Beyond Dehydration: Why Cramping Really Happens And What You Can Do About It.

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Hey folks, it's Ben Greenfield. And one of the journals that I read on a regular basis is the strength and conditioning journal put out by the National Strength Conditioning Association. I always find a few interesting gems in each issue of that journal. And this past October, I actually read an article in there about cramping. Now, I have to be straightforward with you. As a guy who raced triathlon in a lot of really hot places for eight years, I thought I pretty much knew everything that there was to know about cramping and the ways to fix cramping and what really causes cramping. Until I read this article and then I realized, wow, there's a lot about cramping I didn't know and I learned a ton and, and I decided that I wanted to get the author of this article onto the show for you to tell you all about how cramping goes beyond dehydration, what truly causes cramping, and what you can do about it. So my guest today is Andrew Buscard, and he's actually doing his PhD studies in exercise physiology at the University of Miami. Currently he's got a master's degree in strength and conditioning from Springfield College, and he's the guy that wrote this article on cramping. So he's kind of, in my opinion, at this point in my life, the world's leading expert on cramping. So, Andrew, thanks for coming on the call, man.

Great to be here, man.

So this article is obviously jam packed with information, but one of the first things that you throw around here in the article is ea. Can you tell us what EAMC stands for and how that might be different than other types of cramps that might be associated with medical conditions?

Yeah, sure. So EAMC is just how in the literature and the research, how the authors refer to cramping during a race or during any athletic endeavor, really. So part of me wishes I had just read an EAMC once at the beginning of the article and just said cramping for the rest of the article because there's, there's certain synonymous. But I suppose in the terms of cramping during exercise, the real, real key difference between that and, I guess you call it medically, medically associated cramp is that there's a really high EMG activity on it. So really high electrical activity in the muscle. And that ties into the main dysfunction of what we think a cramp is, is that it's a hyper excitability of the, of the motor neuron and the dysfunction of the reflex pathway that, that sends an inhibitory signal back to the back, back to your spinal cord. And so you can kind of think of it as an EAMC is that it's a cramp where we know, we're pretty sure why it happens, whereas you can compare it to an idiopathic cramp or a contracture associated with a medical condition or in the fact that there can be dysfunction in a number of areas that will cause a muscle to contract forcefully and not let go. And those can be associated with different medical conditions. And so I don't quite know how deep you want me to go into those other reasons, but basically an EAMC is really strong motor signal to the muscle that sort of doesn't let up.

Okay. And that stands for Exercise Associated Muscle Cramp. Right?

Yeah.

Okay. Okay, got it. So when we're looking at something like an eamc, when you're talking about the difference between that and something that you might get because of a medical issue, I'm assuming that when we're talking about medical issues, we're talking about like night cramps from severe electrolyte deficiencies or hypothyroid related cramps or any of these other number of cramps that can be caused by medical issues. Right?

Yeah, I suppose so. So I guess we should talk about the physiology of how a muscle relaxes. And so one, one way a muscle needs to relax is you need ATP, you need, you need muscular energy not only to initiate the contraction in the muscle but, but to release it. So you have these myosin and actin cross bridges that they sort of grab onto each other, move a little bit, release, grab on again, move it a little bit. And you need a molecule of ATP to break that rigor bond. And so if you have a condition such as McArdle's disease or PFK, false with fructokinase deficiency is that can impair the energy supply to the muscle to the contractile sarcomere. And if the supply of energy to that sarcomeres is inhibited in any way, you're going to get that cross bridge forming, but it's not going to break. And so that's how you're going to get, you can get a permanent contracture. So that's actually, isn't that also like your mortises?

Yeah, I was going to say that's like what happens when someone dies, right. They, they can no longer generate ATP. So the muscle, like the entire body is in this state of a cramp.

Exactly. And so, and so that, that's one way you can do it. And then also, if you don't have ATP, you can't recycle calcium back into the sarcoplasmic reticulum in the cell. So basically the way the way contraction works is sarcoplasmic reticulum. It's kind of like the storehouse of calcium. And when you, when you move, you release calcium from the sarcoplasmic reticulum. And that's what actually initiates the contraction, the movement of the active myosin heads. But you need ATP to pump that calcium back into the sarcoplasmic reticulum to allow relaxation. So if any way that production of ATP is impaired, you're going to get permanent cross bridges and you're going to get impaired recycling of the calcium back in the sarcoplasmic reticulum. And so if you back it up a step into quote, unquote medical conditions, there's any sort of spectrum of conditions that could impair that, that generation of ATP. And that's also what ties into to some of, some of the theories of cramping that have been suggested in terms of hypoxia or high metabolite buildup in the muscle impairs that recycling and ATP function.

