Muscle Cramps

Fig. 6.1

Altered neuromuscular control theory for the pathogenesis of exercise-associated muscle cramps (dashed arrow used for the sole purpose of improving clarity of the “hot and/or humid environmental conditions” pathway). (Adapted from Schwellnus [10], with permission)


Fig. 6.2

Positive feedback loop demonstrating risk factors which may precipitate maintenance or increased susceptibility to future exercise associated muscle cramping

Support for the Altered Neuromuscular Control Theory

At its core, the altered neuromuscular control theory emphasizes the influence of risk factors on muscle afferents (e.g., muscle spindles and Golgi tendon organs) and neuromuscular control. Several observations from the literature indicate muscle afferents are essential for normal neuromuscular control and may contribute to EAMC development:

  1. 1.

    EAMC most commonly affect muscles that span two joints. The most common muscles to develop EAMC in distance runners were the hamstrings (48%), quadriceps (38%), and calves (14%) [24]. When muscles contract in shortened positions, the alpha motor neuron pool receives less inhibition from Golgi tendon organs [39].


  2. 2.

    Cramps can be alleviated by electrically stimulating Golgi tendon organs [40].


  3. 3.

    Electromyograms from cramping muscles and voluntary contractions demonstrate similar timing and amounts of inhibition. This suggests similar spinal pathways are utilized during normal muscle contractions and cramping [40].


  4. 4.

    Non-crampers produced significantly stronger amounts of inhibition than individuals who developed cramps [40].


  5. 5.

    Cramp duration was shorter, and cramp intensity was less severe when authors induced muscle cramps following a peripheral nerve block [41]. This suggests spinal involvement was necessary for cramp induction and maintenance.


  6. 6.

    Elevations in muscle temperature affect muscle afferent activity, especially muscle spindles [42]. In animal models, muscle spindle discharge frequency was 2–4 times higher when a warm muscle (35 °C) changed length than a cold muscle (25 °C) [43, 44]. By extension, alpha motor neuron excitability would also increase as muscle temperature increased. Since body core temperature and muscle temperatures increase faster under uncompensable conditions, this may explain why EAMC occur more frequently under hot and humid conditions [3].


  7. 7.

    The altered neuromuscular control theory better explains how static stretching relieves EAMC (see Treatment of EAMC section). Since muscle afferents contribute to the pathophysiology of EAMC, it is necessary to discuss the primary risk factors that affect muscle afferent activity and neuromuscular control.


Fatigue may affect neuromuscular control and play a role in the pathophysiology of EAMC. EAMC tend to occur near the end of competitions or exercise sessions when fatigue is the highest. In distance runners, EAMC did not occur until after 24–28 km (14.9–17.4 miles) [8, 24]. Maughan [8] noted 33% of the marathon runners with EAMC developed them in the last 1.5 km (0.9 mile) of the race. EAMC also tend to occur when athletes exercise at intensities higher than anticipated, when exercise intensity is increased, and when specific muscles are targeted [25, 33, 44]. Altering exercise in these ways would tend to induce fatigue faster. In fact, Jung et al. [33] induced EAMC in as little as 15 minutes when a calf-fatiguing protocol was used.

These observations are also consistent with the neurophysiology literature on muscle cramping. Electrically induced fatigue increased resting muscle spindle discharge frequency and firing rate [45] while also decreasing Golgi tendon organ activity [46]. Moreover, the following factors may also influence the onset of fatigue: having a preponderance of less fatigue-resistant muscle fibers (e.g., type II fibers), dehydration, lack of or diminished quality of sleep, exhausted muscle energy stores, age, and lack of conditioning [1, 2, 47]. Consequently, athletes who fail to prepare themselves against the onset of fatigue from any of these sources may be increasing their susceptibility to EAMC via fatigue-induced changes in the neuromuscular system.

Pain and/or psychological stress may also be risk factors for EAMC by influencing neuromuscular control [48, 49]. In three different cohort studies examining risk factors for EAMC, muscle injury, pre-race muscle damage, and pain were predisposing factors to EAMC [5052]. In one study, pre-race creatine kinase (i.e., an indicator of muscle damage) levels were 35% higher in athletes who developed EAMC during an ultramarathon than non-cramping athletes [51]. Summers et al. [52] noted that low back pain that resulted in rugby players missing playing time was a risk factor for calf EAMC. From the neurophysiology literature, the presence of painful illnesses and conditions increased action potential activity in muscles suggesting pain increased muscle activity [53]. Moreover, Golgi tendon organ activity decreased followed experimentally induced muscle pain [54]. Interestingly, when pain was induced by injecting glutamate into a muscle’s latent trigger point, Ge et al. [49] elicited an increase in muscle action potential activity and even elicited muscle cramps. Moreover, when hypertonic saline was injected into a muscle to increase nociceptor activity, scientists could induce cramping with fewer electrical stimulations than when isotonic saline was injected [48]. Similarly, psychological stress may also influence neurological control. Ironman athletes with EAMC predicted they would finish a race approximately 40 minutes faster than their actually time [25]. This may have resulted in higher stress which may have increased central nervous system and/or muscle activity [55]. These observations suggest pain and stress may alter neurological activity and predispose athletes to EAMC.

