-
chloraemia, hyponatraemia, and hypocalcaemia) can cause
generalised skeletal muscle cramping at rest in specific clinical
settings. However, data from well-conducted prospective cohort
studies show that athletes with acute EAMC are not
Figure 1 The ‘‘electrolyte depletion’’ hypothesis for the development of Exercise Associated Muscle Cramping (EAMC).
Review
Br J Sports Med 2009;43:401–408. doi:10.1136/bjsm.2008.050401 403
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hyponatraemic, hypochloraemic, or hypocalcaemic and do not
have an abnormal serum osmolality.
8
Furthermore, there is no
evidence that athletes with a history of EAMC (23 reported
cases) have higher sweat sodium concentration than reported
sweat sodium concentrations from subjects in a number of
other studies. Finally, electrolyte depletion is a systemic
abnormality that will affect all the skeletal muscles in the
body. Yet, the clinical picture of EAMC in the majority of cases
is that of localised cramping in the exercising muscle groups.
This clinical observation, also reported by clinicians who are
proponents of the electrolyte depletion hypothesis, is not in
keeping with the systemic nature of electrolyte depletion.
Scientific evidence in support of the dehydration hypothesis for
the aetiology of EAMC
The dehydration hypothesis for the cause of EAMC also has its
roots more than 100 years ago, when case series reports linked
cramping in mine workers to excessive sweating and presumed
dehydration.
12
These were anecdotal observations and no actual
measures of hydration status were reported in these cases.
Dehydration is still commonly cited as a cause for muscle
cramps in athletes
636
and is linked to the ‘‘electrolyte depletion’’
hypothesis,
62223
and more recently as part of a ‘‘triad’’ of causes
of EAMC.
622
A careful review of the literature did not identify a single
published scientific study showing that athletes with acute
EAMC are more dehydrated that control athletes (athletes of
the same gender, competing in the same race with similar race
finishing times). In contrast, there is evidence from four
prospective cohort studies showing that dehydration is not
associated with EAMC. In these studies, the relationship
between hydration status (indirectly measured as the difference
between pre and post-race body weight) and EAMC was
carefully documented in cramping athletes and
controls.
8916
(Drew N, MPhil Sports Medicine dissertation,
University of Cape Town, 2006) The findings of these studies
consistently show that cramping athletes, at the time of acute
symptoms, were not more dehydrated than control (non-
cramping) athletes. If anything, athletes in the cramping groups
were consistently less dehydrated (not significantly so) than the
control subjects. The results of these studies do not, therefore,
support the hypothesis that there is a direct relationship
between dehydration and muscle cramping. The proposed
mechanism that ‘‘as progressive dehydration occurs, the
extracellular fluid compartment becomes increasingly con-
tracted’’ and that this results in EAMC
22 23
is therefore not
supported by these findings. Both electrolyte depletion and
dehydration are systemic abnormalities, and therefore also do
not explain the localised nature of EAMC.
Summary: scientific evidence in support of the electrolyte
depletion and the dehydration hypothesis for the aetiology of
EAMC
In summary, dehydration and electrolyte depletion are often
considered together (and recently together with muscle fatigue)
as the ‘‘triad’’ causing EAMC. The key components of this
hypothesis (fig 1) are that electrolyte (mainly sodium) depletion
through excessive sweat sodium loss together with dehydration
causes EAMC. However, results from prospective cohort studies
consistently show that athletes suffering from acute EAMC are
not dehydrated, neither do they have disturbances in serum
osmolality or serum electrolyte (notably sodium) concentra-
tions. Furthermore, sweat sodium concentrations measured
during exercise in 23 reported cases with a past history of
EAMC are not higher than those reported in many other
studies. Both electrolyte depletion and dehydration are systemic
abnormalities, and therefore would result in systemic symp-
toms, as has been observed in other clinical conditions.
However, in EAMC, the symptoms classically are local and
are confined to the working muscle groups. Thus, the available
evidence to date does not support the hypotheses that
electrolyte depletion or dehydration cause EAMC — therefore
an alternate hypothesis for the aetiology of EAMC has to be
considered.
