Despite estimates that exercise-associated muscle cramps (EAMC) affect up to 95 percent of the general population , their cause is currently unknown. The two prevailing theories are the dehydration and electrolyte loss theory  and the neuromuscular control theory .
Briefly, the dehydration theory postulates that exercise-induced sweating results in a contracture of the interstitium causing an increase in the pressure on select nerve terminals and EAMC ensue. The neuromuscular control theory suggests EAMC occur when fatigue and other factors coalesce and cause disinhibition of golgi tendon organs and increased excitation of muscle spindles resulting in the hyperexcitability of the alpha motor neuron pool.
Finding the etiology of EAMC is difficult because they are spontaneous and unpredictable and no suitable animal model exists for inducing cramps in a laboratory setting. As a result, scientists have primarily studied EAMC using quasi-experimental or case study research designs. These experiments have usually sought to determine the etiology of EAMC by comparing some physiological characteristic (e.g., body mass loss, plasma sodium concentration) between crampers and non-crampers before and after an athletic competition.
While these experiments are valuable, it is difficult to identify a true etiology with these designs as multiple physiological changes are happening to athletes during exercise besides dehydration, electrolyte loss, or fatigue.
Recent controlled, experimental studies [4,5] indicate that mild to severe dehydration does not affect cramp risk when peripheral fatigue is minimized. These studies [4,5] were the first to try and study cramp etiology by controlling for fatigue but still have subjects lose substantial amounts of body water.
The results are consistent with other scientists’ [6-8] observations that cramps are likely the result of neurological changes rather than dehydration. Further research is needed to identify the factors that coalesce to elicit EAMC so specific strategies to treat and prevent EAMC can be developed.
Dr. Kevin C. Miller, AT, ATC is an Associate Professor in Athletic Training at Central Michigan University. His research interests involve the causes, treatments, and prevention of exercise-associated muscle cramps. He has published numerous articles on muscle cramps in several Tier 1 journals including the British Journal of Sports Medicine, Muscle and Nerve, Medicine and Science in Sports and Exercise, and the Journal of Athletic Training.
1. Norris F, Gasteiger E, Chatfield P. An electromyographic study of induced and spontaneous muscle cramps. Electroencephalogr Clin Neurophysiol 1956;9:139-47
2. Bergeron M. Muscle cramps during exercise–Is it fatigue or electrolyte deficit? Curr Sports Med Rep 2008;7:S50-S55
3. Schwellnus M. Cause of exercise associated muscle cramps (EAMC)-Altered neuromuscular control, dehydration, or electrolyte depletion? Br J Sports Med 2009;43:401-08
4. Miller K, Knight K, Mack G, et al. Three percent hypohydration does not affect the threshold frequency of electrically-induced muscle cramps. Med Sci Sports Exerc 2010;42:2056-63
5. Braulick K, Miller K, Albrecht J, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med 2012;47:710-14
6. Minetto M, Holobar A, Botter A, et al. Mechanisms of cramp contractions: peripheral or central generation. J Physiol 2011;23:5759-73
7. Ge H, Zhang Y, Boudreau S, et al. Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points. Exp Brain Res 2008;187:623-29
8. Merletti R, Botter A, Lanfranco F, et al. Spinal involvement and muscle cramps in electrically elicited muscle contractions. Artif Organs 2011;35:221-25