A history of EAMC is one of the best predictors of future EAMC and is consistent with the altered neuromuscular control theory. Miller et al. [56] observed cramp-prone individuals required fewer electrical stimulations to induce cramping than individuals without a history of cramping. Moreover, almost 90% of their [56] subjects with a history of cramping also had a familial history of cramping. Thus, there may be a genetic predisposition to EAMC. Prior EAMC also appear to predict EAMC recurrence; 71% of distance runners reported having more than three EAMC despite attempts by clinicians or athletes at treatment [24]. Recent laboratory studies confirm this observation; cramp susceptibility was higher for up to 60 minutes following a volitionally induced cramp in rested, unexercised subjects [57]. This increased susceptibility may be due to cramping causing nervous system excitation [58]. Overall, the altered neuromuscular control theory is more consistent with the muscle cramping literature and does not suffer from as many limitations as the dehydration/electrolyte imbalance theory.

Limitations of the Altered Neuromuscular Control Theory

The altered neuromuscular control theory is not without limitations, and several questions remain unanswered. First, it is unclear how fatigue alters muscle spindle or Golgi tendon organ activity. Second, it is unknown to what extent individuals must become fatigued to develop EAMC and whether this fatigue level can be modulated (positively or negatively) by other factors. Numerous highly trained and well-conditioned athletes develop EAMC, and their history of training is often not predictive of EAMC [51, 59]. Third, it is unclear whether central or peripheral fatigue or any other singular factor is more important than another to the pathophysiology of EAMC. Fourth, many of the prospective cohort studies examining athletes with and without EAMC rely on questionnaires for information about past EAMC [23, 25, 51, 52, 59]. Thus, there may be some recall bias in the responses. Finally, while neurophysiology studies on muscle cramping have greatly improved our understanding of how other factors unrelated to fatigue can alter neuromuscular control, uncertainty exists regarding the application of their results to EAMC. Further research is needed to clarify whether exercise induces similar changes in muscle afferents and neuromuscular control.

Recognition of Exercise-Associated Muscle Cramping

Clinically, EAMC are easily recognized. During an acute EAMC, individuals will be in noticeable pain with all, or sections of, their skeletal muscle firm, pulsing, and/or bulging involuntarily. Concomitantly, there may be alterations in joint position due to the sustained involuntary contraction. For example, the ankle and toes may point downward (i.e., plantarflexed) if the calf is actively cramping. Typically, EAMC last a few seconds or minutes and affect the skeletal muscles which cross two joints (e.g., quadriceps, hamstrings, calves) [24]. Moreover, some individuals are able to sense EAMC are imminent or articulate they “feel like they will cramp” [19]. This “cramp-prone state” usually precedes the onset of full EAMC and is often an indicator an individual needs to modify or cease their activity level or EAMC will occur.

Though easily recognized, EAMC severity varies considerably. In most cases, EAMC are mild and do not impair athletic performance [8, 23, 24]. However, some athletes may be unable to complete athletic events because of EAMC. Hoffman and Fogard [30] reported 5% of ultramarathoners were unable to finish a competition because of EAMC. While rare, reports of hospitalization due to EAMC have been reported [60] though advanced diagnostic testing and blood work are often unremarkable in individuals with EAMC [23, 24, 61].

Treatment of Exercise-Associated Muscle Cramping

The immediate treatment for individuals experiencing an acute EAMC is slow, gentle static stretching of the muscle until the EAMC subsides. Static stretching is the most utilized treatment by clinicians to relieve EAMC [16] and is also a common self-treatment used by athletes if they experience EAMC during competitions [24]. Static stretching may alleviate EAMC via two mechanisms. The simplest explanation is static stretching elongates the muscle, thereby physically separating the contractile proteins and prevents the muscle from contracting. When muscles are unable to contract, they cannot cramp [62]. Alternatively, static stretching may increase tension in muscle tendons, thereby increasing inhibitory signals from Golgi tendon organs and lowering the excitability of the alpha motor neuron pool [36, 39].

Once the EAMC has dissipated and the athlete is no longer in pain, clinicians should rule out other potentially dangerous conditions (e.g., low blood glucose, high body temperatures). If athletes do not present with signs or symptoms of other dangerous general medical conditions, clinicians can focus on identifying the potential underlying factors which preceded the EAMC. Since the cause of EAMC is likely multifactorial, clinicians must thoroughly question athletes to determine the underlying cause of EAMC (Table 6.1) and then target those factors with appropriate interventions.

Table 6.1

Questions to aid in the identification of EAMC risk factors



Risk factor

1.  Do you have any illnesses or medical conditions?

Muscle cramping may be associated with diseases [1]

Underlying illness

2.  Did EAMC occur after a change in or start of medication or drug use?

Muscle cramping may be associated with medication use [1].

