Aside from limited talent, one of the barriers I have encountered to quality training and to racing in triathlons has been exercise-associated muscle cramps (EAMC). I am not alone. It has been reported that 67% of triathletes complain of EAMC.
Years ago, at the start of my amateur career (in my 30s) as an endurance athlete, I completed the Marine Corps Marathon and got pretty dehydrated. In the medical tent for IV fluids, I heard a guy shouting and screaming nearby. He was having muscle cramps. I remember thinking to myself, “what a whiner!” Well, karma found me and has never let me out of sight. EAMC are amazingly painful. A muscle, which, inconveniently, is needed for an athletic activity, suddenly and without warning violently clenches and twitches. It feels like the muscle is being ripped apart. For me, EAMC episodes can last for 5-10 seconds, or up to 30 seconds, depending on how much I really need that muscle group for what I am doing. In my scan of the internet it appears that the duration of my muscle cramps is pretty typical, but some people can experience cramps for up to 15 minutes.
It is possible to keep going in spite of EAMC. I rode over 70 miles of an iron-distance triathlon’s bike course last year with repeated EAMC in my hip adductors, quads, hamstrings, and calves. I did it, but I paid. I ended up being unable to complete the rest of the race and I visited the local ER with a host of medical complications. I still doubt that I have fully recovered from this experience.
Why do EAMC happen? Specifically, are there strategies that can be employed that will be helpful for me and you, the reader, to avoid and treat EAMC?
Why do exercise-associated muscle cramps happen?
The following discussion is given with the caveat that other medical conditions (such as diabetes and hypothyroidism), medications (such as diuretics and statins), and other medical causes of muscle cramping (such as nutritional deficiency) need to be considered first.
Most recent good reviews of EAMC present the two leading theories about the cause of this condition: dehydration/electrolyte imbalance and neuromuscular failure. These two theories are often presented as though they are in competition with each other. This is a useful writing technique, but it may not be accurate
The dehydration/electrolyte imbalance concept seems obvious and simple. Since the body cannot store enough water to make up for losses during exercise and since athletes do not or cannot ingest enough water to replace losses, EAMC follow from the sensitization of nerve terminals that occurs as a result of water depletion (and consequent electrolyte imbalances). When muscles contract, there is contracture of the interstitial space, as well, which leads to mechanical pressure on select motor nerve endings and, finally, EAMC. Since there is more loss of fluids and electrolytes in hot and humid conditions, these conditions would be more likely to lead to EAMC.
But this theory is probably not adequate. For example, endurance athletes develop EAMC even in cold temperatures. In a study of marathon runners, those who experienced EAMC did not have significantly different loss of plasma volume, blood volume, or body weight compared to non-sufferers of EAMC. In a variety of studies, there was no difference between EAMC sufferers and non-sufferers in sweat rate and water/sodium losses and there was no correlation found between loss of body weight and EAMC. In addition, water/electrolyte replacement (the treatment that would be predicted to prevent EAMC if this model were correct) has not been shown to prevent EAMC.
As a point of illustration, a small study was published in 2013 that examined cramp frequency with a high degree of dehydration. In this study, of 10 male subjects, average age 24, exercised on a cycle ergometer until 5% loss of body mass or volitional exhaustion. These subjects ended up losing an average of 4.7% of body mass. At this level of dehydration, there was to change in cramp threshold frequency, cramp intensity, or the amplitude of EMG readings with cramps. In other words, a loss of almost 5% of body mass (with loss of water and electrolytes) did not affect muscle cramps in this study.
Similar findings were described in a study of 43 participants in an ultramarathon. About half of the athletes developed EAMC. There were no significant differences between the cramp and non-cramp groups for post-race % change in body weight, blood volume, plasma volume, or red blood cell volume. In the cramp group, the serum sodium concentration (after the race) was lower in the cramp group vs the non-cramp group (139.8 vs 142.3 respectively) and the serum magnesium was higher in the cramp group vs the non-cramp group (0.73 vs 0.67 respectively), but all of these values were within normal ranges.