SCIENTIFIC EVIDENCE SUPPORTING THE ‘‘ALTERED
NEUROMUSCULAR CONTROL’’ HYPOTHESIS FOR THE
AETIOLOGY OF EAMC
Introduction and historical background
The development of muscle fatigue resulting in ‘‘altered
neuromuscular control’’ as a cause for EAMC was first proposed
in March 1996. This was at the time of an international
symposium on ‘‘Muscle fatigue’’ which was held in Cape Town,
South Africa. The main observation that led to the development
of the ‘‘altered neuromuscular hypothesis’’ for EAMC came
from results of a descriptive cross-sectional epidemiological
study that was conducted in our unit in the early 1990s.
37
In this
study, 1383 marathon runners responded to a questionnaire on
EAMC. Of these runners, 536 (26%) reported a past history of
EAMC. The majority (60%) of this group of runners with a past
history of EAMC indicated that muscle fatigue was associated
with, and preceded, the onset of EAMC. This seemingly
incidental finding prompted an in-depth review of the possible
mechanism that may link the development of muscle fatigue to
EAMC. The results of this review were presented at the meeting
that was held in 1996, and the proceedings of the meeting were
published in the following year.
10
In this review, the possible
pathophysiological mechanisms for muscle cramping were
explored from the fundamental physiological principle that
muscle cramping can be considered as an abnormality of skeletal
muscle relaxation.
10 38
For the first time, the lack of scientific
evidence to support the ‘‘electrolyte’’ and dehydration’’
hypotheses was also highlighted in this review,
10
and evidence
that a neurological mechanism resulting from altered reflex
control mechanism in response to muscle fatigue was proposed
as an alternate hypothesis for the aetiology of EAMC.
10
At the same time, a second independent review on the
proposed mechanisms of EAMC was published a few months
after the 1996 ‘‘Muscle fatigue’’ conference.
39
In this review it
was also concluded that ‘‘disturbances at various levels of the
central and peripheral nervous system and skeletal muscle are
likely to be involved in the mechanism of cramp.’’ However, in
this review evidence for ‘‘electrolyte depletion’’ or the ‘‘dehy-
dration’’ hypothesis for EAMC was not explored.
39
Over the past 10 years, a number of research studies have
been conducted to explore possible mechanisms for the
development of muscle cramping in general, and EAMC
specifically. The findings of these studies form the basis for
the current understanding of the ‘‘altered neuromuscular
control’’ hypothesis for EAMC. The sequence of physiological
events that could explain the development of EAMC has
therefore now been refined. The current concepts that link
repetitive muscular exercise, the development of muscle fatigue
and the possible mechanisms by which muscle fatigue and
perhaps other triggers could result in EAMC by altering
neuromuscular control are summarised in fig 2. This scientific
Review
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evidence, including the pathophysiological mechanisms at each
step, will now be reviewed.
Scientific evidence supporting an association between factors
causing premature muscle fatigue and EAMC
It is well established that, during muscular exercise, there are
many factors that can contribute to the development of muscle
fatigue. These factors include exercising in hot and humid
environmental conditions, increasing exercise intensity,
increased exercise duration, and depletion of muscle energy
stores. The evidence that some of these known factors are
associated with the development of EAMC will now be
reviewed.
The observation that EAMC is more common when physical
exercise is performed in hot and humid environmental condi-
tions has its roots in case reports dating to over 100 years
ago,
11 12
and the term ‘‘heat cramps’’ was first used in the
medical literature in the 1930s
12
and is still used today.
6
In
considering the possibility that exercising in hot, humid
conditions causes cramps, there are two fundamental questions
that need to be answered. The first question is whether EAMC
is more common when athletes exercise in hot, humid
environmental conditions, and the second question relates to
the possible mechanism by which exercising in the heat can lead
to EAMC.
