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Qiu and Kang. Scientic Pages Sports Med 2017, 1(1):3-14
Volume 1 | Issue 1
*Corresponding author: Jie Kang, Ph.D, FACSM, Depart-
ment of Health and Exercise Science, The College of New
Jersey, Ewing, 222 Packer Hall, NJ 08628, USA, Tel: 609-
771-2848, Fax: 609-637-5153, E-mail: kang@tcnj.edu
Received: January 12, 2017: Accepted: March 04, 2017:
Published online: March 08, 2017
Citation: Qiu J, Kang J (2017) Exercise Associated Muscle
Cramps - A Current Perspective. Scientic Pages Sports
Med 1(1):3-14
Copyright: © 2017 Qiu J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source
are credited.
Review Article Open Access
THE SCIENTIFIC PAGES
The Scientic Pages of
Sports Medicine
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Exercise Associated Muscle Cramps - A Current Perspective
Jun Qiu1 and Jie Kang1,2*
1Human Performance Laboratory, Shanghai Research Institute of Sports Science, China
2Department of Health and Exercise Science, The College of New Jersey, USA
Abstract
Exercise-associated muscle cramps (EAMC) are a common condition experienced by recreational and competitive athletes
and oen require medical attention during or immediately aer sports events. Despite the high prevalence of this condition,
the etiology of EAMC remains poorly understood, and there is a lack of high levels of evidence to guide the management
of this condition. e previous claim as to how EAMC come about is being challenged by more recent evidence suggesting
a distinctive mechanism. EAMC has been long attributed to an excessive sweat sodium loss together with dehydration.
However, growing evidence suggests that EAMC occurs with sustained and repetitive muscle contraction that results in
fatigue. e purpose of this article is to examine the existing scientic evidence in support of various views on the etiology
of EAMC and to highlight the most current understanding of this complex condition. Various strategies adopted to treat
and prevent EAMC also are discussed even though most of them remain anecdotal and have yet to be substantiated by
research experimentation.
Keywords
Muscle cramps, Dehydration, Electrolytes, Alpha motor neuron, Muscle spindle, Golgi tendon organ, Muscle fatigue
Introduction
Exercise-associated muscle cramping (EAMC) is
a common condition that requires medical attention
during sporting events. It occurs among athletes who
participate in long-distance endurance events, such as the
triathlon, marathon, and ultra-marathon [1,2]. EAMC
also is documented in many other sports, including
basketball, soccer, American football, rugby, tennis, and
cycling [2]. e prevalence of EAMC has been reported
for triathletes (67%), marathon runners (30-50%), rugby
players (52%) and cyclists (60%) [1,2]. Despite the high
prevalence of EAMC, its risk factors and underlying
causes are not completely understood. is review is
intended to examine the existing scientic evidence in
support of various views on the etiology of EAMC and to
highlight the most current understanding of this complex
condition. Various strategies adopted to treat and prevent
EAMC are also discussed. Muscle cramping can occur as
a symptom for a variety of medical conditions including
genetic disorders, muscular diseases, endocrine and
metabolic diseases, hydro electrolyte disorders, and toxic
and pharmacological agents [3]. is review focuses on
cramps that are exercise induced and excludes muscle
cramping that occur in smooth muscle or at rest and
cramping that is associated with any underlying disease
or drugs.
Methods of Literature Search
e literature search not restricted by publication
date was conducted with PubMed and Google Scholar
using key words that included muscle cramps together
with exercise, muscle fatigue, dehydration, electrolyte
imbalance, α-motor neuron, electromyography (EMG),
and treatment. Searchers were set to accept publications
that include original studies involving animals and
humans as well as reviews, commentaries, position
stands, and book chapters relating to both the etiology
and treatment of EAMC. Articles on muscle cramping
caused by factors other than exercise were not included.
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Qiu and Kang. Scientic Pages Sports Med 2017, 1(1):3-14
Initial searches from both search engines generated a
total of 146 citations. Upon further evaluation against
the per-determined criteria, 81 articles were selected
that included 46 original investigations and 35 reviews,
commentaries, position stands, and book chapters
(Figure 1).
