December 13, 2014
[00:00] Greenfield Fitness Systems
[01:17] Introduction about Andrew Buskard
[02:52] What is EAMC?
[10:40] Correlation of Dehydration and Cramping
[18:59] Function of Golgi Tendon Organ
[20:55] Difference Between Central Mechanisms vs. Peripheral Mechanisms
[30:35] Environment, Fatigue and Genetic Theories of Cramping
[32:25] Three Theories of Cramping
[38:00] Are Some People More Genetically Predisposed to Cramping?
[42:10] Andrew’s Suggestions for People who keep getting EAMC
[49:20] The Role of Carbohydrate Depletion
[52:34] End of Podcast
Ben: Hey, it’s Ben Greenfield here. If you want to support this podcast, you can definitely do so by going over to the one website where I store everything that I ever recommended for you to get to your goals as quickly and safely and effectively as possible and that website is greenfieldfitnesssystems.com. So check out greenfieldfitnesssystems.com; it helps to support this show and now, on to today’s interview.
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 and 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 race triathlon in a lot of really hot places for 8 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 I decided that I wanted to get the author of this article on to 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 Buskard 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 leading expert on cramping. So, Andrew thanks for coming on the call, man.
Andrew: Great to be here man.
Ben: So, this article is obviously jam-packed with information but one of the first things that you throw around here in the article is EAMC. 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?
Andrew: Yeah, sure. So EAMC is just how, in the literature, in the research of how the authors refer to cramping during a race or during any athletic endeavor really, so part of me wishes I just wrote EAMC once at the beginning of the article and just said cramping for the rest of the article because they’re sort of synonymous. But I suppose in the terms of cramping during exercise, the real key difference between that, I guess you call it a 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 motor neuron and a dysfunction of the reflex pathway that sends an inhibitory signal back to your spinal cord.
And so you can kind of think of an EAMC is that it’s cramp where we’re pretty sure why it happens, whereas you can compare to an idiopathic cramp or contracture associated with a medical condition in the fact that there can be dysfunction in it and a number of areas that’ll cause the 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 do you want me to go to one of those other reasons but basically, an EAMC is really strong motor signal in the muscle sort of doesn’t let up.
Ben: Okay. So, and that stands for Exercise Associated Muscle Cramp, right?
Andrew: Yeah, yeah.
Ben: 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 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?
Andrew: Yeah, I suppose so. I guess we should talk about the physiology of how muscle relaxes and so, one way a muscle needs to relax is you need muscular energy not only to initiate the contraction in the muscle but to release it. So you have these myosin and actin cross-bridges that grab on to each other, move a little bit, release, grab on again, move it a little bit and you need a molecule of HTP to break that rigor bond. And so if you have a condition such as McArdle’s disease or PFK, Phosphofructokinase, deficiency is I compare the energy supply to the muscle, to the contractile sarcomere. And if the supply of energy to that sarcomere 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, how you can get a permanent contraction. So that’s actually what rigor mortis is.
Ben: Yeah, I was gonna say that’s what happens when someone dies, right? They can no longer generate ATP so the muscle, the entire body, is in this state of a cramp.
Andrew: Exactly, and so that’s one way you can define 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 contraction works is sarcoplasmic reticulums, kind of like the storehouse of calcium, and when you release calcium from the sarcoplasmic reticulum that’s what actually initiates the contraction, the movement of the actin and myosin heads. But you need ATP to put all that calcium back into the sarcoplasmic reticulum to allow relaxation. So if in any way production of ATP is impaired, you’re gonna get permanent cross-bridges and you’re gonna get impaired recycling the calcium back in sarcoplasmic reticulum. And so if back it up a step into “medical conditions”, there’s any sorts of spectrum of conditions that could impair that generation of ATP and that’s also what ties into some of the theories of cramping that have been suggested in terms of hypoxia or high metabolic build-up in the muscle impairs that recycling and ATP function.
Ben: 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.
