Quashing the Myth behind Cramping? The Case of Electrolyte Depletion v Neuromuscular Control Theories
We have all been there… an athlete or player is struck by a painful, spasmodic contracting in a muscle that we know as cramp. The eyes of blame fall to the Physio/Nutritionist/Sport Scientist/Fitness Coach and an electrolyte solution is hurriedly thrown on to fix it.
Now in the hot, humid and exhausting period of preseason, it seems a suitable time to try to understand the pathophysiology of Exercise Associated Muscle Cramps (EAMC).
American readers will also recall the furore around Gatorade’s tongue in cheek responses to LeBron James cramping in the first NBA Finals game earlier this summer:
Although cause and treatment for muscle cramps may be viewed as obvious and well established by the general public with blame falling on dehydration and salt loss, the etiology of cramping is actually fairly poorly understood and these everyday perceptions may be somewhat of a myth.
So let us look into the case between the theories: electrolyte depletion and dehydration versus the neuromuscular control theory…
(Just before we do, it should be well noted that this topic has the obvious potential for conflicts of interest. As a Scientist it is important to consider the influence of marketing and commercial interests against the scientific integrity of research.)
Electrolyte Depletion & Dehydration Theory
The Case For…
- These are two hypotheses that are often considered together. They stem from anecdotal evidence from over 100 years ago of labourers in hot and humid conditions suffering from cramping.
- From this, it had been proposed that a change in serum electrolyte concentrations associated with exercise in hot and humid environments could develop muscle cramps.
- In addition, it has been proposed an increase in sweat sodium concentration or ‘salty sweating’ will deplete sodium in the body and cause cramping.
- As a significant amount of sodium can only be lost in an associated large loss of fluid, this theory must also be coupled with dehydration. Therefore, the theory states; as progressive dehydration and electrolyte depletion occurs the extracellular fluid compartment becomes increasingly contracted, increasing surrounding neurotransmitter concentrations causing selected motor nerve terminals to become hyperexcitable.
The Case Against…
- Sweat is hypotonic (you lose more water than electrolytes) therefore sweating does not actually reduce electrolyte concentration and it may even make you hypertonic (higher electrolyte concentration).
- This is true also for the ‘salty sweaters’ and there is no data actually defining ‘abnormally high’ for sweat sodium concentrations.
- EAMC is localised so how can a systemic abnormality such as electrolyte depletion and/or dehydration that affects the whole body cause such confined symptoms? In fact it seems to affect those muscles that are used repeatedly in the exercise itself (remember that for later!)
- Studies in endurance athletes, marathon runners and triathletes, found a disassociation between EAMC and serum electrolyte concentrations and/or dehydration (Schwellnus et al, 2004; Sulzer et al, 2005; Schwellnus et al, 2007)
- As of 2009, the only published research that linked reportedly ‘high’ sweat sodium concentrations to EAMC were a number of case studies totalling only 23 athletes (Schwellnus, 2009). However, limitations exist within these studies that include a lack of control groups, low sample sizes, being based on past history rather than at the time of an acute bout and not documenting or collection other factors that influence sweat sodium concentration e.g. diet, acclimatisation, anatomical site and seasonal variations. Also, the 23 cases noted as ‘salty sweaters’ compared to normal athletes with no history of cramping in other research are actually in the normal to low range of sweat sodium concentrations.
- Furthermore, various research comparing crampers to non crampers has found no significant differences in serum electrolyte concentrations, plasma volume losses, body weight changes (as a marker of dehydration), sweat rates or sodium losses between the two groups.
- These theories do not explain cramping in cool environments.
- The ingestion of fluid/electrolytes as a treatment for dehydration and electrolyte depletion should consistently resolve the EAMC but does not always.
Neuromuscular Control Theory
- In 1997, Schwellnus and colleagues put forward a new hypothesis that EAMC is in fact associated with the onset of neuromuscular fatigue and consequent altered neuromuscular control.
