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Exercise Associated Muscle Cramps (EAMC)

“A spasmodic, painful, involuntary contraction of the skeletal muscle that occurs during or immediately after exercise”.

Probably about 50% of the people reading this would agree that sounds about right, particularly the painful part. The other 50% have probably never suffered from cramping in races or training. And the good news for those of you who have never experienced this, is that in all probability you never will, as there does seem to be a strong correlation to physical predisposition. Not so great news for those who have, because it will quite likely occur again in the future, unless you take quite aggressive steps to avoid it, but more about that later.

In this article we are only examining EAMC. There are other clinical reasons for cramping but these are not the subject of this present article.

There are not many scientific studies on cramping in sport. One reason for this is that cramping cannot be induced at will. The difficulties of shutting a number of athletes in a hot and humid laboratory and asking them to either run or cycle at a reasonably high intensity until they either get painful cramps or arrive at exhaustion presents both organisational, and almost certainly, ethical problems. Therefore the few studies which do exist have been performed under race conditions, which again presents numerous organisational and logistical problems.

The earliest theories that exist were based upon observational evidence, knowledge of human physiology and logical reasoning (or at least it seemed logical at the time). Later studies would appear to have more scientific bias.

The Dehydration or Electrolyte Depletion Theory

Humans have probably been suffering from muscle cramps for all of their evolution, except no one probably ever thought of asking a neolithic farmer about it, experimenting methods for combating it and documenting results. Quite possibly farmers or labourers in different cultures throughout human history had remedies for cramping but these methods are lost in the mists of time. What we do know is that some of the earliest reports of muscle cramps come from about 100 years ago, when labourers in hot and humid conditions of mines and shipyards suffered from cramps. This was an economic problem because a cramping labourer is not as efficient or productive as a non-cramping labourer. It was easy to note that these labourers were sweating profusely and also clearly losing quantities of sodium and chloride in this sweat. The simple 1 + 1 = 2 conclusion was that the labourers were sweating out valuable electrolytes, causing their muscles (and nerves) to malfunction and that heat and humidity were key factors in this situation. During the construction of the Hoover Dam (Colorado River, Nevada/Arizona border) in the mid 1930s it was similarly noted that workers labouring in the heat of this semi desert area suffered frequent cramps. It was discovered that these cramps could be treated by requiring the labourers to drink salted milk (but perhaps there were other factors in play due to drinking salted milk, which we shall see later in the section on TRP Receptors).

And so the electrolyte depletion theory was born. No controlled or clinical studies, not even some loose “let’s see what happens” studies. We went straight from direct observation and anecdotal evidence to a theory that has been transposed from its original labouring environment to that of sport. According to this theory cramps are caused by loss of sodium, chloride, calcium and magnesium. Heat, high humidity and consequent dehydration were implicated as “accessories”.

Why the electrolyte depletion theory is unsatisfactory

There are a number of problems with this theory. First of all, when you sweat during sports activity, you don’t actually reduce electrolyte concentration.That is, there are certainly electrolytes in the sweat, but the concentration of these electrolytes is so low, that sweating is more likely to make you hypertonic. When you sweat, you lose more water than electrolytes, because the sweat is hypotonic. Therefore, sweating cannot in itself, lead to a fall in electrolyte concentration. What is true however is that drinking excessive quantities of water during sports activities will gradually lead to a dilution of electrolytes, and in particular sodium, leading to problems of hyponatremia but very rarely to cramping, therefore in hot or humid conditions it is important to make sure that liquids ingested do contain a small percentage of electrolytes to avoid this potentially life threatening condition.

The second problem is that if a cramp was caused by a loss of serum electrolytes, there is no reason for the cramp to be limited to one muscle only. Rather, you would cramp everywhere. In fact, studies have shown that people who have diluted their total salt content and have become hyponatremic (not during exercise, but clinically), cramp in all of their muscles. On the other hand exercise associated muscle cramping is observed to occur only in specific muscles, and in particular those that are used extensively in exercise. Studies show that as much as 95% of EAMC occurs in quadriceps, hamstrings and calves.

