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Score tied during the fourth quarter. With less
than a minute to go, a wide receiver makes an
impossible catch and streaks down the sideline
with a cornerback hot on his trail. The crowd
goes wild as the distance between the two lengthen.
The wide receiver and the fans can see that
the end zone is near. Suddenly, the receiver
falls to the turf, curls up into a fetal position,
and grabs his calf. A heavy silence fills the
stadium, thick with worry and apprehension.
The training staff rushes to the player, fearing
the worst case scenario like a ligament tear
or broken bone. "Cramp, cramp!” exclaims
the receiver. “Oh, just a cramp,”
thinks the trainer. “When will these guys
learn to drink more fluids and stretch?”
the trainer mumbles to himself.
But is that really the solution to the age-old
problem of exercise-associated muscle cramping
(EAMC)? As a certified, licensed athletic trainer,
I was always taught that to prevent EAMC, my
athletes had to be flexible, be well hydrated
before practices and games, and had to stay
hydrated during the events. Some of my head
trainers recommended adding electrolytes like
sodium, potassium, calcium, and phosphate to
the athletes’ diets. I believed that EAMC
was due to poor stretching habits, dehydration,
and electrolyte imbalances until I began ensuring
that my athletes stretched, were well hydrated,
and ate a proper diet. Then I knew no one would
cramp, right? To my astonishment, I was wrong.
There were always a couple of athletes that
despite my diligent efforts, were still cramping
up, especially late in a game when it really
mattered. Was I mislead all of these years?
Well, not exactly mislead, but not fully informed.
Cramp
Classification
Although muscle cramps can occur from congenital
abnormalities, acquired medical diseases, or
present as a symptom of a clinical syndrome,
EAMC can be defined as a “painful spasmodic
involuntary contraction of skeletal muscle that
occurs during or immediately after muscular
exercise” [1]. The exact cause of EAMC
still remains a mystery and there is very little
scientific research available. The etiology
of EAMC is intricate and involves the central
(brain and spinal cord) and peripheral (12 pairs
of cranial nerves and 31 pairs of spinal nerves)
nervous systems, as well as the muscle itself
[2]. To help explain the latest theory on what
causes EAMC, let’s first look at some
old theories about EAMC.
Dehydration,
Electrolyte, and Environmental Theory
The story handed down from trainer to trainer
was that exercise in the heat resulted in dehydration
and electrolyte imbalances, and this led to
muscle cramps. The basis for this theory was
descriptions of gold and coal miners at the
turn of the century who developed severe muscular
cramps. The investigators at that time believed
that cramping was caused by the ingestion of
too much water without replenishing sodium chloride,
a medical condition called hyponatremia [3].
Unfortunately, these old studies were only case
reports, and not actual scientific research
[1, 3]. One study of cramps in South African
gold miners supports the hyponatremia theory.
There were no significant differences in electrolyte
changes in the cramp or non-cramp group, but
the cramps group had ingested significantly
more water [4]. Skeletal muscle cramping throughout
the entire body was found in a study where hyponatremia
with sodium loss was induced [5]. But anyone
who has had an EAMC cramp knows that cramps
occur in specific muscles that have been working,
and do not occur spontaneously all over the
body. So it seems that physical disorders that
are associated with altered electrolyte concentrations
may not be applicable to EAMC [1].
The only published study specifically about
fluid and electrolyte balance on EAMC suggested
that EAMC may not be associated with disturbances
of fluid and electrolyte balance at all [6].
The study evaluated the serum electrolyte concentrations,
including sodium and potassium, of 82 male marathon
runners before and after a race. Fifteen (18%)
of the runners reported an attack of EAMC towards
the end of the race. The subjects were the same
in terms of racing performance and training
status and after the race, the serum electrolyte
concentrations were not different between those
suffering from EAMC and those not affected.
With respect to heat alone, it is clearly evident
that heating a muscle at rest does not induce
cramping. Physical therapists and trainers have
been using heat as a relaxation modality for
years. However, there is the possibility in
accordance with the latest theories, that exercise
in the heat and the dehydration that results
may precipitate EAMC [7]. So my teachers may
not have been totally wrong!
