Pickles and Pickle Juice: Healthy or Horrible?

Written by Team Legion | not dated

If you hang out in nutrition and fitness circles like I do, you’ll come across all sorts of interesting recommendations.

Practically everyone has their own personal miracle drug or perfect natural supplement to make their workouts easier.

One of these I keep coming across is pickle juice.

People just can’t seem to get enough of the stuff. And if you follow their logic, you too should be drinking it before and after every workout.

But something about this whole pickle craze hasn’t seemed right to me all along.

Don’t get me wrong, I like the taste of pickles – but should you really drink the juice too?

Today we’re going to find out whether pickles and pickle juice are great for you, or if they’re part of yet another ridiculous trend.

What Are Pickles and Pickle Juice?

Your everyday pickle starts life as a raw cucumber, and then it’s submerged into a concoction of vinegar, salt, and spices, and is fermented. After its fermentation, it becomes a pickle – a vegetable with a different flavor and nutritional value than the original cucumber.

Pickling is an ancient method of food preservation. Before human beings could refrigerate or store foods long-term, pickling was the only way to preserve foods for future consumption.

Cucumbers are fermented by Lactobacillus bacteria, which normally cover the cucumber’s skin.

During commercial processing, these beneficial probiotic bacteria are usually removed once vinegar is added. The liquid remaining after the cucumber has changed into a pickle is its juice.

But when it comes to pickle juice, it’s not really a juice after all. Pickle juice should actually be called pickle brine. Brine is the salt solution meant to preserve food. Anything else added to brine is purely for flavor purposes.

Nutritional Value of Cucumbers and Pickles

A lot of the claims about pickles and pickle juice revolve around the fact that they’re the byproduct of a vegetable – and vegetables are great for you, right?

Let’s take a look at the nutrient content of cucumbers before they become pickles. Your average, unpeeled cucumber contains:

  • 45 calories
  • 4 milligrams of vitamin C
  • 21 micrograms of folic acid
  • 1 milligram of sodium
  • 76 milligrams of potassium

So, let’s compare. Here’s the nutritional breakdown of a serving of pickles:

  • 17 calories
  • 1 milligrams of vitamin C
  • 4 micrograms of folic acid
  • 1251 milligrams of sodium
  • 132 milligrams of potassium

That’s right. The sodium content in pickles is an increase of 1250 milligrams from regular cucumbers. Your biggest positive increase here is in potassium – as a result of the sodium increase.

Pickle Juice: The Claims

Some claim that athletes who experience muscle cramping during their workout sessions should drink pickle juice to replace their electrolytes and reduce cramping. This is based on the idea that vinegar sends signals to your nerves which disrupts the cramping caused during workout sessions.

Would any other brine work just as well? Olive brine or pepper brine for instance? All of these have high levels of sodium and borrow nutrient content from the vegetables in them.

What Does Science Say About Pickles and Pickle Juice?

The real truth is that science has come nowhere close to proving most of these claims.

In fact, if you search PubMed –a website I use constantly to look up scientific studies, you’ll only find a mere 16 results.

The studies that have been performed are underwhelming at best. One study found that drinking pickle juice after exercise was not highly effective at replenishing electrolytes.

Another study found that pickle juice “does not relieve cramps via a metabolic mechanism.”

And yet another study suggested that actually swallowing pickle juice could relieve cramps – something that involves no metabolic processes whatsoever.

The rest of the studies seem to indicate pickle juice is nothing more than a weak water, carbohydrate, and electrolyte replenishing solution. There seem to be no fantastic health benefits here.

But, several of the same studies have shown that the sensation of vinegar and salt on your tongue can help relieve muscle cramps. It’s not clear if this would last long-term, or in everyone, but it certainly couldn’t hurt.

Final Thoughts

There’s nothing special about salt water that once contained floating cucumbers, or pickles themselves for that matter.

I’m sorry, but those are the facts, folks. There’s no evidence for any exclusive advantage you can gain from drinking pickle juice or eating the fermented cucumber, except perhaps a slight ability to ameliorate muscle cramps.

Pickle juice may help with your cramps – and it may not.

If you like the way pickles taste, great! Eat them and drink their juice in safe amounts and you shouldn’t run into any serious health issues.

Just don’t expect any miracles.

Originally Published:

Gastric emptying after pickle-juice ingestion in rested, euhydrated humans.

More research for our science buffs!

J Athl Train. 2010 Nov-Dec;45(6):601-8. doi: 10.4085/1062-6050-45.6.601.
Department of Health, Nutrition, and Exercise Sciences, North Dakota State University, Fargo, ND 58108- 6050, USA.



Small volumes of pickle juice (PJ) relieve muscle cramps within 85 seconds of ingestion without significantly affecting plasma variables. This effect may be neurologic rather than metabolic. Understanding PJ’s gastric emptying would help to strengthen this theory.


To compare gastric emptying and plasma variables after PJ and deionized water (DIW) ingestion.


Crossover study.




Ten men (age  =  25.4 ± 0.7 years, height  =  177.1 ± 1.6 cm, mass  =  78.1 ± 3.6 kg).


Rested, euhydrated, and eunatremic participants ingested 7 mL·kg⁻¹ body mass of PJ or DIW on separate days.


Gastric volume was measured at 0, 5, 10, 20, and 30 minutes postingestion (using the phenol red dilution technique). Percentage changes in plasma volume and plasma sodium concentration were measured preingestion (-45 minutes) and at 5, 10, 20, and 30 minutes postingestion.


Initial gastric volume was 624.5 ± 27.4 mL for PJ and 659.5 ± 43.8 mL for DIW (P > .05). Both fluids began to empty within the first 5 minutes (volume emptied: PJ  =  219.2 ± 39.1 mL, DIW  =  305.0 ± 40.5 mL, P < .05). Participants who ingested PJ did not empty further after the first 5 minutes (P > .05), whereas in those who ingested DIW, gastric volume decreased to 111.6 ± 39.9 mL by 30 minutes (P < .05). The DIW group emptied faster than the PJ group between 20 and 30 minutes postingestion (P < .05). Within 5 minutes of PJ ingestion, plasma volume decreased 4.8% ± 1.6%, whereas plasma sodium concentration increased 1.6 ± 0.5 mmol·L⁻¹ (P < .05). Similar changes occurred after DIW ingestion. Calculated plasma sodium content was unchanged for both fluids (P > .05).


The initial decrease in gastric volume with both fluids is likely attributable to gastric distension. Failure of the PJ group to empty afterward is likely due to PJ’s osmolality and acidity. Cardiovascular reflexes resulting from gastric distension are likely responsible for the plasma volume shift and rise in plasma sodium concentration despite nonsignificant changes in plasma sodium content. These data support our theory that PJ does not relieve cramps via a metabolic mechanism.

