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Skeletal Muscle Cramps During Exercise

Martin P. Schwellnus, MBBCh, MSc (Med), MD


In Brief: Cramps are painful, involuntary contractions of skeletal muscle that occur during or immediately after exercise and are common in endurance athletes. Although cramps can occur in many rare medical conditions, most athletes who have exercise-associated muscle cramping do not have congenital or acquired medical disorders. The cause of cramping is not well understood but may have to do with abnormal spinal control of motor neuron activity, particularly when a muscle contracts in a shortened position. Important risk factors include muscle fatigue and poor stretching habits. Treatment consists mainly of passive stretching, with supportive measures as needed. Special diagnostic studies and conditioning programs may be necessary for recurrent episodes.

Skeletal muscle cramps are one of the most common clinical problems encountered by medical staff who treat athletes at endurance events, especially marathons and triathlons (1,2). The lifetime incidence of skeletal muscle cramping in marathon runners and triathletes has been variously reported to be as high as 30% to 50% (3) and 67% (4). The etiology, diagnosis, and management of this condition have not been definitively elucidated. Muscle cramps can occur in various rare medical conditions, but most athletes who manifest exercise-associated muscle cramping (EAMC) do not have these disorders. The prevalence of EAMC in recreational athletes and differences between rates in elite athletes and recreational athletes are not known.

The purpose of this review is to define and classify skeletal muscle cramping, discuss the pathophysiology and etiology of EAMC, and describe a systematic approach to the clinical diagnosis, management, and prevention of the condition.

Definition and Classification

EAMC can be defined as a painful, spasmodic, involuntary contraction of skeletal muscle that occurs during or immediately after exercise (5-7), as opposed to cramps that occur in smooth muscle and skeletal muscle at rest.

Skeletal muscle cramps can occur as part of the symptom complex of various congenital and acquired disorders (table 1). In some clinical syndromes, skeletal muscle cramping is the principal symptom; besides EAMC, these include occupational cramps, nocturnal calf-muscle cramps, and pregnancy-associated cramps. Detailed discussion of conditions other than EAMC is beyond the scope of this article.

Table 1. Conditions That Cause Skeletal Muscle Cramps

Acquired Skeletal Muscle Cramp Syndromes
Exercise-associated muscle cramps

Occupational cramps

Nocturnal calf-muscle cramps

Pregnancy-associated cramps

Congenital Abnormalities
Autosomal dominant cramping disease

Disorders of carbohydrate, fat, or purine nucleotide metabolism (eg, glycogen storage diseases, carnitine palmityl transferase deficiency, muscle adenylate deaminase deficiency)

Myotonia congenita

Other Acquired Disorders
Endocrine diseases (eg, diabetes mellitus, thyroid disease)

Fluid and electrolyte imbalances (eg, hyperkalemia, hypokalemia)

Neuromuscular diseases (eg, peripheral neuropathy, myotonic dystrophy)

Other acquired diseases (eg, liver cirrhosis, neoplastic disease, diarrhea)

Reactions to drugs or toxins (eg, beta-agonists, ethanol, lead, strychnine)

Pathophysiology and Etiology

Traditional theories. Medical interest in skeletal muscle cramping associated with physical exercise first surfaced at the turn of the century with published reports that described cramping in persons working in hot, humid environments such as steamships and mines (8-13). These early researchers postulated that the pathophysiology was a systemic disturbance of fluid (10) and electrolyte balance (14,15). The observations led to the still-popular serum electrolyte and dehydration theories of etiology (16,17). Recently the validity of these theories has been challenged (18).

Additional theories were subsequently proposed. In the early 1950s, the first case of myophosphorylase deficiency was described (19), and many other similar disorders were identified later (20-32). These discoveries gave rise to the metabolic-abnormality theory. Although cramping is common, there are fundamental differences between EAMC and cramps due to inherited metabolic abnormalities (table 2) (33,34). Finally, case reports of skeletal muscle cramping during exercise in extreme heat or cold have yielded the environmental theory (35), even though most cramps occur in thermoneutral environments.