Historical reports (cases and case series) and clinical anecdotal
observations appear to indicate that EAMC does occur more
frequently when athletes exercise in hot, humid conditions.
11 12
More substantive data to support this observation comes from
only one epidemiological study, in which the incidence of
EAMC in different environmental conditions has been reported
in American Football players.
13
In this study it was reported that
‘‘heat cramps’’ were more common when the Heat Index was
Figure 2 The ‘‘altered neuromuscular control’’ hypothesis for the development of Exercise Associated Muscle Cramping (EAMC).
Review
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‘‘high’’ or ‘‘extreme’’ compared with ‘‘low’’ or ‘‘moderate’’.
13
It
must, however, be noted that these hot and humid conditions
also occurred during the first 2–3 weeks of training in a season,
when players were also likely to be less well conditioned, and
were likely not acclimatised to the environmental conditions. In
this study, however, acclimatisation and training status were
not documented. Therefore, although there is anecdotal
evidence that EAMC occurs more frequently when athletes
exercise in hot, humid environmental conditions, solid scientific
evidence to support this is still lacking.
As indicated, the mechanism by which exercise in hot humid
conditions may cause EAMC also requires discussion.
Historically, when EAMC occurred in athletes who exercised
in hot humid conditions, this has been attributed to dehydra-
tion and/or electrolyte disturbances, rather than the possible
effects of heat alone. The lack of scientific evidence relating
EAMC to dehydration or electrolyte depletion has already been
discussed. It appears, therefore, that if exercising in hot and
humid conditions does result in EAMC this may not be due to
electrolyte depletion or dehydration. Therefore, an alternate
mechanism may be responsible for this observation.
It is well documented that there are a number of mechanisms
by which exercise in the heat will result in the development of
muscle fatigue, independent of electrolyte depletion or dehy-
dration.
40
Therefore, it is possible that the mechanism by which
exercise conducted in hot humid environmental conditions can
cause EAMC, not as a result of dehydration or electrolyte
depletion, but because of the development of muscle fatigue.
The possible mechanisms by which muscle fatigue could result
in EAMC will be reviewed in detail in a subsequent section.
Muscle fatigue during exercise can develop if athletes exercise
at a high intensity or if exercise is performed for a prolonged
time period. In observational studies it has been documented
that there is an association between EAMC in athletes and (1)
self-reported poor conditioning for an event
37
and (2) exercising
at a higher intensity such as during racing and not during
training,
37
and that development of EAMC is more common in
the latter stages of a race (prolonged duration of exercise).
16 37
However, stronger evidence linking increased exercise intensity
and EAMC comes from a recently completed prospective cohort
study in Ironman triathletes. In this study, 210 triathletes
competing in the 2006 South African Ironman triathlon acted as
subjects. All the subjects were assessed pre-race, and informa-
tion from a detailed questionnaire included training history,
personal best performances and a cramping history. During the
race, 44 triathletes developed EAMC (cramp group), while 166
served as a control (non-cramping) group. In a multivariate
analysis, the results of this study showed that EAMC was
related to a faster overall triathlon racing time and a faster
predicted triathlon racing time, despite similarly matched
preparation and performance histories to those in the control
group. The faster racing time (increased exercise intensity) in
the cramp group was an independent risk factor for the
development of EAMC in these triathletes (Drew N, MPhil
Sports Medicine dissertation, University of Cape Town, 2006).
There are no studies that have explored the relationship
between depletion of muscle energy stores (mainly muscle
glycogen) and the development of EAMC. However, in a
recently published study using a laboratory-based exercise
protocol that was specifically designed to cause fatigue of the
calf muscles, a high incidence of muscle cramping during
exercise was documented.
