Category Archives: Endurance Athletics

Defining Winning in Endurance Sports

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About 10 years ago, I participated in a local half-marathon.  My father came out to watch the race.  After the race was over he commented to me, “Brian, a lot of people sped up and sprinted across the finish line.  But they were well behind the winner of the race.  Why did they bother, since their finish times were irrelevant?”

In perhaps 2008 or 2009, Torbjørn Sindballe, a phenomenal professional triathlete, published an article in, I think, Triathlete Magazine.  In this article, he described his perennial struggles with heat in competitions, especially the Ironman World Championship in Kona, Hawaii.  With the help of a creative sponsor, Sindballe developed a number of improvements to his race strategy, including wearing white and using gloves filled with ice.  What I remember most about this article is that, after having used his innovative approach, he came in 3rd place and stated, in the article, that he “won.”

“What?” I thought.  He finished 3rd, right?  That means two people, Chris McCormack and Craig Alexander, finished before him.  How could anyone who can count call this a “win?” I was relatively new to triathlon at that time.

Many non-endurance athletes and even many endurance athletes, themselves, have narrow definitions of success.  First place or bust.  Podium or bust.  Qualify for Kona, Nationals, Worlds, etcetera or bust.

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Attached to this idea is the concept that not achieving such narrowly-defined success reflects a lack of commitment to becoming better.  “That middle-of-the pack guy must have been watching television and munching on chips when he should have been on the bike.”

I wrote an article a few months ago about how it is becoming more difficult to qualify for Kona. This was not meant as a complaint, but instead as a source of information upon which to reflect.  A well-meaning, and highly-motivated, reader looked up my (humble) results from past competitions on Athlinks and wrote me a detailed analysis of how I could qualify for Kona.  I just need to bike a little faster and take, oh, about an hour and a half off my marathon.  But, if I just train really, really hard, I’ll be right there in Kona.

I have had occasional highly-placed finishes and have qualified for Nationals several times. But I have also had surprisingly poor finishes in which I worked just as hard, or harder, as I had for podium finishes.  These experiences, and paying a lot of attention to the athletes around me, have taught me a lot of lessons about winning.

Now, please understand, I do not think that everybody should get a medal just for showing up. I think that graduation certificates for preschool and kindergarten, for instance, are absurd. Winning, however, for some people, can be just showing up (e.g. overweight couch to running a 5K is a wonderful win), but I am trying to make a different point.

Here is my definition of winning in endurance sports:

Winning, in endurance sports, is doing everything you can with what you have been given, without quitting and without feeling self-pity.  

To make an extreme example, recall the story of Jon “Blazeman” Blais.  He had ALS and participated in the Kona race.  His finish, in almost 16 and a half hours, was magical. I will never forget watching footage of him rolling across the finish line. In simply finishing, he won. I have been in a lot of painful places in a lot of long races, but I cannot imagine how much agony he went through to win, on his terms.

This is just the point. Blazeman, and any other endurance athlete who pushes his or her limits, is a winner.  Some of us are born with magnificent athletic gifts, but most of us are not.  But this does not mean that a 50th place finish has any less value to that finisher than the winner of the race if that middle-of-the-pack finisher gave his or her all.

I also hold that the opposite is true.  Losing is not appreciating or using the gifts you possess. For example, I have a friend who is a really strong multi-sport athlete.  In a race a couple years ago, volunteers did not point him the right direction on the bike, and he ended up going some distance off course.  This made it pretty unlikely he was going to podium.  What did he do?  He turned around and biked back to transition, collected his gear and went home.  This behavior may be understandable for a professional who is having a bad day and decides to save his or her energy for the next race.  But this friend is an amateur and this was a short race which would not affect future training or performances.  Essentially, things weren’t going his way and he just quit.

Like everybody else at the start of races I am nervous.  Sometimes I ask myself, “what am I nervous about? Nobody but me really cares about my finishing time and I know I can finish.”  I think sometimes what really scares me is the thought that I may, in the course of a race, lose my commitment to being my best and just become the guy who packs up early and goes home. May this never happen to me or to any of us.

Here is to the winners in all of us.

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Exercise-Associated Hyponatremia: Endurance Athletes Beware

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Exercise-associated hyponatremia (EAH) is an important, amazingly common, and potentially life-threatening condition that affects athletes who participate in sustained activity.  It is also preventable.  The following is a true vignette.

An experienced, very fit, non-anorexic, middle-aged female, accompanied by family members, hiked up to a 14,000+ foot summit on a mountain in the United States. She had spent three days acclimatizing before this hike. Her nutrition on the morning she began the hike may have been an energy bar (at around 6 AM).  During the hike, she had an apple and a handful of nuts, but not much else. She was mainly thirsty, not hungry.  To sate her thirst she drank water that had been collected and filtered from streams along the way.  She did not carry much hydration from the start to minimize weight and she did not add electrolytes to her filtered water.  

She summited the mountain and began to descend back down the trail.  At around 1 PM, at about 10,000 feet of elevation, she began to complain that she felt “weird” and had a headache. She developed increasing disorientation and fatigue and then began to develop very unusual behaviors, which she does not remember.  Her confusion continued to progress to the point at which she was unable to speak.  She then began to stumble and could not stand.  She was carried, using a makeshift litter, by Good Samaritan hikers to a location further down the mountain.  While being carried, the woman experienced a “full body seizure.”  A rescue team had been contacted.  When they arrived on the scene, according to their report, the woman was responsive to painful stimuli only.  She was unable to speak or to follow commands.  She then vomited.  The rescue team, which, along the way, grew in size to 13 individuals, carried the patient down the mountain to a waiting ambulance.

She arrived at the hospital at approximately 3:45 AM and had a very low sodium of 118 and a reportedly normal head CT.  The woman was intubated (a breathing tube was put into her throat so that her airway could be protected and physicians could control her breathing) and she was airlifted to another medical center.  She received IV fluids and a repeat head CT reportedly showed brain swelling.  By noon on that same day, her sodium was normal and she was extubated.  However, her creatinine kinase (which is released when muscle is damaged) was very high at 27,000 and she was kept in the hospital for 3 more days until this level dropped to 3,000.  

This very fortunate woman is alive, well, and, apparently, has no lasting damage from this event. This is fantastic news.  Unfortunately, other people have not done as well with exercise-associated hyponatremia.  There have been a number of known fatalities from this condition (at least 14 in athletes since 1981).  As recently as the summer of 2014, two otherwise healthy 17-year-old high-school football players died from hyponatremic encephalopathy, which is the usual cause of death from EAH. Deaths from EAH have occured during participation in the following activities/sports: marathon, canoe race, hiking, military exercises, police training, American football, and fraternity hazing.

Definition of exercise-associated hyponatremia

The lower limit of normal for sodium is 135 mmol/L. EAH is defined as a sodium value below 135 occurring up to 24 hours after exercise.  This condition is often asymptomatic.  But a much lower level of sodium (below 125) and a more rapid, but smaller fall to higher levels of sodium (as high as 130) can be associated with symptoms.  The individual described, above, with a sodium level of 118 had a critically low level.   

Epidemiology and Presentation of EAH

Prior to 1981, athletes were advised to avoid drinking during exercise (doesn’t this sound nuts today?).  This led to a number of cases of hypernatremia (high blood sodium).  Therefore, authorities, around 1981, began to suggest drinking as much water as possible during exercise. This led to a number of cases of EAH and ongoing misunderstanding about the dangers of overhydration.

EAH can be asymptomatic or symptomatic.  Symptomatic individuals can have mild symptoms such as lightheadedness and nausea or more severe symptoms such as headache, vomiting, confusion, seizures, and respiratory distress.  The confusion and seizures arise from swelling of the brain (exercise-associated hyponatremic encephalopathy) and the respiratory distress arises from non-cardiogenic pulmonary edema.   

