cramp

cramp Muscle cramps are one of the most common clinical problems suffered by athletes in endurance events. A third to a half of marathon runners and two-thirds of triathletes have been reported to experience exercise-associated muscle cramping (EAMC) at some time in their lives. Other forms of cramp affecting healthy people include nocturnal foot and calf muscle cramps, those arising from certain occupations (such as hand cramps in pianists and typists) and those associated with pregnancy. Cramps can also occur in a variety of relatively rare medical conditions, congenital or acquired, including metabolic or neuromuscular disorders, poisonings, and drug effects. This article will focus principally on EAMC — a spasmodic, painful involuntary contraction of skeletal muscle that occurs during or immediately after muscular exercise — since it is the most studied of the common forms, and has recently become better (though still not completely) understood.

The interest in skeletal muscle cramping associated with exercise was first stimulated at the turn of the century by reports that it occurred during physical work in hot, humid environments, including steam ships and mines. In these early studies the proposed explanation was a disturbance of body fluid and salt balance. The early observations led to the ‘serum electrolyte depletion’ and ‘dehydration’ theories for the cause of the cramps. Such theories are consonant with the fact that widespread cramping is one of the symptoms of severe hyponatraemia (salt deficiency). Thus they are still accepted by some clinicians and applied in practice by many athletes who believe adequate salt and water intake to be important cramp-preventatives.

Recent evidence, however, challenges the salt-and-water view. More than one careful study has shown that most runners with acute EAMC are not salt-deficient, dehydrated, or overheated. Also, cramp among sports people can occur in cold conditions (such as cold water, for swimmers). Factors actually associated with EAMC have been identified using three research approaches: epidemiological investigations; studies on spinal reflex activity during muscle fatigue in animals; and recording of muscle electrical activity (electromyography, EMG) in human volunteers during EAMC. The latter technique demonstrates intense electrical activity, at exceptional frequencies (up to 300 Hz), in both EAMC and occupationally cramped muscles, and indeed in the cramps associated with a number of medical conditions, though not quite all. Critical analysis of these factors has led to the development, by Scwellnus and colleagues, of a novel hypothesis for the cause of EAMC.

It seems that most forms of exercise-associated cramp result from an abnormally sustained activity of the nerve cells in the spinal cord which control skeletal muscle, the alpha motor neurons. Fatigue appears to be the central factor in EAMC. Fatigue enhances the input to the alpha motor neurons from the main receptors in the muscles (muscle spindles) and inhibits the input from the receptors in their tendons (Golgi tendon organs) that signal tension. As the spindle signals excite alpha motor neurons, while those from tendon organs are inhibitory, these fatigue effects can combine to promote uncontrolled activity in the relevant regions of the spinal cord. It is a common experience that cramp may be precipitated by contraction of the muscle from an already shortened position, and this of course is when the tension signal from its tendon is weakest.

In a recent epidemiological study of over 1300 marathon runners, risk factors for EAMC were identified. Cramps were more likely with older age, a longer history of running, a higher body mass index, shorter daily stretching time or irregular stretching habits, and if there was a family history of cramping.

In addition, runners themselves identified specific conditions that were associated with EAMC: high-intensity running (racing), long duration of running (most cramps occur after 30 km in a standard marathon), hill running, subjective muscle fatigue, and poor performance in the race.

The two most important observations from these data are that cramp is associated with running conditions that can lead to premature muscle fatigue, and that poor stretching habits appear to increase the risk.

The muscles most prone to cramping are those that span two joints (for example, the gastrocnemius spanning knee and ankle). These muscles are typically activated when shortened — as in swimming, when the gastrocnemius contracts while the toes are already pointed. In runners, the situation is less clear-cut, but activation is common when only one of the two joints is extended. As the foot strikes the ground, the toes are pointed — the ankle is extended by contraction of the gastrocnemius — whilst the knee is also extended. Then in the load-bearing phase of the stride the foot has flexed, which would stretch the gastrocnemius — but now the knee is bent. The gastrocnemius is then activated again in this relatively shortened position. Such contractions are presumed to produce significantly less tension in the tendons than contractions starting near full extension, resulting in less inhibiting effect on motor neuron activity of the sort described above.

In localized cramp, confined to one or 2 muscle groups, the typical scenario is as follows: there is distressing pain in the muscle that develops gradually over a few minutes during intense or prolonged exercise. The muscle is contracted and hard, and an observer can see fasciculation — small twitchings — over its surface. The onset of the cramp is usually preceded by muscle fatigue and more immediately by a feeling of twitching in the muscle (‘cramp prone state’). This is followed by spasmodic spontaneous contractions and frank cramping if the activity is continued. Relief from the ‘cramp prone state’ occurs if the activity ceases or, temporarily, if the muscle is passively stretched. Once activity stops, there may be alternating periods of cramping and relief.

The athlete who has generalized severe cramping, extending to non-exercising muscle groups, or who is also confused or comatose, presents an emergency. This condition is not typical EAMC as a result of fatigued muscle, but a whole body, usually metabolic, disturbance requiring immediate hospitalization and full investigation.

The immediate treatment for acute EAMC occurring in a sports event, or for cramp experienced in bed, should consist of passive stretching of the affected muscle groups, holding the muscle in stretched position until return to normal muscle length does not lead to recurrence of cramp. General supportive treatment includes maintaining a comfortable temperature and providing fluids if required.

The key to the prevention of acute EAMC is to protect the muscle from developing premature fatigue during exercise. The following advice to athletes is recommended: be well conditioned for the activity; perform regular stretching exercises for the muscle groups that are prone to cramping; and have adequate nutritional intake (carbohydrate and fluid) to prevent premature muscle fatigue during exercise. However, athletes who continue to be prone to EAMC must face the need to perform their activity at a lower intensity or a shorter duration.

Martin Schwellnus

Bibliography

McGee, S. R. (1990). Muscle cramps. Archives of Internal Medicine, 150, 511–8.
Maughan, R. J. (1986). Exercise-induced muscle cramp: a prospective biochemical study in marathon runners. Journal of Sports Sciences, 4, 31–4.
Schwellnus M. P. (1999). Skeletal muscle cramps during exercise. Physician and Sportsmedicine, 27(12), 109–15.
Schwellnus, M. P.,, Derman, E. W.,, and and Noakes, T. D. (1997). Aetiology of skeletal muscle cramps during exercise: a novel hypothesis. Journal of Sports Science, 15(3), 277–85.

See also fatigue; reflexes.