In a study of 20 participants in an Ironman triathlon, there were no significant differences between the cramp and non-cramp groups in percent loss of body mass. Interestingly, the cramp group had a lower post-race serum sodium of 140 vs 143 in the non-cramp group. Once more, these values were within the normal range. There were no other significant differences between post-race serum electrolytes, glucose, or hemoglobin.
As illustrated, above, available evidence does not support dehydration or electrolyte disturbance as an explanation for EAMC. It is interesting, however, that post-race serum sodium concentrations were lower for cramp sufferers in two different extended endurance events. I defer to those who know much more than me about cytology and the sodium-potassium channel. However, my understanding is that the human body is designed to buffer large changes in electrolytes. Therefore, a three point difference in sodium in both ultramarathoners and triathletes may hold some significance, even though these values remain within the normal range. Furthermore, perhaps it is not the absolute sodium concentration but the change over the course of an exercise event that can alter action potentials across cell surfaces. [if you, the reader, have more knowledge about this line of reasoning, please share. I have corrected articles in the past and I am happy to improve this one, as well.]
The mechanism for EAMC that is usually offered as an alternative to the fluid and electrolyte theory is the neuromuscular theory. The proposed mechanism of this theory of EAMC has to do with neuromuscular overload and fatigue, which would lead to an imbalance between excitatory impulses from muscle spindles and inhibitory impulses from Golgi tendon organs. Without getting too technical, the bottom line is that, in this theory, there are less inhibitory impulses that would prevent the muscle in question from contracting. So, the muscle contracts into an involuntary cramp.
There is some interesting evidence to support the neuromuscular theory. Some of this evidence comes from studies in cats, which demonstrated that neuromuscular fatigue decreased the inhibitory impulses from the Golgi tendon organs and increased the excitatory activity of the muscle spindles. In humans, EAMC occur more frequently after extended exercise (neuromuscular fatigue) than at the beginning of activity and also occurs more often when a muscle contracts while it is already shortened. The observation about the contraction of already shortened muscles may fit the neuromuscular model because there is already less activity of the inhibitory Golgi tendon organs when a muscle is partially contracted. This would lead the muscle in question, upon further contraction, to be more vulnerable to cramping.
Another line of evidence supporting the neuromuscular theory is the benefit of stretching. Of all the treatment options that have been suggested for EAMC, stretching is the one that has been shown to reliably be effective. Stretching appears to work because it increases tension on the muscle’s tendon, which leads to activation of the Golgi tendon organs, an increase in inhibitory activity, and, therefore, a re-balance between inhibitory and excitatory impulses to the muscle in question.
There are a number of studies that appear to support the neuromuscular theory of EAMC. One of these studies was a prospective cohort study of 49 participants in a 56 kilometer running race. At the end of the event, 20 participants reported EAMC either during or within 6 hours of the event, while 29 reported no cramping. The investigators reported that EAMC in this study was significantly associated with a past history of EAMC and a faster running time for the first 28 km of the race (in spite of being matched with non-crampers for personal best times). EAMC in this study was not associated with age, body mass index, gender, recent and past personal best running times, reports of pre-race muscle pain, and reports of pre-race training (in terms of duration and frequency).
In another similar study of 209 Ironman triathletes, 43 reported EAMC and 166 did not. While there were no differences between the two groups in pre- and post-race serum electrolyte concentrations and changes in body weight, EAMC was found to be associated with faster predicted and actual race times (in spite of similarly matched training and performance histories from subjects in the two groups). Furthermore, a regression analysis showed that faster overall race time (and cycling time) and a history of EAMC within the subjects’ last 10 races were the only two independent risk factors for EAMC.
In a questionnaire-based study of 433 Ironman triathletes, 216 reported having had EAMC, while 217 did not. The investigators in this study reported that the triathletes in the EAMC group were significantly taller and heavier, and predicted and had faster race times in spite of having similar past personal best times to the non-cramping group. The EAMC group was also more likely to have had a past history of EAMC, a history of tendon and/or ligament injuries, and a positive family history for EAMC.