Asymptomatic EAH has most prominently been noted in 161-km ultramarathons, in which the incidence has ranged from 5% to 51%.  In Ironman triathlons, the range of incidence has been negligible to 25%.  For cyclists participating in a 109-km race, the rate was reported as 12%.  In a 26.4-km swim, the incidence was 17%.  For marathoners, the incidence has ranged from 0% to 13% of finishers. After an 80-minute rugby competition, premier league UK players had a rate of 33%.  Finally during a 28-day training camp, 70% of elite rowers had asymptomatic EAH.

Symptomatic EAH is much less common than asymptomatic EAH.  In one study of 2135 endurance athletes drawn from 8 events of varying distances, the incidence of symptomatic EAH was 1% (versus a 6% incidence of asymptomatic EAH in this study).  In another study of 669 161-km ultramarathon runners, there was only one case of symptomatic EAH, an incidence of under 0.1% (versus a 13% incidence of asymptomatic EAH in this study).  

Risk Factors

The most important risk factor for the development of EAH is the over-consumption of water, sports drink, or other fluids with electrolyte content lower than human plasma.  That’s right: guzzling sports drink DOES NOT, repeat DOES NOT prevent dangerous EAH from occurring, due to dilution of the plasma.  

Additional risk factors include being smaller in size and being slower (e.g. marathon times over 4 hours).  The use of NSAIDs (please see my extensive series of articles about NSAIDs and athletes to learn a lot more about this subject), also, at least theoretically, can be a risk factor for EAH by leading the kidneys to retain more water (by strengthening the effects of arginine vasopressin (AVP), which leads to more production of anti-diuretic hormone).  Interestingly, there is not much evidence about the “salty sweater” and relative risk of developing EAH.  

Mechanism of EAH

EAH is a result of dilution.  In this condition, the rate of increase in total body water exceeds the rate of removal of body water (through sweat, respiration, and urine) and the rate of replacement of sodium is inadequate to keep up with needs.  This mostly occurs through drinking too much water or other drinks, including sports drinks, that do not have as much electrolytes as human plasma. Another mechanism at play is decreased clearance of water from the kidneys due to heightened activity of the hormone, AVP.  This hormone is released by the pituitary gland in the brain and is usually responsive to the osmolality of the blood (changes in levels of sodium in the blood change the osmolality).  However, during sustained exercise, AVP production is responsive to other stimuli and (probably from teleological reasons) typically increases, which leads to heightened retention of water by the kidneys.  Interestingly, another source of extra water is the release of water, which had been bound to glucagon, when glucagon is consumed for energy.  

Most of the damage to the body, from EAH, is a result of water entering comparatively salty cells throughout the body (biological forces lead water to go to more salty areas).  The most important area affected by this phenomenon, by far, is the brain.  This leads to swelling of the brain.  In fatalities from EAH, typically the brain swelling becomes so severe that the brain stem is forced into a narrow opening at the base of the skull. This severely damages the brain stem and leads to death.

Treatment of EAH

Most of the treatment of EAH is beyond the scope of this article.  However, there are a few important concepts that medical personnel keep in mind when treating this condition.  The most important of these concepts is that giving routine fluids used for ill people, such as normal saline, can dilute the plasma more and make EAH, with associated brain swelling, worse. Therefore, hypertonic saline (saline with very high salt content) is the mainstay of treatment. The challenge, however, for medical personnel is that athletes can collapse for a number of reasons and, for most of them, normal saline is appropriate.  For example, in a study of over 1300 people who collapsed during Boston Marathon events between 2001 and 2008, only 5% had hyponatremia whereas 28% had hypernatremia.  Therefore, medical personnel need to rely on key aspects of the history to correctly make the diagnosis, such as sustained exercise and consumption of a lot of fluids, along with confusion and other evidence of brain swelling. Some organized events attempt to aid medical personnel by obtaining pre-race weights of athletes. An athlete with signs and symptoms of EAH who has gained weight or has lost less weight than can be expected for the circumstances of the race, is much more likely to, indeed, have EAH.  There has also been a call to have plasma sodium measuring devices available to medical personnel to truly establish the diagnosis.  

Prevention of EAH

If you, the reader, remember nothing else from this article, please remember this:

DRINK TO THIRST!

The thirst mechanism of the human body is finely tuned to respond to small changes in osmolality.  Furthermore, it is difficult to accurately predict sweat rates and other aspects of fluid balance in all conditions, especially for slower athletes, so drinking to thirst is the most appropriate gauge of fluid needs for most athletes. In fact, a small study of 8 female marathon participants demonstrated that drinking to thirst did not lead to overhydration. The Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference (2015) states:

“Earlier published recommendations to begin drinking before thirst was largely meant for situations where sweating rates were high, above maximal rates of gastric emptying, and dehydration would rapidly accrue over time. Unfortunately, this advice has fostered the misconception that thirst is a poor guide to fluid replacement and has facilitated inadvertent overdrinking and pathological dilutional EAH.”

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As mentioned previously, sports drinks have much less sodium than the serum.  Therefore, overdrinking sports drinks can lead to dangerous dilution of sodium and, therefore, EAH.  The take home message is that a sports drink will not protect you from developing EAH if you drink too much.

Another approach to preventing EAH is to provide fewer hydration stations at races.  For example, studies have shown that spacing fluid stations 20 km apart on the bike in an Ironman triathlon or 5 km apart in a stand-alone marathon has reduced or prevented EAH.  

Summary

Exercise-associated hyponatremia is common, dangerous, and preventable.  The most important concept to keep in mind to prevent EAH is to drink to thirst.  Sports drinks are great for a lot of reasons, but they do not prevent EAH.

Please be careful out there!

References:

Hew-Butler T. Arginine vasopressin, fluid balance and exercise: is exercise-associated hyponatremia a disorder of arginine vasopressin secretion?  Sports Med. 2010 Jun;40(6):459-47

Hew-Butler T, Rosner M, Fowkes-Godek S, et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clin J Sport Med. 2015 Jul;25(4):303-320.

Rosner M. Preventing Deaths Due to Exercise-Associated Hyponatremia: The 2015 Consensus Guidelines. Clin J Sport Med. 2015 Jul;25(4):301-302.

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The Zen of Code Yellow: Voiding in Triathlon

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Let me start this article by pointing out that I am an extremely clean person.  It is a long-standing joke in my family that I was destined from an early age to be a physician because of an obvious obsession with hygiene.

However, endurance racing, especially triathlon, is a different thing.  After having survived many dozens of less-than spotless port-a-potties before and, yuck, during races, I have learned to accept race-day hygiene as unavoidably separate from normal-life hygiene.

Another important issue is efficiency.  In triathlon we spend hours practicing transitions and buy expensive slip-on shoes, easy-entry cycling shoes, and other gear all in the interest of saving, truly, just a few seconds.  Well, how much time is “wasted” with a visit to the port-a-potty?  How much ill-will is generated when an athlete pulls over to the side of a race course, in a neighborhood, to void? Think about it.

This brings me to the slightly sensitive topic of this article: taking care of “business” during a race.  How does someone do it?  Are there accepted codes of behavior?  I will share my wisdom and perspective and you can decide for yourself.

The swim:

Is it OK?

It is never, ever, acceptable to void in a pool.  However, a lake or a river is an entirely different story.  As I learned at Med School at Duke: “dilution is the solution to pollution.”  The volume of water in a lake is simply too great for any amount of triathlete-derived urine to create unsanitary, or even noticeable, conditions.

How do you do it?

Just relax, slow down your swim stroke a little bit, and let it go.  With a little practice (in a lake or river, not a pool), you should be able to do this with minimal drop-off in the pace of your swim.

Tips?

Don’t tell your significant other.  My wife will never touch my wetsuit now, even after I have thoroughly cleaned it…

The bike:

Is it OK?

Generally speaking, voiding on the bike is just fine, with some caveats.  There is the possibility to create some spray behind you.  Therefore, always check behind before going Code Yellow. Also, this activity can, for some people, be a little public.  Public nudity/self exposure is not acceptable.