Okay, got it. Yeah. And I wanted to talk to you about some of the traditional theories as to the causes of exercise associated muscle cramps. But we're pretty much at the point now where we know that if this isn't related necessarily to a medical condition, and in many cases it sounds like even medically associated cramps are caused by this same physiology. It's essentially a problem with either you not having enough ATP at that skeletal muscle level or something inhibiting the ability for you to be able to use that ATP to relax the muscle.

Yeah, sure. And there's also normal membrane potential. So for the signal to get, you know, even from your brain, all the way down, all the way down your neurons to the motor nerve, all the way down to the muscle is, it's a process of sodium comes rushing in, potassium goes rushing out, and that's what propagates the signal. But if you, if that ionic balance gets disturbed in any way, that can affect how signals pass, pass along down to the muscle and how the signal from the muscle goes back to the, to the motor neuron to cause relaxation. And so that's, that's one area where you can have cramps. And so there's these central, sort of central areas. I suppose you could say that, you know, there's a five or six key mechanisms that have to be working properly for your muscle to relax. And dysfunction really in any one of those areas could in theory lead to a cramp. But sort of four of those areas are more associated with cramping due to medical conditions, so to speak, or idiopathic cramps. You call them silent cramps, whereas exercise induced ones. We really think it has to do with these spinal reflex pathways that we'll get into.

Okay, gotcha. All right, let's do that. Let's talk about the traditional theories of how exercise associated muscle cramps happen, because I know there's a few of them and I'd like you to describe them for us if you could.

Yeah, so I mean, researchers have been looking into why we cramp for over a hundred years. And some of the early research is actually kind of funny because you get these. Mostly they're German. They're these German researchers and they have just.

The Germans must cramp a lot, huh?

Yeah, I guess. But just the tone with which they write is super, super patrizing and kind of sexist sometimes, you know, they'll say, oh well, cramps are more prevalent in people who are insecure and those who get lasting stiff, who don't get lasting satisfaction from their endeavors and pretty funny things. But ever since the 100 years, they've really thought it's had something to do with sort of heightened sympathetic nervous activity and spinal reflex loops, although they didn't, didn't quite phrase it that way. But the real big one, I suppose that's had a lot of, a lot of people believing for a long time is that cramps during exercise EAMC are caused by dehydration when you get dehydrated and low electrolyte levels. That's what precipitates cramps. It was first noticed in minors working really, really hot, humid conditions that they would cramp. And it just, it just seems that there's no, there's no evidence, so to speak, that this is what, that dehydration and electrolyte deficiencies is what causes cramps. There's two, two real, real big studies that sort of highlight this point, or at least there's researcher, this guy Schwelnitz, and also a guy, Timothy Noakes, who Wrote water logs.

Yeah, he's been on the podcast a couple of times.

Yeah. Okay, there you go. So him and his colleague, this guy, this guy Shloma down in University of Cape Town, what they did is they looked, they were interested in cramps. And so they went to, they recruited people who were doing triathlon and sort of an ironman triathlon and a marathon. And they said, all right, let's look at, let's look at if dehydration and electrolyte depletion are what are causing cramps here. And what they did is they took so serum electrolyte levels, so they took a blood draw and they saw where their electrolyte levels were at, and they did that pre and post race. And then they also looked at their body weight changes, which is indicative of dehydration. And what they found is that the people who did cramp and the people who didn't cramp, no difference in final serum electrolyte concentrations, nor is there any difference in how dehydrated they were. So you'd think if dehydration and electrolyte and low electrolyte levels were what were causing cramps, you'd think that those who cramped would have greater body weight loss and lower electrolytes. But, yeah, I don't, I don't think.

I don't think Gatorade liked the results of that study too much.

No, no, I don't, I don't think. I don't think they did either. And so, interestingly enough, they did. They did come up with another. A bunch of risk factors that correlated to a higher, higher chance of cramping. But, but none of them had to do with electrolyte and dehydration. Another theory is they. Is one of the real or real early ones was a psychosomatic origin. So that's basically a relationship between your mental state and cramping. And so these early German guys talking about people who are really anxious, intense, and while the way they phrase it would never fly today, they kind of have a point in terms of those sort of conditions, would being in that state correlates to a higher sympathetic, higher sympathetic state or sort of a mild fight or flight condition? And then, you know, when we get into real nitty gritty, the abnormal spinal reflex and the muscle spindles is that when you have a really high sympathetic activation, you get that muscle spindle closer to the threshold of where, where it's going to, may cause you problems. And so, and so it's, it's sort of a. These guys, this Psychosomatic origin is kind of, kind of out of left field the way they describe it. But there's, there's kind of a, the underlying sort of kernel of truth underneath there. But they sort of phrase it wrong. Right. There's another, there's, there's another one is a vascular origin of muscular, muscular cramp. It's just, is when you get claudication, when you get a cease of blood flow to the area. And that, that, that makes, that makes sense because what we talked to about, about the ATP levels, when you block the blood flow, you're eventually gonna, you're eventually gonna exhaust your ATP, your personal exhaust, your oxidative energy pathways and your non oxidative pathways. So you're gonna have no ATP, then you're gonna have a huge hydrogen buildup from your lactic acid dissociating. And all those factors are going to contribute to the, to the muscle basically stopping to function. And so that's, that could be one contributing mechanism. And so I guess all these researchers is there, they're trying to find like the, this is the main, it's, this is it, this is the reason why we cramp. And really, it's really more seems like it's a constellation of factors that sort of contribute in different amounts in different situations. So in some situations, sure, occluded blood flow may cause a cramp, but when it comes to at least prolonged endurance events, that the spinal reflex loop dysfunction is sort of the key one to look at.