Andrew: Yeah, sure. And there's also normal membrane potential, so for signaling that from your brain all the way down your neurons, to the motor nerve, all the way down to the muscle, it’s a process of sodium comes rushing in, potassium goes rushing out and that’s what probably is the signal but if that balance gets disturbed in any way, that can affect how signals pass along down to the muscle and how the signal from the muscles goes back to the motor neuron to cause relaxation. And so that’s one area where you can have cramps; there’s the central sort of, central areas I suppose you could say, that there’s 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 certain medical conditions so to speak or idiopathic cramps, side cramps, whereas exercise-induced ones, we really think it has to do with the spinal reflex pathways that we’ll get in to.
Ben: Okay, gotcha. Alright, 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.
Andrew: Yeah, so the research that I’ve been looking into, to why cramps for over a hundred years and some of the brilliant research is actually kind of funny because you get these, mostly they’re German researchers…
Ben: The Germans must cramp a lot, huh?
Andrew: Yeah I guess, but just the tone which they write is super patronizing, kind of sexist sometimes; they’ll say “well cramps are more probable in people who are insecure and those who don’t get lasting satisfaction from their lovers” and pretty funny things.
Andrew: Ever since, for a hundred years they really thought it had something to do with heightened sympathetic nervous activity and spinal reflex loops, although they didn’t quite phrase it that way. But the real big one I suppose that’s had 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 in really, really hot, humid conditions that they would cramp, and it just means that there’s no evidence, especially that dehydration and electrolyte deficiencies is what causes cramps. So there’s two real big studies that sort of highlight this point; this researcher, this guy Schwellnus and also a guy, Timothy Noakes, he wrote “Waterlogged”.
Ben: Yeah, his name has been on a podcast a couple of times.
Andrew: Yeah, okay, there you go. So him and his colleague, this guy Schwellnus, down in University of Cape Town, what they did is they were interested in cramps and so they recruited people who were doing triathlon and Ironman triathlon and marathon and they said “alright let’s look at dehydration and electrolyte depletion or what are causing cramps here.” And what they did is they took serum electrolyte levels, so they took a blood log and saw what 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 the people who did cramp and the people who didn’t cramp, no difference in final serum electrolyte concentrations, nor was there any difference in how dehydrated they were, so you’d think if dehydration and low electrolyte levels were what causing cramps, you’d think that those who cramped had greater body loss and lower electrolytes but that wasn’t the case.
Ben: Yeah, I don’t think Gatorade liked the results of that study too much. (laughs)
Andrew: (laughs) No, I don’t think they did either. And so interestingly enough, they did come up with a bunch of risk factors that correlated to a higher chance of cramping but none of them had to do with electrolyte and dehydration. Another theory is one of the real early ones is a psychosomatic origin, so that’s basically correlationship between your mental state and cramping. And so these early German guys talking about people who’re really anxious and tense and they kind of have a point in terms of those sort of condition, being in that state, correlates to a higher parasympathetic state or sort of a mild fight-or-flight condition and when we get into the 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 it may cause problems. And so, it’s sort of a, these guys, the psychosomatic origin is kinda out of left field, the way they describe it but there’s kind of an underlying kernel of truth underneath there but they sort of raise it wrong.
Andrew: There’s another one that’s a vascular origin of muscular cramp; it’s when you get claudication, when you get a cease of blood flow to the area, and that makes sense because what we talked about the ATP levels, when we block the blood flow you’re eventually gonna first exhaust your oxygen energy pathway then your non-oxidated pathways, so you’re gonna have no ATP. Then you’re gonna have a few pathogen buildup from your lactic acid dissociating and all those factors are gonna contribute to the muscle basically stopping to function, and so that could be one contributing mechanism. And so I guess all these researchers are trying to find the “this is it, this is the reason why we cramp” and 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 for long endurance that the spinal reflex dysfunction is sort of the key one to look at.
Ben: Yeah, and that’s one that it seemed that that neurological stimulus for exercise associated muscle cramps really seem 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 tightness in the muscle, etcetera. But I’d like, if possible, to hear kinda your explanation on what exactly you mean when you say that the neurological stimulus for cramping is probably the most common reason that a cramping occurs and kinda what’s going on physiologically when that happens.
Ben: I know it’s a loaded question but we’re all geeks here in the Ben Greenfield Fitness Show so we’re okay with you diving into the science if you need to.