How do you do it?

This is much harder to do on the bike than during the swim. My suggestion is to find a portion of the race in which there is some degree of separation between you and other athletes and, especially, spectators.  Pedal a little harder, then sit up or stand, then relax.  It can take a few tries to find the Zen of Code Yellow, but it gets easier with practice.

Tips?

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Once you start Code Yellow, you will have a damp crotch.  If the weather is cool, this, by normal human reflex, may lead you to “go” again and again.  Be prepared. Also, since your bottom will be damp for, potentially, hours, you are at risk for nasty chafing: “baboon butt.”  If you plan to void on the bike, be very liberal with the Body Glide, or similar product, over broad areas of your nethers.

The run:

I have read accounts of professional triathletes who are able to achieve Code Yellow while running.  This is an expert-level accomplishment and, I am sorry to say, I have no guidance to give.  If you have information to offer, please share it in the “comments” to this article, so we can all learn from your gift.

The Zen of Code Yellow is, with some guidelines, an acceptable way to enhance your triathlon experience.  I hope that this information is entertaining and helpful to you.

Race and train safe and clean.

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What Every Doctor Should Know About Athletes

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Years ago I saw a patient in my practice who was in his early 60s.  This gentleman had been lifting heavy weights for years and had an amazing physique.  After I listened to his concerns and started to address them, he said to me “thanks for thinking about my medical problems and not being distracted by how I look.”  He felt the need to say this because many health care providers seemed, to this patient, to be so impressed by his appearance that they seemed to be unwilling to consider that he may truly have an illness.

In more than 17 years of practice I have found that the experience of this athlete is not uncommon.

This article is intended as a basic guide, for athletes and their health care providers, to some of the unique characteristics and concerns of athletes.  As an amateur athlete of modest ability, I will take the liberty of using the term “we” rather than “they”

We have unusual laboratory findings:

Athletes often demonstrate laboratory results that would appear abnormal in the sedentary population.  The most well-known of these is pseudoanemia.  Because, by conditioning, there is an increase in the volume of blood plasma, hemoglobin in the blood becomes diluted.  This can lead to hemoglobin levels commonly 0.5g/dl lower than “normal,” but sometimes up to 1g/dl lower than “normal.”  However, the total amount of hemoglobin in the blood, and, hence, the blood’s ability to carry oxygen, is not reduced.

Another common finding in athletes who are actively training and competing is a positive urine dip test for blood.  When the athlete’s urine is examined under a microscope, there is no blood. This finding on the dip test is a false positive because the dip test cannot differentiate between hemoglobin (in red blood cells) and myoglobin (which is released from muscles that are injured during exercise).

Similar to myoglobin in the urine, signs of muscle damage are also detectable in the blood after strenuous exercise.  These laboratory findings include elevated levels of myoglobin, creatine kinase, and aspartate aminotransferase (AST).  Since AST is usually considered a measure of liver function, an elevated level may be taken to indicate liver damage.

Our hearts are different:

Athletes often have big hearts in every sense of the word.  The physiologic version of our big hearts is called the “athlete’s heart.”  A review on this subject stated that, in roughly 50% of athletes, their training induces:

“some evidence of cardiac remodeling, which consist of alterations in ventricular chamber dimensions, including increased left and right ventricular and left atrial cavity size (and volume), associated with normal systolic and diastolic function.”

In addition, marked enlargement of the left ventricular chamber (greater than or equal to 60 mm) occurs in approximately 15% of highly trained athletes.

In addition to, or, more likely, a function of, our enlarged hearts, our hearts can have strange-looking electrical patterns, with approximately 40% of trained athletes demonstrating abnormalities on 12-lead electrocardiograms.

Our heart rates are often ridiculously low.  It is not unusual for highly trained male and female athletes to have resting heart rates in the 30s and 40s, respectively.  This low heart rate is reflective of the increased efficiency of the cardiovascular system.

But we can still have serious heart disease:

There is significant overlap diagnostically between a physiologically unsurprising athlete’s heart and the potentially life-threatening condition, hypertrophic cardiomyopathy.  Tragically, athletes die of this condition, as well as conduction abnormalities, coronary arteriosclerosis, and other heart abnormalities.  The bottom line is that an unusual heart finding in an athlete should lead to serious consideration given to having an evaluation by a cardiologist who has experience differentiating between an athlete’s heart and dangerous heart disease.

We obsess about “small” health concerns:

Athletes train for months and years.  For some athletes, training and racing is their full-time job. Often times, all of this training is directed toward a single race event.  For some events, like the Olympics, there is no second chance.  Either an athlete arrives and performs to his or her peak ability, or the years of intense training can be “wasted.”  Therefore, a “little cough” or sore throat, a sore joint, or even a blister in a bad spot can be extremely important to an athlete. Even if “minor” health concerns do not appear to be at a level that could affect performance, lingering doubt can be a factor.  It is extremely difficult for non-athletes to understand the degree of dedication it takes to reach a high  level of athletic prowess and the amount of emotional and physiologic stress an athlete experiences before and during an event.

This is, actually, an area in which non-athletic physicians and athletes can find common ground. Physicians often make huge sacrifices of time and social relationships to get through the education and training that is required to practice.  Just imagine, after years of stress and poor sleep, while your friends were going out to bars, buying homes, and starting families, not getting your medical diploma because you have a cold or a sore shoulder!

Fitness is not a hobby – athletes can’t just stop:

Aside from the loss of fitness (deconditioning) that occurs when athletes stop training, fitness is a lifestyle, a part of personal identity, and, for some, a career.  When an athlete sees a physician about a health concern that could affect his or her ability to participate in exercise, the expectation is that every effort will be made to help him or her to return to full participation.

We are prone to fads and experimentation:

When I first got into triathlon, small wheels and beam bikes were a trend.  Then there was barefoot running.  Similarly, nutritional trends (avoiding gluten or milk, taking antioxidants, taking other nutritional supplements, etc.), whether based on evidence or not are very attractive to athletes.  If an athlete believes that a legal nutritional intervention will lead to an improvement in performance, no matter how small, he or she may try it.  It is important for physicians to ask athletes if they are taking supplements and what, from the athletes’ perspectives, are the expected effects of these supplements. Physicians who treat athletes should have some familiarity with such supplements and should be able to offer constructive, evidence-based, guidance.

We fear aging and decrepitude:

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We athletes understand, intellectually, that most of us will not be running marathons with our grandchildren, but we don’t know how we will deal emotionally with loss of fitness and activity. Every year I look at my performances and think to myself “is this the year I am starting to decline?”  Sadly, however, it is inevitable.  This is why, when a middle-aged athlete like me visits his physician, a gain of a couple pounds of weight or of 5 points of blood pressure can seem like a crushing defeat.

Many athletes doctor-shop:

Many athletes have limited budgets and time.  They will not put up with health care that they do not feel is helpful. If a brilliant physician gives excellent care in every regard, but is tone-deaf about the importance of peak fitness to patients who are athletes, those patients will seek care elsewhere.

Many of us have the same failings as everybody else:

I often find myself amazed when I read about a top athlete in his or her sport who is addicted to alcohol or drugs. These substances are so clearly detrimental to performance that it seems obvious that serious athletes would avoid them.  Sadly, this is not true. Physicians need to ask the same questions about smoking, drugs, and addiction of their chiseled patients who are athletes as they do of any other patient.

It is essential for physicians who treat athletes to understand their patient’s concerns, even if they seem trivial, and become fully engaged in becoming part of the athlete’s “team.”  This term, “team,” is not used trivially.  When an athlete trains or competes, there often is an entire team of people (coaches, physical therapists, massage therapists, dietitians, physicians, etc.) who has supported that athlete.

From a physician’s perspective, it’s fun to be part of a top athlete’s team. I saw a patient for follow-up recently who is a superb runner and has asthma.  He told me that he had recently broken the 4-minute mile.  I can’t run that fast.  Ever.  But I feel like my small contribution, as his asthma doctor, gave me a tiny piece of that achievement.