In a study (*1) on runners in the Two Oceans 56km endurance race in Cape Town researchers measured organic variables between athletes who cramped and those who didn’t. The result showed that the crampers did have slightly lower sodium levels, though not clinically relevant, but that they also had slightly higher levels of magnesium. The slightly lower sodium concentration would suggest that these athletes would have been overhydrated rather than dehydrated.

Another study (*2) on Ironman athletes showed similar results. Again, those athletes who suffered cramps did show slightly lower sodium levels (suggesting overhydration) but higher levels of magnesium and potassium.

Trail runners were studied (*3) during the Ultra Trail du Mont Blanc race to ascertain if there was any relationship between sodium intake and cramping. Yet again no relationship was found.

It has been noted both clinically and anecdotally that passive stretching of a cramping muscle tends to reduce the amount of contraction and in many cases may eliminate the problem. If the lack of electrolytes were to blame this would not happen. Only the replenishment of the electrolytes would resolve the problem. Stretching seems to be the most effective treatment and therefore it is more probable that some form of neuromuscular activity may better explain cramping.

It is also worthwhile to mention that cramping also occurs in swimmers, who are clearly not sweating and unlikely to have any form of electrolyte depletion.

The Muscle Fatigue and Spinal Reflex theory for Muscle Cramps
Muscles are stimulated to contract by a group of nerves known as alpha motor neurons – in order for you to perform any motor task (touching your finger to your nose, cycling, running etc.), a signal from the motor cortex of the brain travels down the spinal cord, it then leaves the spinal cord and travels to the muscle fiber along the motor nerve.
Muscle fibres contain small organs called muscle spindles. These tiny structures are there to make sure that the muscle doesn’t stretch too much. Because of this whenever muscles are stretched, as they would be during sports or heavy activity, muscle spindle activity increases. This sends a signal back to the spinal cord through nerve impulses known as Type 1a afferents, which is then communicated through the alpha motor neuron back to the muscle causing a contraction.

There is a second organ in the muscle fiber that also plays a part in the regulation of movement. This is called the Golgi tendon organ (GTO) and it performs an almost opposite role to muscle spindles. It becomes active when muscles are lengthened and contracted and makes sure that muscles are not contracted too forcefully which could cause damage. Therefore when the muscle is placed under a load, causing a contraction, the GTO sends a signal along the spinal cord through what is known as a Type 1b afferent. Contrary to the type 1a afferents of the muscle spindles this signal tells the Alpha motor neurons to stop firing. It is an inhibitory signal and has a protective function. Therefore if GTO signaling is strong Alpha motor neuron activity will be lessened. On the contrary if GTO signaling is inhibited Alpha motor neuron activity will increase and lead to more contraction.

Muscle fatigue has the effect of increasing muscle spindle activity that leads to more forceful contraction, and at the same time it decreases GTO activity leading to increased alpha motor neuron activity and yet more forceful contraction. Therefore fatigue can play an important role in sustained but involuntary muscle contraction.

Evidence for the Muscle Fatigue theory

It has been noted previously that only some muscles cramp and that these muscles are the ones that have been working harder. For runners and cyclists this means within the leg muscles and in particular the quadriceps, hamstrings and calf muscles that are being actively used.

It may also be noted that there is a far higher incidence of cramping during racing than during training, and that these tend to occur towards the end of a race rather than in the beginning. Logically we may presume that athletes are more likely to push themselves towards fatigue in a race than in training and that the greatest fatigue will occur towards the end of a race. Evidence for this may be found in the previously cited works by Schwellnus. The researchers found that the Ironman triathletes (*2) who paced themselves poorly and tried to cycle or run faster than they were capable of (based on previous performances) were more likely to cramp. Similarly during the study on the Two Oceans Ultra Marathon (*1) they measured the electrical activity of muscles at the end of the race, finding that alpha motor neuron activity was higher in cramping runners compared to non-cramping runners. In another study (*4) concerning the UTMB it was seen that cramping in runners was associated with having suffered previous episodes and with greater muscle damage during the race.

As mentioned previously, stretching the cramping muscle appears to be the most effective treatment and it is known that stretching increases Golgi tendon organ activity. When GTO activity increases it is known that muscular contraction decreases and would therefore lead to the reversal of cramping.