Looking
Back
The latest theory on EAMC has its basis in some
very old information about cramps. Back in the
late 40’s and early 50’s during
electromyographic (EMG) studies, a researcher
described muscle cramps as being different from
tetany in that they only affected one muscle
group [8]. Low calcium concentrations in the
extracellular fluid (blood and plasma) stimulate
nerve endings. This results in tetany in many
muscles throughout the body [9]. The researcher
also stated that cramps began with fasciculations
(small twitches of the muscle) and then spread
to the entire muscle. He reasoned from these
EMG studies that cramps originated in the nerves
of muscles [7], which is part of the peripheral
nervous system. Another researcher then studied
EMG activity on cramps induced by isometric
contractions of a shortened muscle [10]. These
studies seemed to point to a central nervous
system origin. However, the origin of EAMC seems
multifactorial and is based on a combination
of physiologic factors occurring simultaneously
[2].
Tired
Muscles
Recently, researchers have been pointing to
muscle fatigue as the precipitating factor to
EAMC. As the fatiguing muscle continues to contract,
it also relaxes slower, which increases the
time its contracting [2]. Then a positive feedback
loop develops where each fatigued motor unit
of the muscle calls upon more motor unit recruitment
until the entire muscle cramps [11]. This phenomenon
relies on sensory feedback information from
the muscle to the spinal cord by two muscle
proprioceptors: the muscle spindles, located
throughout the muscle belly, and the golgi tendon
organs (GTOs), located in the muscle tendons.
The muscle spindles send information about muscle
length or rate of length change, and the GTOs
send information about the muscle tension or
the rate of tension change [12]. When the muscle
fatigues, it becomes stiff and resistant to
lengthening [13]. While this fatigue is increasing
muscle spindle activity, it is reducing GTO
activity [14]. These mixed signals result in
abnormal spinal reflex activity, which is way
the spinal cord handles simple motor movement.
This theory is strengthened by the fact that
the muscles more prone to cramping are those
that cross two joints and are contracted in
a shortened position during exercise, like the
gastrocnemius and hamstring [10]. This contraction
in a shortened position decreases GTO activity
[1]. Another theory to consider is that the
motor nerves get hyperexcited by the muscular
shortening, and this results in EAMC [7]. Closely
related to this theory is that nerve excitation
can occur from the fluid loss caused by exercising
in the heat. It is thought that the dehydration
contracts the extracellular space, and this
put pressure on the motor nerves [7]. There
are no scientific studies to back this up, yet.
Matthew Vukovich, Ph.D., thinks that we need
to be careful when drawing conclusions about
the cause of EAMC, because research seems to
be pointing to the fact that EAMC is due to
a number of physiological factors.
“We know that the majority of cramps occur
when the muscle is fatigued and sometimes the
subjects may be experiencing hyperthermia from
the loss of plasma volume through sweating.
Sweating does result in a loss of electrolytes,
however, that does not mean there is a direct
cause and effect relationship. Research does
appear to be providing more insight to the cramping
issue and one day we may know exactly what is
causing EAMC,” he says.
Prevention
and Treatment
So was my athletic training treatment regimen
all wrong? Well, not exactly. It is proven in
many studies that stretching can reduce EAMC
[10, 15, 16]. I also told my cramping athletes
to keep walking and moving, and this is still
good advice. Gentle motion will change the shortened
muscle position and reset the muscle spindle
[2]. Increasing or replacing electrolytes does
not seem to be the answer for putting out the
fire of cramps, but keeping hydrated may play
a role in the hyperexcitability of nerves [7]
and in fighting fatigue [2]. Increasing cardiovascular
fitness can also help delay fatigue [2]. The
involvement of muscle proprioceptors in EAMC
points to the possibility that plyometric exercises,
along with balance and coordination drills,
may prevent EAMC [2].
An
Old Trainer Can Learn Some New Tricks
You can see that there still is quite a lot
to learn about muscle cramps. The theories about
dehydration and electrolytes that my fellow
trainers and I always ascribed to may not be
totally wrong, yet new theories point to a more
neuromuscular connection. Whatever the cause,
some old recommendations are still applicable.
Prevention is the key and with proper stretching,
strengthening, and nutrition, that receiver
can catch the touchdown pass and be a hero instead
of a casualty.
Sidebar
–Bodybuilders and Cramping: Myths vs.
Reality
You’ve seen it before – the posing
is perfect, the bodybuilder is getting call-outs
and comparisons, and then every muscle in his
body looks like it’s balling into knots.
