A Novel theory for Exercise-associated muscle cramps
Today sees the third part of our series on muscle cramps. It was going to be the final installment in this particular series, but we've received some excellent and thoughtful questions and comments on the issue, so have decided that we'll do a fourth post, just summarizing some of those key "sticking" points. It seems from the feedback that this issue - electrolytes and cramps - is one of the more contentious ones around. So in our FOURTH post of the series, we'll look back and try to tie up any loose ends and conceptual issues.
In Part I and Part II, we have introduced some of the problems in the Electrolyte theory. These problems - gaps in the theory - are what Stephen Hawking referred to as "creaking, ugly edifices". In science, we establish a hypothesis, and when the data do not support that hypothesis, it is time to find an alternative. Clearly, the data on electrolytes do not support the electrolyte or dehydration theories (though they don't rule it out 100% either), so it's time for a new proposed theory. And that's what this post is all about...
The Muscle Fatigue and Spinal Reflex theory for Muscle Cramps
This theory has its orgins in a paper published in 1997 in the Journal of Sports Sciences, in which Professor Martin Schwellnus and some colleagues looked at the electrolyte-dehydration issue and concluded that on the basis of insufficient evidence, a new theory was required. They proposed, in this paper, that a cramp was the result of dysfunctional reflex control of the motor nerve as a result of fatigue. That sounds like a mouthful, and if we go into huge detail, then it could well be a very technical post. But we'll pull it apart step by step, hopefully without allowing the issue to become incredibly complex!
This of course means potentially oversimplifying things and leaving out some details that are not directly relevant, but hopefully it'll be understandable for everyone, and stimulating to encourage further discussions, where desired!
A summary of the theory
But because we know it's a highly technical issue, we decided to give you the "executive summary" right at the start. For those who like the detail, read on. For those who just want the answer, here's the take-home message:
- Muscle contraction is initiated by a nerve, called the alpha motor neurone. The alpha motor neurone receives inputs from the higher brain areas (when you make conscious movements) as well as from the spinal reflexes
- These reflexes are responsible for protecting the muscle against either excessive stretching or loading - they are the muscle spindles and Golgi tendon organs, respectively
- There is evidence that fatigue causes increased firing from the muscle spindles, and decreased activity from the Golgi tendon organs
- The net result of this change in the activity of these reflexes is that the alpha motor neuron activity is increased, and the muscle thus contracts involuntarily
We begin with a brief overview of how muscle contraction happens in the first place.
Normal control of the alpha motor neuron
Your muscles are stimulated to contract by a group of nerves known as alpha motor neurons - in order for you to perform any motor task (touching your finger to your nose, cycling, running etc.), a signal from the motor cortex of the brain travels down the spinal cord, before leaving the spinal cord and traveling to the muscle fiber along the motor nerve. Once at the muscle, the electrical signal being delivered is responsible for muscle contraction (via a process we won't go into here).
There are other pathways that also affect movement, and of course, it's not so simple as a single impulse traveling down the spinal cord to the muscle - the complexity of a simple motor task, like placing your finger on your nose is absolutely astonishing, and it involves many other brain areas and muscle groups. But for our purposes, what is important is that when the alpha motor neuron activity is increased, then the muscle contracts.
The Reflex modulation of alpha motor neuron activity
Now, we can introduce a slightly greater level of complexity. We've just said that the alpha motor neuron is responsible for stimulating muscle contraction. This alpha motor neuron is itself stimulated by three pathways - any of these three pathways will activate the motor neuron and thus cause muscle contraction:
- Firstly, there are the higher central control we already described above;
- Second, you have spinal inter-neurones which we won't discuss in detail here;
- Third, and most important for our cramp discussion, it's also regulated by what is called spinal reflex activity, and there are two particular reflexes that need to be addressed
You've all probably heard of, or experienced, the classic "knee jerk" reflex, where a doctor (or a friend) taps on the knee tendon with a small hammer and you can't help but to kick out with your foot. Well, that simple test demonstrates the first important reflex.
The muscle spindle is a tiny structure in each muscle fiber, whose job it is to make sure that the muscle does not stretch too much. So what happens is that every time your muscle is stretched, the muscle spindle activity increases. This sends a signal back to the spinal cord (along what are called Type Ia AFFERENTS), where the nerve impulse is passed on to the alpha motor neuron, and then back to the muscle. Hopefully, you will see that the end result of all this is that the alpha motor neuron will be active, leading to muscle contraction - in other words, if you stretch the muscle, the response is to eventually cause it to contract - this is protective, and prevents over stretching of the muscle.
So referring back to the knee-jerk reflex, the tapping on the knee causes your quadriceps muscle to stretch. As a result, the spindle fires, the Type Ia afferent activity to the spinal cord increases, and then the alpha motor neuron activity increases. When the alpha motor neuron fires, it causes the SAME muscle to contract, and that is why your quadriceps contract and you kick out your leg in response!
The bottom line, if you would like to forget about the details above, is that if the muscle spindle firing rates go up, then the muscle will contract.
The Golgi Tendon organ reflex
Now, there is a second organ in the muscle that plays a role in reflex regulation - it's called the Golgi tendon organ. The Golgi tendon organ performs almost the opposite role to muscle spindle it monitors the tension in the muscles and tendons, and it is active when the muscle is contracted and lengthened (which puts load on the tendons). It's role is to make sure that the muscle does not contract too forcefully or under too much load. So when the muscle is placed under load (any contraction), the Golgi tendon organ fires, and it sends a signal to the spinal cord along what is called a Type Ib afferent (remember the spindles had Type Ia afferents).