References:

Maron BJ and Pelliccia A. Contemporary Reviews in Cardiovascular Medicine: The Heart of Trained Athletes, Cardiac Remodeling and the Risks of Sports, Including Sudden Death. Circulation 2006;114:1633-1644.

Fieseler, C. What Runners Need to Know About Their Blood Test Results. http://www.runnersworld.com/health/blood-test-results-for-runners

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Exercise-Associated Muscle Cramps: Causes, Prevention, And Treatment

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Aside from limited talent, one of the barriers I have encountered to quality training and to racing in triathlons has been exercise-associated muscle cramps (EAMC).  I am not alone.  It has been reported that 67% of triathletes complain of EAMC.

Years ago, at the start of my amateur career (in my 30s) as an endurance athlete, I completed the Marine Corps Marathon and got pretty dehydrated.  In the medical tent for IV fluids, I heard a guy shouting and screaming nearby.  He was having muscle cramps.  I remember thinking to myself, “what a whiner!”  Well, karma found me and has never let me out of sight.  EAMC are amazingly painful.  A muscle, which, inconveniently, is needed for an athletic activity, suddenly and without warning violently clenches and twitches.  It feels like the muscle is being ripped apart.  For me, EAMC episodes can last for 5-10 seconds, or up to 30 seconds, depending on how much I really need that muscle group for what I am doing.  In my scan of the internet it appears that the duration of my muscle cramps is pretty typical, but some people can experience cramps for up to 15 minutes.

It is possible to keep going in spite of EAMC.  I rode over 70 miles of an iron-distance triathlon’s bike course last year with repeated EAMC in my hip adductors, quads, hamstrings, and calves.  I did it, but I paid.  I ended up being unable to complete the rest of the race and I visited the local ER with a host of medical complications.  I still doubt that I have fully recovered from this experience.

Why do EAMC happen? Specifically, are there strategies that can be employed that will be helpful for me and you, the reader, to avoid and treat EAMC?

Why do exercise-associated muscle cramps happen?

The following discussion is given with the caveat that other medical conditions (such as diabetes and hypothyroidism), medications (such as diuretics and statins), and other medical causes of muscle cramping (such as nutritional deficiency) need to be considered first.

Most recent good reviews of EAMC present the two leading theories about the cause of this condition: dehydration/electrolyte imbalance and neuromuscular failure. These two theories are often presented as though they are in competition with each other.  This is a useful writing technique, but it may not be accurate

The dehydration/electrolyte imbalance concept seems obvious and simple.  Since the body cannot store enough water to make up for losses during exercise and since athletes do not or cannot ingest enough water to replace losses, EAMC follow from the sensitization of nerve terminals that occurs as a result of water depletion (and consequent electrolyte imbalances). When muscles contract, there is contracture of the interstitial space, as well, which leads to mechanical pressure on select motor nerve endings and, finally, EAMC.  Since there is more loss of fluids and electrolytes in hot and humid conditions, these conditions would be more likely to lead to EAMC.

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But this theory is probably not adequate. For example, endurance athletes develop EAMC even in cold temperatures.  In a study of marathon runners, those who experienced EAMC did not have significantly different loss of plasma volume, blood volume, or body weight compared to non-sufferers of EAMC.  In a variety of studies, there was no difference between EAMC sufferers and non-sufferers in sweat rate and water/sodium losses and there was no correlation found between loss of body weight and EAMC.  In addition, water/electrolyte replacement (the treatment that would be predicted to prevent EAMC if this model were correct) has not been shown to prevent EAMC.

As a point of illustration, a small study was published in 2013 that examined cramp frequency with a high degree of dehydration.  In this study, of 10 male subjects, average age 24, exercised on a cycle ergometer until 5% loss of body mass or volitional exhaustion.  These subjects ended up losing an average of 4.7% of body mass.  At this level of dehydration, there was to change in cramp threshold frequency, cramp intensity, or the amplitude of EMG readings with cramps.  In other words, a loss of almost 5% of body mass (with loss of water and electrolytes) did not affect muscle cramps in this study.

Similar findings were described in a study of 43 participants in an ultramarathon.  About half of the athletes developed EAMC.  There were no significant differences between the cramp and non-cramp groups for post-race % change in body weight, blood volume, plasma volume, or red blood cell volume.  In the cramp group, the serum sodium concentration (after the race) was lower in the cramp group vs the non-cramp group (139.8 vs 142.3 respectively) and the serum magnesium was higher in the cramp group vs the non-cramp group (0.73 vs 0.67 respectively), but all of these values were within normal ranges.

In a study of 20 participants in an Ironman triathlon, there were no significant differences between the cramp and non-cramp groups in percent loss of body mass.  Interestingly, the cramp group had a lower post-race serum sodium of 140 vs 143 in the non-cramp group.  Once more, these values were within the normal range.  There were no other significant differences between post-race serum electrolytes, glucose, or hemoglobin.

As illustrated, above, available evidence does not support dehydration or electrolyte disturbance as an explanation for EAMC.  It is interesting, however, that post-race serum sodium concentrations were lower for cramp sufferers in two different extended endurance events.  I defer to those who know much more than me about cytology and the sodium-potassium channel.  However, my understanding is that the human body is designed to buffer large changes in electrolytes. Therefore, a three point difference in sodium in both ultramarathoners and triathletes may hold some significance, even though these values remain within the normal range.  Furthermore, perhaps it is not the absolute sodium concentration but the change over the course of an exercise event that can alter action potentials across cell surfaces.  [if you, the reader, have more knowledge about this line of reasoning, please share.  I have corrected articles in the past and I am happy to improve this one, as well.]

The mechanism for EAMC that is usually offered as an alternative to the fluid and electrolyte theory is the neuromuscular theory.  The proposed mechanism of this theory of EAMC has to do with neuromuscular overload and fatigue, which would lead to an imbalance between excitatory impulses from muscle spindles and inhibitory impulses from Golgi tendon organs. Without getting too technical, the bottom line is that, in this theory, there are less inhibitory impulses that would prevent the muscle in question from contracting.  So, the muscle contracts into an involuntary cramp.

There is some interesting evidence to support the neuromuscular theory.  Some of this evidence comes from studies in cats, which demonstrated that neuromuscular fatigue decreased the inhibitory impulses from the Golgi tendon organs and increased the excitatory activity of the muscle spindles.  In humans, EAMC occur more frequently after extended exercise (neuromuscular fatigue) than at the beginning of activity and also occurs more often when a muscle contracts while it is already shortened.  The observation about the contraction of already shortened muscles may fit the neuromuscular model because there is already less activity of the inhibitory Golgi tendon organs when a muscle is partially contracted. This would lead the muscle in question, upon further contraction, to be more vulnerable to cramping.

Another line of evidence supporting the neuromuscular theory is the benefit of stretching.  Of all the treatment options that have been suggested for EAMC, stretching is the one that has been shown to reliably be effective.  Stretching appears to work because it increases tension on the muscle’s tendon, which leads to activation of the Golgi tendon organs, an increase in inhibitory activity, and, therefore, a re-balance between inhibitory and excitatory impulses to the muscle in question.

There are a number of studies that appear to support the neuromuscular theory of EAMC.  One of these studies was a prospective cohort study of 49 participants in a 56 kilometer running race.  At the end of the event, 20 participants reported EAMC either during or within 6 hours of the event, while 29 reported no cramping.  The investigators reported that EAMC in this study was significantly associated with a past history of EAMC and a faster running time for the first 28 km of the race (in spite of being matched with non-crampers for personal best times).  EAMC in this study was not associated with age, body mass index, gender, recent and past personal best running times, reports of pre-race muscle pain, and reports of pre-race training (in terms of duration and frequency).