Staying on top of your nutrition will help offset the cramping process.

Muscle Cramps: Causes and Remedies Based on Latest Science

CTS Coach Corrine Malcolm lays down the latest science

When it comes to cramping, especially exercise-associated muscle cramping (EAMC) almost everyone has a story. A story about that one time, in that one race, where that one muscle seized. Exercise-associated muscle cramps are defined as painful spasms, and involuntary contractions of skeletal muscles that occur during or immediately post exercise. So, for the purpose of this article, that would exclude cramps that occur outside of the context of exercise, or that are caused by underlying medical conditions such as nocturnal cramps, hypo/hyperthyroidism, and central or peripheral nervous system diseases such as Parkinson’s disease.

Cramping is by no means a new topic in the endurance community, and because EAMC can be debilitating in a race scenario cramping remains a hot topic. There have been decades of research dedicated to trying to figure out how we cramp, why we cramp, and how to stop cramps once they start. Despite our long affair with EAMC, we are not much closer to fully understand their etiology. If anything, our new understanding of EAMC is that they are complicated and likely stem from multiple compounding factors that make any one treatment or preventative technique unlikely to work for everyone, every time.

The Old Theories About Cramping

The advancement that has happened over the past 5 to 10 years however, is a clear move away from the original “dehydration & electrolyte imbalance theory” and an increased focus on the “altered neuromuscular control theory”. Starting in the early 2000s, study after study appeared that looked at hydration status and blood-electrolyte concentrations in endurance athletes, and over and over again there was no significant difference in the hydration status or blood-electrolyte concentrations of athletes who cramped and athletes who did not cramp on race day. Moreover, if you think about it, dehydration and electrolyte imbalances are a system-wide issue, which should cause system-wide muscle cramping. However, EAMC is most commonly localized two one or two major muscle groups and frequently occurs unilaterally. What that means is that EAMC primarily occur in asymmetry (one calf cramps). However, if muscles are cramping bilaterally (both calves) or become generalized/full body cramping, this can be tied more closely to extreme dehydration or hyponatremia, or a more serious medical condition.

What this means is that although we should not completely eliminate dehydration or electrolyte imbalances entirely from the EAMC guidebook, there is likely more going on. Most likely, hydration and fueling problems act as one of the many players that work together to lead to EAMC.

The New Theories About Cramping

The newest theory knocking at the door is the altered neuromuscular control theory. The premise of this new theory is that EAMC is most closely linked to the tenuous relationship between your nervous system and muscles contractions. This theory suggests that EAMC are a combination of several factors coalescing in a perfect (terrible) storm, overexciting your alpha motor neuron, ultimately resulting in a cramp. The variables that are seemingly most important to causing this heightened fatigued state are: inadequate conditioning (particularly for heat or altitude), muscle damage, previous injury to both the cramping muscle or in the compensating muscle group, and certain medications like albuterol, conjugated estrogen, and statins. These variables can easily build off each other, snowballing into that cramp-prone state we’ve all seen happen on race day. These factors also explain why EAMC seem to been seen more frequently at hot races where muscles fatigue more quickly at the same work load, and why athletes with a history of previous cramping are most likely to experience cramping again. This also explains why we almost always see EAMC in races and not during training because we are placing a heavier demand on our muscles than we normally do.

What Happens When A Muscle Cramps

So how exactly do cramps happen and how do we try and treat them?

As mentioned above, cramping is the result of your alpha motor neuron becoming overexcited. Your alpha motor neurons are the largest neurons in your spinal chord and they directly innervate your muscle fibers, the stretch sensor, of your skeletal muscle. Their job is to send the message to your muscle to, “Contract! Contract! Contract!” We only move, pedal, kick, or stride when our alpha motor neurons work in perfect harmony with our Golgi Tendon Organs (GTOs). GTOs are the other half of the contraction-relaxation pattern our muscles rely on.

When alph motor neurons and GTOs are both functioning properly, the GTOs act as the inhibitor to muscle spindle contractions. Basically, your alpha motor neurons and muscle spindles are the active “Contract! Contract! Contract!!!” command and action, while the GTOs are the inhibition to the contraction and allow the muscle to relax. As our muscles fatigue, there is an increased firing from the muscle spindles to keep “Contracting-contracting-contracting!!!” while, at the same time, there is a decreased response from the muscle GTOs to relax. When both of these things happen, we get an over excited alpha motor neuron that causes the contraction to win out time and time again, resulting in a contraction that won’t stop or, as we’ve all experienced, a cramp.

What Muscles Are Prone To Cramping

Muscles that are most likely to experience EAMC are muscles that are contracting in a shortened position. This is particularly true of muscles that cross two joints including your muscles that make up your hamstrings, quadriceps, calves, your biceps brachii, and the long head of your triceps. EAMC are not limited to biarticulated muscles but they are the most common locations of cramping in runners, swimmers, and cyclists. Part of the reason for this is that when muscles have to contract in a shortened position, or through a small arc of movement, your GTOs produce less inhibition to the contraction than normal, due to altered muscle tensions. This can be made worse if you have an injury or an imbalance that causes you to decrease your normal range of motion.

The beauty of this knowledge is that one of the ways to stop EAMC once they’ve started is to stop and give your muscles the opportunity to lengthen. You can do this by stopping and passively stretching the muscle or by moving that muscle through its full range of motion. What you accomplish by doing this is creating a change in tension in the muscle, thereby increasing the GTOs’ inhibitory input to the alpha motor neuron and relaxing the muscle.

So why do people drink pickle juice?

Pickle juice appears to be more than folklore when it comes to stopping EAMC in their tracks. In a now famous 2010 study, researcher Kevin Miller and his colleagues brought pickle juice mainstream. For decades, athletic trainers and coaches had anecdotally been prescribing pickle juice, apple-cider vinegar, and mustard to treat EAMC, but there had been no concrete evidence as to why these various concoctions were stopping cramps. Playing into the electrolyte and dehydration theory, it was initially believed that the sodium in pickle juice was aiding in correcting an electrolyte balance in the cramping athletes. However, the result was happening so rapidly (30 seconds) it was deemed unlikely that the small amount of pickle juice ingested could possibly alter the athlete’s blood sodium concentrations in that short timeframe. What the scientific community began to conclude was that something in the pickle juice was abating the cramps via another mechanism. A new idea emerged that a neural reflex in the mouth, oropharynx, or esophagus could quickly disrupt the alpha motor neuron, stopping a cramp. This discovery has led to the development of several new anti-cramping products.