Taken together, the three trials summarized above indicate that poor pacing may play a large role in the development of EAMC. This concept supports the model of neuromuscular overload and fatigue as the cause of EAMC.
Oh no...This form doesn't exist. Head back to the manage forms page and select a different form.
It was also interesting to find an association, in the last study, with family history of EAMC. This suggests, of course, that there may also be a genetic factor, entirely independent of fluids, electrolytes, and neuromuscular fatigue, that can predispose athletes to EAMC. In fact, a study has recently demonstrated an association between the collagen gene COL5A1 and the development of EAMC. In this study, the CC genotype of COL5A1 was significantly under-represented in the EAMC group vs the non-cramping group (11.1% vs 21.8%, respectively).
The neuromuscular model of EAMC does have some gaps. For example, the electrical stimulation that was used in models of EAMC is not an exact match for real-life neuromuscular stimulation in humans. Another point is that there does not appear to be a set level of fatigue at which EAMC occurs. Instead, this level is probably unique to each athlete. It is also unclear if the neuromuscular fatigue, in this model, is occurring peripherally (in the muscle) or centrally (in the spinal cord and brain). Indeed, a recent study demonstrated that static stretching does not lead to the autoinhibition of contraction that the Golgi tendon organ confers. In other words, this study showed that stretching before exercise does not affect the Golgi tendon organ. Therefore, concluded the investigators of this study, if stretching before exercise reduces EAMC (which is unproven), the mechanism for this effect is not through inhibition of contraction by the Golgi tendon organ.
How to treat and prevent EAMC
Since EAMC are so challenging, so prevalent, and so poorly understood, a remarkable variety of treatment options have been suggested. The following is a list of many of the options I have found in the literature and on the internet:
- DMSO (dimethylsufloxide): I have used this chemical in the laboratory in the distant past and it SMELLS. The concept is to rub it over muscles that either are prone to spasming or have spasmed. DMSO is then, according to its proponents, absorbed into the muscle and the problems are solved. The obvious weakness of this approach is that muscle spasms involve huge areas of muscle that can be very deep under the skin. There is simply no way for a topical chemical to penetrate that amount of tissue and cause a beneficial effect.
- Biting/pinching a lip: The technique here is to pinch the upper lip for 20-30 seconds, but sometimes for up to 3 minutes. It is supposed to work up to 90% of the time. The first and most obvious weakness of this approach is that the lips are not connected to any muscles except the muscles surrounding the lips. There is no known nerve or chemical pathway that passes from the lips to any cramping muscle around the body. The next point is that most muscle cramps do pass in well under 30 seconds. So, a muscle cramp would pass, just as reliably, by singing “Yankee Doodle Dandy.” This is, I believe, an example of confirmation bias.
- Replacing calcium deficiency: a chiropractor named Dr. David Williams states, on his website, that: “I believe that 90% of muscle cramps are caused by calcium deficiency.” It would be truly great news if this were true. That would mean that 90% of EAMC would be prevented simply by checking calcium levels and correcting deficiencies. Unfortunately, Dr. Williams’ “I believe” is just that, a belief. He does not offer any scientific evidence. This is because there is no scientific evidence to show that 90% of muscle cramps are caused by calcium deficiency.
- Quinine: Some sources suggest that tonic water, which contains a small amount of quinine, can be consumed before exercise to prevent cramping. The rationale for this is that quinine is a mild muscle relaxant. Because of safety issues (most importantly, the risk of thrombocytopenia, which is a dangerous drop in platelet counts that can lead to bleeding and other problems), the dose of quinine in tonic water is limited to 83 mg per liter and quinine, in larger doses, is no longer available by prescription in the U.S.. In a Cochrane Review of research about quinine and muscle cramps of any cause, the authors concluded: “Compared to placebo, quinine [at doses of 200 to 500 mg per day] significantly reduced cramp number over two weeks by 28%, cramp intensity by 10%, and cramp days by 20%. Cramp duration was not significantly affected.” But note the dose required to achieve this effect is above the safe range.
