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  Muscle Cramp
  By Lori Incledon, LPTA, LATC, CSCS, NSCA-CPT, RPT

 

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 cramps. Am J Sports Med, 1998. 26(6): p. 820-824.

 






 




 

 

 

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