This new area of research (and the associated sports products) is based on stimulating transient receptor potential (TRP) channels. TRP channels are ion channels in the body that help mediate a variety of different sensations including pain, tastes, hot, cold, and pressure. Many TRP channels that help us differentiate temperatures are also activated by various molecules found in spices, such as capsaicin (chili peppers), menthol (mint), cinnamaldehye (cinnamon), shogaol (ginger), and allyl isothiocyanate (wasabi). Two channels of particular interest to researchers in this are the TRPA1 and TRPV1 channels that are found in our mouth, oropharynx, esophagus, and stomach. Given how fast the acetic acid in pickle-juice works to abate a cramp, it is very likely it stimulates TRP channels above the stomach, which makes this a particularly interesting way to address cramps once they start.

What this means is that strong sensory stimuli activated at these specific TRP channels, by a TRP agonist, or activators for each channel, like capsaicin, could potentially cause the alpha motor neurons to become less excited, which would in turn diminish or stave off a cramp (16). There are two possible scenarios being considered by researchers and companies cashing in on this new theory: 1) pre-ingestion of a TRP agonist might increase the threshold one has to reach in order to cramp, thereby keeping the individual out of a cramp prone state longer, and 2) ingestion of a TRP agonist at onset of a cramp will “trip” our electrical wiring, causing our muscle spindles and GTOs to work in harmony once again by decreasing the excitability of our alpha motor neurons.

What You Can Do About Cramping Today

So what does this mean for us right now? What the literature is currently telling us is that, although there is not yet strong evidence to support the idea that ingesting a TRP agonist pre-activity will successfully stave off a cramp, there is fairly strong evidence that ingesting a TRP agonist at the onset of cramping is likely to help abate the cramp and temporarily prevent subsequent cramps from occurring. I would add that at this time more research needs to be conducted on the most researched TRP agonist, HotShot, and other products containing TRP agonists like mustard, apple-cider vinegar, menthol etc. We are just at the beginning stages of understanding the complexities of TRP channels, the electrical component of EAMC, and their physiological intricacies.

So what can you do right now?

  • Experiment! Anecdote is not science. The brain is incredibly powerful, and placebos can have very real effects on physiological symptoms and performance. It doesn’t mean that something will not work, but the reliability of such methodologies remains unproven.
  • Train yourself specifically for the event you are undertaking. It’s thought that when the demand you put on your muscles does not match up with the training you’ve done, you are more susceptible to cramping, as evidenced by most cramp occurring during a race or event. This applies to athletes who go into events without acclimating to heat or altitude, who go faster than they train, and who fail to prepare for the types of terrain they will be competing on. Nothing can protect you from being underprepared for an event, not even the powerful miscalculation of our own limitations.
  • Work on form, mobility, and range of motion. Muscles most affected by EMAC are those that are confined to a small arc of motion, in a shortened state, and used repetitively. For runners, avoid heavy braking and focus on manipulating your stride length (in training for race day) so that you can maintain adequate hip and knee flexion and extension. For cyclists, make sure you’re seat position is high enough to allow for greater range of motion.
  • Fuel adequately. Glycogen depletion and inadequate fueling can lead to premature muscle fatigue and increase your risk of cramping.
  • Learn to recognize your body’s pre-cramping state and respond accordingly. Slowing down or stopping to stretch cramp-prone muscles could save you from that DNF, or from crawling into the next aid station.
  • Be reflective. Evaluate the training or race-day scenarios that may have brought you to your knees. What factors may have combined to lead to the over-fatigued state? For me personally it’s been a journey of rejiggering my biomechanics and imbalances.

By Corrine Malcolm, CTS Coach

Originally Published:

The science behind Pickle Juice: Reflex Inhibition of Electrically Induced Muscle Cramps in Hypohydrated Humans

For our science buffs!

Source: Medicine & Science in Sports & Exercise: May 2010 – Volume 42 – Issue 5 – p 953-961
doi: 10.1249/MSS.0b013e3181c0647e
Author information: Department of Health, Nutrition, and Exercise Sciences, North Dakota State University, Fargo, ND; Department of Exercise Sciences, Brigham Young University, Provo, UT; and Department of Statistics, Brigham Young University, Provo, UT Address for correspondence: Kevin C. Miller, Ph.D., ATC, CSCS, North Dakota State University, Health, Nutrition, and Exercise Sciences, NDSU Dept #2620, PO Box 6050, Fargo, ND 58108-6050; E-mail:

Skeletal muscle cramps that occur during or shortly after exercise have been termed exercise-associated muscle cramps (EAMC). These muscle cramps are highly prevalent in athletic populations (3,8,36) and the physically active (25). In fact, 73% (102/139) of heat-related injuries experienced in American football were EAMC (8). In triathletes, 67% (1631/2438) complained of EAMC under a variety of training conditions (14). Despite their prevalence, the etiology of EAMC is unclear.

Traditionally, EAMC have been associated with fluid and electrolyte disturbances (6,32,35). Proponents of this theory hypothesize that the loss of fluids and electrolytes owing to exercise-induced sweating causes a contracture of the interstitial space, which results in mechanical deformation of nerve endings and leads to cramp genesis (4,16). This theory is based on the observation that athletes who develop EAMC often have significant fluid and electrolyte losses at the time of cramp (3,32). However, losses in plasma and blood volume, electrolytes, and body weight are often similar in individuals who develop EAMC as in noncramping individuals (18,30). In addition, EAMC can be relieved by moderate static stretching of the cramping muscles (17,30,35) or activation of Golgi tendon organs (15). Neither of these treatment strategies has any impact on fluid or electrolyte balance, yet both adequately relieve a skeletal muscle cramp.

The unclear etiology and conflicting results of observational studies regarding EAMC have resulted in several anecdotal treatments, many with little or no scientific credibility. One such treatment is the ingestion of small volumes (30-60 mL) of pickle juice, a highly salty and acidic brine. This treatment is claimed to relieve an EAMC within 35 s (38). Several athletic trainers (25%, 92/370) seem to be treating athletes who develop EAMC with pickle juice (22) despite the lack of scientific evidence of its efficacy and the warnings against its ingestion (10). Many of these health professionals attribute pickle juice’s efficacy to the high sodium (Na+) and electrolyte content (22).

