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The Evolution of Exercise-Associated Muscle Cramp Research

Miller, Kevin C., Ph.D., AT, ATC

ACSM's Health & Fitness Journal: July/August 2018 - Volume 22 - Issue 4 - p 6–8
doi: 10.1249/FIT.0000000000000395
Departments: Health & Fitness A to Z

Kevin C. Miller, Ph.D., AT, ATC, is a full professor in the Athletic Training Program at Central Michigan University. His research interests include the causes, treatments, and prevention of exertional heat illness with a specific emphasis on exercise-associated muscle cramping. He has published more than 40 peer-reviewed manuscripts including the National Athletic Trainers Association (NATA) Position Statement on Exertional Heat Illness; the Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference; and the NATA round table on Malignant Hyperthermia in Physically-Active Populations. He serves on several journal editorial boards and the Korey Stringer Institute’s Medical and Science Advisory Board.

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INTRODUCTION

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Muscle Cramp Research: the Early Years (1900–1990)

In the early 1900s, there was little known about muscle cramps, even as the condition sometimes resulted in hospitalization. Edsall (1) recorded one of the earliest cases of exercise-associated muscle cramps (EAMC) in 1904 and attributed it to heat exposure. However, few systematic investigations in this area occurred over the ensuing 20 years until Moss (2) and colleagues began to notice EAMC occurring in workers who performed physical activity in the heat, such as miners or stokers. Moss and his colleagues speculated that hard work in high air temperatures, excessive fluid consumption, and substantial losses in chloride all contributed to the incidence of EAMC.

Years later, Talbott (3) concurred with Moss (2) when he noted five Hoover Dam workers with EAMC had low blood chloride concentrations. Following these early observations and growing intrigue into the genesis of EAMC, Ladell (4) performed a series of experiments and noted EAMC rarely occurred without salt deficiencies; he further noted EAMC seemed to dissipate shortly after injection of intravenous sodium chloride. Therefore, Ladell’s (4) hypothesis that EAMC occurred primarily because of overhydration and significant losses in chloride, generally from exercise-induced sweating, largely concurred with the clinical findings from earlier in the century. Together, this early evidence established what became the long-held belief that EAMC was a function of hard physical labor in hot and humid conditions that resulted in substantial loss of fluid from the interstitial fluid space and critical deficits in salt. This belief generated what would become known as the dehydration/electrolyte imbalance theory of EAMC. Two small observational studies in American football players supported this theory (5,6). In these studies, players with a history of EAMC had considerably higher sweat sodium concentrations than their peers without a history of EAMC. This finding seemingly supported the term salty sweater, to describe those at higher risk for EAMC. This term is still used today.

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Muscle Cramp Research: Current Thinking (1990s–Present)

In the mid-1990s, an alternative theory for EAMC was proposed by Schwellnus et al. (7), known as the altered neuromuscular control theory. Initially, Schwellnus’ group hypothesized EAMC occurred as a consequence of fatigue-induced changes to neuromuscular control, which was a stark contrast to the dehydration/electrolyte theory. They suggested fatigue, not dehydration/electrolyte changes, was responsible for increasing muscle spindle activity and decreased golgi tendon organ inhibition. Combined with other excitatory impulses, these fatigue-induced alterations in spinal feedback increased alpha motor neuron activity and induced EAMC. The altered neuromuscular control theory has been updated and expanded to include other factors which may independently or collectively affect alpha motor neuron control (e.g., muscle injury, genetic predisposition) (8).

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Evaluating the Evidence

The past 15 years has seen a substantial increase in the number of observational and laboratory studies investigating muscle cramping. Contrary to conventional wisdom, most of these studies are not consistent with the dehydration/electrolyte imbalance theory. Many studies do not show any differences in plasma volume (9,10), body mass losses (6,9–11), or sweat rates (5,6) between athletes with or without a history of EAMC. Other studies show that no EAMC occurred despite athletes losing more than 10 g of sodium during exercise (5,12). In two well-controlled laboratory studies, neither mild (13) nor serious (14) dehydration, with associated sodium losses, altered muscle cramp susceptibility when fatigue was minimized. In fact, even when subjects ingested fluids that matched their sweat losses during exercise, EAMC still occurred 70% of the time (15). Moreover, an acute muscle cramp increased subjects’ susceptibility to subsequent cramps for up to 1 hour, even when no exercise-induced fluid losses were present (16). And maybe the most damaging evidence to dispute the dehydration/electrolyte imbalance theory is that static stretching is known to relieve acute EAMC, yet it adds no fluids or electrolytes to the body. If EAMC were due to dehydration, stretching should not relieve acute EAMC.

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Future Research Directions

If the altered neuromuscular control theory is true, then the main clinical implication is that there may be numerous risk factors that are responsible for producing EAMC, and these factors may act independently or in some combination with each other. Therefore, future investigations should continue to identify possible risk factors for EAMC and test if these factors affect cramp susceptibility when confounding variables (e.g., muscle injury, pain, fatigue) are controlled. Specifically, greater clarity is needed on how fatigue (i.e., central and/or peripheral) may affect EAMC development and whether prophylactic strategies that target neuromuscular control (e.g., plyometric training) can effectively prevent EAMC.

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SUMMARY

What is increasingly clear, thanks to the evolving EAMC research over the last 100 years, is that evidence overwhelmingly supports that EAMC are due to changes within the nervous system.

In contrast, the evidence supporting the dehydration/electrolyte imbalance theory is weak, as indicated by several expert-written position statements (17,18). However, it is unlikely any one factor is completely responsible for EAMC genesis. Instead, it is more probable that risk factors vary from person to person and may even vary within a given individual, particularly as environmental or physiological conditions change. Therefore, individuals struggling with EAMC should try to identify their unique EAMC risk factors and target these with appropriate interventions. By better understanding individual risk factors that lead to EAMC development, clinicians can develop individualized evidence-based intervention strategies. Such prevention strategies should prove far more productive than nonspecific treatment recommendations, especially those based on outdated models of EAMC pathology (e.g., drink more fluids, consume more potassium).

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References

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13. 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(11):2056–63.
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17. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2015;50:986–1000.
18. Armstrong LE, Casa DJ, Millard-Stafford ML, Moran D, Pyne S, Roberts WO. American College of Sports Medicine position stand: Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39:556–72.
© 2018 American College of Sports Medicine.