Yeah. And that's one that it seemed that neurological stimulus for exercise associated muscle cramps really seemed to be something that you felt in the article was the primary culprit or at least one of the really true underlying factors. And that's one that you don't hear talked about as much, of course, compared to dehydration, lack of electrolytes occasionally like tightness in the muscle, etc. But I'd like, if possible to hear kind of your explanation of what exactly you mean when you say that the neurological stimulus for cramping is probably the, the most common reason that a cramping occurs and kind of what's going on physiologically when that happens. I know it's a loaded question, but we're all geeks here on the Ben Greenfield Fitness. Yeah. So we're okay with you delving into the science if you need to.

Sure. Okay. So I guess we should start off is we really need to know the function of muscle spindles and golgi tendon organs. And they're both these sensory Receptors in the muscle that help regulate tension. And so they really help us use with fine motor skills. One analogy you can kind of think of, it is when you, if you're packing your car into a parking spot, you don't just hit on the gas and then slam on the brake. You know, you kind of do a little bit of gas, you know, a little bit of brake, little bit of gas, and sort of ease your car in there. And that's how these muscle spindles and Golgi tendon work is there. They work together in a negative feedback loop to really regulate the fineness of our motor skills. And so what a muscle spindle does is it's within the main belly of the muscle, and in essence, it's there to prevent hyperextension injuries. And so if a muscle stretches really fast, it's going to send a signal through the afferent or through its main feedback pathway to the motor neuron, or sort of. You kind of think of it like a regional control center. So, so your brain is the brain, the main control center of your body, but it has these regional control centers for these reflex loops. So if you touch a hot pan really quickly, that signal doesn't go all the way up to your brain, and your brain sends a signal back, oh, better pull the hand away. The signal just goes to this, the motor neuron in your spine, and it sends the impulse back out. So it speeds it up. And so what the spindle does is if your muscle stretches really fast or if it's getting to the end range of the motion, these muscle spindles fire and they send a signal back to the motor neuron, and it reflexively sends a signal back to the muscle to contract it.

Hey, quick break here. This is Jessa Greenfield, Ben's boss. I mean, wife. I'm not sure if you know this, but Ben, being the complete nerd that he is, keeping track of everything he's ever recommended and found to work really well and puts it all over@greenfieldfitness systems.com from books to lab tests to supplements, he has it all there. So whether you want to build muscle, burn fat, fix your gut, sleep, better, balance hormones, learn about smart drugs, whatever, it's all there. Check it out@greenfieldfitnesssystems.com okay, now back to the podcast.

So, totally random question. I've heard one of the reasons that, like, chimps and gorillas and animals like that are much stronger than humans, even though they have similar amounts of muscle mass, is because they actually don't have the same type of neurological mechanisms. To inhibit the muscle from contracting over and above what it would normally be able to do to, you know, keep the muscle from tearing or straining or spraining something. Is that true? Do they have less of a Golgi tendon organ reflex?

You know, I've never heard of that, but I think that could just be a function of me, not sort of directing. Directing my interest in that way. But it makes sense. Yeah, we have a ton of. That's the function of the Golgi tendon is to prevent us from having such a strong contraction that in fear, you could rip your. You know, rip a tendon off its insertion. And so, interestingly, one of the initial adaptations to strength training is there's no. You get stronger, not because you're adding muscle or anything like that, just that your body is sort of taking off the brakes, so to speak, because it's desensitizing these Golgi tendons to let you access more of your muscle fiber. So to complete the sort of. The story of muscle spindles and Golgi tendons is the Golgi tendons are in. Or the Golgi tendon organs are right where the muscle meets the tendon. And what they do is they prevent the muscle from generating too much amounts of force. And so they're these little capsules. And when they get deformed, they send a signal back up. Back up to the spine through something called an inhibitory interneuron, which. Which shuts down how much. How much output is coming from the motor neuron. And so you can kind of think of. Kind of think of bulgy tendon is sort of like the stop button on the treadmill. When you're getting. When you're getting going too fast, you can't quite handle it. The Golgi tendons will slow that down. And so the essence of the neurological perspective on cramping is that fatigue, so actual actual damage at the muscular level results in a hyperactivity of the muscle spindle where it's sending out stronger impulses than normal, and concurrently, an inhibition or a down regulation of how these Golgi tendons fire. And so you get this positive feedback loop where the system that's supposed to be putting on the brake, that's supposed to be causing relaxation in the muscle, it's dysfunctional. And so the spindle just keeps firing around and the motor neuron sends its contractile output, and that's how you get the permanent state of cramp.