In another similar study of 209 Ironman triathletes, 43 reported EAMC and 166 did not.  While there were no differences between the two groups in pre- and post-race serum electrolyte concentrations and changes in body weight, EAMC was found to be associated with faster predicted and actual race times (in spite of similarly matched training and performance histories from subjects in the two groups).  Furthermore, a regression analysis showed that faster overall race time (and cycling time) and a history of EAMC within the subjects’ last 10 races were the only two independent risk factors for EAMC.

In a questionnaire-based study of 433 Ironman triathletes, 216 reported having had EAMC, while 217 did not.  The investigators in this study reported that the triathletes in the EAMC group were significantly taller and heavier, and predicted and had faster race times in spite of having similar past personal best times to the non-cramping group.  The EAMC group was also more likely to have had a past history of EAMC, a history of tendon and/or ligament injuries, and a positive family history for EAMC.

Taken together, the three trials summarized above indicate that poor pacing may play a large role in the development of EAMC.  This concept supports the model of neuromuscular overload and fatigue as the cause of EAMC.

It was also interesting to find an association, in the last study, with family history of EAMC.  This suggests, of course, that there may also be a genetic factor, entirely independent of fluids, electrolytes, and neuromuscular fatigue, that can predispose athletes to EAMC.  In fact, a study has recently demonstrated an association between the collagen gene COL5A1 and the development of EAMC.  In this study, the CC genotype of COL5A1 was significantly under-represented in the EAMC group vs the non-cramping group (11.1% vs 21.8%, respectively).

The neuromuscular model of EAMC does have some gaps.  For example, the electrical stimulation that was used in models of EAMC is not an exact match for real-life neuromuscular stimulation in humans.  Another point is that there does not appear to be a set level of fatigue at which EAMC occurs.  Instead, this level is probably unique to each athlete.  It is also unclear if the neuromuscular fatigue, in this model, is occurring peripherally (in the muscle) or centrally (in the spinal cord and brain). Indeed, a recent study demonstrated that static stretching does not lead to the autoinhibition of contraction that the Golgi tendon organ confers. In other words, this study showed that stretching before exercise does not affect the Golgi tendon organ.  Therefore, concluded the investigators of this study, if stretching before exercise reduces EAMC (which is unproven), the mechanism for this effect is not through inhibition of contraction by the Golgi tendon organ.

How to treat and prevent EAMC

Since EAMC are so challenging, so prevalent, and so poorly understood, a remarkable variety of treatment options have been suggested.  The following is a list of many of the options I have found in the literature and on the internet:

  1. DMSO (dimethylsufloxide): I have used this chemical in the laboratory in the distant past and it SMELLS. The concept is to rub it over muscles that either are prone to spasming or have spasmed. DMSO is then, according to its proponents, absorbed into the muscle and the problems are solved.  The obvious weakness of this approach is that muscle spasms involve huge areas of muscle that can be very deep under the skin.  There is simply no way for a topical chemical to penetrate that amount of tissue and cause a beneficial effect.
  2. Biting/pinching a lip: The technique here is to pinch the upper lip for 20-30 seconds, but sometimes for up to 3 minutes.  It is supposed to work up to 90% of the time.  The first and most obvious weakness of this approach is that the lips are not connected to any muscles except the muscles surrounding the lips. There is no known nerve or chemical pathway that passes from the lips to any cramping muscle around the body.  The next point is that most muscle cramps do pass in well under 30 seconds. So, a muscle cramp would pass, just as reliably, by singing “Yankee Doodle Dandy.”  This is, I believe, an example of confirmation bias.
  3. Replacing calcium deficiency: a chiropractor named Dr. David Williams states, on his website, that: “I believe that 90% of muscle cramps are caused by calcium deficiency.” It would be truly great news if this were true.  That would mean that 90% of EAMC would be prevented simply by checking calcium levels and correcting deficiencies.  Unfortunately, Dr. Williams’ “I believe” is just that, a belief. He does not offer any scientific evidence.  This is because there is no scientific evidence to show that 90% of muscle cramps are caused by calcium deficiency.
  4. Quinine: Some sources suggest that tonic water, which contains a small amount of quinine, can be consumed before exercise to prevent cramping.  The rationale for this is that quinine is a mild muscle relaxant.  Because of safety issues (most importantly, the risk of thrombocytopenia, which is a dangerous drop in platelet counts that can lead to bleeding and other problems), the dose of quinine in tonic water is limited to 83 mg per liter and quinine, in larger doses, is no longer available by prescription in the U.S..  In a Cochrane Review of research about quinine and muscle cramps of any cause, the authors concluded: “Compared to placebo, quinine [at doses of 200 to 500 mg per day] significantly reduced cramp number over two weeks by 28%, cramp intensity by 10%, and cramp days by 20%. Cramp duration was not significantly affected.” But note the dose required to achieve this effect is above the safe range.
  5. Pickle juice: A number of athletes and coaches have been advocating the consumption of pickle juice for years, apparently largely as a method to consume a lot of salt quickly. A study has shown that pickle juice can, in fact, help relieve EAMC.  In this study, when 1 mL per kg of body weight of pickle juice or deionized water was consumed immediately after the experimental induction of a muscle cramp in hypohydrated male subjects, the duration of the cramp was 49.1 seconds shorter for the group who consumed pickle juice (84.6 seconds vs 133.7 seconds) (please note, again, that these were experimentally-induced muscle cramps).  5 minutes after consumption of pickle juice or water, there was no change in plasma electrolyte levels.  Therefore, the investigators concluded that the improvement could not be explained by the restoration of fluids and electrolytes.  Instead, they postulated that the tart pickle juice initiated a neural reflex from the oropharyngeal region that led to inhibition of the alpha motor neurons of the cramping muscle.
  6. Mustard: Some athletes have used mustard in the same manner as pickle juice, with similar logic.  However, there is no published evidence to demonstrate a benefit.  In an interview in the November 2014 issue of Runner’s World magazine, investigator Kevin C. Miller, PhD (an investigator in the pickle juice trial, above) stated that he studied athletes consuming as much as ¾ of a cup of mustard with no relief of EAMC.
  7. Replacing fluids and electrolytes: Dehydration and electrolyte imbalances have been shown, per above, to not be a satisfactory explanation for EAMC.  However, there is no question that dehydrated athletes under-perform and are susceptible to serious or even life-threatening medical complications.  Therefore, even if the replacement of fluids and electrolytes does not prevent or relieve EAMC, it is strongly advocated for a number of other reasons.
  8. Eating bananas: This appears to be ineffective for a couple of reasons.  First of all, since the intended effect of bananas is to restore potassium, and since electrolyte imbalances do not appear to be the main cause of EAMC, consuming bananas would be predicted to be ineffective.  Furthermore, even if the restoration of potassium were important to EAMC, it takes 30-60 minutes for the potassium from bananas (depending upon how much is consumed) to get into the circulation.  This is a case of too little, too late.
  9. Stretching: This simple approach to muscle cramps addresses the most widely accepted mechanism for EAMC, muscle fatigue and misfiring. While stretching before exercise may or may not prevent EAMC, stretching immediately upon the onset of a muscle cramp can be very helpful.  I think of it as “re-calibrating” muscles.
  10. Contracting opposing muscles: Similar to the concept of stretching, this method is to take advantage of the reflexive relaxation of a muscle when the opposing one contracts (e.g. hamstrings relax when quadriceps are contracted).  Practically speaking, this technique appears to be reasonable and may be most useful when it is too painful to stretch a cramped muscle.
  11. Massage: at least for me, sometimes all I can do with a bad cramp is to rub it.  I have not found studies on this subject, but my impression is that massage would lead to some mild stretching (by compression) and relaxation of a cramped muscle, perhaps by activating the Golgi tendon organs.
  12. Exercise: plyometric and endurance. The concept here is to train neuromuscular units to operate more effectively with increasing levels of intensity. Explosive plyometric exercises are reasoned to be especially effective to make cramp-prone muscles more resistant to cramping.  But, to truly simulate race conditions (which, of course, is when an athlete would most want to avoid muscle cramps), intense endurance training is necessary.  As endurance fitness increases, muscles would be predicted to be less prone to cramp at a given level of intensity. Some experts state: “the better shape you are in, the less likely you are to cramp.” This statement, however, is not supported by the evidence, since athletes matched for fitness appeared to experience EAMC or not based upon their pacing and effort and not baseline fitness.  In other words, if an athlete trains and races within his or her abilities, he or she is less likely to experience muscle cramps.  But every race is a calculated gamble, in a sense.  If an athlete chooses to push his or her limits, then he or she needs to be prepared for muscle cramps.