This time, however, a key difference is that the Type Ib afferents tell the Alpha Motor neurones to STOP FIRING - they are inhibitory. In otherwords, when the Golgi tendon organ fires, then the alpha motor neuron activity goes DOWN. This would cause a reduction in muscle contraction. The effect, of course, is again protective, because it prevents the muscle from taking on too much load.
So, the bottom line here is that if the Golgi tendon organ is stimualted, the end result is that muscle contraction is switched off. However, if the Golgi tendon organ is inhibited, then the alpha motor neuron activity will increase, and the muscle will contract even more - this is called "disinhibition".
So what happens with fatigue, and can it explain cramp?
In studies of muscle function and fatigue, the following has been found:
- When muscle becomes fatigued, the firing rate of the Type Ia Afferent fibers from the muscle spindle INCREASES;
- and the firing rate from the Type Ib Afferent fibers from the Golgi tendon organ DECREASES.
Therefore, FATIGUE causes the following:
- Spindle activity increases - alpha motor activity increases - MUSCLE CONTRACTION
- Golgi tendon organ activity decreases - alpha motor activity increases - MUSCLE CONTRACTION
This theory is supported by a number of observations, which cannot be explained by the serum electrolyte depletion theory:
1. Which muscles are more likely to cramp?
This is a pretty important question. The answer, of course, is the active muscles. This theory explains why, because the fatigue, which alters the activity of these two important reflexes, is most manifest in the active muscle. The electrolyte theory doesn't explain why only the muscles being used for exercise tend to cramp - in fact, if low electrolyte levels were the cause of cramp, we'd expect generalized cramping, as occurs in clinical conditions where people lose a lot of salt and become hyponatremic. It does not happen in exercise, but the Fatigue Theory can explain it.
2. What kind of muscle cramps most often?
Here, the answer is that a muscle that crosses two joints will cramp more often. This makes sense according to the Neural Fatigue theory, because if a muscle spans two joints, then it means that the muscle is going to be in a shortened position when it contracts. Think of the calf muscle during swimming - your toes are pointed (the ankle is in plantar flexion), which means the muscle is contracting in a shortened position. When the muscle is in this position, then the activity of that Golgi tendon organ is going to reduced even more than normal. Add to this the contraction, which stimulates the muscle spindle, and the net result is that the inhibition of the motor neuron is reduced even further, predisposing one to cramp.
This is why calf muscle cramps are so prevalent in swimmers (the only time I've ever cramped, incidentally), and also why, when you wake up in the middle of the night or sit in a strange position for a really long time, it's when you point your toes that you suddenly go into a fully-fledged cramp!
In other words, it's actually the position of the muscle that predisposes to cramp.
3. When is cramp most likely to occur?
Here, the answer is a little less overwhelmingly in favour of the neural fatigue model, but it is still a good argument for it, and against the electrolyte theory. The answer, of course, is that cramps happen during racing and not training, and it happens only at the end of the race, when the athlete is most fatigued. One could of course argue that it's only at the end that the electrolyte levels drop to the point where it causes cramps, but we described in Part II that there's zero evidence for this. So the explanation now would be that the muscle becomes more and more predisposed to cramp as it fatigues.
Supporting this, Schwellnus et al found that Ironman triathletes who paced themselves poorly and tried to cycle or run faster than they were capable of (based on previous performances) were going to be the ones to cramp. In other words, if a guy was capable of a 6 hour 180km cycling leg in the IronMan, and he tried to do it in 5h45, he would cramp. Note that this has nothing to do with electrolytes - he replaces the same amount, would lose the same volume of fluid, but he cramps because his muscles are not able to do the work he is asking them to! The resulting fatigue is what causes the cramp.
4. Is there any evidence for the theory?
The entire theory is built around this "end-result" that the activity of the alpha motor neuron is increased, due to the increased firing from the spindle Type Ia and the Golgi tendon organ Type Ib afferent fibres. Well, there is evidence that this is the case - the electrical activity of the muscles of cramping runners was measured after the 56 km Two Oceans marathon, and it was found that the alpha motor neuron activity was HIGHER than in non-cramping athletes.
Note that the electrolyte theory cannot explain this finding. Even more important, with 20 seconds of passive stretching, the EMG activity goes down. This means that stretching relieves cramps. Why would this be the case if electrolytes were to blame? Surely if the cause was low electrolyte levels, then the only solution would be to replace them? But instead, the most effective treatment is stretching, and it has been shown that the alpha motor neuron activity goes down. The act of stretching restores the normal balance, because suddenly, the Golgi tendon organ activity goes up again, and the muscle eventually relaxes.
Of course, this evidence is by no means the "definitive proof," and as Jonathan mentioned in Part II, we need to figure out a way to study cramps in a controlled, prospective fashion. Then we would be able to analyse exactly what is happening. Until that happens, we have theories and models. But this neural fatigue theory is certainly the best available theory for the observations of cramps at the moment. I have little doubt it will evolve over time, however!
Well done if you made it this far! I realise this is a pretty heavy post, and it relies on some level of physiology or anatomy knowledge, because there's a lot of jargon in the theory. That's something we prefer to steer clear of, but for this particular post, I felt it important to put out the necessary details. Of course, for some, we have probably oversimplified it, and please feel free to ask question.
For the others, the take home message really is that "Fatigue causes cramps, by interfering with the normal balance of spinal reflex control - it switches on the alpha motor neuron and the muscle contracts involuntarily."
Monday's post, which will be Part IV of the series, is a recap of some of the key issues in the electrolyte-fluid-cramp debate. I promise it'll be less technical than this one!