7
In this study of 13 healthy men (91.8
(SD 15.1) kg) the administration of an oral solution containing
carbohydrate and electrolytes (given at a rate of 1.0 to 1.5 litres/
h), compared with no fluid administration, resulted in a delay in
the onset of EAMC (from a mean of 14.6 (SD 5.0) min to a
mean of 36.8 (SD 17.3) min). The main limitation in this study
was that the intervention consisted of administration of a drink
that contained fluid, electrolytes, and carbohydrate. It is
therefore not possible to determine whether the act of drinking,
the fluid, the electrolytes, the carbohydrate or a combination of
these interventions was responsible for the delay in the onset of
EAMC. However, as EAMC occurred after a mean of 15 min
into the exercise bout, and the mean sweat rate reported in this
group was 2.0 litres/h, the mean fluid loss after 15 min can be
estimated as 500 ml, which is not enough to result in significant
dehydration. Furthermore, if the sweat sodium concentrations
in the subjects were in the range reported as ‘‘salty sweaters’’
(mean of ,50 meq/litre) total sodium loss in the 15 min of
exercise would have been ,25 meq, again not enough to result
in significant sodium depletion. Therefore, it is unlikely that
either clinically significant dehydration or sodium depletion
could occur in this short time period. In contrast, it has been
documented that short-duration, intermittent, high-intensity
exercise can significantly reduce muscle glycogen stores.
41
Although speculative, as measurements of muscle glycogen
were not done, the delay in EAMC following the combination
drink in the Jung et al study could have been due to the
carbohydrate supplementation in the drink, thereby delaying
the depletion of muscle energy stores (glycogen).
7
In summary, there are some data to support the observations
that some factors responsible for the development of muscle
fatigue may also be associated with the development of EAMC.
There is some evidence that exercising in hot, humid environ-
mental conditions increases the risk of developing EAMC.
13
The
possible mechanism for this increased risk is not as a result of
dehydration or electrolyte depletion, but could be related to the
development of muscle fatigue. There is only limited evidence
that other factors which can cause muscle fatigue, such as
increased exercise duration, poor conditioning and depletion of
muscle energy stores, are related to the development of EAMC,
and this requires further investigation. However, participating
at higher exercise intensity during racing (compared with
training) has recently been shown to be an independent risk
factor for the development of EAMC.
Scientific evidence that fatiguing muscular exercise can cause
muscle cramping
One of the first studies showing that fatiguing muscle
contraction can induce cramping in normal healthy subjects
was reported in 1957.
42
In this study, among 115 college
students, sustained maximal muscle contraction, with the
muscle in a shortened position, resulted in muscle cramping in
18% of the subjects before an exercise bout, and in 26% after a
20–30 min exercise (swimming or callisthenics) bout. This was
also one of the first studies documenting that these episodes of
cramping were electrically active (using electromyography), and
that acute cramping could be treated by passive stretching.
42
These authors concluded that it was probable that ‘‘the motor
activity in cramps was originating in the central nervous
system’’. This observation, that cramping can be induced by
voluntary sustained muscle contractions, has now been
confirmed by a number of investigators.
43–45
Furthermore, there
is evidence that muscle cramping can be caused by repetitive
electrical stimulation of the nerves supplying the motor input to
muscle,
45 46
and that this can be used as a reliable laboratory test
to induce cramping in humans.
47
Review
406 Br J Sports Med 2009;43:401–408. doi:10.1136/bjsm.2008.050401
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In these laboratory studies investigating muscle cramping in
human subjects, factors that have been shown to increase the
likelihood of inducing cramping have also been explored. It has
been documented in the voluntary contraction model that
contraction of the muscle in a shortened position,
42–45
and first
performing muscular exercise and then performing the volun-
tary contraction to induce cramping,
42
increases the likelihood
of inducing muscle cramping. In the case of the electrical
stimulation model, stimulation of the nerve to reach a specific
‘‘threshold frequency’’ of stimulation reliably induces muscle
cramping.
45 46
In summary, these laboratory-based studies show that, in
humans, voluntary muscle contraction and electrical stimula-
tion of the muscle reliably induce muscle cramping.
Furthermore, performing muscular exercise, as well as contract-
ing the muscle in a shortened position, increases the likelihood
of inducing muscle cramp. These data indicate that the
mechanism for muscle cramping is neuromuscular in nature.