Like many medical conditions, EAMC are possibly not a single medical condition (some researchers divide EAMC into “local” and “generalized,” for instance), but the endpoint of a variety of pathways.  In other words, different athletes may have different mechanisms leading to very similar-appearing EAMC.  [Incidentally, this is one big reason why the neighbor’s or friend’s anecdotal advice: “it worked for me” is often useless and sometimes harmful in dealing with medical conditions].

Recommendations (based on current research and informed expert opinion)  to prevent and treat EAMC

  • Train at race-intensity (or, conversely, race according to the level of ability that was attained in training).
  • Pace and use power carefully (learn, in training, how many “matches” are available to burn, then use them carefully).
  • Consider plyometric training of key muscle groups.
  • Pay attention to fluids and electrolytes.  I am not fully convinced that this is irrelevant to EAMC, but, even if it is, careful attention to hydration and electrolytes is critical to safe athletic performance.
  • Learn to recognize early warning signs of EAMC (for me it is a little tightness) and respond accordingly.
  • Learn how to train and race through cramps, and when to stop.
  • When cramps begin, STOP!! and stretch immediately. The seconds “wasted” for stretching will likely be more than gained back by the end of the race.
  • Along with stretching, consider corollary activities like flexing opposing muscles and massaging cramped muscles.
  • Consider drinking pickle juice once a cramp begins.  However, note that pickle juice has been shown to shorten the duration if cramps, but not prevent them.  Furthermore, the study involved consuming 1 mL per kg of body weight.  This means that a 70 kg person would have to consume  almost 2 1/2 ounces of pickle juice.  This must be tried in training first; some people’s stomachs cannot tolerate that much pickle juice.

Take it from me, EAMC are painful and frustrating. But, for many people, with careful attention to current medical research, EAMC can be managed.

References:

Bergeron MF. Muscle cramps during exercise – is it fatigue or electrolyte deficit? Curr Sports Med Rep. 2008;7(4):S50-55.

Braulick KW, Miller KC, Albrecht JM, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med. 2013 Jul;47(11):710-714.

El-Tawil S, Al Musa T, Valli H, et al. Quinine for muscle cramps. Cochrane Database Syst Rev. 2015 Apr 5;4:CD005044.

Kantarowski P, Hiller W, Garrett W. Cramping studies in 2600 endurance athletes. Med Sci Sports Exerc.1990;22:S104.

Maughan R, Exercise induced muscle cramp: a prospective biochemical study in marathon runners. J Sports Sci. 1986;4:31-34.

Miller KC and Burne JA. Golgi tendon organ reflex inhibition following manually applied acute static stretching. J Sports Sci. 2014;32(15):1491-1497.

Miller KC, Mack GW, Knight KL, et al. Reflex inhibition of electrically induced muscle cramps in hypohydrated humans. Med Sci Sports Exerc. 2010 May;42(5):953-961.

Miller KC, Stone MS, Huxel KC, et al. Exercise-associated muscle cramps: causes, treatment, and prevention. Sports Health. 2010 Jul;2(4):279-283.

O’Connell K, Posthumus M, Schwellnus MP, et al. Collagen genes and exercise-associated muscle cramping. Clin J Sport Med. 2013 Jan;23(1):64-69.

Schwellnus MP. Cause of exercise associated muscle cramps (EAMC) – altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med. 2009 Jun;43(6):401-408.

Schwellnus MP, Allie S, Derman W, et al. Increased running speed and pre-race muscle damage as risk factors for exercise-associated muscle cramps in a 56 km ultra-marathon: a prospective cohort study. Br J Sports Med. 2011 Nov;45(14):1132-1136.

Schwellnus MP, Drew N, Collins M. Increased running speed and previous cramps rather than dehydration or serum sodium changes predict exercise-associated muscle cramping: a prospective cohort study in 2010 Ironman triathletes. Br J Sports Med. 2011 Jun;45(8):650-656.

Schwellnus MP, Nicol J, Laubscher R, et al. Serum electrolyte concentrations and hydration status are not associated with exercise associated muscle cramping (EAMC) in distance runners. Br J Sports Med. 2004 Aug;38(4):488-492.

Shang G, Collins M, Schwellnus MP. Factors associated with a self-reported history of exercise-associated muscle cramps in Ironman triathletes: a case-control study.  Clin J Sport Med. 2011 May;21(3):204-210.

Sulzer NU, Schwellnus MP, Noakes TD. Serum electrolytes in Ironman triathletes with exercise-associated muscle cramping. Med Sci Sports Exerc. 2005 Jul;37(7):1081-1085.

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Meb Keflezighi Versus A Horse

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Anyone who follows distance running knows that American Meb Keflezighi, Olympic silver medalist and winner of the New York and Boston Marathons, is a phenomenal athlete.  But few people know he can outrun a horse.  Here’s how.

Unlike horses and most other animals, humans can sweat.  This is of critical importance to endurance running because sweating prevents overheating.  Most mammals are dependent upon panting to cool themselves.  But panting occurs by taking shallow breaths at about ten times the usual rate of breathing.  This is a problem for galloping mammals because they have 1:1 coupling of locomotion with respiration to satisfy their oxygen demands.  Therefore, galloping mammals cannot pant and quickly become overheated.  This is dramatic in the case of sprinting cheetahs, which are famously fast but must stop due to overheating after approximately 1 kilometer.  Horses, of course, gallop much faster than humans can sprint, but they also have to slow down to prevent overheating after about 10-15 minutes.

[Since this article was published, I have been informed my sources were incorrect and that horses do, indeed, sweat.  Thank you for the correction, Julie Moffitt. However, the overall fact remains that humans do cool much more efficiently than other mammals, including horses.]

The speed of a galloping horse is approximately 30 mph (48 km/h), whereas the speed of a trotting horse (the sustainable speed for a horse) is approximately 8-12 mph (13-19 km/h).  I have limited experience with horses, but my expectation is that in a Meb vs Horse race, the horse either would have to gallop then trot slowly or gallop slowly then trot normally, to prevent overheating. This would be especially true in warm weather conditions.

The speed Meb Keflezighi maintained over his 2 hour, 8 minute, 37 second victory in the Boston Marathon in 2014 was 12.2 mph (19.7 km/h).  So, on paper, Meb vs Horse is simple algebra.

Assuming that the horse is able to gallop at full speed for 15 minutes then maintain a trot of 17.5 km/hour and that Meb is able to maintain his speed throughout, he will catch the horse in 3.22 hours.  If Meb slows down 5% because of added distance and the horse is like Gandalf’s Shadowfax and does not slow down, he catches the horse in 5.82 hours.

But you don’t have to take my word for it.  The “Whole Earth Man vs. Horse Marathon” has been held in Wales every year since 1980.  Here is a quote from the website of this event:

The Man v Horse Marathon began in June 1980 following a chat over a pint (or three) in the back bar of Neuadd Arms Hotel. The then Landlord, Gordon Green overheard two men discussing the relative merits of men and horses running over mountainous terrain. The enterprising Gordon, never one to miss an opportunity to promote Llanwrtyd Wells and improve business at his hotel, decided to put it to the test. And so began Green Events and its first, longest standing and now internationally acclaimed event, The Man versus Horse Marathon.

