- The hugely popular commercial sports drinks have no effect on performance or muscle cramping.
- The only potential performance benefit of drinks like Powerade or Gatorade may be the sugars they contain.
- There are no scientific data to support the efficacy of low-dose electrolytes in boosting performance.
- No data exist to support the notion that electrolytes (at the dosages in the commercial drinks) prevent muscle cramping.
- Evidence appears to support the “altered neuromuscular control” hypothesis as well as other causes and solutions.
The conventional, commercial wisdom suggests that low levels of electrolytes—potassium, sodium, calcium, and others—is what causes exercise-associated muscle cramps (EAMCs). However, the scientific data refute this wisdom on every level. Studies have shown that serum electrolyte levels are not influenced by the oral intake of electrolyte-containing drinks.
The picture appears to more scientifically complicated than simply drinking a bottle of Gatorade. This writer has frequently engaged in endurance training and competition. I have run 5 marathons and have cycled more than 120 miles on many occasions, often in very hot weather. And, I have suffered muscle cramps on many occasions. Personally, the cramping did not seem to correlate with my level of fitness, the degree of exertion, or anything that I could eat or drink.
That was until I discovered pickle juice. I have found pickle juice to be 99% preventive and 99% curative with respect to muscle cramping. I am a heavy, salty sweater. Often after a long bike ride my face will be crusted with salt crystals. I now drink pickle juice before a long, hard, hot workout. If I cramp following a workout, I drink pickle juice and the cramps nearly always disappear within about 15 minutes. Obviously, this is purely anecdotal.
While there are numerous scientific studies examining the influence of pickle juice on muscle cramping, they seem to further cloud the picture as to what causes muscle cramps in endurance athletes. A roundup of the scientific findings offers no consistent cause of EAMC, nor it does offer consistent advice on how to reverse them.
One area of consistent agreement: drinking commercial sports drinks such as Gatorade or Powerade does not delay, prevent, or treat EAMCs.
A Complicated Medical and Scientific Picture
It appears that some other dietary element may be causing the cramps, or relieving the cramps. Many competitive endurance athletes swear by drinking pickle juice or by eating mustard packs. Could it be the vinegar that’s making the difference? MDalert.com explores the potential causes and relief of muscle cramping in light of the scientific literature on the topic.
Here are some of the potential causes of muscle cramping elucidated by scientific research:
- High intensity exercise
- Over exertion
- Low sodium
- Low magnesium
- Altered neuromuscular control
The range of suggested treatments include:
- Stretching the affected muscle
- Electrolyte replenishment
- Maintenance of appropriate serum sodium levels
- A high level of fitness
- Drinking pickle juice
- Eating mustard
Findings of Scientific Studies: A Brief Literature Review
A report published in Muscle & Nerve in 2016, “A narrative review of exercise-associated muscle cramps: Factors that contribute to neuromuscular fatigue and management implications,” came to these conclusions:
“Based on the findings of several large prospective and experimental investigations, the available evidence indicates that EAMC is multifactorial in nature and stems from an imbalance between excitatory drive from muscle spindles and inhibitory drive from Golgi tendon organs to the alpha motor neurons rather than dehydration or electrolyte deficits. This imbalance is believed to stem from neuromuscular overload and fatigue. In concert with these findings, the most successful treatment for an acute bout of EAMC is stretching, whereas auspicious methods of prevention include efforts that delay exercise-induced fatigue.”
A study published in the Journal of Athletic Training in 2014, “Electrolyte and plasma responses after pickle juice, mustard, and deionized water ingestion in dehydrated humans,” examined the effects of drinking pickle juice and eating mustard, among other potential cramping interventions. The findings, as with many of the studies reviewed herein, were inconclusive:
“Pickle juice and mustard are 2 anecdotal treatments believed to be effective for treating EAMCs by restoring plasma electrolytes; however, no appreciable changes occurred to [Na+]p, [K+]p, percentage changes in plasma Na+ content, percentage changes in plasma volume, or OSMp of hypohydrated humans within 60 minutes of PJ or mustard ingestion. Pickle juice is unlikely to exacerbate exercise-induced hypertonicity, delay rehydration, or cause hyperkalemia. Moreover, ingesting 80 mL of PJ or a mass of mustard with a similar Na+ content cannot fully replace the Na+ or K+ lost due to exercise-induced sweating. The effects of drinking multiple boluses of PJ after exercise in the heat on electrolytes are unknown and worthy of future research.”