Andrew: Sure, okay; so I guess we should start off, 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 with fine motor skills. One analogy to kind of think of it is when you’re backing your car into a parking spot, you don’t just hit on the gas and then slam on the brake; you kinda put a little bit of gas and 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 they work together in a negative feedback 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 gonna send a signal through the [0:16:51] ______, through its main feedback pathway to the motor neuron. You kind of think of it like a regional control center, so your brain is the main control center of your body but it has 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 the motor neuron in your spine and it sends the impulse back out so it speeds it up. And so what the spindle does, 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 reflexly sends a signal back to the muscle to contract it.
Jessa: 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, keeps track of everything he’s ever recommended and found to work really well, and puts it all over at greenfieldfitnesssystems.com. From books to lab tests to supplements, he has 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 at greenfieldfitnesssystems.com. Okay, now back to the podcast.
Ben: So totally random question, I’ve heard one of the reasons that 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 keep the muscle from tiring or straining or spraining something. Is that true, do they have less of a golgi tendon organ reflex?
Andrew: You know, I’ve never heard of that but I think that could just be a function of me not directing my interest in that way, but it makes sense, yeah. That’s the function of the golgi tendon is to prevent us from having such a strong contraction that, in theory, you could rip your tendon off as an insertion, and so interestingly one of the initial adaptations to strength training is you get stronger not because you’re adding muscle or anything like that, just that your body is sorta taking off the brakes, so to speak, as it desensitizing these golgi tendons to let you access more of your muscle fibers, so to complete the story of muscle spindles and golgi tendons is the golgi tendons are right where the muscle meets the tendon, and what they do is 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 to the spine through something called an inhibitory interneuron which shuts down how much output is coming from the motor neuron, and so you can kinda think of the golgi tendon as sort of like a stop button on a treadmill; when you’re 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, actual damage on the muscular level results in a hyperacting of the muscle spindle, where it’s sending out stronger impulses than normal and concurrently an inhibition or downregulation of how these golgi tendons fire, and so you get this positive feedback where the system that’s supposed to be putting on the brake, that’s supposed to be causing relaxation in the muscle is dysfunctional, and so the spindle just keeps firing around and the motor neuron sends it contractual output and that’s how you get the permanent state of cramp.
Ben: One of the things that you talk about in the article is the big question mark about whether this hyperexcitability 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?
Andrew: Sure, so both central and peripheral mechanisms relate to this dysfunction at the neurological level so in a way you can think of it as researchers having different explanations for the same phenomenon, and so what I just explained, that would be considered the central mechanism, because the main affector, so to speak, comes from the motor neuron, sorta the regional control center in your spine, where the reflex sends and afferent signal to the motor neuron and then the motor signal back to the muscle. But the peripheral way where some researchers think about this is a dysfunction at the neuromuscular junction, so where the neuron that sends a signal from the spine connects to the muscle. And so the way that signal, it comes as an electrical signal down the motor neuron, cross into the muscle, they call it the neuromuscular junction, is actually a release of these neurotransmitters; it’s a release of acetylcholine, these fill the chemical vesicles, transfer across this tiny little gap and then when they reach the motor end plate, they call it, when it reaches the muscle itself, the acetylcholine molecules bind to the receptors, then they open the sodium-potassium channels and then the signal becomes electrical again, 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 source, the area that releases it, and so you get this accumulation of acetylcholine in the synaptic cleft, and so that just continues; because it doesn’t get removed, it just continues to activate those receptors and continue to fire the signal a lot. And so 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 of certain electrolytes and the acetylcholine receptors, and also because of the volume lost, some researchers have suggested that there’s a physical deformation of the neuromuscular junction at the motor end plate, and so that’s essentially the thinking behind the peripheral mechanism is that it have to do with the dysfunction where the motor neuron meets the muscle and that’s what’s continuing to send the signal 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 put a nerve block, basically, what it is is they blocked the ability of that reflex pathway to go to the motor neuron and they electrically stimulated the muscle, and they found that it took a much stronger stimulus to get the contraction elicited without the motor neuron because you can kinda think of it as sort of like an amplifier. You have a pretty small signal sent from the muscle spindle but the motor neuron can really jack up the signal at its end back out, and so that’s what would make even a small dysfunction at the motor spindle could magnify into a large dysfunction in the muscle.