Humans have won the race twice over that time (and a total of three humans were faster than their equine competitors).

In 2014, the winner, Leo the horse, won in 2:22:53 with an average pace of 14.84 km/h. Meb, sadly for the running universe, was not in this race.  Fortunately, we have access to the “Chrissie Wellington-conversion factor.”  Chrissie is a legendary multiple Ironman World Championship winner and for reasons that only she understands, participated in Man vs Horse in 2014.  Her fastest Ironman marathon (there are no stand-alone marathon results to compare) was 2:44:35 in the 2011 Challenge Roth in Germany.  This makes her speed about 15.4 km/h.  In the Man vs Horse Marathon in 2014, she ran 73.5% slower at 11.3 km/h.  If Meb’s fastest marathon performance (yes, it is a stand-alone and, therefore, different from an Ironman) were slowed by a similar 73.5%, his pace in Man vs Horse would be about 14.5 km/h.  Very close to Leo the horse.  Also, Man vs Horse is run over 23.6 miles (shorter than the standard 26.2 miles of a marathon) and over rough cross-country terrain.  This shorter, more challenging course would likely favor the panting horse over the sweating man.

There is another, smaller, event in Prescott, Arizona called “Man Against Horse.” Results are only available online for the past eight years.  In these results, humans were unable to win until finally beating the horses in 2014.  In that year, in fact, in the 25 mile event, there were three humans who were faster than the fastest horse.  In the 50 mile event, one human was faster than the fastest horse.

[Since this article was published, it was pointed out to me that the 100 mile Western States Endurance Run started out in 1974 as a horse event.  Humans then started to participate and, eventually, horses stopped participating.  Please see the comments attached to this article for more details. Thank you Cal Nef!]

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So, on a good day, Meb could probably beat a horse in a marathon.  If the weather is hot, his ability to withstand overheating would give him an additional advantage over his equine competitor.  If Meb could not overtake a horse by the end of a marathon, he almost certainly would over a greater distance.

Go Meb!

References:

Bramble DM and Lieberman DE. Endurance running and the evolution of Homo. Nature 2004 Nov;432:345-352.

Carrier DR. The energetic paradox of human running and hominid evolution. Curr Anthropol. 1984;25(4):483-495.

Heglund NC and Taylor CR. Speed, stride frequency and energy cost per stride: how do they change with body size and gait? J Exp Biol. 1988 Sep;138:301-318.

Lieberman DE, Bramble DM, Raichlen DA, et al. Brains, brawn, and the evolution of human endurance running capabilities. In: Grine , Fleagle , Richard , Leakey , editors. The First Humans—Origin and Early Evolution of the Genus Homo. Springer; 2006.

Minetti AE. Physiology: efficiency of equine express postal systems. Nature 2003 Dec;426:785-786.

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NSAIDs And Athletes: Part 4, Effects Of NSAIDs On Exercise-Induced Pain And Inflammation

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This is the fourth installment of the series NSAIDs and athletes.  This article will address the question of why athletes use NSAIDs so often and if the intended benefits are supported by clinical research.  The first article in this series dealt with the mechanism of action of NSAIDs and the prevalence of use of these medications.  The second article dealt with potential adverse effects of NSAIDs.  The third article dealt with demonstrated adverse effects of NSAIDs in athletes participating in endurance sports.

Given the important adverse effects of NSAIDs as discussed in the second and third articles in this series, it is reasonable to ask: “why would any athlete take NSAIDs?”  There appear to be a number of reasons, all of which are underpinned by the observation that most athletes are unaware of the full potential for harm from NSAIDs.  An example of this lack of awareness is given in a study of the 2010 Bonn Marathon, in which approximately one half of participants (who responded to a survey) took NSAIDs, and 93% stated that they were unaware of the negative consequences of the use of NSAIDs in connection with endurance sports.

One reason athletes may take NSAIDs before and during exercise is to reduce pain.  For example, an injured, but fit, athlete may want to use an NSAID as a crutch to allow him or her to train for or participate in an event without being limited by pain from a pre-existing injury.  Another example is using NSAIDs to prevent pain that is anticipated to arise naturally during the course of an event.  In this sense, NSAIDs can be considered to be ergogenic aids: preventing pain that would distract an athlete or otherwise degrade performance. Finally, NSAIDs may be used with the intention of preventing pain or soreness that may arise after exercise, such as delayed-onset muscle soreness (DOMS).

Since NSAIDs reduce the production of prostaglandins, and since prostaglandins help mediate inflammation, many athletes also use NSAIDs before, during, and after exercise to prevent inflammation.  The rationale may be that inflammation from exercise may cause injury and prevent or prolong the healing process.  Therefore, since NSAIDs are anti-inflammatory medications, the use of these medications would promote recovery.

Are these suppositions about pain and inflammation and the effects of NSAIDs substantiated? Let’s look at the clinical data.

In a study published in March, 2015, 20 male endurance runners, average age 18.8 years, were divided into two equal groups.  Both groups performed running trials of time until self-reported fatigue 48 hours before a muscle-damaging activity called isokinetic dynamometry.  48 hours after this muscle-damaging activity, participants again performed running trials of time until self-reported fatigue. One group received 1.2 grams of ibuprofen 1 hour before the second time trial, whereas the other group received placebo.  The researchers found that both groups had more muscle pain and decreased performance with the second time trial, but that there was no difference between the groups.  The authors conclude:

“Ibuprofen did not reduce the effect of muscle damage and pain on performance. Prophylactic use of nonsteroidal anti-inflammatory drugs did not have an ergogenic effect on running performance after exercise-induced muscle damage in male long-distance runners.”

Similar findings were reported in another study of runners.  32 subjects participated in a two-period crossover trial in which ibuprofen was compared to placebo for its effectiveness in reducing muscle soreness and laboratory measures of muscle damage after two trials of downhill running.  While the downhill runs led to muscle soreness, reduced muscle strength, and reduced isometric endurance time at 50% of maximum strength, there was no difference between the ibuprofen and placebo groups.  With regard to laboratory measures of muscle damage, serum creatine kinase and urea levels were higher in the ibuprofen group after both runs.  This indicates that ibuprofen does not improve performance or reduce soreness and may worsen muscle damage when taken before exercise.

There were somewhat different findings in another study of the effects of ibuprofen on muscles.  In this small study, 10 volunteers performed one-arm eccentric bouts of exercise on opposite arms separated by three weeks. The volunteers received 2400 mg of ibuprofen (a high dose) or placebo for 5 days before exercise and for 10 days after exercise.  The investigators found that isometric strength, soreness, tenderness, and arm angles were similar between the groups who received ibuprofen vs placebo.  Laboratory measurements were made, at 7 different points in time, of neutrophil counts, neutrophil O2* production, and creatine kinase.  The only significant difference in these measures between the ibuprofen and placebo groups was at 3 days post-exercise.  At this point, creatine kinase levels were lower in the ibuprofen group relative to placebo.  This indicates that ibuprofen taken before exercise, even in high doses, does not improve strength, reduce soreness, or significantly reduce muscle damage.

One of the most important studies on this subject was done with 54 ultramarathoners who participated in the Western States Endurance Run.  29 of the participants in this study took 600 mg of ibuprofen on the day before the race and 1200 mg of ibuprofen on race day.  These participants were compared to 25 ultramarathoners who did not consume ibuprofen or any other medications before the race.  The study found that finishing time and ratings of perceived exertion did not differ significantly between the ibuprofen and control groups.  Furthermore, muscle soreness in the week following the race (DOMS) did not differ significantly between the two groups.  The main difference between the two groups was in indicators of endotoxemia and inflammation, which was worse (not better!) in the ibuprofen takers.  For example, plasma levels of lipopolysaccharide, C-reactive protein, interleukin (IL)-6, IL-8, IL-10, IL-1ra, granulocyte colony-stimulating factor, monocyte chemotactic protein 1, and macrophage inflammatory protein 1 beta, but not tumor necrosis factor alpha, were elevated in the ibuprofen group relative to the control group.  Therefore, and very importantly, the authors concluded that:

“Ibuprofen use compared to nonuse by athletes competing in a 160-km race did not alter muscle damage or soreness, and was related to elevated indicators of endotoxemia and inflammation.”