We examined whether pickle juice could relieve an electrically induced muscle cramp in mildly hypohydrated humans by inducing skeletal muscle cramps with low-frequency percutaneous electrical stimulation. The ability to initiate a cramp via low-frequency activation of the alpha motor neuron (5,34) supports the hypothesis that the muscle cramp is generated peripherally, either at the level of the alpha motor neuron or motor end plate (24). This cramp induction model effectively induces skeletal muscle cramps and is generally well tolerated and reliable and has a close correlation with the occurrence of EAMC (21,33).

If pickle juice relieves an electrically induced muscle cramp, we questioned how quickly it relieved the muscle cramp and if the cessation of the cramp was associated with a change in plasma electrolyte concentration or other plasma constituents. We hypothesized that pickle juice would alleviate an electrically induced muscle cramp but that this effect would not occur within 35 s of ingestion. In addition, we did not expect any appreciable changes in plasma constituents within 5 min after ingestion.



Twelve healthy, unacclimated college-aged males volunteered for this study. Two volunteers were excluded from participating because we could not induce a cramp on the first day of testing. Therefore, 10 subjects (mean ± SE, age = 23.5 ± 1.0 yr, height = 177.8 ± 1.8 cm, mass = 73.9 ± 2.8 kg) completed the study. Volunteers were excluded from participating if they 1) had experienced any lower extremity injury or surgery within the last 6 months or 2) self-reported any neurological, cardiovascular, or blood-borne diseases. All subjects had experienced EAMC within 6 months of experimentation. All procedures were approved by our university’s institutional review board, and subjects provided written informed consent. To protect against a placebo effect, subjects were not informed what they would be drinking or the beverage’s purported effects on muscle cramps.

Testing procedures.

Subjects reported for a familiarization session and two experimental trials. No data were collected on the familiarization session. This session was used to screen potential subjects to ensure that an electrically induced cramp could be induced in the flexor hallucis brevis (FHB) and that subjects could tolerate the electrical stimuli. The familiarization session occurred 24 h before the first experimental trial for all subjects.

On the familiarization day, subjects were taught how to perform a maximum voluntary isometric contraction (MVIC) with their dominant leg’s FHB by performing 15 practice MVIC. Each 2-s MVIC was separated by 1 min of rest. After the last practice MVIC, subjects rested for 15 min, and we attempted to induce a cramp in the FHB via low-frequency percutaneous electrical stimulation of the tibial nerve. If successful (see criteria in the next paragraph), EMG and stimulating electrode placements were marked for replication, and subjects were invited back the following day for the first experimental trial. Subjects were instructed to fast for 12 h before the experimental trials, to drink water consistently throughout the evening and morning before these trials, and to avoid exercising for 24 h before testing.

On the first experimental trial day, subjects reported to the laboratory and were weighed, and a venous catheter was inserted into a superficial vein in the forearm. Subjects ingested 5 mL of tap water per kilogram body weight within 5 min to help ensure hydration and lay supine for 30 min during which they were prepared for several measurements. A portion of the right midforearm was shaved in preparation for sweat patch placement. Subjects’ legs were then prepared for EMG analysis using standard preparatory procedures (34). After this equilibration period, subjects voided their bladders completely, and their urine was collected (first urine collection). Subjects were weighed and then lay supine for an additional 30 min after which they practiced performing 15, 2-s MVIC with 1 min of rest separating each contraction. After the last practice MVIC, subjects rested for 5 min and then performed three consecutive 2-s MVIC. The mean EMG activity (V) of these MVIC was recorded and averaged for statistical analysis. After 15 min of rest, subjects voided their bladders (second urine collection) and were weighed.

An HR monitor was placed on the chest (Polar Electro, Inc., Lake Success, NY). The right forearm was washed with distilled water and dried. A sterile sweat patch was placed on the forearm. Subjects then began a 30-min bout of one-leg (nondominant), semirecumbent cycle ergometer exercise at 41°C and 15% relative humidity. Subjects exercised at a moderate intensity that generated an HR between 145 and 150 bpm. After 30 min of exercise, subjects were towel-dried, weighed, and rested for 5 min. This cycle of 30-min exercise/5 min rest continued until subjects lost ∼3% of their body mass (2.1 ± 0.1 h). None of our subjects experienced EAMC as a result of the exercise protocol.

When subjects became sufficiently hypohydrated, they exited the heat chamber, voided their bladders (third urine collection), and lay supine on a treatment table for 30 min to allow body fluid compartment equilibration. Subjects’ MVIC EMG activity was reassessed. A cramp in the FHB was induced, and cramp duration and FHB EMG activity were recorded. No fluids were ingested during this cramp. Subjects were instructed to remain relaxed for the duration of the cramp and to let the cramp proceed for as long as possible. On cramp cessation, subjects voided their bladders (fourth urine collection).

Subjects lay supine for 30 min after cramp induction after which we collected a 5-mL blood sample (baseline). Subjects then sat up slightly to facilitate fluid ingestion. The primary investigator and subject donned nose plugs to prevent discovery of the drink composition. Subjects were instructed to allow the upcoming cramp to persist as long as possible, not make any sounds, gestures, or facial expressions after fluid ingestion, which may have notified the primary investigator of the contents of the water bottle, and to wait until signaled to ingest the treatment fluid. A cramp was then induced at the same frequency and parameters that had been used to induce the first cramp (e.g., stimulation frequency, intensity). The primary investigator verified cramping (2 s after cramp induction) and then signaled to the subjects to ingest 1 mL·kg−1 body weight of either pickle juice or deionized water. They drank the fluid as quickly as possible (3-5 s). At 1 and 5 min after ingestion, 5-mL blood samples were collected. After collection of the last blood sample, subjects voided their bladders (fifth urine collection) and were excused. Each subject completed two identical experimental trials separated by at least 1 wk. The two trials differed only by the composition of the fluid ingested during the electrically induced muscle cramp: pickle juice or deionized water. No other fluids were ingested at any other point by the subjects during experimentation.

Subjects were instructed to not drastically alter their diet and activity level the week in between experimental trials and to remark the locations of the EMG and stimulating electrodes if they noticed the marks were fading during the course of the week. Compliance of these instructions was assessed via a diet/exercise log on the final day of testing.

We collected the pickle juice by straining it from commercially available sliced dill pickles (Vlasic Pickles, Pinnacle Foods Corp., Cherry Hill, NJ). Both treatment fluids were kept in sealed, unmarked, opaque containers and chilled in a refrigerator at 3°C until needed. A research assistant prepared each drink after the first body weight measurement, so both the subject and primary investigator were blinded to its contents. Drink order was randomized and counterbalanced.

Muscle cramp induction and determination criteria.

