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Rethinking the Cause of Exercise-Associated Muscle Cramping: Moving beyond Dehydration and Electrolyte Losses

Miller, Kevin C. PhD, AT, ATC

doi: 10.1249/JSR.0000000000000183
Invited Commentary
Free

School of Rehabilitation and Medical Sciences, Central Michigan University, Mount Pleasant, MI

Address for correspondence: Kevin C. Miller, PhD, AT, ATC, School of Rehabilitation and Medical Sciences, Central Michigan University, Mount Pleasant, MI 48859; E-mail: mille5k@cmich.edu.

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Introduction

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.

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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.

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Conclusion

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.

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Acknowledgment

The author declares no conflicts of interest and does not have any financial disclosures.

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