Table 2. Comparison of Exercise-Associated Muscle Cramps and Cramping Due to Metabolic Disorders (18)

Exercise-Associated Metabolic Disorders
Lifetime prevalence reported as 30% to 67% (3,4) Rare

Intermittent, variable severity during exercise Recurrent and severe during exercise

Myoglobinuria usually absent Myoglobinuria common

Myalgia or rhabdomyolysis usually absent Myalgia and rhabdomyolysis usually present

Electrical activity present during cramping Often electrically silent (rigor)

Weak familial tendency Strong familial tendency

A novel hypothesis. A recent critical analysis of the evidence does not support any of the existing theories (18). A novel hypothesis for EAMC etiology has been proposed and is supported by data from epidemiologic studies, animal experimental data on spinal reflex activity during muscle fatigue (36,37), and electromyographic (EMG) data obtained during and between bouts of acute EAMC (18,38).

The hypothesis proposes that EAMC occurs as a result of an abnormality of sustained alpha motor neuron activity, which stems from aberrant control at the spinal level. The central factor is muscle fatigue that causes lack of control through an excitatory effect on the muscle spindle afferent activity (types Ia and II) and an inhibitory effect on the type Ib Golgi tendon organ afferent activity (36,37). An additional contributing factor is a contraction of the muscle in its shortest position (inner range), which also inhibits type Ib afferent activity from the Golgi tendon organ. This may be the factor that precipitates the cramp (figure 1) (18).

[Figure 1]

It is well known that the muscles most prone to cramping are those that span two joints. These muscles are often contracted in a shortened position during exercise—a fact that seems to confirm the role of inner-range contractions in muscle cramping. Contraction in this state produces decreased tension in the tendons of the muscles as well as decreased Golgi-tendon activity. The best example is a calf-muscle cramp in a swimmer. During swimming, the ankle is maximally plantar flexed as the calf muscle contracts. The tension in the Achilles tendon is decreased compared with the ankle in full dorsiflexion. Golgi-tendon activity is thus decreased in plantar flexion compared with dorsiflexion, resulting in less inhibition of the gastrocnemius alpha motoneurons.

Passive stretching results in almost immediate relief of the cramp and reduction in EMG activity; stretching increases tension in the Achilles tendon and increases Golgi activity (36). This phenomenon is compatible with the hypothesis that abnormal spinal reflex activity is an important etiologic factor in EAMC, and it may account for the increase in nocturnal cramping in athletes who train heavily. Nocturnal cramps may well be due to contractions (perhaps during REM sleep) of the gastrocnemius while in the plantar flexed position.

Risk Factors for EAMC

In an epidemiologic study of over 1,300 marathon runners, the identified risk factors for EAMC included older age, longer history of running, higher body mass index, shorter daily stretching time, irregular stretching habits, and family history of cramping (39). Runners also identified exercise-related conditions that were associated with EAMC: high-intensity running (racing), long duration of running (most cramps occur after 30 km in a standard marathon), subjective muscle fatigue, hill running, and poor performance in the race (38).

The two most important observations from these data are, first, that EAMC is associated with running conditions that can lead to premature muscle fatigue, and, second, that poor stretching habits appear to increase the risk for EAMC. Poor stretching habits could lead to an exaggerated myotonic reflex, thereby increasing spindle activity.

Management of Acute EAMC

The diagnostic approach to the athlete with suspected acute EAMC is outlined in figure 2.

[Figure 2]

History. Athletes usually manifest cramping at or near the end of a bout of intense or prolonged exercise. In the typical clinical history, prodromal muscle pain or twitching usually develops over a few minutes and is preceded by muscle fatigue and twitching (cramp-prone state). The twitching is followed by spasmodic spontaneous contractions and frank muscle cramping if activity is continued. The cramp-prone state is relieved if activity ceases or if the muscle is passively stretched (temporary relief only). Once activity ceases, cramping episodes are usually followed by cramp-free periods. Cramping episodes can be precipitated by contraction of the muscle in a shortened position (inner range).

Physical signs. Clinical examination of athletes who have localized acute EAMC (confined to one or two muscle groups) reveals obvious distress and pain, a hard contracted muscle, and visible fasciculation over the muscle belly. In most instances, athletes are conscious, respond normally to stimuli, and are able to converse. Vital-sign and general examinations usually reveal no abnormalities; most runners with acute EAMC are not dehydrated or hyperthermic. In general, they require no special investigations.

Treatment. The immediate treatment for acute EAMC is as follows:

  • Passive stretching of the affected muscle groups;
  • Holding the muscle in a stretched position until fasciculation ceases and a return to normal muscle length does not precipitate a cramp;
  • General supportive treatment (keeping the patient at a comfortable temperature and providing oral fluids if required); and
  • Admission to the medical care facility at the sports event if cramps are severe.