Now, one of the things that you talk about in the article is the Big question mark about whether this, this hyper excited ability of the, of the Golgi organ or the inability of the muscle to relax when it's in that state of a cramp is because of central mechanisms or what you call peripheral mechanisms. Can you differentiate between the two?

Sure. So both, both central and peripheral mechanisms relate to this dysfunction at the neurological level. So you can, in a way you can think of it as researchers having different explanations for the same phenomena. And so what I just explained, that would be considered the central mechanism because the, the main effector, so to speak, comes from the motor neuron, sort of the regional control center in your spine where, you know, it's the reflex, it's the afferent signal to the motor neuron and then the motor signal back to the, back to the muscle. But the peripheral, peripheral way research, some researchers think about this is that it's a dysfunction where the, at the neuromuscular junction. So where the neuron that sends a signal from the, from the spine connects to the muscle. And so the way, the way that signal, it comes as an electrical signal down the motor neuron, but to cross into the muscle, they call it the neuromuscular junction, is actually a release, these neurotransmitters, it's a release of acetylcholine. These little chemical vesicles trans, go across this tiny little gap and then when they reach the, the motor end plate, they call it, when it reaches the muscle, the muscle itself, these acetylcholine molecules bind to their receptors. Then they open the sodium potassium channels and then the signal becomes electrical again, fired down the fires down the muscle. And that's what causes contraction. And so the peripheral theory here is that there's a dysfunction at that neuromuscular junction. And so it could be because there's so many action potentials firing that the acetylcholine can't be recycled back into the terminal bulb, so to speak, or into the area that releases it. And so you get this accumulation of acetylcholine in the synaptic cleft. And so that just continues because it, it doesn't get removed, it just continues to activate those receptors and continue and continue to fire the signal along. And so that, that actually ties into how some people have said that that's how dehydration could manifest this peripheral dysfunction or how dehydration could play a role in cramping at the neurological level. Because when you get dehydrated, in theory, that would cause a concentration increase in, in the, in the concentration of certain electrolytes and the acetylcholine receptors. And also because, because, because of the volume loss, some researchers have suggested that there's a physical deformation of the, of the, of the neuromuscular junction of the. At the motor end plate. And so that's essentially the, essentially the thought, the thinking behind the peripheral mechanism is that it has to do with the dysfunction where the motor neuron meets the muscle, and that's what's continuing to send the signals down the muscle to contract. And sort of, that's the balance. But it looks like that it's more significantly the central mechanism. There's a big study that looked at. They put a muscle, they put a nerve block. So basically what they did is they blocked the, the ability of that, that reflex pathway to go to the, to the motor nerve. And then they, they electrically stimulated the muscle. And they found that it took a much stronger stimulus to get the, to get the contraction elicited without the, without the central. Without the, without the motor neuron. Because you can kind of think of it as like a sort of like an amplifier. So you can have, you can have a pretty small signal sent from the muscle spindle, but the motor neuron can really jack up the signal that it sends back out. And so that's what would make. Even a small dysfunction at the motor spindle could magnify into a large dysfunction causing a large contraction in the muscle.

Right, and that you just described would be more of a peripheral mechanism, right?

Yeah, exactly. Exactly. Yeah.

And so what you're saying is that we rarely see that type of cramp occurring compared to, like, a central nervous system cramp that originates more from the spinal cord.

Yeah, I mean, yes, I guess all these, all these, these answers are qualified because there's not, there's not a huge, huge amount of research that goes into the specific mechanisms that we're talking about. And then, and so, and so also there's a problem with sort of the nature of these research studies is that they're. The way they're designed. I mean, you can really say that it's. It's an issue with all sort of scientific. The nature of all scientific research is that you really have to go out and you have to say, make a firm hypothesis. And so it's. It's either this or it's either that, and it doesn't really leave a lot of. A lot of room for a gray area of sort of a relative contribution of both. And so at this point, it seems like the central mechanism, the abnormal reflex pathway Plays a much more significant role. But at this point, you can't really say that there's no contribution of a peripheral mechanism. But I guess the qualified answer is it appears to be mostly that the abnormal spinal reflex.

So if it is an abnormal spinal reflex, then that means that a big, big part of this could potentially be neurologically related in terms of overexcited ability, perhaps a lot of cortisol, a lot of nervousness, a lot of tension, and even returning to some of the woo woo stuff that, you know, those, those old school German research we're talking about that you mentioned that there is potential, it appears if this neurological form of cramping and this, you know, more specifically the central mechanism of the neurological stimulus for cramps is occurring, it could, a very, very big part of this could be your mental state when you cramp.