Overview of Exercise Associated Muscle Cramps
Dening Exercise Associated Muscle Cramps
(EAMC)
EAMC is dened as a syndrome of involuntary painful
skeletal muscle spasms that occur during or immediately
aer physical exercise [4]. It presents as localized muscle
cramping that happens spasmodically in dierent exercising
muscle groups, usually the gastrocnemius, hamstrings,
or quadriceps. e gastrocnemius is the most commonly
aected [4].
Signs and symptoms of EAMC
Clinically, EAMC may be recognized by acute pain,
stiness, visible bulging or knotting of the muscle,
and possible soreness that can occur suddenly with no
warning and last for several days [5,6]. e aected
muscles oen appear to be randomly involved, and as
one bundle of muscle bers relax, an adjacent bundle
contracts, giving the impression that the spasms wander
[7,8]. For example, twitches rst may appear in the
quadriceps and subsequently in another muscle group
[7]. Most EAMC incidents last 1-3 min, but athletes
oen complain of EAMC symptoms up to 8 hours
aer exercise [9]. is post-exercise period of increased
susceptibility to EAMC has been termed as the cramp-
prone state [10]. EAMC can be completely debilitating
[11,12] although in some cases EAMC do not appear to
aect athletic performance [13,14].
Risk factors
EAMC seems to be more frequent in long-duration,
high-intensity events. Indeed, the competitive schedule
of certain athletic events may predispose to EAMC. In
multi-day tennis tournaments, competitors oen play
more than one match a day, with only an hour between
matches. is competition format induces muscle fa-
tigue, impedes uid and electrolyte replacement between
matches, and oen results in debilitating muscle cramps
Article identified through
search by PubMed and Google
Scholar:
(n = 146)
(n = 65)
Articles excluded for not
meeting the criteria:
Articles remained after these
that were duplicate or did not
meet the pre-determined
criteria were removed:
(n = 81)
(n = 46)
Articles that are orginal
investigations including case
reports and observational and
intervention studies:
Articles that are reviews,
commentaries, position
stands, and book chapters:
(n = 35)
▼
▼
▼▼
Figure 1: Selection process for the articles included in the review.
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peated exercise bouts when sweat sodium and chloride
losses signicantly exceed salt intake [25,26]. An estimat-
ed sweat-induced loss of 20-30% of the sodium pool has
been linked to severe muscle cramping [15,27]. Other
electrolytes lost in sweat to a much lesser degree, namely
calcium, magnesium, and potassium, have also been im-
plicated as the cause of muscle cramping during or aer
exercise when purported deciencies are suspected [28-
31]. e chief premise behind the electrolyte imbalance
theory is that an increased sweat sodium concentration
or ‘‘salty sweating” results in sodium depletion, which
then causes EAMC [25,32]. However, the pathophysio-
logical basis for this hypothesis remains poorly dened.
e more sensible explanation for how the electro-
lyte-imbalance-and-dehydration theory works seems
to be more dehydration-driven. Because sweat sodium
concentration is always hypotonic [33,34] a signicant
loss of sodium through sweat can therefore only occur if
there is a large loss of bodily uid. is would mean that
dehydration would accompany any signicant sodium
loss in athletes experiencing EAMC. Excessive sweating
will reduce plasma volume. To compensate for the loss
in plasma volume, water from the interstitial uid com-
partment shis to the intravascular space to maintain
central blood volume [35-37]. As sweating continues,
the interstitial uid compartment becomes increasing-
ly contracted [35]. is can persist even aer exercise as
sweating continues and body temperature returns to a
pre-exercise level [36]. Consequent to a contracted in-
terstitial compartment, certain neuromuscular junctions
(especially in muscles that are heavily used) could be-
come hyper-excitable by mechanical deformation. e
resulting change in mechanical pressure can then induce
spontaneous discharges of the aected motor neurons,
thereby causing cramps [6,38]. Figure 2 illustrates a step-
by-step process of how sweat-induced dehydration may
trigger EAMC.
Cramp discharges may also be attributed to the fact
that terminal branches of motor axons are exposed to
increased concentrations of excitatory extracellular
substances such as acetylcholine or electrolytes (i.e.,
sodium and potassium) [39-41]. As more water is
shied away from the interstitial compartment to the
intravascular space, adjacent and other nerve terminals
and post-synaptic membranes could be similarly aected.
is may explain why cramping is oen observed in
various muscle bundles alternately contracting and
relaxing [42].