Ben: Right, and what you just described would be more of a peripheral mechanism, right?
Andrew: Yeah, exactly.
Ben: And so what you’re saying is that we rarely see that type of cramp occurring compared to a central nervous system cramp that originates more from the spinal cord?
Andrew: Yeah, I mean, yes. I guess all these answers are qualified coz there’s not a huge amount of research that goes into the specific mechanisms that we’re talking about and so also there’s a problem with some of the nature of these research studies is that the way they’re designed, and you can really say that it’s an issue with all scientific research, is that you really have to go out and make a firm hypothesis, and so it’s either this or it’s either that. And it doesn’t really leave a whole lot of room for a gray area or 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 a qualified answer is they appear to be mostly the abnormal spinal reflex.
Ben: 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 overexcitability, perhaps a lot of cortisol, a lot of nervousness, a lot of tension and even returning to some of the woo-woo stuff; those old school German research we we’re talking about that you mentioned. There is potential, it appears, if this neurological form of cramping and more specifically, the central mechanism of the neurological stimulus for cramps is occurring; it could, a very, very big part of this, be your mental state when you cramp.
Andrew: Yeah, definitely. I suppose the reason the central mechanisms have no support is that they’re the only one with a clear mechanism. For research you could say “yeah, this is clearly how we think it happens, this is kinda the research that supports it” and so in terms of how the nervousness or increased sympathetic activity would manifest that is not only do you have motor nerves echo to the muscle to cause the contraction, these actual muscle spindles, in order for them to be sensitive at all muscle lengths, for example when a muscles almost completely contracted versus when it’s lengthened, the actual muscle spindle itself has a little muscle fiber in it. And so in order to be functional at all lengths of muscle, this muscle spindle itself needs to lengthen and shorten; and so it has its own itty-bitty motor neuron itself, and so the more motor output to these little muscle spindles, the more sensitive they are. And so that’s the adaptation of strength training.
So when we talk about the neurological adaptations of strength training, the first couple of weeks, a lot of it has to do with the desensitization of your sympathetic motor, to these little muscle spindles, and so it’s sort of letting you tolerate more tension in the muscle, so to speak. And so I guess the way to think of both cramping, everyone has a cramp threshold, so to speak; once you exceed a certain number of impulses per second, then the muscle is gonna cramp. The way I look at it, the way to explain this is, so imagine you work in a sandwich shop, it’s not very busy at all, one customer an hour; one customer comes in, you get up, you make him a sandwich, then you go sit down, you relax for the rest of the hour. And then okay, maybe you get two customers in, so you get up, make two sandwiches and sit down;, and there comes a point where the customers are coming so frequently, you never get to sit down. You’re always on your feet the whole time making sandwiches.
And so different individuals have a different cramp threshold; so some people, once’ they’re getting 15 signals per second, then that muscle’s gonna tense and that’ muscle’s gonna cramp, whereas other individuals, well that threshold is at 20 impulses per second, and so one theorized mechanism or one pre-disposing factor we think to cramps is that inherently some people have a lower frequency threshold for cramping, and so the way that high nervousness or higher sympathetic tone we call it is that increases the number of signals you’re sending just at baseline. So just standing, waiting for your race to get going, may be already sending seven signals per second. And so you have less of a buffer of increase toward; you hit that cramp threshold and your muscle’s gonna permanently cramped.
Ben: Right, that makes sense. Now when it comes to 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 taste something extremely salty, like the famous pickle juice reverses cramping study, it causes almost this instant reflex reaction where you stop that cramp, I believe it’s via the alpha motor neuron, but it’s all via the spinal cord versus like “boom”, it happens so fast that there’s no way that the salts could’ve actually gotten to the muscle. Does that help to support this central mechanism?
Andrew: Yeah, I suppose so, completely. I mean it’s a placebo effect, if you think it’s working then you’re gonna relax and it’s gonna drop the amount of tone or baseline signals you’re sending just by nurturing your mental state, sure.