Skeletal muscle cramps induced with this low-frequency, percutaneous electrical stimulation model have both high intrasession (intraclass correlation coefficients (ICC) [3,1] > 0.844) (34) and intersession reliability (ICC [3,1] > 0.963) (20,34). Scientists have used this model to investigate the effects of various interventions (31,40) as well as their correlation with EAMC (21,33).

Subjects lay supine with their dominant ankle hanging off a table and were instructed to relax for the duration of testing. Standard EMG preparatory procedures (34) were performed at the medial plantar aspect of the foot, at the area around the medial malleolus, and at the ipsilateral tibial tuberosity. An 8-mm Ag-AgCl stimulating electrode was placed slightly inferior to the medial malleolus. The tibial nerve was submaximally stimulated two to four times with 1-ms electrical stimuli at 80 V to determine the site around the medial malleolus that caused the greatest hallux flexion. An 8-cm square dispersive electrode was placed over the lateral malleolus. Electrodes were secured with medical tape and an elastic wrap at these locations. Two EMG measurement electrodes were placed 2 cm apart over the midbelly of the FHB with a single-ground measurement electrode over the ipsilateral tibial tuberosity.

The compound muscle action potentials of the FHB were sampled at 2000 Hz and filtered (band-pass low-frequency = 10 Hz and high-frequency = 500 Hz) using the MP150 analog-to-digital system and operated by AcqKnowledge v3.7.3 software (Biopac Systems, Santa Barbara, CA). Disposable long-term recording electrodes (EL502-10; Biopac) were used to collect EMG data. The total EMG recording consisted of baseline (1 s), stimulation (2 s), and poststimulus activity (5 min).

A Grass S88 stimulator with SIU5 Stimulus Isolation Unit (Astro-Med, Inc., West Warwick, RI) with an 8-mm Ag-AgCl shielded active electrode (EL258S; Biopac) and an 8-cm square dispersive electrode was used to deliver the train of electrical stimuli to the tibial nerve. Stimulus intensity and duration were set at 80 V and 2 s, respectively, because this intensity and duration have been shown to induce muscle cramps in healthy subjects (20). Subjects received two consecutive trains of electrical stimuli (one train per second; no rest intervals between trains) beginning at a train frequency of 4 Hz (eight total stimuli on the first trial). If a cramp did not occur at 4 Hz, subjects rested for 1 min, and train frequency was increased by 2 Hz. This process continued until the FHB cramped.

A muscle cramp was defined as an involuntary painful contraction of the FHB immediately after stimulation and was verified by involuntary sustained great toe flexion, subject verification that a cramp had occurred, and an average EMG root mean square amplitude >2 SD above the 1-s baseline EMG average root mean square amplitude (34). Also, induced cramps must have lasted ≥90 s, and cramp intensity must have been approximately 50% of MVIC EMG activity. The stimulation frequency required to induce cramps with the previously mentioned criteria was termed the minimal treatment frequency (MFtrt). This is not to be confused with “cramp threshold frequency” that has been reported in previous studies and is defined as the minimal electrical stimulation frequency (Hz) required to elicit mild and short-lasting (i.e., <10 s) cramps (20,21,34).

The FHB EMG activity during each cramp was recorded until it seemed to return to resting activity. The filtered and rectified EMG measurements were saved and placed into an algorithm that calculated cramp duration. Cramps were considered alleviated when the cramp EMG activity was <2 SD above baseline EMG activity. Cramp intensity (%) was calculated by dividing the 2 s of cramp EMG activity immediately after the end of the electrical stimuli by MVIC EMG activity and multiplying by 100.

MVIC EMG activity determination.

The dominant legs’ big toe was placed in a toe harness that was attached to a strain gauge rated for loads <11 kg and calibrated with a 4-kg weight. Four-centimeter nylon straps were tightened over the subject’s midthigh and shin to prevent movement of the hip and knee. The subject’s dominant ankle was placed in a foam block with a foot pad at 120° to keep the ankle in slight plantarflexion and to prevent the ankle from extreme inversion and eversion (Fig. 1). The subjects were instructed to keep the plantar aspect of their foot against this foam block when performing their MVIC. The compound muscle action potentials of the FHB during MVIC were sampled using similar parameters as described above for FHB cramps.FIGURE 1

Gastrocnemius muscle activity was monitored with a biofeedback unit (Pathway TR-10C; Prometheus Group, Dover, NH) to ensure that the subjects were not producing force by using the incorrect muscles. Gastrocnemius EMG activity exceeding 8 mV constituted a failed MVIC attempt. If subjects performed an MVIC incorrectly, they rested for 1 min and then reattempted the contraction. These settings have been used successfully in previous experiments (unpublished observations).

Blood analysis procedures.

Five-milliliter blood samples were collected before and at 1 and 5 min after ingestion of each fluid. One milliliter of blood from each sample was used to analyze hematocrit (Hct) and hemoglobin (Hb; 0.5 mL for each); the 4 mL of blood remaining was sealed and stored in a 6.0-mL lithium heparin vacutainer (BD, Franklin Lakes, NJ) and placed into an ice bath until the last blood sample was collected.

Blood for Hct analysis was drawn into heparinized microcapillary tubes and centrifuged at 3000 rpm (IEC Micro-MB; International Equipment, Co., Needham Heights, MA) for 5 min and read using a microcapillary reader (Model IEC 2201; Damon/IEC, Needham Heights, MA). Hemoglobin concentration ([Hb]) was measured by mixing 20 µL of whole blood with 5 mL of cyanomethemoglobin reagent, and the absorbance was read at 540 nm on a standard spectrophotometer (Smartspec 3000; Bio-Rad, Hercules, CA). Hct and [Hb] were measured in triplicate immediately after sampling and averaged for each blood sample for statistical analysis and calculations. Hct and [Hb] measurements were used to calculate changes in plasma volume (PV) per the Dill and Costill equation (11).

The remaining 4 mL of blood was centrifuged at 3000 rpm for 15 min at 3°C (Eppendorf Centrifuge 5403; Eppendorf North America, Inc., New York, NY). Plasma was removed from the packed red blood cells, and plasma sodium concentration ([Na+]p), plasma potassium concentration ([K+]p), plasma magnesium concentration ([Mg2+]p), and plasma calcium concentration ([Ca2+]p) were analyzed using an ion-selective electrode system (NOVA 8 electrolyte analyzer; Nova Biomedical, Waltham, MA). Plasma osmolality (OSMp) was determined using freezing point depression osmometry (Model 3D3 Osmometer; Advanced Instruments, Inc., Norwood, MA). Plasma electrolyte concentrations and OSMp were measured in duplicate and averaged for statistical analyses. An OSMp of ≥290 mOsm·kg−1 H2O was used to indicate hypohydration (28).

