In August 2014, two healthy high school American football athletes died due to exercise-associated hyponatremic encephalopathy. In both cases, copious volumes of fluid were ingested to prevent exercise-associated muscle cramping (EAMC). In one case, 15.1 L (4 gallons) of fluid was purported to be ingested (20). Underlying these tragedies is the belief held by many medical professionals (22) and the general public that EAMC is caused by dehydration and electrolyte (e.g., sodium) losses. Yet, new experimental and observational data in the last 15 years suggest that cramping may be due to changes in the nervous system. Therefore, in light of this new evidence and the tragic deaths of these teenagers, it is vital to reevaluate the evidence for each theory on EAMC genesis.
The dehydration/electrolyte loss theory was originally proposed to explain why EAMC occurred in individuals who did intense work in the heat (e.g., miners). In its current iteration (2), proponents postulate that exercise-induced sweating causes a contracture of the interstitium thereby increasing mechanical pressure on nerve terminals. This, in addition to an increased concentration of excitatory neurochemicals in the interstitium, initiates EAMC. The dehydration/electrolyte loss theory is supported primarily by case studies (1) or observational research studies (7,21) that examine fluid and electrolyte losses in athletes with or without a prior history of EAMC.
In addition to the low strength of evidence of these studies (1,7,21), several observations argue against the dehydration/electrolyte loss theory. First, no evidence has ever been reported of an increase in interstitial fluid compartment pressure or build-up of excitatory neurochemicals in athletes with acute EAMC. In contrast, some evidence in animals suggests that interstitial fluid compartment pressure is lower when the interstitium is dehydrated compared with hydrated (6). Second, if a build-up of excitatory neurochemicals occurred in the interstitium, one would expect the muscles’ resting membrane potential to become less negative (i.e., easier to depolarize) as dehydration progressed. However, some authors observed slight decreases in resting membrane potential as dehydration progressively worsened with exercise (4). Third, serum electrolyte concentrations are often within normal limits or not different in athletes with and without EAMC (9,16,18,23). Thus, it is reasonable to conclude that both groups had similar osmotic fluid pressures driving fluid from the interstitium to the vasculature. Yet, some athletes developed EAMC, whereas others did not. Finally, this theory cannot explain why static stretching, which adds no electrolytes or fluids to the body, effectively relieves EAMC. Accordingly, the authors of the 2007 American College of Sports Medicine Position Statement on Exercise and Fluid Replacement concluded that the level of evidence for the association between EAMC and dehydration was not strong (i.e., SORT level C) (13).
In contrast, the altered neuromuscular control theory (15) suggests that EAMC ensue when several factors (e.g., fatigue, inadequate conditioning, and muscle damage among others) coalesce to increase alpha motor neuron excitability. Recently, higher H-reflex amplitudes were observed up to 60 min after a volitionally induced cramp in rested subjects (my unpublished observations). This suggests that muscle cramping, in and of itself, may alter the excitability of the central nervous system. In two other experimental studies (3,11), muscle cramp susceptibility was unchanged when cramps were induced with low frequency electrical stimulation in a rested, unexercised muscle before and after subjects became 3% to 5% dehydrated and had sodium deficits up to 4 g. Even when athletes with a history of EAMC have large sodium (up to 10 g) and fluid losses over the course of a day, EAMC still did not occur (1,7,21). In fact, studies have repeatedly shown that EAMC was not associated with body mass losses (16,18,23), blood volume or plasma volume losses (9,16), or red cell volume (16) in endurance contests. Instead, EAMC predictors consistent across several cohort studies include a prior history of EAMC (10,17,24), faster race times (14,17–19), and previous muscle injury or damage (17). These observations are consistent with other data from neurophysiology studies (3,11), cohort studies (16,18,19,23,24), and case reports (25), which support the altered neuromuscular control theory.
The altered neuromuscular control theory, although supported by a greater number of higher quality studies, is not perfect and several questions remain unanswered. First, how do fatigue or other risk factors (e.g., muscle injury) alter spinal excitability? Second, does central fatigue influence EAMC development, and if so, could this be an explanation for the “whole body cramp” phenomena described in the literature? Third, why do some athletes develop EAMC despite similar performance times and training histories as noncrampers (9,16,23)? Fourth, is the practice of administrating IV fluids prophylactically to athletes with EAMC effective, and if so, how do these fluids relieve or prevent EAMC (5)? Finally, how do the studies in laboratory animals (8,12) and the neurophysiological studies on electrically induced cramping correlate with EAMC (3,11)? Answering these questions would further clarify the genesis of EAMC because it pertains to the altered neuromuscular control theory.
Implications for Prevention
If EAMC is the result of alterations in the nervous system brought about by a confluence of extrinsic or intrinsic factors, it is imperative for clinicians to identify these factors for each athlete to effectively prevent EAMC. This requires working closely with the patient to identify trends in their medical history and to note when EAMC occurs. For example, the athlete or clinician could keep a “cramp journal” and document what was done (e.g., exercise duration and intensity, recent diet, and injury status) in the days or hours preceding the EAMC occurrence. Although laborious, such a targeted strategy will likely prove more fruitful in preventing EAMC than a one-size-fits-all recommendation of consuming more fluids or electrolytes. Overall, the literature is lacking in well-designed randomized controlled trials on EAMC prevention and is an area ripe for further exploration.