Ben: And even that pickle juice study wasn’t even suggesting it was a placebo as much as it was that reflexive gag to tasting something incredibly salty just cause that cramp to release just based off a really quick alpha motor neuron inhibition of the cramp. When I was reading through the description of the peripheral versus central mechanism, I thought “well the fact that he’s leaning towards the central mechanism is what causes this cramp”; could possibly lend the [0:32:21] ______ to this whole “taste something salty” theory.
Now you also get into just a few other, there are three other theories that you talk about: the environmental theory of cramps, the fatigue theory and the possible genetic predisposition 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?
Andrew: Sure, sure. The environmental theory is simply that extreme environmental conditions could cause you to cramp, so super hot environments or super cold; and I guess it’s a way to think about the environmental theory is that’s not what’s directly causing it, but it could be a predisposing factor to other mechanisms that are gonna cause your cramp.
So for example, in the extreme heat, higher masses of heat 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 play a role; so I guess the way to think of electrolyte depletion and dehydration is not exactly to throw it out the window and say it doesn’t; it’s not a factor at all. The research hasn’t really shown that this causes cramps nor does it have a proposed mechanism but by no means has it been disproven, so to speak, so you kinda wanna be careful and sorta think that the absence of evidence is not evidence of absence.
Ben: Right, and even if dehydration or lack of electrolytes may not actually causes cramps, even in these hot and humid environmental conditions, and I kinda tend to personally think that’s the case 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’d 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 or you’re just so tight ‘coz it’s so hot or so cold, or maybe you think being hot or cold could cause more cramping ‘coz that’s what you’re been led to believe and that could actually also cause the cramping.
Andrew: Yeah, I think that’s thoroughly fair, and one way I think of cramping is there’s a possibility that this idea of task dependency might factor into it, and we can kinda think of task dependency as the cramping is dependent on the task that you’re doing. So this concept comes from the general idea of fatigue in general. So the reason you fatigue, say a maximal deadlift, the reason you can’t do more than one or two of your real heaviest; the reason you fatigue there is gonna be different from the reason we fatigue during a 400 meter sprint, it’s gonna be different from the reason you fatigue running a marathon. And so in 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, so the way I kinda think of it is, yeah, spinal reflex seems to be a heavy hitter but we can’t really wipe off these other mechanisms off the table.
Ben: What about just pure fatigue, pure muscle fatigue? Because you hear about that a lot too, you simply get to a point where the muscles just give up, almost. Is that a credible theory?
Andrew: Yeah, definitely. So that’s actually a contributing factor to the central mechanism is that the fatigue correlates to physical damage at the microscopic level. And so the article written by Noakes and this guy Schwellnus is that they think the reason we get this abnormal spinal reflex is that it’s the physical damage to the muscle that causes damage to the muscle spindles, causing the hyperactivity, adding critical damage to the golgi tendon organs, causing them to desensitize. And so fatigue is basically the key reason, and so the outcomes of what they found was their research, in the cramping Ironman triathletes, when they didn’t find anything to do with dehydration and low electrolyte levels, they found that the biggest predisposing factor to cramping were improper tapering, so not tapering enough before the event, and also faster training pace; I’m sorry, a faster race pace than they trained at. And both of those factors made sense in terms of muscle fatigue.
Ben: Asking the muscle to do something in competition that you haven’t asked them to do in training, basically.
Andrew: Yeah, well I mean you’re speeding up the rate at which you got the muscle fatigue, just that muscle’s gonna hit that critical fatigue or damage level sooner, and then you’re gonna get that cramp.
Ben: Yeah, now are some people, do you think, more genetically predisposed to cramping?
Andrew: Yeah, I guess that’s the third topic that I kinda got off on a tangent on, but yeah. It seems to be only one study and Schwellnus was in this as well. There’s some evidence that you can have genetic variations and predisposed individuals to soft tissue and musculoskeletal injuries. And so what they think it relates to is extracellular structural proteins, so you can kinda think of a muscle as a collection of millions of these tiny little muscle cells but they exist in 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 factors; there’s a number of genetic variations and so again, you kinda think of it as a scaffolding. You could build scaffolding out of different kinds of wood; you have pine or oak or whatever, and each are gonna have different strengths, different structural properties and that’s sort of the same thing, genetic variations of collagen. And what they found is that certain collagen variations are just weaker, they hold up until the repetitive stress of running or doing whatever for eight hours, and so if your scaffolding, if you’re structure’s not as strong, then it’s gonna fail sooner then you’re gonna get to that break point where you get physical distortion of spindles and the golgi tendons. So that’s sort of the essence of the genetic theory, is that you can have certain gene variations that can impact the durability of sarcomere at the cellular level of resisting damage.