Although intravenous diazepam, magnesium, or even calcium has been used for severe cramping, these agents are not generally recommended because they may lead to complications such as hypotension or respiratory depression.

All patients with acute EAMC should be cautioned to seek medical help immediately if they do not pass any urine or pass very dark urine in the first 24 hours after the episode. They should also seek additional medical advice if they experience recurrent acute EAMC.

Generalized cramping. The athlete who has generalized severe cramping (in nonexercising muscle groups) or has localized cramping accompanied by confusion, semicoma, coma, or other central nervous signs must be treated as a medical emergency. This patient does not suffer from EAMC caused by a fatigued muscle, but more likely has a systemic, usually metabolic, disturbance (33-39). Such a patient requires immediate hospitalization in an intensive care unit and a full diagnostic workup to rule out imbalances of serum electrolyte concentrations, acute renal failure, or intracranial or other systemic pathology.

Management of Recurrent EAMC

Physicians often see the athlete who presents with a history of episodic EAMC. The challenge is to identify whether the athlete has EAMC or a related medical condition (see table 1). At the Sports Medicine Clinic of the Sports Science Institute of South Africa, we follow a stepwise diagnostic approach that often requires more than one visit.

First visit. At the first visit, the physician takes a careful, comprehensive medical history. The history is the key to distinguishing EAMC from other disorders that cause cramping. Key questions include:

  • Is the cramping precipitated by physical exercise, or does it also occur at rest?
  • Are there any associated symptoms, such as paresthesia, pain, decreased sensation, or muscle weakness?
  • What is the timing of the onset and clinical course of the cramping episode?
  • Does passive stretching relieve the cramping?
  • Is there a strong family history of cramping?
  • Does the athlete use any drugs?

Answers to these questions, and a supplementary comprehensive clinical history, allow the clinician to determine whether the cramps are EAMC only or due to some underlying condition.

In addition, a complete physical exam that includes neurologic and musculoskeletal assessment must be performed. In patients with EAMC, the findings are generally unremarkable, but care should be taken to rule out neurologic disease, chronic infections, endocrine disease, and cancers.

In our facility, routine blood tests to exclude other causes of cramping are taken at the end of the first visit. Tests include a complete blood count, plasma viscosity, and levels of serum electrolytes, serum creatine kinase, and thyroid-stimulating hormone. In athletes with EAMC, these blood tests are generally normal.

Second visit. This visit is used to confirm that the blood tests are normal and therefore confirm the diagnosis of EAMC. In addition, the physician seeks to identify risk factors for EAMC by testing muscle flexibility, strength, and endurance (isokinetic), and by making a full dietary assessment. The dietary assessment is also used to gain information about the patient's nutritional patterns.

Once risk factors have been identified, the appropriate advice is given. Athletes are usually referred for a muscle conditioning and flexibility program. They are asked to keep a training diary and note cramping episodes, and to report regularly to the clinician on their progress. Return to sport is gradual. A few athletes do not respond to this approach and require a review of the diagnosis and other special investigations such as a muscle biopsy to deduce the cause of cramping and to rule out a myopathy. Some nonresponsive patients may be carriers or have a cellular defect not detected by a blood test.

EAMC Prevention

The key to preventing acute EAMC is protecting the muscle from developing premature fatigue during exercise. This may be accomplished by advising athletes to:

  • Be well conditioned for the activity;
  • Regularly stretch the muscle groups that are prone to cramping;
  • Maintain adequate nutrition (carbohydrate and fluid) to prevent premature muscle fatigue during exercise; and
  • Reduce their exercise intensity and duration if necessary.

Summing Up

The etiology of EAMC is not well understood, but recent studies indicate that it is related to muscle fatigue from exhaustive exercise. Acute EAMC can be diagnosed clinically and is best managed by rest and passive stretching. Recurrent cramping calls for a stepwise diagnostic approach with an emphasis on the history. EAMC can be prevented by a flexibility program, measures that delay muscle fatigue, and/or reduction of exercise intensity and duration.


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Dr Schwellnus is professor of sports medicine in the department of physiology at the University of Cape Town Medical School and in the Bioenergetics of Exercise Research Unit, Sports Science Institute of South Africa, Cape Town. Address correspondence to Martin P. Schwellnus, MBBCh, MSc (Med), MD, Sports Medicine, Dept of Physiology, University of Cape Town Medical School, Sports Science Institute of South Africa, Boundary Rd, Newlands 7700, South Africa; e-mail to: [email protected].