- The theory states that as muscle fatigue develops it disrupts the peripheral receptors with increased excitatory (e.g. muscle spindle) and decreased inhibitory (e.g. Golgi tendon organ) signals to the ?-motor neuron. This abnormal firing of motor neurones first presents as muscle twitches and if muscle contraction continues, EAMC ensues.
- This theory would support the observation that cramp is localised and occurs in the working and therefore fatigued muscle.
- The muscles most susceptible to cramp are those contracting in a shortened position across two joints i.e. the calf muscle especially when plantar flexing. In this position the activity of the Golgi tendon organ is further inhibited, as per the neuromuscular fatigue theory.
- There is evidence that increased exercise duration, self-reported poor conditioning and depletion of muscle energy stores, which are all associated with muscle fatigue can lead to the development of cramping (Schwellnus, 2009).
- Further evidence suggests that increased exercise intensity, represented as a faster race time in cramping Ironman triathletes, is an independent risk factor for EAMC, along with a history of cramping (Schwellnus et al, 2011).
- Laboratory studies that reliably induce muscle cramping using electrical stimulation or voluntary muscle contraction suggest the mechanism is neuromuscular.
- One of the most effective treatments for EAMC is passive cramping, which supports the neuromuscular control theory given that stretching increases muscle tension and the inhibitory activity of the Golgi tendon.
I have to admit, it was not until I looked into the research on Exercise-Associated Muscle Cramping that I discovered just how unknown the pathophysiology is. I presumed the established electrolyte deficiency theory was thoroughly supported, which reaffirms the importance of working as an evidence based scientist.
I am not suggesting there is definitive proof for the neural fatigue theory as of yet and it is likely that EAMC is in fact a multifaceted phenomenon. The novel hypothesis Professor Schwellnus and colleagues presented in 1997 was just the first step of a long and still ongoing journey to truly understand the etiology of cramping but questioning the established electrolyte deficit/hydration model was a good start!
There is still much more to understand regarding the mechanisms of cramping as well as the genetic predisposition factor and there is a clear need for controlled, prospective studies into the etiology and the possible altered neuromuscular control theory. I am also very interested in the mechanisms and treatment of players that appear to suffer anxiety-related cramping; examples with no history of cramping and seemingly no changes or issues with conditioning, training load, environmental conditions, diet or hydration status but cramp in important games such as the later stages of cup competitions.
It seems some factors that can help in the prevention of cramping are stretching, good conditioning, progressive training loads and/or pacing strategies and maintaining hydration status (even if they may just be a placebo effect!).
As you can tell from the references in this article Professor Martin Schwellnus is clearly the leading researcher in this area. If this blog has left you wanting further reading on this area, the ever-brilliant Dr Ross Tucker and colleagues on the Science of Sport website have a whole series of articles on cramping here: http://sportsscientists.com/2007/11/muscle-cramps-part-i/
Miller KC, Stone MS, Huxel KC et al. (2010) Exercise-associated muscle cramps. Sports Health 2: 279-283.
Schwellnus MP (2007) Muscle cramping in the marathon: aetiology and risk factors. Sports Med 37: 364-367.
Schwellnus MP (2009) Causes of Exercise Associated Muscle Cramps (EAMC) – altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med 43: 401-408.
Schwellnus MP, Derman EW & Noakes TD (1997) Aetiology of skeletal muscle ‘cramps’ during exercise: A novel hypothesis. J Sports Sci 15: 277-285.
Schwellnus MP, Drew N & Collins M (2011) 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 45: 650-656.
Schwellnus MP, Nicol J, Laubscher R et al. (2004) Serum electrolyte concentrations and hydration status are not associated with exercise associated muscle cramping (EAMC) in distance runners. Br J Sports Med 38: 488-492.
Sulzer NU, Schwellnus MP & Noakes TD (2005) Serum electrolyte in Ironman triathletes with exercise-associated muscle cramping. Med Sci Sports Exerc 37: 1081-1085.