Yeah, definitely. I suppose the reason that essential mechanisms have the most support is that they're the only ones with a really clearly clear mechanism where research you can say, yeah, this is clearly how we think it happens. This is kind of the research that supports it. And so in terms of how the nervousness or the increased sympathetic activity would manifest, that is, not only do you have motor nerves that go to the muscle that causes a contraction, these actual muscle spindles, in order for them to be sensitive at all muscle lengths. So for example, when a muscle's almost completely contracted versus when it's, when it's lengthened, there needs to be. The actual muscle spindle itself has a little muscle fiber in it. And so in order to be functional at all lengths of the muscle, this muscle spindle itself needs to lengthen and shorten. And so it has its own tiny little itty bitty motor neuron itself. And so the more, the more a 12 gamma motor output, so the more motor output to these little muscle spindles is, the more sensitive they are. And so that's, that's the main, that's the adaptation of strength training. So when we talk about the neurological adaptations of strength training in the first couple weeks is a lot of it has to do with the desensitization of the mode of your sympathetic motor output to these little motor, to these little muscle spindles. And so it's sort of letting you tolerate more, letting you tolerate more tension in the muscle, so to speak. And so the way, I guess the way to think about cramping is that everybody has a, everybody has a cramp threshold, so to speak, is that a certain number, once you exceed a certain number of impulses per second, then the Muscle is going to cramp. And so kind of the way I look at it, there's a way to explain this is sort of. Imagine you worked in, maybe you worked in a sandwich shop. It's not very busy at all. You only get one customer an hour. So, you know, one customer comes in, you get up, you know, you make them a sandwich, and you go, you go sit down, you relax for the.

Rest of the hour.

And then, okay, maybe you had two customers in. So you get up, make two sandwiches, and sit down. And so there comes a point where the customers are coming so frequently, you know, you never get to sit down. You're on your feet the whole time, you know, making sandwiches. And so there's differences. Different individuals have a different cramp threshold. Whereas so some people, once they're getting 15 signals per second, then that muscle's in a tetanus, then that muscle is in a cramp. Whereas other, other individuals, well, that threshold isn't at, is not maybe 20 hertz, 20, 20 impulses per second. And so one, one theorized mechanism or one predisposing factor, we think, to cramps is that inherently some people have a lower threshold, lower frequency threshold for cramping. And so the, the, the way that higher nervousness or a higher sort of sympathetic tone we call it, is that that increases the number of signals you're sending just at baseline. So just, just standing, waiting for your race to get going, maybe you're already sending seven signals down per second, and so you have sort of less of a buffer of increase before you hit that threshold, that cramp threshold, and your muscle is going to be permanently cramped.

Right, that makes sense. Now, when it comes to the central fatigue mechanism, would this also be why, when you, for example, swallow an electrolyte or a salt capsule, it may not reverse the cramp. Whereas when you simply taste something extremely salty, you know, like the famous pickle juice, reverses cramping study, it causes almost like this instant reflex reaction where you stop that cramp. I believe it's via the alpha motor neuron, but it's all like via the spinal cord. It's just like, boom. It happens so fast that there's no way the salts could have actually gotten to the muscle. Does that help to support this central mechanism?

Yeah, I mean, I suppose so completely. Yeah. I mean, there's a placebo effect. If you think, if you think it's working, then you're going to relax and it's going to drop the amount of tone or amount of baseline signals you're sending Just by nature of your mental state. Sure.

And even that pickle juice study, I think, was not even suggesting it was a placebo as much as it was that that reflexive gag to tasting something incredibly salty just caused that cramp to release. Just based off a really quick alpha motor neuron inhibition of the cramp. When I was reading through your description of the peripheral versus central mechanism, I thought, well, you know, the fact that he's leaning towards a central mechanism as being what causes this cramp could possibly lend credence to this whole like taste something salty theory. Now you also, you get into just a few other, you know, there were three other theories that you talk about. The environmental theory of cramps, the fatigue theory, and then the possible genetic predisposition to cramp to cramps. Can you delve into those really briefly just to outline a few of the other theories that may hold a little bit of credence here when it comes to cramping?

Sure. So the environmental theory is simply that extreme environmental conditions could cause you to cramp. So super hot environments or super cold. And I guess the way to think about the environmental theory is that's not, that's not what directly is causing it, but they could be a predisposing factor to other mechanisms that are going to cause your cramp. So for example, in the extreme heat, higher muscles of heat actually within the muscle could cause an abnormal function of your contractile mechanisms or your ATP recycling. And also the extreme heat profuse sweating that could, that could play a role. And so I guess the way to think of electrolyte depletion or dehydration electrolyte depletion is not exactly to throw it out the window and say it's not a factor at all. So yes, there's no scientists or the research hasn't really shown that this causes cramps, nor is it has a proposed mechanism, but it by no means has it been sort of disproven, so to speak. So you kind of want to be careful and sort of think that the absence of evidence is not evidence of absence.