This 2011 study published in the British Journal of Sports Medicine, “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," found that exercise intensity predicted EAMC:
“The results from this study add to the evidence that dehydration and altered serum electrolyte balance are not causes for EAMC. Rather, endurance runners competing at a fast pace, which suggests that they exercise at a high intensity, are at risk for EAMC.”
A study published in the Clinical Journal of Sports Medicine in 2011 found that:
“There is evidence from this study that a history of EAMC is associated with (1) exercising at a higher intensity during a race that may result in premature muscle fatigue, (2) an inherited risk (positive family history), and (3) a history of tendon and/or ligament injury.”
Results of a study published in Medicine & Science in Sports & Exercise, “Reflex inhibition of electrically induced muscle cramps in hypohydrated humans,” found that EAMC lasted for a shorter duration in participants who drank pickle juice—about 50 seconds less than in participants who drank water. The conclusions were as follows:
“Anecdotal evidence suggests that ingesting small volumes of pickle juice relieves muscle cramps within 35 s of ingestion. No experimental evidence exists supporting the ingestion of pickle juice as a treatment for skeletal muscle cramps.
“Pickle juice, and not deionized water, inhibits electrically induced muscle cramps in hypohydrated humans. This effect could not be explained by rapid restoration of body fluids or electrolytes. We suspect that the rapid inhibition of the electrically induced cramps reflects a neurally mediated reflex that originates in the oropharyngeal region and acts to inhibit the firing of alpha motor neurons of the cramping muscle.”
Another report published in 2010 in Medicine & Science in Sports & Exercise, “Three percent hypohydration does not affect threshold frequency of electrically induced cramps, found that:
“Mild hypohydration with minimal neuromuscular fatigue does not seem to predispose individuals to cramping. Thus, cramps may be more associated with neuromuscular fatigue than dehydration/electrolyte losses. Health care professionals may have more success preventing exercise-associated muscle cramp by focusing on strategies that minimize neuromuscular fatigue rather than dehydration. However, the effect of greater fluid losses on cramp threshold frequency is unknown and merits further research.”
A study published in British Journal of Sports Medicine in 2009, “Cause of Exercise Associated Muscle Cramps (EAMC)—altered neuromuscular control, dehydration or electrolyte depletion?,” found that:
“Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case–control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC.”
“Recovery and maintenance of water and sodium balance with oral or intravenous salt solutions is the proven effective strategy for resolving and averting exercise-associated muscle cramps that are prompted by extensive sweating and a sodium deficit.”
A study of magnesium supplementation conducted in 1998, published in Medicine & Science in Sports & Exercise, “Lack of effect of oral Mg-supplementation on Mg in serum, blood cells, and calf muscle,” came to the following conclusion:
“These results indicate that Mg supplementation in athletes with low-normal serum Mg did not improve performance and failed to increase the body's Mg stores. Serum Mg appears to be a poor indicator for Mg in skeletal muscle or most other cellular compartments, but the concentration of Mg in mononuclear leukocytes might be used as an indicator of skeletal muscle Mg when NMR is not available.”
The results of a review study, “Exercise-induced muscle cramp. Proposed mechanisms and management” were published in Sports Medicine in 1996. The conclusions were as follows:
“Disturbances at various levels of the central and peripheral nervous system and skeletal muscle are likely to be involved in the mechanism of cramp and may explain the diverse range of conditions in which cramp occurs. The activity of the motor neuron is subject to a multitude of influences including peripheral receptor sensory input, spinal reflexes, inhibitory interneurons in the spinal cord, synaptic, and neurotransmitter modulation and descending CNS input. The muscle spindle and golgi tendon organ proprioceptors are fundamental to the control of muscle length and tone and the maintenance of posture. Disturbance in the activity of these receptors may occur through faulty posture, shortened muscle length, intense exercise and exercise to fatigue, resulting in increased motor neuron activity and motor unit recruitment. The relaxation phase of muscle contraction is prolonged in a fatigued muscle, raising the likelihood of fused summation of action potentials if motor neuron activity delivers a sustained high firing frequency. Treatment of cramp is directed at reducing muscle spindle and motor neuron activity by reflex inhibition and afferent stimulation. There are no proven strategies for the prevention of exercise-induced muscle cramp but regular muscle stretching using post-isometric relaxation techniques, correction of muscle balance and posture, adequate conditioning for the activity, mental preparation for competition and avoiding provocative drugs may be beneficial. Other strategies such as incorporating plyometrics or eccentric muscle strengthening into training programmes, maintaining adequate carbohydrate reserves during competition or treating myofascial trigger points are speculative and require investigation.