Evidence against the original etiology of EAMC
As mentioned earlier, support for the electrolyte-
imbalance-and-dehydration theory comes mainly from
case reports or observations with no actual measures
[15]. Risk factors associated with EAMC in running
also have been examined in a cross-sectional survey of
1300 marathon runners [16]. In this survey, the specic
conditions found to be associated with EAMC included
high-intensity running, long distance running (> 30km),
subjective muscle fatigue, all of which are intense and ex-
haustive physical eorts. Other risk factors identied in
this survey were older age, a longer history of running,
higher body mass index, shorter daily stretching time, ir-
regular stretching habits, and a positive family history of
cramping [16]. In a prospective study of Ironman triath-
letes, the only independent risk factors for EAMC were a
history of the condition and competing at a higher than
usual exercise intensity [17]. A review on muscle cramp-
ing in marathon also suggests that EAMC is associated
with running conditions, e.g., high intensity, long dura-
tion, and hilly terrain, that can lead to premature muscle
fatigue in runners who have a history of the condition
[18].
History and Original Etiology of EAMC
Early reports of muscle cramps
e earliest reports of muscle cramps come from 100
years ago, when labors in hot and humid conditions of
the mines and shipyards suered from cramps [19,20].
Upon further analysis, it was noticed that the builders
had a high chloride level in their sweat. In these reports, it
was noted not only that muscle cramping occurred in the
heat, but also that cramps were accompanied by profuse
sweating [20]. More recently, by monitoring external
heat illness among American football players, Cooper,
et al. [21] observed that 95% of the cramping incidents
occurred in hot months when the risk of developing heat
illness was “high” or “extreme” [21]. It was because of
these early observations that the “electrolyte imbalance
and dehydration” theory was developed as an underlying
cause for EAMC. In principle, this theory suggests that
overly sweating and thus loss of electrolytes can cause
muscles and nerves that innervate them to malfunction,
thereby producing muscle cramps. It is now a common
belief that EAMC happens because athletes exercise in
the heat, lose electrolytes in their sweat, and the resulting
electrolyte imbalance and dehydration combines with
high body temperature [22,23].
e electrolyte-imbalance-and-dehydration theory
e electrolyte-imbalance-and-dehydration theory
suggests that EAMC is related to the decreased concen-
tration of serum electrolytes, particularly sodium and
chloride, resulting from excessive sweating or overcon-
sumption of water [4,8,24]. Indeed, a sizable whole-body
exchangeable sodium decit always develops following a
single long race, match, game or training session or re-
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heat illness was high [21]. Other evidence for this theory
comes from case studies and observational work in
which large sweat losses occurred in exercising athletes
[15,25,26].
e electrolyte-imbalance-and-dehydration theory
seems to contradict many recent evidences. Four
prospective cohort studies have shown no relationship
between serum electrolyte abnormalities and EAMC
in marathon runners or triathletes [13,14,17,43]. e
ndings have led to the suggestion that increased sweat
concentration (or salty sweating) resulting in sodium
depletion is the mechanism for EAMC [44,45]. However,
the physiological explanation for how sodium depletion
may cause EAMC remains unclear. Hyponatremia
resulting from a signicant loss of sodium has been
associated with generalized muscle cramping at rest
[46]. Nevertheless, in most athletes experiencing
EAMC, cramping occurs in the localized muscle groups
involved in repetitive contractions during exercise. At
the present, no data is available to support the possibility
that a systemic imbalance of electrolytes could result in
localized muscle cramps [10].
As for dehydration, it has been argued that excessive
sweating is the primary cause of EAMC [4]. However, in
the four prospective cohort studies previously mentioned
in which calculated body mass changes and volume of
blood or plasma were used as indicators of hydration
status, it was found that cramping athletes were not more
dehydrated than non-cramping athletes [13,14,17,43].
Additionally, using an electrical stimulation model,
Braulick, et al. [47] and Miller, et al. [48] observed that
both mild (3% body mass) and severe (5% body mass)
hypohydration with moderate electrolyte losses did not
alter cramp susceptibility when fatigue and exercise
intensity were controlled. us, the hypothesis of a direct
relationship between dehydration and muscle cramping
was not supported.
e electrolyte-imbalance-and-dehydration theory
also does not stand when it is used to explain EAMC
that occurs in athletes exercising in cool and tempera-
ture-controlled environments [49,13]. For example,
Maughan [13] reported that some marathoners (~18%)
still developed EAMC even though the ambient tem-
perature was 10 to 12 °C. us, it is unlikely that a hot
and humid environment is required for the development
of EAMC, although EAMC may occur more frequently
under conditions of elevated ambient temperatures [21].
is same study also revealed no signicant dierences
in losses of plasma volume and body mass between run-
ners with and without EAMC [13].