Scientific evidence that the mechanism by which fatiguing
muscular exercise causes muscle cramping is muscle fatigue
resulting in altered neuromuscular control
There is a growing body of evidence to suggest that the
mechanism for muscle cramping has a neuromuscular basis.
Firstly, as has been discussed, voluntary muscle contraction or
stimulation of the motor nerve can reliably cause muscle
cramping. Secondly, there is evidence from experimental work
in human subjects that stimulation of the 1a afferents through
electrical stimulation
48
or using the tendon tap (activating the
1a afferents)
48
can induce cramping. Thirdly, it has repeatedly
been shown that the most effective treatment for cramping
induced in this manner is muscle stretching.
42 45
An increase in tension in the Golgi tendon organ during
stretching, which will result in increased afferent reflex
inhibitory input to the a-motor neuron,
44
is a plausible
mechanism to explain why stretching is an effective treatment
of cramping. This mechanism would also support the finding
that voluntary contraction of the muscle in a shortened position
increases the likelihood of cramping
42–45
because the tension in
the tendon (and therefore the Golgi tendon organ) would be
less. Strong evidence, from a recently published study, support-
ing this inhibitory mechanism is that electrical stimulation of
the tendon afferents has been shown to successfully relieve
muscle cramping.
44
Collectively, these data indicate that the
mechanism responsible for muscle cramping is a result of altered
neuromuscular control, whereby increased a-motor neuron
activity as well as reduced inhibitory feedback from the tendon
both have an important role in generating cramp.
44
There is also evidence that the development of muscle fatigue
alters spinal neuromuscular control mechanisms that are
responsible for muscle activation and inhibition.
49 50
In an
animal model, muscle fatigue has been shown to disrupt the
functioning of the peripheral muscle receptors by causing (1) an
increased firing rate of the muscle spindle’s type 1a and II
afferents, and (2) a decrease in the type Ib afferent activity from
the Golgi tendon organ.
49 50
Therefore, as muscle fatigue
develops during prolonged intense exercise, it is possible that a
combination of the increased excitatory activity of the muscle
spindle and a reduced inhibitory effect of the Golgi tendon
organ with muscle fatigue would result in a sustained a-motor
neuron activity.
10
Clinically, and when measuring electromyo-
graphic activity, this would initially present as muscle
fasciculation (muscle ‘‘twitches’’) and increased electromyo-
graphic (EMG) activity respectively. This has been termed the
‘‘cramp prone state’’.
35
If fatiguing exercise continues, a full-
blown muscle cramp will develop.
There is some evidence from a field study in support of this
‘‘cramp prone state’’. It has been documented that there is
increased EMG activity at rest (baseline activity between bouts
of acute episodes of EAMC) in athletes who suffer from EAMC.
9
In this study, baseline EMG activity in triathletes suffering from
EAMC was significantly higher in the cramping muscle than in
a non-cramping control muscle in the same athlete.
9
This
finding indicates that cramping muscles, in between bouts of
acute EAMC, exhibit increased neuromuscular excitability —
notably in the exercising muscle groups only. In these subjects
EAMC was not associated with systemic abnormalities such as
electrolyte depletion or dehydration. Although these findings
have to be interpreted with caution because of a small sample
size,
9
the observed heightened neuromuscular excitability
(‘‘cramp prone state’’) could be explained by the development
of muscle fatigue and the resultant changes in spinal neuro-
muscular control that have already been reviewed.
Finally, further evidence in support of the ‘‘abnormal
neuromuscular control’’ hypothesis for EAMC comes from an
analysis of the effective therapeutic approaches to EAMC. As
has already been discussed, passive stretching is the most
common and effective therapy to relieve acute muscle cramp-
ing.
42 44 51–53
It is also regarded as effective treatment by those
who mainly support the electrolyte depletion and dehydration
hypotheses of EAMC.
6
As previously discussed, passive stretch-
ing increases the tension in a muscle, thereby increasing the
Golgi tendon organ’s inhibitory activity,
44 50
and this mechanism
offers further support for the hypothesis that abnormal
neuromuscular control is associated with EAMC.