Right. And even if, if like dehydration or lack of electrolytes may not actually cause cramps, you know, even in these, these hot and humid environmental conditions. And I, I kind of personally tend to think that's the case, but because when I first talked to Tim Noakes two months later, I decided I'd put it to the test and I went and raced Ironman Hawaii without using any electrolytes at all. I drank normal amounts of water, but I didn't use a single salt capsule and no electrolytes and did just fine. However, it's possible, I suppose, that if you were very hot or very cold, you would also be very uncomfortable. And if you're very uncomfortable, you might have a lot of sympathetic nervous system activation and that could potentially cross over into causing this central neurological related fatigue where you're just like so tight because it's so hot or so cold. Or maybe even you think being hot or cold could cause more cramping because that's what you've been led to believe, that that could actually also cause a cramp.

Yeah, yeah, I think that's totally fair. And sort of one way I think of cramping is there's possibility that this idea of task dependency might, might factor into it and that you can kind of think of task dependency is that the cramping is dependent on the task that you're doing. So this concept comes from the general idea of fatigue in general. So sort of the reason you'd fatigue, say you're doing a maximal deadlift. The reason you can't do more than one or two of your real heaviest. The reason you fatigue there is going to be different from the reason you fatigue during a 400 meter sprint is gonna be different from the reason you fatigue running a marathon. And so by the same token, I think there might be room to consider that depending on the task that you're doing, certain mechanisms might be contributing differently. And so the way, the way I, how I kind of think of it is that, yeah, spinal reflex, that seems to be the heavy hitter, but we can't really wipe off these other mechanisms off the table.

What about just pure pure fatigue, Pure muscle fatigue? Because you hear about that a lot too, right?

Okay, yeah.

So, yeah, yeah, you simply get to a point where the muscles just give up almost. Is that, is that a credible theory?

Yeah, definitely. So that's actually, that's actually a contributing, A contributing factor to the central mechanism is that the fatigue correlates to physical damage at the, at the microscopic muscular level. And so the article written by, written by Noakes and this guy Schwalmis is that they think that the reason we get this abnormal, this abnormal spinal reflex is that it's the physical damage to the muscle that causes damage to the muscle spindles, causing their hyperactivity and the physical damage to the Golgi tendon organs that causes them to desensitize. And so fatigue is basically the key reason. And so the outcomes of what they found was their research into Cramping in these Iron man triathletes, where they didn't find anything to do with dehydration and low electrolyte levels is they found that the biggest predisposing factors to cramping were a failure. So improper tapering, so not tapering enough before the event, and also a faster training pace than. Or, sorry, a faster race pace than they trained at. And both of those factors make sense.

Asking the muscle to do something, competition, that you have an asset to do in training, basically. Yeah.

Well, I mean, it's just, you're just, you're speeding up the rate at which you get the muscle fatigue. Just that muscle is going to hit that critical fatigue or damage level. So sooner, and then you're gonna. You're gonna get that cramp.

Yeah. Now, are some people, do you think, more genetically predisposed to cramping?

Yeah, that's. I guess that's the third. The third topic that I kind of got off on a tangent on. But yeah, it's. It's only. It seems to be only one study, and it was Sholom, he was in this as well, is that there's some evidence that genetic. You can have genetic variations that predispose individuals to soft tissue and musculoskeletal injuries. And so what they think it relates to is extracellular structural proteins. So you can kind of think of a muscle as. Obviously, it's a collection of millions of these tiny little muscle cells, but they exist within the structure, sort of scaffolding, if you will, a sort of a scaffolding that gives them structure. And this scaffolding is made largely out of these things called collagen fibers. And so there's not just one gene for collagen fibers. There's a number of genetic variations. And so again, you kind of think of it as if this is scaffolding. You know, you could, you know, you could drink, there's. You could build scaffolding out of different kinds of wood. You know, you have pine or oak or whatever, and each you're going to have different strengths, different structural properties, and that's sort of the same thing as genetic variations of collagen. And what they found is that certain, certain collagen variations are just. They're weaker. They don't hold up to the repetitive stress of running or, you know, doing whatever for eight hours. And so if, you know, if you're scaffolding, if your structure is not as strong, then it's going to fail sooner than you're going to get to that breakpoint. Where you're getting physical distortion of the, of the spindles and, and the Golgi tendons. So that's, that's sort of the essence of the genetic, genetic theory is that you can have a certain, certain gene variations can impact the durability of the, of the, you know, start to be a very cellular level of resisting damage.