Not so simple and what to do to avoid cramping.

It would therefore appear that the Muscle Fatigue theory explains cramping better than the Dehydration and Electrolyte Depletion theory, however the reality is most probably a multifaceted and more complicated mechanism.

There are certainly some steps (ranked in their order of importance), that any athlete can take to avoid cramping if this is a recurrent problem.

  1. Appropriate training. A consistent, gradual but steadily progressive training plan is always the best strategy and even more so if you are susceptible to cramping. Bringing your fitness levels to the required level for the race distance is fundamental.

  2. Appropriate race strategy. If you are capable of finishing a race within a certain time frame (according to your talent, physical condition and training) it is asking for trouble to race at a higher speed. Muscular fatigue will almost certainly catch up with you.

  3. Regular Stretching. This strategy is often utilised in order to improve overall performance or prevention of injury although there is little evidence that this works. However stretching does decrease alpha motor neuron activity and could possibly help those athletes who regularly suffer from cramping.

  4. Electrolyte pills. This may be a placebo effect but anecdotally it does work for some athletes who suffer from cramps. Certainly taking an electrolyte pill or drink will not do any harm.

TRP Receptors

TRP channels are found in the oral cavity and connect the mouth to the central nervous system. Ther is some evidence that stimulating these receptors somehow causes a ‘jolt’ reaction down the nerves, disrupting the signals that are causing a cramp. Substances that stimulate TRP channels are things like wasabi, mustard oil and ginger (possibly also the salted milk being administered to workers on the Hoover Dam was having a similar effect).

There is a great deal of evidence from USA, where pickle juice is consumed during trail and ultra running events, that this can have an inhibitory effect on cramping. Pickle juice contains acetic acid and it would seem to be this, rather than the high levels of sodium, that stimulates the TRP receptors and helps relieve cramps. This is consistent with the muscle fatigue theory that postulates the root cause of cramping is to be found in the nervous system.

It is not known whether the ingestion of a TRP stimulator can prevent the onset of cramps but there is a growing body of both anecdotal and scientific (*9) (*10) material pointing in this direction (though a placebo effect may be involved). In this case the author would suggest that a more easily carried and more palatable solution may be found in ginger (dried or candied).


(*1)“Increased running speed and pre-race muscle damage as risk factors for exercise-associated muscle cramps in a 56 km ultra-marathon: a prospective cohort study”. Schwellnus, Allie, Derman, Collins. British Journal of Sports Medicine November 2011.

(*2) “Increased running speed and previous cramps rather than dehydration or serum sodium changes predict exercise-associated muscle cramping: a prospective cohort study in 210 Ironman triathletes.” Schwellnus, Drew, Collins. British Journal of Sports Medicine, June 2011.

(*3) “Sodium Intake During an Ultramarathon Does Not Prevent Muscle Cramping, Dehydration, Hyponatremia, or Nausea.” Hoffman, Stuempfle, Valentino. Sports Med Open, 2015.

(*4) “Muscle Cramping During a 161-km Ultramarathon: Comparison of Characteristics of Those With and Without Cramping.” Hoffman, Stuempfle. Sports Med. Open, 2015.

(*5)“Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis.” Schwellnus, Derman, Noakes. Journal of Sports Science, June 1997.

(*6) “Cause of exercise associated muscle cramps (EAMC)--altered neuromuscular control, dehydration or electrolyte depletion?” British Journal of Sports Medicine, June 2009.

(*7) “Serum electrolyte concentrations and hydration status are not associated with exercise associated muscle cramping (EAMC) in distance runners.” Schwellnus, Nicol, Laubscher, Noakes. British Journal of Sports Medicine, August 2004.

(*8) “Serum electrolytes in Ironman triathletes with exercise-associated muscle cramping.” Sulzer, Schwellnus, Noakes. Med. Sci. Sports Exerc., July 2005.

(*9) “Transient receptor potential channels and exercise-associated muscle cramping: A tale of multiple complexities.” Schwellnus, Hoffman. Muscle Nerve, September 2017.

(*10) “Ingestion of transient receptor potential channel agonists attenuates exercise-induced muscle cramps.” Craighead et al. Muscle Nerve, September 2017.

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