Acute Sports Injuries - CRAMP

Muscle cramps are sudden, painful, involuntary contractions characterised by repetitive firing of motor unit action potentials

When they occur during or immediately after exercise in healthy individuals with no underlying metabolic, neurological or endocrine pathology, they are referred to as 'Exercise Associated Muscle Cramps' (EAMC). These are usually temporary (lasting <60 seconds) but often incapacitating and tend to recur if activity at the same exercise intensity level is continued without an adequate recovery period. EAMC can significantly impair athletic performance. The most common sites for EAMC are in the calf and foot muscles, followed by the hamstring and quadriceps muscles.

Historically, EAMC were thought to be due to dehydration and/or electrolyte depletion, but this hypothesis has not been supported by scientific evidence. EAMC most commonly occurs towards the end of or following fatiguing exercise, or after a rapid increase in exercise intensity. The current leading theory is that EAMC result from abnormal neuromuscular control at the spinal level in response to fatiguing exercise. EAMC is linked to increased excitatory and decreased inhibitory afferent inputs to motor neurons during fatigue. The net result is sustained motor neuron activity and the production of a cramp-inducing discharge.

Immediate treatment of EAMC aims to reduce motor neuron activity, with the most popular and effective technique being passive stretching. This increases the Golgi tendon organ's inhibitory activity to reduce muscle electromyographic activity within 10-20 seconds and provide symptomatic relief. Ideally, passive tension should be maintained to the affected muscle for up to 20 minutes or until fasciculation ceases. If the EAMC were particularly intense or prolonged, icing while the muscle is on stretch may be considered to offset any potential delayed onset muscle soreness (resulting from microscopic muscle fibre damage). Other potential methods of reducing motor neuron activity during EAMC include electrical stimulation of tendon afferents and antagonist contraction to induce reciprocal inhibition.

The incomplete knowledge of the aetiology of EAMC has limited the development of preventative strategies. Fluid and electrolyte replacement has not been shown to be beneficial, consistent with the now debunked dehydration-electrolyte imbalance theory. Strategies aimed at modulating fatiguability and altering neuromuscular control may be beneficial. Fatiguability may be modified by improving generalised conditioning and endurance, whilst ensuring adequate carbohydrate reserves. Neuromuscular control can be targeted by performing plyometric and eccentric exercises, which may elicit changes in muscle spindle and Golgi tendon organ firing to enhance efficiency and sensitivity of reflexive and descending pathways used for neuromuscular control. Regular stretching is also recommended because EAMC often occur when the muscle is in its shortened position. Massage and treatment of myofascial trigger points can also be used to help improve muscle efficiency and reduce fatiguability.

REFERENCES

Brukner, P., 2012. Brukner & Khan's clinical sports medicine. North Ryde: McGraw-Hill.