Yeah, it's very interesting and I'm always curious about whether or not those differences in connective tissue and tendons that might predispose someone to cramping could be something that you would be able to size up from a qualitative standpoint.

Right.

Like look at somebody's body type, like whether they're like ectomorphic skinny or mesomorphic muscular, like endomorphic apple shape. And if there's any type of way to see just by looking at someone versus like I guess a muscle biopsy to look at connective tissue or something like that, whether or not someone might be predisposed to cramping just based off of their body type. Just because like, from what I've found, just, and this is totally observation based and not research based, over a decade of coaching, it seems that my skinnier, more slow twitch athletes simply cramp less. And possibly that's because of weight, it's because of fatigue, it's because of muscle damage, whatever. But I'd be curious if there's connective tissue differences as well and if those connective tissue differences manifest themselves in changes in body type.

Yeah, I mean, you bring up something interesting about the, your quote unquote slower twitch athletes because that makes sense. So the lesser amount of highly glycolytic fiber, so your type two, those are the main contributors that are going to dump out a lot, dump a lot of, a lot of hydrogen because when you break up a glucose without oxygen, you produce, you produce two hydrogen molecules. And also those fast switch muscle fibers they receive, they send out a much, they're much more electrically active. And so if we're looking at cramping being related to hyperactivity of the muscle units, these big strong electrical ones that send out a strong electrical signal, then those are, those are more likely to contribute to cramping. So that's interesting that you've noticed that because, you know, based on why we think we cramped, there's a lot of reasons to think that that would make sense, that the slower twitch athletes would be less, have a lower disposition to cramp.

Now ultimately, let's say that someone doesn't have an electrolyte imbalance, right? They've got their bases covered from a mineral standpoint and they're hydrated. We know that hydration based off of what you were talking about with no, for example, may not be as important as we've been led to believe. Unless, unless you are severely dehydrated. But let's say someone you know has their, their electrolytes balanced, they're not severely dehydrated. What would you suggest to someone who just keeps on getting exercise associated muscle cramps based off of what you found when writing this article?

Yeah, I mean I'd be curious to ask them if they, if they strength train. Because, because strength training will be, it's sort of like, it's almost like flushing the pipes. Like you're just, you're reinforcing the, the normal function of a muscle spindle. And then also, also by strength, strength training is you're going to reduce the sensitivity of your muscle spindles and you're going to reduce the sensitivity of the Golgi tendon organs. You're going to sort of get the muscle to realize, okay, you know, this is, this is the amount of tension that I can handle that, you know, don't freak out. This is the muscles working like it's supposed to. And so, you know, so for a lot of, a lot of movements, you know, you can talk about sort of grooving the pattern. You know, if you're trying to teach someone to squat or do whatever, you know, blotter has to groove the pattern. And you can, you could almost think of, you want to groove the pattern of your spinal reflex to work normally. And so it's possible if someone, someone doesn't strength train, they can have abnormal, abnormal firing patterns. You can also have like something called synergistic dominance where, you know, sleepy butt syndrome, for example, where your quads are doing all the work when, when you're, when your glutes should be kind of contributing. And so say for example, you have synergistic dominance in that your calves are doing a ton of, a ton of work. And so that's just going to speed up the point until they cramp. And so I was thinking about this earlier. It's possible that a midfoot strike seems like it's beneficial for so many ways and better than a heel foot strike. But one thing about a, about a mid, mid foot strike is that the calves are being subjected to a much higher stretch and stretch with each stride and so part of, part of the reflex. So when you, when you hit the ground, particularly in a midfoot strike, you get the stretch shortening cycle. So all these elastic components in the, in the calf stretch and that's also what causes the muscle spindle to fire and reflexively sends a signal back. Let's contract this muscle. Your foot pops up and you spring into the next step. But so the midfoot strike could lead into. You're pushing that muscle spindle further towards hyperactivity. And so that could be one component of it.

Yeah, and you certainly do hear about that quite a bit. And people who switch shoes or who make significant changes to their running gait as they start to experience cramping. That makes sense. So we've got strength training, we've got actual biomechanics of movement. Any other recommendations for folks?

I don't know. I mean if they have a genetic predisposition, there's not much you can do. I mean if they have a lower cramp frequency, there's not much you can do. I'd be wary of static stretching before an event.

Yeah, yeah, there's a pretty bad trade off there with, with power production. Of course. You know, we, we talk so much about this central mechanism and about the potential for sympathetic over activation. How much do you think mental training comes into play? Focusing on relaxation, visualization, breathing, you know, focus and you know, even potentially using, you know, things like, you know, there's all sorts of like relaxation soundtracks to increase alpha brainwave production and different ways of kind of staying focused and relaxed during activity. Do you think that that is something that is underplayed with respect to cramping and a potential strategy to mitigate it?

You know, I've never thought about that and I mean there's, I thought about it a lot.