- Pickle juice: A number of athletes and coaches have been advocating the consumption of pickle juice for years, apparently largely as a method to consume a lot of salt quickly. A study has shown that pickle juice can, in fact, help relieve EAMC. In this study, when 1 mL per kg of body weight of pickle juice or deionized water was consumed immediately after the experimental induction of a muscle cramp in hypohydrated male subjects, the duration of the cramp was 49.1 seconds shorter for the group who consumed pickle juice (84.6 seconds vs 133.7 seconds) (please note, again, that these were experimentally-induced muscle cramps). 5 minutes after consumption of pickle juice or water, there was no change in plasma electrolyte levels. Therefore, the investigators concluded that the improvement could not be explained by the restoration of fluids and electrolytes. Instead, they postulated that the tart pickle juice initiated a neural reflex from the oropharyngeal region that led to inhibition of the alpha motor neurons of the cramping muscle.
- Mustard: Some athletes have used mustard in the same manner as pickle juice, with similar logic. However, there is no published evidence to demonstrate a benefit. In an interview in the November 2014 issue of Runner’s World magazine, investigator Kevin C. Miller, PhD (an investigator in the pickle juice trial, above) stated that he studied athletes consuming as much as ¾ of a cup of mustard with no relief of EAMC.
- Replacing fluids and electrolytes: Dehydration and electrolyte imbalances have been shown, per above, to not be a satisfactory explanation for EAMC. However, there is no question that dehydrated athletes under-perform and are susceptible to serious or even life-threatening medical complications. Therefore, even if the replacement of fluids and electrolytes does not prevent or relieve EAMC, it is strongly advocated for a number of other reasons.
- Eating bananas: This appears to be ineffective for a couple of reasons. First of all, since the intended effect of bananas is to restore potassium, and since electrolyte imbalances do not appear to be the main cause of EAMC, consuming bananas would be predicted to be ineffective. Furthermore, even if the restoration of potassium were important to EAMC, it takes 30-60 minutes for the potassium from bananas (depending upon how much is consumed) to get into the circulation. This is a case of too little, too late.
- Stretching: This simple approach to muscle cramps addresses the most widely accepted mechanism for EAMC, muscle fatigue and misfiring. While stretching before exercise may or may not prevent EAMC, stretching immediately upon the onset of a muscle cramp can be very helpful. I think of it as “re-calibrating” muscles.
- Contracting opposing muscles: Similar to the concept of stretching, this method is to take advantage of the reflexive relaxation of a muscle when the opposing one contracts (e.g. hamstrings relax when quadriceps are contracted). Practically speaking, this technique appears to be reasonable and may be most useful when it is too painful to stretch a cramped muscle.
- Massage: at least for me, sometimes all I can do with a bad cramp is to rub it. I have not found studies on this subject, but my impression is that massage would lead to some mild stretching (by compression) and relaxation of a cramped muscle, perhaps by activating the Golgi tendon organs.
- Exercise: plyometric and endurance. The concept here is to train neuromuscular units to operate more effectively with increasing levels of intensity. Explosive plyometric exercises are reasoned to be especially effective to make cramp-prone muscles more resistant to cramping. But, to truly simulate race conditions (which, of course, is when an athlete would most want to avoid muscle cramps), intense endurance training is necessary. As endurance fitness increases, muscles would be predicted to be less prone to cramp at a given level of intensity. Some experts state: “the better shape you are in, the less likely you are to cramp.” This statement, however, is not supported by the evidence, since athletes matched for fitness appeared to experience EAMC or not based upon their pacing and effort and not baseline fitness. In other words, if an athlete trains and races within his or her abilities, he or she is less likely to experience muscle cramps. But every race is a calculated gamble, in a sense. If an athlete chooses to push his or her limits, then he or she needs to be prepared for muscle cramps.
Like many medical conditions, EAMC are possibly not a single medical condition (some researchers divide EAMC into “local” and “generalized,” for instance), but the endpoint of a variety of pathways. In other words, different athletes may have different mechanisms leading to very similar-appearing EAMC. [Incidentally, this is one big reason why the neighbor’s or friend’s anecdotal advice: “it worked for me” is often useless and sometimes harmful in dealing with medical conditions].