Although the cause of EAMC remains unknown, more evidence is accumulating supporting a neurological origin. Most likely, the cause of EAMC is multifactorial, unique to each athlete, and caused by alterations in the nervous system. If EAMC are multifactorial in nature, this may explain why there are so many anecdotal treatment and prevention strategies perpetuated to be effective in the literature. Clearly, ingesting copious volumes of fluid is not the cure for all EAMC and carries a serious risk if too much fluid is ingested (20). Clinicians will likely be more successful preventing EAMC if they identify the unique risk factors in their athletes with EAMC and then target those risk factors with interventions.
The author declares no conflicts of interest and does not have any financial disclosures.
1. Bergeron MF. Heat cramps: fluid and electrolyte challenges during tennis in the heat. J. Sci. Med. Sport
. 2003; 6: 19–27.
2. Bergeron M. Muscle cramps during exercise — is it fatigue or electrolyte deficit? Curr. Sports Med. Rep.
2008; 7: S50–5.
3. 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; 47: 710–4.
4. Costill D, Coté R, Fink W. Muscle water and electrolytes following varied levels of dehydration in man. J. Appl. Physiol.
1976; 40: 6–11.
5. Fitzsimmons S, Tucker A, Martins D. Seventy-five percent of National Football League teams use pregame hyperhydration with intravenous fluid. Clin. J. Sport Med.
2011; 21: 192–9.
6. Guyton AC. Interstitial fluid pressure. II. Pressure–volume curves of interstitial space. Circ. Res.
1965; 16: 452–60.
7. Horswill CA, Stofan JR, Lacambra M, et al. Sodium balance during U. S. football training in the heat: cramp-prone vs. reference players. Int. J. Sports Med.
2009; 30: 789–94.
8. Hutton RS, Nelson DL. Stretch sensitivity of Golgi tendon organs in fatigued gastrocnemius muscle. Med. Sci. Sports Exerc.
1986; 18: 69–74.
9. Maughan RJ. Exercise-induced muscle cramp: a prospective biochemical study in marathon runners. J. Sports Sci.
1986; 4: 31–4.
10. Miller KC, Knight KL. Electrical stimulation cramp threshold frequency correlates well with the occurrence of skeletal muscle cramps. Muscle Nerve
. 2009; 39: 364–8.
11. Miller KC, Mack GW, Knight KL, et al. Three percent hypohydration does not affect threshold frequency of electrically induced cramps. Med. Sci. Sports Exerc.
2010; 42: 2056–63.
12. Nelson DL, Hutton RS. Dynamic and static stretch responses in muscle spindle receptors in fatigued muscle. Med. Sci. Sports Exerc.
1985; 17: 445–50.
13. Sawka MN, Burke LM, Eichner ER, Maughan RJ, Montain SJ, Stachenfeld NS. American College of Sports Medicine Position Stand: exercise and fluid replacement. Med. Sci. Sports Exerc.
2007; 39: 377–90.
14. Schwabe K, Schwellnus MP, Derman W, Swanevelder S, Jordaan E. Less experience and running pace are potential risk factors for medical complications during a 56 km road running race: a prospective study in 26 354 race starters — safer study II. Br. J. Sports Med.
2014; 48: 905–11.
15. Schwellnus MP. Cause of exercise associated muscle cramps (EAMC)—altered neuromuscular control, dehydration or electrolyte depletion? Br. J. Sports Med.
2009; 43: 401–8.
16. Schwellnus MP, Nicol J, Laubscher R, Noakes TD. Serum electrolyte concentrations and hydration status are not associated with exercise associated muscle cramping (EAMC) in distance runners. Br. J. Sports Med.
2004; 38: 488–92.
17. Schwellnus MP, Allie S, Derman W, Collins M. 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; 45: 1132–6.
18. 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 210 Ironman triathletes. Br. J. Sports Med.
2011; 45: 650–6.
19. 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; 21: 204–10.
21. Stofan J, Zachwieja JJ, Horswill C, et al. Sweat and sodium losses in NCAA football players: a precursor to heat cramps? Int. J. Sport Nutr. Exerc. Metab.
2005; 15: 641–52.
22. Stone M, Edwards J, Stemmans C, et al. Certified athletic trainers’ perceptions of exercise associated muscle cramps. J. Sport Rehabil.
2003; 12: 333–42.
23. Sulzer NU, Schwellnus MP, Noakes TD. Serum electrolytes in Ironman triathletes with exercise-associated muscle cramping. Med. Sci. Sports Exerc.
2005; 37: 1081–5.
24. Summers KM, Snodgrass SJ, Callister R. Predictors of calf cramping in rugby league. J. Strength Cond. Res.
2014; 28: 774–83. doi: 10.1519/JSC.0b013e31829f360c.
25. Wagner T, Behnia N, Ancheta WK, et al. Strengthening and neuromuscular reeducation of the gluteus maximus in a triathlete with exercise-associated cramping of the hamstrings. J. Orthop. Sports Phys. Ther.
2010; 40: 112–9.