Medication side effect

3.  How hard were you exercising before you developed EAMC?

EAMC occur in athletes with the fastest actual and predicted race times [2, 25, 59]


4.  When did the EAMC occur during exercise (i.e., beginning, middle, end)?

EAMC tend to occur near the end of exercise or competitions [8, 24]


5.  How much sleep did you get the night before your exercise session when EAMC occurred?

Sleep loss reduced muscle glycogen [63] and time to exhaustion and increased energy needs [64]

Premature fatigue

6.  How hot and humid was it when you developed EAMC?

EAMC can occur under any environmental conditions though they do occur most frequently in summer months (e.g., August) [3]

Hypohydration, premature fatigue, unacclimatized to environment

7.  Was the exercise session during which EAMC occurred novel in any way?

EAMC tended to occur more in untrained individuals [12] or during harder than anticipated events [65]

Overexertion and/or fatigue

8.  What was your diet like in the days preceding the EAMC? Was it balanced and nutritious?

Diets low in carbohydrates may reduce muscle glycogen and the amount of work or exercise performed [66]

Premature fatigue

9.  Did you consume stimulants (e.g., caffeine) before your exercise session?

Stimulants can increase excitability of the nervous system

Overexcitation of the nervous system

10. Were you recently injured?

Pain [48, 49, 52] and prior injury [51] are predictors of cramping

Overexcitation of the nervous system

11. What was your psychological state during the exercise session when EAMC developed?

Stress [55] or unrealistic expectations [25] may increase nervous system and/or excitability

Overexcitation of the nervous system

12. Did you consume enough fluids and/or electrolytes to replace your sweat losses?

Contribution of sweat losses to EAMC genesis is equivocal [2124]. American football players with an EAMC history may benefit from fluid and electrolyte monitoring [29]

Hypohydration; premature fatigue

13. Did the EAMC tend to stop once you stopped the activity?

Activity cessation and/or reduced pace can relieve EAMC [44]

Overexcitation of the nervous system

14. Do the EAMC tend to occur only in the muscles that were doing the most work?

EAMC tend to affect working muscles and may be mitigated with reeducation of synergistic muscles [44]

Overexcitation of the nervous system

15. Did EAMC occur during training or during competition?

EAMC tend to affect athletes more during competitions than training [25]

Overexcitation due to stress of competition; premature fatigue due to overexertion

EAMC exercise-associated muscle cramps. Questions appear in no particular order or level of importance after Questions 1 and 2

Many individuals use food, drinks, and other home remedies to treat EAMC. Most of these ingestible remedies are associated with the belief that EAMC are due to electrolyte losses. For example, bananas and mustard are often advocated to cramp-prone athletes because of their electrolyte content. However, individuals must consume at least 2 servings of bananas (~3 bananas) and wait 30 minutes before a meaningful increase in blood potassium content occurs post-exercise [67]. Similarly, eating the equivalent of 30 mustard packets (141 grams) did not alter blood electrolytes up to 60 minutes post-ingestion in dehydrated subjects [68]. Thus, banana or mustard ingestion is too slow to relieve an acute EAMC.

Another popular EAMC remedy is ingestion of pickle juice. Pickle juice is sometimes recommended because of its high sodium content, and the assumption EAMC are caused by sodium losses [69]. Interestingly, ingesting small volumes (~80 mL) of pickle juice during an electrically induced muscle cramp relieved the cramps 37% faster than water and 45% faster than drinking nothing at all [70]. However, like mustard and bananas, the nutrients in pickle juice are not absorbed by the body quickly post-ingestion. Miller et al. [71] observed small volumes of pickle juice stayed in the stomach for at least 25 minutes. Moreover, several experimental studies showed blood electrolyte concentrations do not change significantly following ingestion of small volumes of pickle juice [68, 70, 72]. Consequently, Miller et al. [70] hypothesized pickle juice ingestion relieved cramping through an oropharyngeal reflex rather than electrolyte restoration. They further hypothesized it was the acetic acid (vinegar) in pickle juice that elicited the reaction. Further research is required to elucidate the ingredients that trigger this reflex as well as the pathway and receptors through which pickle juice relieves cramping.

A popular and dangerous misconception is sports drinks can be consumed to treat EAMC because they contain electrolytes. Most commercially available sports drinks are hypotonic. This means they contain less sodium in them than the blood. Consequently, drinking sports drinks tends to reduce blood sodium concentration [73]. If hypotonic beverages, like sports drinks, are overconsumed, a rare but deadly condition known as exertional hyponatremia (i.e., low blood sodium) may occur [74]. Table 6.2 demonstrates the dangerous volume of a variety of popular sports drinks a person would need to ingest to fully replace ~5 grams of sodium and ~1 gram of potassium. While the volumes in Table 6.2 are already dangerous, even more concerning is that some authors [20, 21] report athletes with a history of EAMC can lose up to 10 grams of sodium during exercise! Sadly, athletes overconsuming dangerous volumes of fluid to prevent and treat EAMC are not hypothetical. In 2014, two otherwise healthy secondary school American football athletes died from exercise-associated hyponatremia. In both cases, the young men died because they were trying to treat and prevent EAMC by consuming sports drinks and/or water [75].
Nov 7, 2020 | Posted by in SPORT MEDICINE | Comments Off on Muscle Cramps
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