Sweat analysis procedures.

Sweat patches were collected after 45 min of exercise. Sweat was separated from the sterile patches via centrifugation and analyzed in duplicate with an ion-selective electrode analyzer for sweat sodium concentration (Sw[Na]), sweat potassium concentration (Sw[K]), sweat magnesium concentration (Sw[Mg]), and sweat calcium concentration (Sw[Ca]). Whole-body sweat rate (L·h−1) was calculated by subtracting postexercise body weight from preexercise body weight and dividing by total exercise duration (1 kg of body mass lost represented 1 L of fluid lost). Total sweat electrolytes lost (mmol) were estimated by multiplying electrolyte concentration (mmol·L−1) by total sweat volume (L).

Urine analysis procedures.

Urine volume was measured using appropriately sized graduated cylinders. Urine sodium concentration (U[Na]), urine potassium concentration (U[K]), urine magnesium concentration (U[Mg]), and urine calcium concentration (U[Ca]) were measured in duplicate using an ion-selective electrode system. Urine electrolyte content (mmol) was calculated by multiplying urine volume (L) at each sampling point by electrolyte concentration (mmol·L−1). Total urinary electrolytes lost were determined by adding the electrolytes lost at each time point.

Fluid analysis procedures.

Pickle juice and deionized water were analyzed for [Na+], [K+], [Mg2+], [Ca2+], pH, and osmolality in duplicate and averaged for statistical analysis. Electrolytes were analyzed using an ion-selective electrode analyzer. Fluid pH was measured with a pH meter (AR15; Fisher Scientific, Pittsburgh, PA). Osmolality was measured by freezing point depression osmometry.

Statistical analysis procedures.

Data are presented as means ± SE. To determine the effects of pickle juice and deionized water ingestion on cramp duration, we used an ANCOVA with MFtrt and cramp intensity as covariates. Because the covariates were insignificant, we removed the covariates from the analysis and used a 2 × 2 repeated-measures ANOVA. The cramp duration after the dehydration protocol (i.e., no fluid ingested) was compared with the cramp duration after ingestion of each drink using repeated-measures ANOVA. Similarly, the intensity of the cramps induced when subjects ingested each fluid and the MFtrt was compared with a repeated-measures ANOVA.

Mean plasma, sweat, and urine electrolyte concentrations and contents, osmolality, and volume were analyzed with a 2 × 3 repeated-measures ANOVA (fluid and time) to assess differences between fluids over time for these variables. Because the fluid × time interaction was insignificant for all variables but several time effects were significant, we reexamined each fluid trial separately using a one-way ANOVA for repeated measures on time and used the Tukey-Kramer post hoc multiple-comparison test to identify which time points were different from baseline. All statistical analyses were performed with Number Cruncher Statistical Software (NCSS 2007, Kaysville, UT). Significance was set at P ≤ 0.05.


Effects of deionized water and pickle juice ingestion on electrically induced muscle cramps.

Subjects self-reported compliance with testing instructions before each experimental day. Cramp duration, intensity, and MFtrt data before and after fluid ingestion can be found in Table 1. Cramp duration (F1,9 = 0, P = 0.95), cramp intensity (F1,9 = 0.85, P = 0.4), and MFtrt (F1,9 = 1.2, P = 0.3) were similar during the initial cramp induction before each fluid’s ingestion. During muscle cramp induction combined with fluid ingestion, cramp intensity was again similar between fluids (F1,9 = 3.1, P = 0.11). Also, compared with before ingestion, cramp intensity was not different after ingestion of pickle juice (F1,9 = 0.1, P = 0.79) and deionized water (F1,9 = 0, P = 0.96).TABLE 1

Cramp duration was 49.1 ± 14.6 s shorter after pickle juice ingestion than after deionized water ingestion (F1,9 = 11.3, P = 0.008). Moreover, cramp duration after ingestion of pickle juice was 68.6 ± 23.2 s shorter than before ingestion (F1,9 = 8.7, P = 0.02). In contrast, ingesting deionized water did not significantly affect cramp duration compared with before ingestion (F1,9 = 4.1, P = 0.1).

Fluid composition.

Subjects ingested 73.9 ± 2.7 mL of pickle juice and 73.9 ± 2.8 mL of deionized water. Pickle juice contained a higher [Na+], [K+], [Mg2+], and [Ca2+], had a higher osmolality, and had a lower pH than deionized water (F1,1 > 615.9, P < 0.02; Table 2). Total electrolyte content ingested was 72.4 ± 2.6 mmol of Na+, 0.5 ± 0.02 mmol of K+, 0.9 ± 0.03 mmol of Mg2+, and 1.7 ± 0.06 mmol of Ca2+ with pickle juice and 0 mmol of Na+, K+, Mg2+, and Ca2+ with deionized water.TABLE 2

Blood analysis.

Plasma osmolality did not differ between pickle juice and deionized water over time (F2,18 = 0.2, P = 0.82; Table 3). However, OSMp increased slightly over time; OSMp increased to 296.4 ± 1.2 mOsm·kg−1 H2O 1 min after pickle juice ingestion (P < 0.05) but quickly returned to baseline levels after 5 min (296.2 ± 1.4 mOsm·kg−1 H2O, P > 0.05). Similar changes occurred after deionized water ingestion, although OSMp remained elevated at 5 min after ingestion (P < 0.05). The increase in OSMp after ingestion of each fluid is likely due to a shift of hypotonic fluid out of the intravascular space rather than to an increase in osmoles because of fluid ingestion. This hypothesis was confirmed by the small, but significant, decreases in PV after ingestion over time (F2,18 = 13.15, P < 0.001). However, no differences in PV occurred between pickle juice and deionized water over time (F2,18 = 0.14, P > 0.05), and PV returned to baseline 5 min after ingestion of each fluid (P > 0.05; Table 3).TABLE 3

Despite pickle juice having a significantly higher electrolyte content than deionized water, there were no significant differences between fluids after ingestion for [Na+]p (F2,18 = 1.26, P = 0.31), [K+]p (F2,18 = 0.14, P = 0.87), [Mg2+]p (F2,18 = 0.39, P = 0.68), or [Ca2+]p (F2,18 = 0.06, P = 0.94; Table 3). However, deionized water ingestion resulted in a small increase in [Na+]p at 1 min after ingestion (P < 0.05), which returned to baseline after 5 min (P > 0.05). This increase in [Na+]p is also likely due to the decrease in PV rather than to an increase in Na+ content in the intravascular space. Contrastingly, [K+]p decreased over time (F1,9 = 15.09, P < 0.001) and was significantly lower at 5 min after ingestion for both pickle juice and deionized water (P < 0.05) but was not outside normal clinical values. No changes in [Mg2+]p or [Ca2+]p occurred between drinks (F1,9 < 1.11, P > 0.32) or up to 5 min after ingestion of pickle juice or deionized water (F2,18 < 1.98, P > 0.17).