He’s got to get off stage and eat some
bananas and drink some water, right? Maybe,
but maybe not. New cutting edge research on
football players may give us some insight on
severe generalized muscle cramps. A study on
professional football players in need of intravenous
hydration for severe generalized muscle cramps,
showed a 300% increase in serum nitric oxide
(NO) concentrations [17]. The researchers did
not determine if the increase was due to exercise
alone, muscle cramps alone, or a combination
of both. Nitric oxide is a chemical messenger
and science is just beginning to discover all
of its physiological functions. But because
NO can modify nerve excitability, some top scientists
think that research in the area of muscle cramping
will be taking this direction.
“Perhaps in competitors that are ‘cramp
prone’ for whatever reason there is a
link between NO concentrations and the incidence
of whole body affects, for example, cramping,
while on stage and during competition,”
says Conrad Earnest, Ph.D. “There is so
much more research that needs to be done on
this topic.”
Sidebar
- Extinguish the Fire of a Cramp
Keep moving – this will reset the muscle
spindle
Stretching and posture – stretch daily
to improve flexibility, stretch when a cramp
is felt, and lengthen muscles by improving posture
Improve balance – work on challenging
the muscle proprioceptors with balance exercises
like catching a ball standing on one leg
Increase cardiovascular fitness - to decrease
muscle fatigue
Strength training with an emphasis on sport-specific
and functional drills – training muscles
like they are going to be used for a specific
sport improves coordination and pattern learning
Incorporate eccentric movements – muscle
contraction movements while the muscle lengthens
(eccentrics) may help muscles adapt better during
deceleration
Plyometrics –hopping, skipping, and jumping
involve the muscle proprioceptors and also strengthen
tendons
References:
1. Schwellnus, M.P., E.W. Derman, and T.D. Noakes,
Aetiology of skeletal muscle 'cramps' during
exercise: a novel hypothesis. J Sports Sci,
1997. 15(3): p. 277-285.
2. Bentley, S., Exercise-induced muscle cramp.
Proposed mechanisms and management. Sports Med,
1996. 21(6): p. 409-420.
3. Noakes, T.D., The hyponatremia of exercise.
Int J Sport Nutr, 1992. 2(3): p. 205-228.
4. Shearer, S., Dehydration and serum electrolyte
changes in South African gold miners with heat
disorders. Am J Ind Med, 1990. 17(2): p. 225-239.
5. McCance, R.A., Proceedings of the Royal Society
of London. Series B--Biological Sciences, Volume
119, 1935-1936: Experimental sodium chloride
deficiency in man [classical article]. Nutr
Rev, 1990. 48(3): p. 145-147.
6. Maughan, R.J., Exercise-induced muscle cramp:
a prospective biochemical study in marathon
runners. J Sports Sci, 1986. 4(1): p. 31-34.
7. Layzer, R.B., The origin of muscle fasiculations
and cramps. Muscle & Nerve, 1994. 17: p.
1243-1249.
8. Denny-Brown, D., Clinical problems in neuromuscular
physiology. Am J Med, 1953. 15: p. 368-390.
9. Guyton, A.C. and J.E. Hall, Textbook of Medical
Physiology. Vol. Ninth Edition. 1996, Philadelphia:
W.B. Saunders Company. 65.
10. Norris, F.H., Jr., E.L. Gasteiger, and P.O.
Chatfield, An electromyographic study of induced
and spontaneous muscle cramps. EEG Clin Neurophysiol,
1957. 9: p. 139-147.
11. Ross, B.H. and C.K. Thomas, Human motor
unit activity during induced muscle cramp. Brain,
1995. 118(Pt 4): p. 983-993.
12. Guyton, A.C. and J.E. Hall, Textbook of
Medical Physiology. Vol. Ninth Edition. 1996,
Philadelphia: W.B. Saunders Company. 695-696.
13. Nelson, D.L. and R.S. Hutton, Dynamic and
static stretch responses in muscle spindle receptors
in fatigued muscle. Med Sci Sports Exerc, 1985.
17(4): p. 445-450.
14. Hutton, R.S. and D.L. Nelson, Stretch sensitivity
of Golgi tendon organs in fatigued gastrocnemius
muscle [published erratum appears in Med Sci
Sports Exerc 1986 Apr;18(2):251]. Med Sci Sports
Exerc, 1986. 18(1): p. 69-74.
15. Bertolasi, L., et al., The influence of
muscular lengthening on cramps. Ann Neurol,
1993. 33(2): p. 176-180.
16. Guissard, N., J. Duchateau, and K. Hainaut,
Muscle stretching and motoneuron excitability.
Eur J Appl Physiol, 1988. 58(1-2): p. 47-52.
17. Maddali, S., et al., Postexercise increase
in nitric oxide in football players with muscle
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