Overall, the electrolyte-imbalance-and-dehydration
theory has limitations. Its supporting evidence was based
of hydration status reported. Miners develop cramps
because of their sweat losses while working in hot
and humid conditions [6,20]. More recently, research
on American football revealed that most cramping
incidents occurred in hot months when football players
trained in an environment where the risk of developing
Sustained or repetitive strenuous
physical effort
Excess sweat loss
Decrease in plasma volume (w/increase
in plasma osmolality)
Fluid shifting from interstitial space
into the intravascular space by osmosis
Deceased interstitial fluid
compartment volume
Mechanical deformation of motor
neuron axon terminals
Spontaneous discharge of the affected
motor neurons
Muscle cramping
▼
▼
▼
▼
▼
▼
▼
Figure 2: Schematic illustration of the electrolyte -
imbalance - and - dehydration theory of exercise associated
muscle cramps (EAMC).
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loading on selected muscles can lead to localized muscle
fatigue. e altered neuromuscular control theory sug-
gests that muscle fatigue disrupts the normal functioning
of peripheral muscle receptors, causing an increase in ex-
citatory aerent activity within the muscle spindle and a
decrease in inhibitory aerent activity within the Golgi
tendon organ, both of which then lead to an increase in
alpha motor neuron discharge to the muscle bers, pro-
ducing a localized muscle cramp [4,52].
Muscle spindles and the Golgi tendon organs are two
important proprioceptors involved in working together
reexively to regulate muscle length and tone via alpha
and gamma motor neurons. When the Golgi tendon organ
is excited, it causes the muscle to relax, which is opposite of
a muscle spindle that causes it to contract (Figure 3). Dis-
turbance in the activity of these proprioceptors can occur
through faulty posture, shortened muscle length, intense
exercise and exercise to fatigue, thereby resulting in in-
creased motor neuron activity and motor unit recruit-
ment [53].
e altered neuromuscular control theory is sup-
ported by animal studies that used isolated gastrocne-
mius muscles derived from cats and electromyographic
recordings [54,55]. In these studies, muscle fatigue was
introduced via electric stimulation, and experiments
were terminated when the maximum force obtainable
decreased by 25%. It was found that as muscle fatigue
developed, there was an increased ring rate of the mus-
cle spindle’s type Ia and II aerents concomitant with a
decrease in the type Ib aerent activity from the Golgi
tendon organ [54,55]. In other words, muscle cramps
can be viewed as a consequence of a sustained alpha
motor neuron discharge that occurs when the enhanced
excitatory activity of the muscle spindle that triggers an
involuntary muscle contraction is unopposed by Golgi
tendon organs designed to inhibit such a muscular re-
on observational studies that could not provide cause-
eect conclusions. Although EAMC may appear in the
presence of signicant electrolyte and/or uid losses
during exercise, the underlying cause can be due to other
factors such as neuromuscular fatigue, fuel deciency,
and accumulation of metabolic wastes, muscle damage,
and a lack of conditioning and/or acclimatization.
“Heat cramps” - a misnomer
Case reports and anecdotal observations oen related
the development of cramping to physical activity per-
formed in hot and humid conditions, and this has led
to the use of ‘‘heat cramps’’ or ‘‘exertional heat cramps’’.
ese terms are oen used synonymously with EAMC
[15,42,44,50]. More substantive data to support the use
of this terminology came from a study in which the term
“heat cramps” was reported to be more common when
American Football players trained in an environment
where the heat index was ‘‘high’’ or ‘‘extreme’’ com-
pared with “low” or “moderate” [21]. It must be noted
that these hot and humid weather conditions occurred
during the rst 2-3 weeks of training in a season when
players were also most likely less well-conditioned and/
or acclimatized to the heat. EAMC is known to also occur
in individuals exercising in moderate to cool tempera-
tures [13,49] and exposure to extreme cold also has been
associated with EAMC in swimmers [51]. In addition, it
has been found that the development of EAMC does not
correlate with an increased core temperature [13]. Clear-
ly, heat alone is not a direct cause of muscle cramping
during exercise. As such, the term ‘‘heat cramps’’ is inac-
curate and its use should be discouraged.