I thought about it a lot when I was reading your article. It's like, yeah, okay man, a lot of the time has got to be mental.

Yeah, well, I mean that, that perspective fits right into, right into the, to what we're talking about here. I mean anything that, anything that increases your baseline sympathetic tone will ask you to push you closer to cramping and anything that, that lowers your sympathetic tone is going to pull you further away. And so yeah, I think you're, I think you're bang on there. I think you're. That, that's, you know, a fine explanation. And what I would add to that is that what you're talking about doing is there's benefits to that, to your performance above and beyond just cramping, you know, so working on the mental side of your race. That's great for a lot of reasons besides cramping and so, yeah, give you a thumbs up for that.

Yeah. So I can think of, you know, and I always like to leave people with a few actions, steps. Just based off of everything that you've told me so far, Andrew, I can think of a few things that people can try if they are okay on electrolytes and they're okay on hydration. And we talked about three of them already. You know, strength training, looking at biomechanics, maybe even like going to a lab and getting a biomechanical gait analysis to see if you're running properly, looking at relaxation and figuring out ways to train your brain. Right. Don't. Don't discount the importance of brain training. You talked about muscle damage and how muscle damage could be an issue and improper tapering could be an issue. So maybe if you find yourself cramping a lot going into races, maybe try making your taper a little bit longer or better, like, learn how to really, truly go into a race or a big event. You know, whether you're competing in the CrossFit games or you're doing a triathlon or whatever, go in a little bit more relaxed than you think you should be. Potentially even, as they say, 10% under trained is better than 1% over trained. That could be a good one. I know that weight. When you're running or you're exercising and you've got a lot of excessive weight, your muscles are susceptible to more damage. They're simply having to absorb more impact. And so I would say if you're not taking into account your weight and aspects of your diet that go above and beyond electrolytes and hydration, such as how much face stuffing you're doing, that might come into play as well, potentially. Especially if you're like a, A chronic repetitive motion athlete, like. Yeah, like a runner, for example. And then, of course, there's always that genetic theory. You could always go back and be born to different parents. You know, it's always.

Yeah, yeah. I mean, you can always just sort of just back off, you know, back off the face a little bit. Yeah. And that might help as well.

Yeah. Interesting. Oh, and one other thing I wanted to ask you about, and I know we got a rumble pretty soon, but did you come across anything as far as carbohydrates, as far as like, glycogen depletion? Would that be a part of the fatigue mechanism that you discussed? I'm just curious because we have a lot of folks listening in who are like, experimenting with ketosis and low carb diets. And things along those lines. So I'm curious if there's a link between cramping and glycogen depletion.

Well, I mean there was one study that looked at, took a bunch of college students and looked at the time, at how long it took for the time to cramp onset. And one was in a low electrolyte, low electrolyte, low carbohydrate state. And another one was they, they, I think they gave them Gatorade and there are no dietary restrictions that they found that the time to onset of, of cramp was, was extended when you did have, when you did have enough, when you did have enough carbohydrate stores. So yeah, I'd say, I think it's fair to think say that having, having sufficient glycogen stores are going to, are gonna, may, may, may prolong the time to fatigue. And also just burning fats and burning proteins is just such a, such a more complex by, you know, the, the metabolic processes to break them down is so much more complex. And so there's just, there's just many more steps that something could go wrong that could possibly, you know, precipitate fatigue. And so you're, I mean your body, your body certainly can perform on.

Yeah, I would say, I would say especially if you haven't trained yourself to do so. Right. Like that's even one of the things you talk about. Nokes. Like that's what he's talking a lot about now is like sure, you can, you can do just fine and probably not experience a lot of deleterious effects during exercise from a low carbohydrate diet.

Yeah.

If you've actually trained yourself in training to be able to up regulate those mechanisms or even like trained yourself to have enough mitochondrial density to be able to handle oxidation. So yeah, you know, if you, if you, if you restrict carb for two weeks and then you know, maybe taper for a week and go compete, that's probably not such a great idea.

No, it takes a while to get your body to shift over.

Well, what I'm going to do is in the show notes for this podcast, you can grab them over@BenGreenfieldFitness.com YCramping that's BenGreenfieldFitness.com yCramping I will put a link to the original article that Andrew wrote if you happen to want to get access to that article. I believe on most peer reviewed research websites there's a little bit of like a pay access if you want to pay to grab the article and read it yourself, you can do so. Or if you happen to subscribe to the National Journal of Strength Conditioning Research or you want to grab it from your local library, you can always look at it there, too. And I'll put a link to the resources that we talked about during today's episode all over there@BenGreenfieldFitness.com YCramping and Andrew, thanks so much for coming on the call today. Man, this was fascinating.

Yeah, I appreciate it. Yeah, no worries. All right. Cool.

Well, folks, this is Ben Greenfield and Andrew Buscard signing out from BenGreenfieldFitness.com have a great week.

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