Exercise-induced hypohydration.

Subjects lost similar amounts of body weight (F1,9 = 0.38, P = 0.55) and were similarly hypohydrated on each experimental day (F1,9 = 0.09, P = 0.78). Thus, data were combined (n = 10). Subjects lost 3.04% ± 0.1% body weight via exercise-induced sweating, which resulted in significant hypohydration after exercise (OSMp = 295.1 ± 1.1 mOsm·kg−1 H2O).

Sweat volume and electrolyte losses.

Subjects lost similar amounts of sweat (F1,9 = 0.1, P = 0.76) and had similar Sw[Na] (F1,9 = 0, P = 0.96), Sw[K] (F1,9 = 0.1, P = 0.75), Sw[Mg] (F1,9 = 0.07, P = 0.79), and Sw[Ca] (F1,9 = 0, P = 0.99) on each experimental day. Therefore, sweat data were combined (n = 10). Subjects had an Sw[Na] of 65.9 ± 4.2 mmol·L−1, Sw[K] of 5.1 ± 0.2 mmol·L−1, Sw[Mg] of 1.5 ± 0.1 mmol·L−1, and Sw[Ca] of 1.4 ± 0.1 mmol·L−1. Subjects lost a total of 2.2 ± 0.1 L of sweat, 144.9 ± 9.8 mmol of Na+, 11.2 ± 0.4 mmol of K+, 3.3 ± 0.3 mmol of Mg2+, and 3.1 ± 0.1 mmol of Ca2+ as a result of the exercise protocol. The high Sw[Na] indicated that our subjects were unacclimated to exercising in a hot environment (1,7).

Urine volume and electrolyte losses.

Because the first and second urine samples were collected before exercise while the subjects were euhydrated, the data from these samples were combined and represent the preexercise condition. Urine sample 3 was collected immediately after the last bout of exercise and therefore represents the urine produced during exercise. Urine samples 4 and 5 were collected 90 and 120 min after exercise. Because these samples were representative of subjects in a hypohydrated state, they were combined for analysis and represent urine produced after exercise.

Subjects had similar urine volumes (F1,9 = 0.7, P = 0.43), urine flow rates (U˙, F1,9 = 0.7, P = 0.43), U[Na] (F1,9 = 3.2, P = 0.11), U[K] (F1,9 = 0.05, P = 0.84), U[Mg] (F1,9 = 0.55, P = 0.48), and U[Ca] (F1,9 = 0.47, P = 0.51) on each experimental day over time. There were also no differences between drinks (F1,9 < 3.22, P > 0.11); thus, the urine data were combined (Table 4). However, Uvol, U˙, U[Na], U[K], and U[Mg] changed over time (F2,18 >10.6, P < 0.001). Urine volume and U˙ were lower after exercise and after ingestion than before exercise (P < 0.05). Urine [Na] was higher after ingestion than during and before exercise (P < 0.05). Urine [K] increased after exercise as well as after ingestion (P < 0.05). Urine [Mg] was only elevated after ingestion compared with baseline (P < 0.05), and no changes in U[Ca] occurred during the experiment (F2,18 = 2.3, P = 0.12). Overall, subjects lost a total of 1.0 ± 0.1 L of urine, 45.1 ± 3.7 mmol of Na+, 23.7 ± 1.4 mmol of K+, 0.35 ± 0.1 mmol of Mg2+, and 0.47 ± 0.1 mmol of Ca2+ via urination.TABLE 4

Total fluid and electrolyte losses.

Overall, subjects lost a total fluid volume of 3.2 ± 0.2 L, 190.0 ± 8.1 mmol of Na+, 34.9 ± 1.6 mmol of K+, 3.7 ± 0.3 mmol of Mg2+, and 3.6 ± 0.1 mmol of Ca2+ on each experimental day.


The most significant and novel observation of this study was that ingesting small volumes (73.9 ± 2.7 mL) of pickle juice alleviated electrically induced muscle cramps in mildly hypohydrated (3%) humans. Pickle juice required approximately 85 s to alleviate muscle cramps (cramp duration after ingestion ranged from 12 to 219 s). Although this was much longer than the purported claims of pickle juice’s efficacy (38), it still relieved a cramp 45% (85 vs 153 s) faster than when no fluid was consumed. In contrast, ingesting similar volumes of deionized water had no therapeutic effect on cramp duration (cramp duration after ingestion ranged from 71 to 246 s). Discrepancies between anecdotal claims of pickle juice’s efficacy and our data may be because of the type of cramp alleviated (EAMC vs electrically induced muscle cramps) or errors by these clinicians (38) in their estimation of cramp duration.

The rapidity with which pickle juice relieves electrically induced muscle cramps likely cannot be attributed to spontaneous cramp cessation, weakness of the induced muscle cramps, a placebo effect, or a lack of fluid and electrolyte losses because of our experimental protocol. Cramps induced 30 min before pickle juice ingestion lasted almost twice as long (150 s) as when subjects ingested pickle juice, making it unlikely that the cramps dissipated spontaneously. Moreover, subjects experienced moderately intense cramps on ingestion of pickle juice (66% of MVIC EMG activity) and deionized water (55% of MVIC EMG activity). Although a substantial placebo effect can exist when studying skeletal muscle cramp treatments (24), both the primary investigator and subjects were blinded as much as possible to the fluid being ingested. Subjects had their noses plugged while ingesting the fluids and were not told what they were going to drink or any potential effects of the fluid on the electrically induced muscle cramps. However, subjects were likely able to identify one fluid as pickle juice on tasting it. Regardless, it is unlikely that pickle juice’s efficacy can be attributed to a psychological phenomenon. Finally, our subjects lost significant amounts of Na+, K+, Mg2+, and Ca2+ as a result of the experimental protocol. In fact, our subjects lost similar amounts of fluid and electrolytes as athletes who develop EAMC during athletic competitions (32). Therefore, a lack of electrolyte or body mass losses because of our experimental protocol is an unlikely explanation for the pickle juice’s effects on electrically induced muscle cramps.