Recent Discoveries on EAMC
e altered neuromuscular control theory
During sports competition, training, and a variety of
other intense physical activities, repeated or extended
Figure 3: A muscle spindle (left) and a golgi tendon organ (right).
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contracted. e potential risk factors associated with
overload and fatigue-related muscle cramping also in-
clude older age, poor stretching habits, insucient con-
ditioning, cramping history, excessive exercise intensity
and duration, and related metabolic disturbances (i.e.,
muscle glycogen depletion) [18,53].
Evidence supporting the altered neuromuscular
control theory
e theory is rst brought up in the early 1990s by an
observational study in which 1383 marathon runners re-
sponded to a questionnaire on EAMC [16]. Of these run-
ners, 536 (26%) reported a history of EAMC and a major-
ity (60%) of them indicated that the onset of EAMC was
sponse. Figure 4 illustrates more detailed explanations of
how muscle cramps may come about based on the al-
tered neuromuscular control theory.
EAMC are more likely to occur when the muscle is
contracting in an already-shortened position [4,40]. is
is because when muscle is in a shortened position, the
inhibitory activity of the Golgi tendon organ will reduce
even more than normal, causing a greater imbalance
between inhibitory and excitatory drives to the alpha
motor neuron [56]. e observation that the shortened
muscle is more prone to cramping may explain why calf
muscle cramps are prevalent in swimmers because in
most swimming races a swimmer must swim with point-
ed toes that require the calf muscle to remain somewhat
Increased
exercise
intensity
Increased
exercise
duration
Decreased
muscle
energy fuels
Hot and
humid
conditions
Lack of
conditioning
/acclimation
Development of muscle fatigue
Increased excitatory afferent
activity of muscle spindles
Decreased inhibitory afferent
activity of Golgi tendon organs
Altered sensory inputs received in the
spine
Increased alpha motor neuron
discharge
Increased muscle cell membrane
excitability
Muscle cramping
▼
▼▼
▼
▼
▼
▼
▼
Figure 4: Schematic illustration of the altered neuromuscular control theory of exercise associated muscle cramps (EAMC).
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muscular control at the spinal cord level, thereby con-
tributing to the development of EAMC. e rst of these
is the possibility that muscle injury or damage, resulting
from fatiguing exercise, could cause a reex ‘‘spasm’’,
and thus lead to a sustained involuntary contraction. e
second possibility is that changing signals from other
peripheral receptors, such as chemically sensitive intra-
muscular aerents, pressure receptors, or pain receptors,
could elicit a response from the central nervous system,
which may alter neuromuscular control of the muscles
[56]. In a prospective cohort study involving triathletes,
one independent risk factor associated with EAMC was a
previous history of EAMC [17]. In addition, studies that
surveyed marathon and ultra-marathon runners and
Ironman triathletes, a positive family history of cramp-
ing also has been reported as a risk factor for EAMC
[16,62,63]. In this context, a genetic predisposition to
EAMC cannot be ruled out. Indeed, mutation of a gene
(i.e., COL5A1) that provides instruction for synthesizing
collagen has been identied as a potential marker for a
history of EAMC [64]. Among other theories that have
been proposed for the etiology of EAMC are an inade-
quate intake of carbohydrate, glycogen depletion, poor
biomechanics or running gait, hilly terrain and lack of
adequate massage before and during a game [2].
Treatment and Prevention
Treatment
With multiple theories about the cause of EAMC,
it is dicult to provide a single answer for a treatment
or prevention strategy. Consequently, there are many
interventions available for the treatment of muscle
cramps. ese treatment options include stretching
of the aected muscle, decreasing exercise intensity,
massage, thermotherapy, cryotherapy, sports drinks,
salt and electrolytes, pickle juice, intravenous infusion,
and transcutaneous electric nerve stimulation. Many of
these treatment options are anecdotal or not supported
by experimental research. EAMC can be viewed as the
endpoint of a variety of pathways and dierent athletes
may have dierent mechanisms leading to very similar-
appearing EAMC. erefore, a treatment that works for
one athlete may not be eective one for others. Some of
the commonly used treatment options aimed to combat
against EAMC are discussed in the following sections.
