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According to wikipedia, muscle cramps are caused by myosin fibers not being able to break free from the actin filaments during contraction, resulting in a prolonged contraction.

Obviously a lack of ATP would produce cramping, as myosin requires ATP to become free from actin.

However I have heard that potassium and sodium etc. are useful for treating cramps, and their deficiencies can lead to cramping.

So how does a deficiency in sodium or potassium etc. result in myosin being stuck to actin causing the cramp?

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check this article. It is not accessible to me. –  WYSIWYG Apr 10 '13 at 14:04

4 Answers 4

up vote 7 down vote accepted

The quick and simple answer:

Cramps of a hypokalemic origin are much more common than those of a hyponatremic origin because the Na-K pump is more effective at moving potassium in comparison to sodium. At the onset of a muscle contraction, the presence of calcium triggers the opening of the Na-K channels in the membrane. Potassium is a calcium inhibitor, so as the potassium flows out of the cell, it eventually reduces the presence of calcium. This causes the closure of the Na-K channel (negative feedback mechanism). In a hypokalemic state, the lack of sufficient K doesn't inhibit the calcium channel, and in turn doesn't properly terminate the muscle contraction at the cellular level.

The continued presence of calcium, which has a lot to do with nerve impulses, means that the nerves keep firing, and in some cases such as a 'charlie horse', these impulses fire fast and continuously. The body at this point is reaching a small local state of metabolic acidosis resulting from the extremely high oxygen consumption, increasing levels of CO₂ (the acidosis component) and reducing blood partial oxygen levels. Since the oxygen is no longer as abundant as it was, it inhibits the bodies ability to locally produce the ribose and phosphate necessary for ATP. Less ATP = more myosin that can't be disconnected from actin = continued muscle cramp.

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still doesn't answer why low sodium causes cramps.. the exercise cramps dont happen because of hypokalemia.. potassium is hardly lost in sweat.. Potassium is not a calcium inhibitor.. calcium release in muscles in voltage gated, which is triggered by sodium influx –  WYSIWYG Apr 11 '13 at 4:32

Muscle contarction is when the brain tell the body to move. the brain then starts an action potential down the motor neurons. The action potential moves down motor neuron and reached the terminal bouton. At the terminal bouton, it releases the neurotransmitter acetylcholine. Acetylcholine travels through myoneural junction and into myoneural cleft. ACH binds to the receptor which causes an action potential in both directions along the cell membrane. Action potential repels potassium which travels down cell membrane until it falls into a transverse tubule. K+ continues to fall into transverse tubule and accumulates which increases voltage (-70 to -50 mV). The voltage change causes the calcium gates to open and calcium diffuses out. Calcium then binds to troponin. Troponin binds to tropomyosin and pulls it exposing the g-actin binding site which allows myosin and actin to bind. the myosin head changes shape (called power or working stroke) and pulls the actin towards the M line and the muscle contracts. similar to Tug-of-War, the myosin heads (your hands) pull on the actin (the rope) to contract a muscle. like team members for tug of war, the myosin heads alternate between pulling and holding on to the actin... the only way myosin will release actin is to add ATP which forces the two apart and thus relaxing the muscle. (as mentioned above)..

Now a lack of potassium, sodium, or calcium would prevent the muscle from contracting but wont relieve a muscle cramp. the common advice of eating a banana actually does help relieve cramps but not because of the potassium. Bananas also have sugar and fat. the sugar and fat then make ATP..

Muscle Cramps are primarily caused by lack of ATP in the body. ATP is what forces the myosin to release the actin and thus the muscle relaxes and the cramp is relieved.

another cause could be lack of magnesium which helps the ATPase sodium/potassium pump which is what changes the voltage back to resting potential and relaxes the muscle..

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Anaid, welcome to Bio SE, and thank you for resurrecting this question with an answer. If you can try to add in line citations as mentioned in the help section. I also think there are some more topics that might should be covered here like Ca2+-ATPase. –  Atl LED Nov 5 '13 at 3:55

non of these answer makes sense, and there a few minor errors in them. i know that action potential may keep on firing continuously down the axon. one reason may be because acetylcholinesterase is not coming to the rescue and cleaning up all the acetylcholine in the synaptic cleft. but that only happen usually if there are drugs involve. so in term of natural muscle cramps, it really does not make any sense what so ever.

a really good reason is mainly because of lack of potassium. the function of potassium inside the muscle cell is to repolarize the membrane. however if there are not enough potassium, the time it takes for it to repolarize is pretty damn slow. on the other hand, sodium is used to depolarize the membrane. As a result, since there are an unequal distribution of sodium to potassium, less potassium is flowing out the membrane while more sodium will flow in the membrane causing it to depolarize faster than it suppose to repolarize. since the inside of the cell is becoming more positive with the help of sodium and the outside of the cell is becoming negative with the help of potassium, the inside of the cell is pulling back the potassium. but again, there is an unequal distribution of potassium compare to sodium so it will never achieve that electrochemical equilubrium (resting membrane potential). since electrochemical equilibrium can not be achieve, sodium is flowing inside the membrane causing it depolarize across the membrane at a rapid rate forming an unfused tentanus at a rapid rate.

the rate in which this is happening is so fast that it wont let the myosin head detach from actin for a long period of time, so it continuously making the sacromere shorter and shorter causing a pain receptor to travel toward the CNS. these is my hypothesis.

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Can you please expand your answer with some references? –  Chris Dec 12 at 15:22

One of the thing i would like to point out is that ATP detached the myosin head but does not control the powerstroke! If there are no more ATP being produce, then it is rigor mortis. You will just be really tense/sore because the myosin head is not being released and its staying contracted (perhaps a fused tentanus) but it does not make the sacromere shorter if ATP are no longer able to be produced. And if there are no more ATP being produce, it can't hydrolyzed into ADP and inorganic phosphate (Pi). that would help in create the cross bridge. in addition, inorganic phosphate is the essential compound when you want the power stroke to happen, not ATP.

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