It is also unlikely that pickle juice’s effects on muscle cramp duration are due to the changes in plasma electrolytes or body fluid chemistry, as believed by 64% (226/353) of athletic trainers who provide pickle juice to their cramping athletes (22). Three reasons refute this hypothesis. First, the amount of electrolytes ingested with 1 mL·kg−1 body weight of pickle juice has a negligible effect on extracellular fluid electrolyte concentrations (<1.5 mmol·L−1) (23). Previous work in our laboratory has demonstrated that no changes in [Na+]p, [K+]p, [Mg2+]p, [Ca2+]p, PV, or OSMp occur after ingestion of 1 mL·kg−1 body weight of pickle juice or water in euhydrated rested humans (23). The results of the present study not only confirm these observations but also extend them to include hypohydrated individuals. Second, 85 s is not enough time for the nutrients in pickle juice to be emptied from the stomach, absorbed by the small intestines, and assimilated into the extracellular fluid compartment. Small volumes of pickle juice (150 mL) require approximately 30 min to leave the stomach in rested euhydrated humans (unpublished observations). The slow gastric emptying is likely due to the high osmolality, low pH, and small volume of the pickle juice ingested. Moreover, hypohydration would, theoretically, further impair gastric emptying (27), making it even more unlikely that the electrolytes in pickle juice were absorbed quickly enough to cause cessation of the electrically induced muscle cramp. Third, even if all the electrolytes present in pickle juice were immediately absorbed and circulated to the cramping muscle, subjects would still have substantial electrolyte and fluid losses. On the basis of the volume of pickle juice ingested, its electrolyte content, and the volume and electrolytes lost during experimentation, pickle juice would only restore 2% (0.074/3.2 L) of fluid, 38% (72.4/190.0 mmol) of Na+, 1% (0.5/34.9 mmol) of K+, 24% (0.9/3.7 mmol) of Mg2+, and 47% (1.7/3.6 mmol) of Ca2+.

Considering these points, we speculate that pickle juice ingestion triggers a reflex, likely somewhere in the oropharyngeal region, which acts to reduce alpha motor neuron pool activity in cramping muscles. Oropharyngeal stimulation is known to elicit simple and complex reflexes that involve the modulation of alpha motor output in the cephalic region (e.g., glossopharyngeal-hypoglossal reflex), upper gastrointestinal tract, and airway (2,19). Chemical stimulation by acetic acid (a primary ingredient in pickle juice) is effective at eliciting these oropharyngeal reflexes (13). Because acetic acid has been shown to elicit reflexive motor responses in the oropharyngeal region, it may not be outside the realm of possibility that its ingestion triggers an inhibitory motor reflex to skeletal muscles undergoing cramp.

We propose two scenarios by which pickle juice ingestion may cause inhibition of a cramping muscle’s alpha motor neuron pool. First, pickle juice may trigger an inhibitory stimulus from a supraspinal source that activates inhibitory interneurons. Activation of these interneurons may postsynaptically inhibit the alpha motor neuron pool of the cramping muscle. In rats, intraperitoneal injection of acetic acid increases the release of inhibitory neurotransmitters (e.g., serine and glycine) in the dorsal horn of the spinal cord (12). Glycine is a specially potent inhibitory neurotransmitter in the spinal cord that may increase inhibitory interneuron activity (e.g., Renshaw cells) or decrease ventral horn neuron activity (9) because these neurons have a high affinity for glycine (37). Suppression of inhibitory neurotransmitters has been implicated as a possible mechanism for cramp genesis (26). Thus, an increase in inhibitory neurotransmitter activity, triggered by pickle juice ingestion, could be involved in the alleviation of electrically induced muscle cramps.

Second, this inhibitory supraspinal signal may override stimuli of an excitatory nature coming from a small group of muscle afferent fibers that were activated by the percutaneous electrical stimulation, muscle contraction/cramp, or both. Although the cramp induction model we used is generally well tolerated (20,34), some pain and, thus, small-diameter muscle afferent (e.g., Types III and IV) stimulation undoubtedly occurred. Activation of these small group muscle afferents can affect cramp generation or sustainability (31). Serrao et al. (31) observed that injection of hypertonic saline into the FHB-induced muscle pain and facilitated the generation of muscle cramp. They concluded that enhanced activation of these small-diameter muscle afferents resulted in an increased susceptibility to cramp. Because we did not apply a proximal nerve block to the tibial nerve, we cannot rule out the possibility that small-diameter muscle afferent activation occurred and helped maintain the cramp.

Regardless of where the inhibition is occurring, pickle juice’s apparent reduction of alpha motor neuron activity is consistent with current thought on the etiology of EAMC. Schwellnus et al. (29) proposed that EAMC were due to neuromuscular fatigue. Neuromuscular fatigue is thought to create an imbalance between muscle spindle and Golgi tendon organ activity, resulting in increased alpha motor neuron excitability. Thus, if EAMC are caused by an imbalance between excitatory and inhibitory stimuli at the alpha motor neuron pool, pickle juice ingestion may cause an increase in inhibition from supraspinal sources, thereby resulting in cramp alleviation.

It is unknown which ingredient in pickle juice may initiate this inhibitory reflex. We propose that it is the acetic acid (vinegar) in pickle juice, not the electrolyte content, which triggers this reflex. Acetic acid has been shown to cause motor reflexes in the muscles of the larynx and pharynx (13). Moreover, there is anecdotal support for acetic acid ingestion also relieving EAMC. Williams and Conway (39) observed in one subject that when vinegar was ingested instead of pickle juice, less vinegar was required to alleviate the EAMC and the EAMC was alleviated faster. Therefore, anecdotally, acetic acid seems capable of alleviating EAMC irrespective of the Na+ content of the drink. These claims remain to be verified scientifically, however, and must be used cautiously because they only occurred in one subject.

In conclusion, pickle juice, and not deionized water, significantly shortens electrically induced muscle cramp duration in mildly hypohydrated humans. How pickle juice decreases cramp duration is unknown; however, we hypothesize that it triggers an inhibitory oropharyngeal reflex shortly after ingestion, which reduces alpha motor neuron activity to cramping muscles. The decrease in cramp duration after pickle juice ingestion is likely not due to the changes in body fluid chemistry, a placebo effect, spontaneous cessation, or a lack of fluid and electrolyte loss because of experimentation. The ingredient in pickle juice that elicits the decrease in cramp duration is also unknown, although acetic acid could play a role in triggering an oropharyngeal reflex.

The results of the present study do not constitute endorsement by the American College of Sports Medicine.

The authors thank Samantha R. Miller for help with data collection and Brigham Young University Graduate Studies for partially funding this research.

Submitted for publication July 2009.

Accepted for publication September 2009.

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