e electrolyte-imbalance-and-dehydration theory
suggests that ingesting uids containing electrolytes
helps normalize the interstitial or extracellular volume,
thereby alleviating EAMC. However, owing to a small
quantity of electrolytes in many sports drinks, it may be
dicult to suciently replace the volume of electrolytes
lost during exercise even if the athlete has modest sweat
losses and sweat sodium content. Note that uids and
associated with muscle fatigue. is nding concurs with
those of Maughan [13] who found that the occurrence of
EAMC was more common in the later stages of a mara-
thon race. Stronger evidence linking potential muscle fa-
tigue and EAMC comes from a prospective cohort study
in Ironman triathletes [17]. In this study, 210 triathletes
competing in an Ironman triathlon acted as subjects, and
all the subjects were surveyed for their training history,
personal best performances, and cramping history prior
to the race. Results of this study showed that those who
developed EAMC (n = 44) exercised at a higher intensity
during the race and had faster overall race time despite
similar preparation and performance histories as com-
pared to those who did not develop EAMC [17]. ese
ndings indicate that the increased exercise intensity in
the cramp group was a risk factor for the development of
EAMC. In a study using an exercise protocol specically
designed to induce calf muscle fatigue, a high incidence
of muscle cramping during exercise was documented
[57]. is study also revealed that supplementing carbo-
hydrate orally, compared with no uid administration,
resulted in a delay in the onset of EAMC following a calf
fatiguing protocol [57]. It appears that providing athletes
with more energy fuels can alleviate EAMC.
More objective evidence that supports the theory
come from studies that used EMG to trace the discharge
of alpha motor neurons in fatigued muscles as EAMC
developed [54,55]. For example, a modest increase in
EMG was noticed as muscle twitches prior to EAMC.
However, as fatiguing exercise continues, there was
a much greater change in EMG that coincided with a
full-blown muscle cramp. By using EMG to compare
ironman triathletes with and without EAMC, Sulzer, et
al. [43] found that baseline EMG activity in triathletes
who suered from EAMC was signicantly higher in a
cramping than a non-cramping muscle. Interestingly,
this study revealed no signicant dierences in serum
electrolyte concentrations between cramping and control
groups matched for race nishing time and body mass.
e theory also seems consistent with the use of pas-
sive stretching in treating EAMC. Passive stretching is
the most common and eective therapy to relieve acute
muscle cramping [1,58-60]. It is regarded as eective
treatment by those who support the electrolyte-imbal-
ance-and-dehydration theory [42,61]. Passive stretching
increases the tension in a muscle, thereby increasing the
Golgi tendon organ’s inhibitory input to the alpha mo-
tor neuron [6,56]. is mechanism oers further support
for the hypothesis that abnormal neuromuscular control
mediates EAMC.
Other etiological factors in EAMC
Other factors have been speculated to alter neuro-
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stretching of the aected muscle to alleviate the cramp is
recommended. Passive stretching increases the tension
in a muscle, thereby increasing the Golgi tendon organ’s
inhibitory input to the alpha motor neuron [55,56]. is
will then reduce the activity of alpha motor neurons,
making EAMC less likely to occur. Other methods
that have been implicated for reducing motor neuron
activity, thereby alleviating EAMC include massage,
active contraction of the antagonist muscle group, and
icing of the aected muscles. Certainly, lowering overall
exercise intensity and altering the load on the distressed
muscles are eective as well [38].
Recently, an eort has been devoted to evaluate a
method of using food extractslike peppers, ginger, mus-
tard, and cinnamon to resolve EAMC [68]. Consum-
ing these food extracts does not seem to aect plasma
electrolyte concentrations [68]. Instead, it is thought
that these food extracts can activate transient receptor
potential channels (TRP channels) that are capable of
disrupting hyper excited motor neurons [73]. TRP chan-
nels are a group of ion channels located in the mouth,
esophagus and stomach that regulate the ow of ions,
i.e., charged particles like sodium and potassium, across
cell membranes. Recent evidence suggests that oral in-
gestion of TRP channel agonists like cinnamon, peppers,
or mustard may attenuate the intensity and/or duration
ofmuscle cramps, presumably by dampening alpha mo-
tor neuron excitability [74,75]. ese studies produced
muscle cramps by electrical stimulation. erefore, this
preventive approach has yet to be examined in clinical
trials where cramps can be more naturally induced by
physical exercise.