Ben: Yeah, it’s very interesting and I’m always curious about whether or not those differences in connective tissue in tendons that might predispose someone to cramping could be something that you could size up from a qualitative standpoint; like looking at somebody’s body type, like whether they’re ectomorphic skinny or mesomorphic muscular, endomorphic apple shape and if there’s any type of way to see, just by looking at someone versus 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 I can, from what I found and this is totally observation-based and not research-based over a decade of coaching, it seems that my skinnier, slow-twitch athletes simply cramp less and possibly that’s because of weight, it’s because of fatigue, it’s because of muscle damage or 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.
Andrew: Yeah, you bring up something interesting about the slower-twitch athletes coz that makes sense. The lesser amount of highly glycolytic fibers, your type 2 flows the main contributor that dump a lot of hydrogen, because when you break up a glucose without oxygen, you produce two hydrogen molecules. And also, those fast-twitch muscle fibers, they’re much more electrically active and so if we’re looking at cramping being related to hyperactivity in the muscle units, these big, strong electrical ones that send out electrical signal, then those are more likely to contribute to cramping. So that’s interesting that you noticed that based on why we think we cramp; there’s a lot of reasons to think that would make sense, that the slower-twitch athletes would be less of a lower disposition to cramp.
Ben: Hmm. 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 Noakes, for example, may not be as important as we’ve been led to believe unless you are severely dehydrated. But let’s say someone has their electrolytes balances, 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?
Andrew: Yeah, I’d be curious to asking if they strength train, because strength training will be sort of like flushing a pipe; you’re reinforcing the normal function of the muscle spindle, and also by strength training you’re gonna reduce the sensitivity of your muscle spindles and you’re gonna reduce the sensitivity of the golgi tendon organs; you’re gonna sort of get the muscle to realize “okay, this is an amount of tension that I can handle, don’t freak out”, this is the muscles working like it’s supposed to. And so a lot of movements, you can talk about grooving the pattern; you can try to teach someone to squat or whatever. You can almost think of you wanna groove the pattern of your spinal reflex to work normally, and so it’s possible that someone that doesn’t strength train they can have abnormal firing patterns.
You can also have synergistic dominance where sleepy butt syndrome, for example, where your quads are doing all the work when your glutes should be kinda contributing and so, say for example you have synergistic dominance and your calves are doing a ton of the work, and so that’s just gonna 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 midfoot strike is that the calves are being subjected to a much higher stretch and stretch with each strike. And so when you hit the ground, particularly in a midfoot strike, you gotta stretch working cycles, so all of these elastic components 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”, pops up, and you spring into the next step. But so the midfoot strike could lead into your pushing that muscle spindle further towards hyperactivity, and so that could be one component of it.
Ben: Yeah, and you certainly hear about that quite a bit in people who switch shoes or make significant changes to their running gait is susceptible to experience cramping; that makes sense.
Ben: So we’ve got strength training, we’ve got actual biomechanics of movement; any other recommendations for folks?
Andrew: Uhmm, I dunno, I mean if they have a jagged 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 dynamic static stretching before an event.
Ben: Yeah, there’s a pretty bad trade-off there, with power production of course.
Ben: Uhmm, 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, focus, and even potentially using, there’s all sorts of relaxation soundtracks to increase alpha brainwave production and different ways 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?
Andrew: Hmm, yeah; I never thought of that, and I mean…
Ben: I thought about it a lot when I was reading your article, so like (laughs), man, a lot of this has gotta be mental.
