Muscle cramp

Why do cramps seize a player late in a match even when they have drunk plenty and taken salt all day?

Eighty minutes into a match, a player goes down clutching a calf that has locked solid. They have been drinking all afternoon and taking salt with everything since breakfast, on advice given confidently by people who have given it for decades. The cramp arrives anyway.

The folk account says the player is dehydrated or short of electrolytes. But this player is neither, or at least not more so than the twenty-one others on the pitch who are fine. And the cramp did not seize the whole body, or even both calves — it seized that muscle, the one that has been working hardest, and it seized it while the player was pushing off. A whole-body deficiency ought to produce a whole-body problem. Something more local is going on.

Begin with what a cramp actually is. It is not a muscle that has stopped working. It is a muscle contracting furiously and refusing to stop — and electrical recordings during a cramp show exactly that: a burst of motor unit firing, at high rates, in a muscle nobody is asking to contract. So the question is not why the muscle failed. It is why the nervous system is sending a signal that nobody ordered.

That reframing is most of the work. Ask what normally stops a muscle contracting. Two sensory systems sit inside every muscle and report on it. Muscle spindles, embedded among the fibres, sense stretch and excite the motor neurons supplying that muscle — stretch it, and it contracts back. Golgi tendon organs, sitting at the junction with the tendon, sense tension and inhibit those same motor neurons — pull too hard, and the drive is damped. The motor neuron sits between an accelerator and a brake, and its output is the balance of the two.

Now ask what fatigue does to that balance. As a muscle fatigues, spindle activity increases and Golgi tendon organ activity decreases. The accelerator is pressed and the brake released, both at once, by the same underlying condition. Push that far enough and the motor neuron pool becomes hyperexcitable: a small input produces sustained firing that will not switch off.

Two predictions fall straight out, and both match what anyone who has watched cramps will recognise. First, the cramp should hit the muscle that is most fatigued, not the body generally — which it does. Second, it should be worse when the muscle is shortened, because a shortened muscle has slack spindles and low tendon tension, which is the same imbalance the fatigue produced. That is why cramps strike the calf when the foot is already pointed, why swimmers cramp with the foot extended, and why the immediate remedy is not to drink but to stretch: stretching loads the tendon, drives the Golgi tendon organs, and restores the inhibition that had gone missing.

That last observation is close to decisive. If the cramp were caused by a shortage of something in the blood, a stretch would not fix it in ten seconds, because nothing has been supplied.

The electrolyte account is poorly supported, and this deserves to be said plainly rather than hedged. Studies comparing athletes who cramp during an event against those who do not, sampling at the moment of cramping, have generally failed to find the expected differences in hydration status or serum electrolytes. Cramps occur in cool weather and in swimmers immersed in cold water, where sweat losses are modest. Whole-body deficiency also fails the localisation test above. The related file on exercise-associated hyponatremia makes a neighbouring point from the other direction — the fluid-and-salt advice given to endurance athletes has been confidently wrong before, and in that case actively harmful.

I should be careful about how strong a claim that licenses. The evidence against a primary electrolyte cause in exercise-associated cramp is reasonably good; the claim that electrolytes are irrelevant in every cramp is not. Cramps in dialysis patients and with certain drugs do track measurable disturbances. The athlete's late-match cramp and the clinic's metabolic cramp are probably different things wearing the same name.

The pickle-juice observation is the sharpest available clue, and it points away from the stomach. Athletes given a small volume of strongly flavoured acidic liquid report cramp relief in well under a minute — faster than the fluid could plausibly leave the stomach, let alone be absorbed and distributed. The leading explanation is a reflex triggered by receptors in the mouth and throat, which inhibits the runaway motor output centrally. If that is right, the substance is not replacing anything; it is pulling a lever. Note what this does to the folk theory: a remedy widely cited as evidence for the electrolyte account turns out, on its timing alone, to refute it.

The neuromuscular account is not fully settled either. It explains the localisation, the shortened-position dependence, the stretch remedy and the association with unaccustomed intensity. It is less good at explaining why some individuals cramp repeatedly and others never do under the same conditions — prior cramp history is the strongest known predictor, and that is a fact in search of a mechanism.

The falsification test. If the cramp is a local reflex imbalance rather than a systemic deficiency, then passively stretching the cramping muscle should abolish it within seconds, while drinking an electrolyte solution should not. If a salt drink reliably released cramps as fast as a stretch does, the reflex account would be in serious trouble.

• Why prior cramp history predicts future cramping better than any physiological measure.
• How exercise-associated hyponatremia shows the same advice failing in a more dangerous direction.
• Why nocturnal leg cramps in older adults may or may not share this mechanism.

Every term the collection defines is gathered in the glossary.