Prevention
e pathophysiology causing EAMC is most like-
ly multifactorial and complex. As such, prevention of
EAMC will need a multifactorial approach [42,66].
EAMC that occur in hot conditions seems to be pre-
vented by maintaining uid and salt balance. Moni-
toring an athlete’s body mass is an easy method of en-
suring adequate uid replacement. Both the National
Athletic Trainers’ Association and the American Col-
lege of Sports Medicine recommend a volume of uid
that allows for less than a 2% body mass reduction from
training or competition [42,66]. An athlete who ingests
a liter of water or hypotonic sports drink at least 1 hour
before competition can be condent that the majority of
the uid, electrolytes, and nutrients would be absorbed
and become available in the body when the competition
begins. Additionally, uids should be available and easily
accessible throughout practices and competitions. Ath-
letes with high sweat rates and sodium loss or who have
a history of EAMC may need to consume supplemental
sodium during prolonged activities to maintain salt bal-
electrolytes are not absorbed immediately aer ingestion;
that is, even hypotonic uids require at least 13 minutes
to be absorbed into the circulatory system [65]. Based on
the assumption that a relationship between dehydration-
electrolyte imbalance and EAMC exists, the National
Athletic Trainers’ Association recommends that athletes
prone to muscle cramping add ~1.3 g∙L-1 of salt to
their drinks to avert muscle cramps [66]. Others have
recommended adding higher amounts of sodium (about
3 to 6 g∙L-1) to sports drinks based on the frequency of
EAMC [50]. At the rst sign of muscle twitches or mild
cramps, a prompt oral bolus of a high-salt solution (e.g.,
0.5 L of a carbohydrate-electrolyte drink with 3 g of salt
added consumed all at once or over 5-10 min) has been
proven eective in preventing muscle twitches from
developing into a full-blown EAMC [15]. Aer such a
high-salt solution bolus, athletes can oen promptly
resume training or competition eectively without
muscle cramping or twitching symptoms for an hour or
more [7], although additional lower-sodium uid should
be consumed at regular intervals.
Other substances oen chosen to relieve EAMC are
pickle juice, quinine and electrolytes such as magnesium,
potassium, and calcium. A case report for using pickle
juice to treat EAMC revealed that ingesting of a small
volume of highly salty and acidic brine (30 to 60 mL)
could relieve cramp within 35 seconds [67]. is eect
was, however, attributed to the fact that pickle juice
contains acetic acid that can trigger a reex, probably in
the oropharyngeal region, that acts to increase inhibitory
neurotransmitter activity in cramping muscles [67]. In
fact, consuming pickle juice was found to be ineective
in raising plasma electrolyte concentrations in both
hydrated and dehydrated humans [68,69]. Quinine is
a medication used to treat malaria caused by mosquito
bites, but also oen prescribed totreat cramps of all causes.
A systematic review of 23 clinical trials has concluded
that quinine reduces cramp frequency, intensity, and
days, but not duration, compared with placebo, and that
there is a signicantly greater risk of thrombocytopenia
for quinine compared with placebo [70]. ough
magnesium supplementation has been reported to be
the most treatment used to prevent recurrent cramping
[71], most users report this method to be of little or no
help. Additionally, potassium-rich supplements or foods
or other mineral supplements such as calcium have not
been proven eective in relieving symptoms associated
with muscle cramps [15,32].
If the athlete has no underlying illness, then the most
common treatment for EAMC is stretching [40]. In fact,
moderate stretching of the aected muscle has proven to
be eective for muscle cramps of all types including those
that are heat related [5,7,10,72]. erefore, moderate
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to the level of ability that was attained in training.
• Know the dierences in humidity, temperature,
indoor versus outdoor, altitude and terrain between
competition and usual training conditions.
• For those who have cramped in the past, think about
all factors that could have played a role, i.e., drastic
change in intensity, volume, altitude, terrain, so they
can plan their training and competition accordingly.
• Learn to recognize early warning signs of EAMC and
respond accordingly.
• Muscles most aected by cramping are those
repetitively used and conned to a small arc of motion,
so focus on form in training to avoid heavy "braking"
and try to stretch out the stride with adequate hip and
knee exion and extension.