Andrew: Yeah, well that perspective fits right into what we’re talking about here. Anything that increases your baseline sympathetic tone will ask you to push you closer to cramping. And anything that lowers your sympathetic tone is gonna lure you further away, and so yeah, I think you’re right on there; that’s a fine explanation and what I would add to that is that what you’re talking about doing, there’s benefits to your performance, above and beyond just cramping. So working on the mental side of your race, that’s great for a lot of reasons besides cramping. And so, I give you a thumbs up for that.
Ben: Yeah, so I can think of, and I always like to leave people with a few action 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: strength training, looking at biomechanics, maybe even 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 discount the importance of brain training. You talked about muscle damage and how muscle damage can be an issue and improper tapering could be an issue. So maybe if you find yourself cramping 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, 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 should be; potentially even, as they say, 10% undertrained is better than 1% overtrained.
Ben: And that can be done. I know that weight, when you’re running or you’re exercising, you’ve got a lot of excessive weight. Your muscles are susceptible to more damage, 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 (laughs), that may come into play potentially as well, especially if you’re a chronic repetitive motion athlete 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, it’s always (laughs)…
Andrew: Yeah, you can always just back off the pace a little bit and that might help as well.
Ben: Yeah, interesting. Oh, and one of the things I wanted to ask you about, and I know we gotta rumble pretty soon but did you come across anything as far carbohydrates, as far as 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 experimenting with ketosis and low-carb diets and things along those lines; I’m curious if there’s a link between cramping and glycogen depletion.
Andrew: Uhh, well there was one study that looked in, took bunch of college students at the time, at how long it took for the time-to-cramp onset, and one was in a low electrolyte-low carbohydrate state, and another one was, I think they give Gatorade to her, no dietary restrictions, and the time-to-onset of cramp was on and was extended when you did have enough carbohydrates, so I think it’s fair to say that having some glycogen storage may prolong the time of fatigue. Also burning fat and burning protein is just such a more complex… the metabolic process of breaking down is so much more complex and so there’s many more steps that something could go wrong and possibly precipitate. I mean your body can certainly perform…
Ben: Yeah, I would say, especially if you haven’t trained yourself to do so, that’s even one of the things we were talking about Noakes, like that’s what he’s talking about now. It’s like sure, you can do just fine and probably not experience a lot of deleterious effects during exercise from a low carbohydrate diet if you’ve actually trained yourself in training to be able to upregulate those mechanisms or even trained yourself to have enough mitochondrial density to be able to handle that oxidation.
Andrew: Yeah, that’s exactly it.
Ben: And so, if you restrict carbs for two weeks and then taper for a week then go compete, that’s probably not such a great idea (laughs).
Andrew: Takes a while to get your body to shift over.
Ben: Well what I’m gonna do is, in the show notes for this podcast, you can grab ‘em over at bengreenfieldfitness.com/whycramping, that’s bengreenfieldfitness.com/whycramping; 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-viewed research websites and there’s a little bit of a pay-access if you wanna pay to grab the article and read it yourself or if you happen to subscribe to the National Journal of Strength & Conditioning Research or you wanna grab it from your local library you can always look at it there, too. And I’ll put a link to the resources we talked about during today’s episode, all over there at bengreenfieldfitness.com/whycramping; and Andrew, thanks so much for coming on the call today, man, this was fascinating.
Andrew: Yeah, appreciate it. No worries.
Ben: Alright, cool. Well folks, this is Ben Greenfield and Andrew Buskard signing out from bengreenfieldfitness.com. Have a great week.
Last month, I read one of the best scientific treatises on cramping that I’ve ever seen. The title of the article was “Cramping In Sports: Beyond Dehydration“, and was written by today’s podcast guest, Andrew Buskard.
If you’ve ever scratched your head about why the heck you won’t stop cramping during your workouts or races, this episode is for you! During our discussion, you’ll discover:
-Why a cramp during exercise is way different than a medically associated cramp…
-What’s really happening inside your body when you cramp…
-Why the traditional theories of what causes exercise associated muscle cramping are incorrect or have been mostly disproven…
-Why neurologically related cramps are the primary cause of cramping during exercise…
-Why simply tasting something very salty can reverse a cramp…
-How your environment, your relaxation level and even your genetics can affect your susceptibility to cramping…
-Strategies to stop cramping when you have adequate electrolytes and hydration but you’re still cramping…