Recommendations (based on current research and informed expert opinion) to prevent and treat EAMC
- Train at race-intensity (or, conversely, race according to the level of ability that was attained in training).
- Pace and use power carefully (learn, in training, how many “matches” are available to burn, then use them carefully).
- Consider plyometric training of key muscle groups.
- Pay attention to fluids and electrolytes. I am not fully convinced that this is irrelevant to EAMC, but, even if it is, careful attention to hydration and electrolytes is critical to safe athletic performance.
- Learn to recognize early warning signs of EAMC (for me it is a little tightness) and respond accordingly.
- Learn how to train and race through cramps, and when to stop.
- When cramps begin, STOP!! and stretch immediately. The seconds “wasted” for stretching will likely be more than gained back by the end of the race.
- Along with stretching, consider corollary activities like flexing opposing muscles and massaging cramped muscles.
- Consider drinking pickle juice once a cramp begins. However, note that pickle juice has been shown to shorten the duration if cramps, but not prevent them. Furthermore, the study involved consuming 1 mL per kg of body weight. This means that a 70 kg person would have to consume almost 2 1/2 ounces of pickle juice. This must be tried in training first; some people’s stomachs cannot tolerate that much pickle juice.
Take it from me, EAMC are painful and frustrating. But, for many people, with careful attention to current medical research, EAMC can be managed.
Bergeron MF. Muscle cramps during exercise – is it fatigue or electrolyte deficit? Curr Sports Med Rep. 2008;7(4):S50-55.
Braulick KW, Miller KC, Albrecht JM, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med. 2013 Jul;47(11):710-714.
El-Tawil S, Al Musa T, Valli H, et al. Quinine for muscle cramps. Cochrane Database Syst Rev. 2015 Apr 5;4:CD005044.
Kantarowski P, Hiller W, Garrett W. Cramping studies in 2600 endurance athletes. Med Sci Sports Exerc.1990;22:S104.
Maughan R, Exercise induced muscle cramp: a prospective biochemical study in marathon runners. J Sports Sci. 1986;4:31-34.
Miller KC and Burne JA. Golgi tendon organ reflex inhibition following manually applied acute static stretching. J Sports Sci. 2014;32(15):1491-1497.
Miller KC, Mack GW, Knight KL, et al. Reflex inhibition of electrically induced muscle cramps in hypohydrated humans. Med Sci Sports Exerc. 2010 May;42(5):953-961.
Miller KC, Stone MS, Huxel KC, et al. Exercise-associated muscle cramps: causes, treatment, and prevention. Sports Health. 2010 Jul;2(4):279-283.
O’Connell K, Posthumus M, Schwellnus MP, et al. Collagen genes and exercise-associated muscle cramping. Clin J Sport Med. 2013 Jan;23(1):64-69.
Schwellnus MP. Cause of exercise associated muscle cramps (EAMC) – altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med. 2009 Jun;43(6):401-408.
Schwellnus MP, Allie S, Derman W, et al. 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. Br J Sports Med. 2011 Nov;45(14):1132-1136.
Schwellnus MP, Drew N, Collins M. Increased running speed and previous cramps rather than dehydration or serum sodium changes predict exercise-associated muscle cramping: a prospective cohort study in 2010 Ironman triathletes. Br J Sports Med. 2011 Jun;45(8):650-656.
Schwellnus MP, Nicol J, Laubscher R, et al. Serum electrolyte concentrations and hydration status are not associated with exercise associated muscle cramping (EAMC) in distance runners. Br J Sports Med. 2004 Aug;38(4):488-492.
Shang G, Collins M, Schwellnus MP. Factors associated with a self-reported history of exercise-associated muscle cramps in Ironman triathletes: a case-control study. Clin J Sport Med. 2011 May;21(3):204-210.
Sulzer NU, Schwellnus MP, Noakes TD. Serum electrolytes in Ironman triathletes with exercise-associated muscle cramping. Med Sci Sports Exerc. 2005 Jul;37(7):1081-1085.
Photo Credit: N08/18262611639/”>micolumnasana via Compfight cc