• For those who are heavy sweaters, be sure to increase
salt intake and consume uids higher in sodium
content, especially in the hotter, more humid months.
• Salt tabs or pills are an easy method, but practice using
them in training as they can cause upset stomach in
some individuals.
• Have adequate nutritional intake, particularly carbo-
hydrates, to prevent premature muscle fatigue during
exercise.
• Consider plyometric training of key muscle groups.
• Along with regular stretching, consider corollary
activities like exing opposing muscles and massaging
cramped or cramp-prone muscles.
Conclusion
EAMC are a common condition experienced by rec-
reational and competitive athletes. As such, it is impera-
tive for clinicians to identify underlying causes and eec-
tive strategies for treating and preventing the condition.
Despite the high prevalence of EAMC, few experimental
data exist on their cause, treatment, and prevention to
date. EAMC has long been explained by the electrolyte
imbalance-and-dehydration theory. However, its sup-
porting evidence comes mainly from anecdotal observa-
tions and case reports. In addition, the theory does not
oer plausible pathophysiological mechanisms, and it
has been reported that EAMC can occur without elec-
trolyte depletion or dehydration. More recent evidence
suggests that EAMC may be mediated by muscle fatigue
that altered neuromuscular control. e evidence that
support this “altered neuromuscular control” theory
stems from the laboratory-based experiments that used
EMG to monitor spinal reex activities in response to
muscle fatigue and cramping. Although more exper-
imental evidence is still needed, muscle fatigue and al-
ance [7] and may need to increase daily dietary salt to
5-10 g∙day-1 when sweat losses are large [42]. is is espe-
cially important during the heat acclimatization phase of
training. Bergeron [15] demonstrated that by calculating
sweat sodium losses and replacing them during and aer
activity, two athletes with previously debilitating EAMC
were able to compete successfully in hot conditions.
As mentioned earlier, an important etiology for
EAMC is muscle fatigue. As such, prevention strategy
should also focus on proper conditioning of an athlete.
To truly simulate race or game conditions, intense
endurance training is necessary. As endurance capacity
increases, muscle would be less prone to cramp at a given
level of intensity. Endurance training may also serve as
an eective means of preventing EAMC by expanding
plasma volume and the extracellular uid compartment
and delaying neuromuscular fatigue [76,77]. e
conditioning regimen should also consider resistance
training of the aected muscle as well as its synergists. In a
case report involving a male triathlete [78], strengthening
gluteus maximus was found to be eective in preventing
EAMC of the hamstrings, a nding that was attributed to
a reduced relative strain placed on the hamstrings [78].
Athletes who are returning to competition aer injury
are particularly susceptible to EAMC as they are likely to
experience early muscle fatigue, to be less acclimatized
to a hot environment, and to have diminished sweating
capacity [79]. Proper progression during rehabilitation
will prevent overstressing the athlete while ensuring
adequate sport specic conditioning before the return to
competition.
Prevention exercises that target muscle spindle and
Golgi tendon organs should also be implemented to delay
the onset of neuromuscular fatigue and, hence, EAMC.
Plyometrics may be such exercise to be considered. e
explosive nature of this exercise can train neuromuscular
units to operate more eectively with increasing levels of
intensity. It has been reported that plyometric training
can improve the eciency of neuromuscular control
by muscle spindles and Golgi tendon organs, thereby
making them more resistant to fatigue [80,81].
Other preventive measures that have been taken in-
clude 1) correcting technique errors, muscle imbalance,
and/or posture, 2) stretching muscle regularly, 3) having
adequate warm up, 4) applying massage therapy before
and during competition, 5) wearing compression gar-
ments, 5) becoming heat acclimatized, and 6) optimizing
footwear and/or orthotics. ese preventive measures,
however, are not evidence-based.
To prevent or attenuate EAMC, the following
recommendations should be used:
• Train at race-intensity or, conversely, race according
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tered neuromuscular control seem more plausible in ex-
plaining many of the unanswered questions with regard
to the cause, treatment and prevention of this complex
condition. ere are numerous strategies existed for the
treatment and prevention of EAMC. However, most of
them are anecdotal and unsupported by experimental
research. Research that involve both humoral and neu-
rological systems and provide high levels of evidence is
needed to substantiate the etiology, treatment options,
and prevention strategies of EAMC.
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