What is the cause of muscle cramps?

Question

According to Wikipedia, muscle cramps are caused by the inability of myosin fibers to break free from the actin filaments during contraction, resulting in a prolonged contraction.

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

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

So, how does a deficiency in sodium or potassium result in the inability of myosin fibers to break free from the actin filaments during contraction?

Answer 1

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.

Answer 2

Muscle contraction occurs when the brain tells the body to move. The brain then starts an action potential down the motor neurons, until it reaches the terminal bouton. At the terminal bouton, it releases the neurotransmitter, acetylcholine, which travels through the myoneural junction and into the myoneural cleft. ACH binds to the receptor, which causes an action potential in both directions along the cell membrane. The action potential repels the potassium, which travels down the cell membrane until it falls into a transverse tubule. K+ continues to fall into a transverse tubule and accumulates, which increases voltage (-70 to -50 mV). The voltage change causes the calcium gates to open and to diffuse the calcium. Calcium then binds to troponin, which in turn binds to tropomyosin and pulls it, exposing the g-actin binding site that 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 a tug of war, the myosin heads (your hands) pull on the actin (the rope) to contract a muscle. Like team members in a tug of war, the myosin heads alternate between pulling and holding on to the actin; the only way that myosin will release actin is to add ATP, which forces the two apart and thus relaxes the muscle (as mentioned above).

Now, a lack of potassium, sodium, or calcium would prevent the muscle from contracting but won't 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, which are converted into ATP.

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

Another cause could be the lack of magnesium, which helps the ATPase sodium/potassium pump, which, in turn, returns the voltage to resting potential and relaxes the muscle.

Answer 3

One possible reason why low sodium levels induce cramps may lie in the cation selectivity of the nicotinic acetylcholine receptor (nAChR), which is an ion channel. When ACh binds to the receptor site on the nAChR protein, the protein changes shape to open a pore formed by the protein in the cell membrane. This pore allows the influx of both sodium and calcium ions, which induce depolarisation (a positive shift in the membrane voltage) to trigger the voltage-dependent ion channels responsible for action potentials. A reduction in sodium ions would mean more calcium is able to enter the cell through the nAChR. The calcium ion carries greater charge as it is formed by the loss of two electrons from its outer shell, while the sodium ion is formed by the loss of one electron. This means that, each time the nAChR channel opens, the cell undergoes greater depolarisation. The muscle response is harder and faster to the same neural stimulus, which results in a depletion of energy stores.

Answer 4

None of these answers makes sense, and there some minor errors in them. I know that action potentials may continue to fire 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 usually happens if there are drugs involved. So, in terms of natural muscle cramps, it really does not make any sense whatsoever.

A really good reason is mainly because of a lack of potassium. The function of potassium inside the muscle cell is to repolarize the membrane. However, if there is not enough potassium, the time it takes for it to repolarize is very slow. On the other hand, sodium is used to depolarize the membrane. As a result, since there is an unequal distribution of sodium to potassium, less potassium flows out the membrane while more sodium flows into the membrane, causing it to depolarize faster than it repolarizes. Since the inside of the cell is becoming more positive with the help of sodium, and since 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 compared to sodium, so it will never achieve that electrochemical equilubrium (resting membrane potential). Since electrochemical equilibrium can not be achieved, sodium is flowing inside the membrane, causing it to depolarize across the membrane and to form an unfused tentanus at a rapid rate.

The rate in which this is happening is so fast that it won't let the myosin head detach from actin for a long period, so it is continuously making the sacromere shorter, causing a pain receptor to travel toward the CNS. This is my hypothesis.

Answer 5

One of the things that 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 rigor mortis results. You will just be really tense/sore because the myosin head is not being released, and it's 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 be hydrolyzed into ADP and inorganic phosphate (Pi). That would help to create the cross bridge. In addition, inorganic phosphate, not ATP, is the essential compound when you want the power stroke to happen.

Answer 6

A quote from Flex Pharma:

Most muscle cramps are not caused by dehydration, lactic acid, electrolyte imbalance, or muscle tightness. That is why popular remedies like sports drinks, bananas, magnesium tablets, and stretching are usually ineffective. New research has shown that cramps and spasms do not originate in the muscle itself, but are caused instead by a neural mechanism: excessive firing of the motor neurons in the spinal cord that control muscle contraction.

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Activation of transient receptor potential (TRP; TRPV1 and TRPA1) ion channels reduces muscle cramps.

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http://www.flex-pharma.com/scientific-presentations.php