10
In summary, there is growing scientific evidence from studies
in human and animal models that muscle cramping occurs with
repetitive muscle contraction. As muscle fatigue develops there
is evidence that this is associated with increased excitatory and
decreased inhibitory signals to the a-motor neuron. If muscle
contraction (or electrical stimulation of the muscle) continues,
muscle cramping results. Effective immediate treatment of the
cramping is by increasing inhibitory input to the muscle, either
by stimulating the Golgi tendon organ afferents through
stretching or by electrical stimulation of the tendon. Finally,
there is some evidence that athletes with acute EAMC exhibit
this increased muscular hyperexcitability in between bouts of
acute EAMC (‘‘cramp prone state’’). These data suggest that
altered neuromuscular control during fatiguing muscular
exercise is the principal mechanism in the aetiology of acute
EAMC.
Other aetiological factors in EAMC that have to be considered in
future research
There are other factors that may have to be considered in the
aetiology of EAMC. These factors may well also alter
neuromuscular control during exercise, but need further
investigation. Recently, it has been shown in a prospective
cohort study that one of the two independent risk factors
associated with EAMC in triathletes (multivariate analysis) was
a previous history of EAMC (Drew N, MPhil Sports Medicine
dissertation, University of Cape Town, 2006). A positive family
history of cramping has also been reported as a risk factor for
EAMC in a cross-sectional study.
37
Therefore, a genetic
predisposition to EAMC cannot be excluded, but the precise
mechanism for such a predisposition requires further investiga-
tion.
Review
Br J Sports Med 2009;43:401–408. doi:10.1136/bjsm.2008.050401 407
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There are other possible mechanisms that could alter
neuromuscular control at the spinal cord level, and therefore
may contribute to the development of EAMC. The first of these
is the possibility that muscle injury or muscle damage, resulting
from fatiguing exercise, could cause a reflex ‘‘spasm’’, and
thereby result in a sustained involuntary contraction. The
second possibility is that increased or decreased signals from
other peripheral receptors (such as chemically sensitive intra-
muscular afferents, pressure receptors or pain receptors) could
elicit a response from the central nervous system that can alter
neuromuscular control of the muscles.
44
These other mechan-
isms have not been investigated in athletes with EAMC, but
would be important to explore in the future.
SUMMARY
In summary, scientific evidence in support of the ‘‘electrolyte
depletion’’ and ‘‘dehydration’’ hypotheses for the aetiology of
EAMC comes mainly from anecdotal clinical observations, case
series totalling 18 cases, and one small (n = 10) case–control
study. Results from four prospective cohort studies do not
support these hypotheses. In addition, the ‘‘electrolyte deple-
tion’’ and ‘‘dehydration’’ hypotheses do not offer plausible
pathophysiological mechanisms, with supporting scientific
evidence that could adequately explain the clinical presentation
and management of EAMC.
Scientific evidence for the ‘‘altered neuromuscular control’’
hypothesis is based on evidence from human laboratory models of
cramping,animalexperimentaldataonspinalreflexactivity
during fatigue, and field studies where EMG data were recorded
during bouts of acute cramping after fatiguing exercise.
34
Whilst it
is clear that further evidence to support the ‘‘altered neuromus-
cular control’’ hypothesis is also required, research data are
accumulating that support this as the principal pathophysiologi-
cal mechanism for the aetiology of EAMC (fig 2).
Acknowledgements: Funding for the studies by the author who contributed to this
review came mainly from the University of Cape Town and the Medical Research
Council of South Africa. No funding was received from any company that may have
benefited from results of the scientific studies conducted by the author.
Competing interests: The author has been reimbursed by Gatorade, the
manufacturer of Gatorade sports drinks, for the costs to attend the ‘‘Sodium and
Exercise’’ conference in Vail, Colorado in July 2007 and to produce the original
manuscript for the proceedings of this conference.
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