These studies demonstrate that taking NSAIDs before exercise to reduce pain and inflammation and to enhance performance is ineffective.  Why does this approach fail?  A large part of the reason for the failure of this approach is the underlying mechanism of sports-related injuries. While NSAIDs have undeniable anti-inflammatory properties, histopathological studies have shown that the mechanism of many sports-related injuries is degenerative rather than inflammatory.  One way to visualize this concept of injury is to consider muscles as ropes: ropes become frayed, not swollen, from overuse.

I sincerely hope you have learned a lot from reading all four parts of this series about NSAIDs and athletes.  This is important information that can impact the health of the athletic community.  Please help me spread the word!

References:

Da Silva E, Pinto RS, Cadore EL, et al. Nonsteroidal anti-inflammatory drug use and endurance during running in male long-distance runners. J Athl Train. 2015 Mar;50(3):295-302.

Donnelly AE, Maughan RJ, Whiting PH. Effects of ibuprofen on exercise-induced muscle soreness and indices of muscle damage. Br J Sports Med. 1990 Sep;24(3):191-195.

Küster M, Renner B, Oppel P, et al. Consumption of analgesics before a marathon and the incidence of cardiovascular, gastrointestinal and renal problems: a cohort study. BMJ Open 2013;3:e002090.

Nieman DC, Henson DA, Dumke CL, et al. Ibuprofen use, endotoxemia, inflammation, and plasma cytokines during ultramarathon competition. Brain, Behavior, and Immunity 2006 Nov;20(6):578-584.

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Pizza FX, Cavender D, Stockard A, et al. Anti-inflammatory doses of ibuprofen: effect on neutrophils and exercise-induced muscle injury. Int J Sports Med. 1999 Feb;20(2):98-102.

Warden SJ. Prophylactic use of NSAIDs by athletes: a risk/benefit assessment. Phys Sportsmed. 2010 Apr;38(1):132-138.

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NSAIDs And Athletes: Part 3, Effects During Endurance Racing Events

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This is the third part in a series about NSAIDs and athletes. This article will explore the effects of NSAIDs on athletes during endurance events. The first part of this series examined the mechanism of action of NSAIDs and the prevalence of use of these medications by athletes. The second part explored the adverse effects of NSAIDs for anybody, but especially athletes.

As described in the first article in this series, an amazingly high proportion of athletes use NSAIDs before and during events. This is so commonplace that may be hard to imagine that these athletes could be doing harm to themselves. But they may be doing just that. A number of studies address this issue in great detail.

One such study, by Kuster et al, was conducted as a survey of approximately 4000 of the 7000 participants in the 2010 Bonn Marathon and Half-Marathon. Overall, the researchers found no difference in the rate of withdrawal from the race between the NSAID consumers and non-consumers. However, withdrawal because of gastrointestinal adverse events was significantly higher in the consumer group, while withdrawal because of muscle cramping was higher in the non-consumer group. More remarkably, in this study there was almost a 5x higher incidence of adverse events, overall, in the consumer group compared to the non-consumer group. This incidence also increased significantly with increasing dose of NSAIDs. Of the analgesic users, there were nine who reported hospital admittance: three (who had taken ibuprofen) were admitted for kidney failure, four (who had taken aspirin) for GI bleeds, and two (who had taken aspirin) for heart attacks. There were no non-users of NSAIDs who required hospital admittance. Note that the NSAIDs taken by 90% of participants in this study were either diclofenac or ibuprofen. Also the rate of adverse events in the NSAID-taking group was almost three times higher for the marathon participants than the half-marathon participants, so duration of exercise does appear to have an effect.

In 2005, there was a widely-publicized paper in the New England Journal Medicine that reported that 13% of finishers of the Boston Marathon in 2002 had hyponatremia (low blood sodium). Furthermore, 0.6% had critical levels of hyponatremia. Mechanistically, since NSAIDs reduce the removal of water by the kidneys, it is a realistic concern that the use of NSAIDs could independently raise the rate of hyponatremia (since sodium is diluted by retained water). However, in this study, while 50-60% of participants reported having taken NSAIDs in the week before the race (this was a survey study), there was no linkage between the use of NSAIDs and the incidence of hyponatremia.

In contrast, a study of participants in the 2004 Ironman triathlon in New Zealand did demonstrate such a linkage. Overall, 30% of athletes used NSAIDs and the rate of hyponatremia was 1.8%. Statistically, there was a highly significant association in this study between having taken NSAIDs and developing hyponatremia.

In yet another study of endurance athletes, having taken NSAIDs was found to be statistically associated the the development of hyponatremia. This study was of the Kepler Challenge 60 km mountain run in New Zealand in 2003. Of note is that 20% of participants in the study had used NSAIDs within 24 hours of the start of the event, whereas 15% had used selective COX-2 enzyme inhibitors, called COXIBs (although these are also NSAIDs) within 24 hours of the start of the race.

After the 2009 Western States Endurance Run, which is an ultra-marathon of 161 km, 5 out of 400 participants were hospitalized with rhabdomyolysis (severe muscle damage) and hyponatremia. The authors of the scientific report about these adverse events stated that “these individuals tended to be younger, faster, more likely to have had an injury that interfered with training, and more likely to have used NSAIDs during the race.”

Abdominal complaints are very common in distance runners (including me). In a study of participants in the 1996 Chicago Marathon, researchers assessed the effects of prolonged exercise and NSAID ingestion on gastric and intestinal permeability during the first five hours following completion of the race (side note: anyone who has completed this race will remember that most of that first hour post-race is spent limping through huge crowds of people to get out of the finish area, then additional limping through downtown Chicago to finally arrive at a parking deck or CTA station- not a good time to have intestinal cramping!). Remarkably, 75% of participants reported having taken aspirin or ibuprofen before or during the race (the highest percentage I have seen in researching this subject area). Those runners who took ibuprofen, but not those runners who took aspirin, had significant elevations in measures of small intestinal permeability. This study only had 34 participants. Of the 26 participants in the study who had taken NSAIDs, 13 reported GI complaints whereas 4 out of the 8 participants who had not taken NSAIDs also reported GI complaints (no difference between these two groups).

In another study of the effects of exercise and NSAIDs on the function of the gut, nine healthy, trained male cyclists were studied on four occasions. These occasions were as follows: after having received 400 mg of ibuprofen twice before cycling, cycling without having taken ibuprofen, 400 mg of ibuprofen twice taken at rest, rest without having taken ibuprofen. The researchers reported that both having taken ibuprofen and cycling independently led to evidence of injury to the small intestine. The greatest injury was associated with the first test, in which ibuprofen was taken before cycling.

As alluded to above, most of the studies used in this article were based on survey information and have inherent weaknesses.  The study of participants in the Chicago Marathon was unfortunately very small.  But the last study, of cyclists, was more scientifically rigorous.  Taken together, however, the scientific evidence appears to be strong that the use of NSAIDs before or during endurance events can lead to dangerous, potentially life-threatening, conditions including hyponatremia and intestinal injury.  This potential for harm appears to be true even at more routine doses, such as the 800 mg of ibuprofen that was used in the cycling study.

The final installment in this series about NSAIDs and athletes will explore why athletes rely on NSAIDs and if these intended beneficial effects are scientifically-supported.

Please stay tuned!  By subscribing to our mailing list, you can make sure you do not miss this, or any other, update.

References:
Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. N Engl J Med. 2005 Apr 14;352(15):1550-1556.

Bruso JR, Hoffman MD, Rogers IR, et al. Rhabdomyolysis and hyponatremia: a cluster of five cases at the 161-km 2009 Western States Endurance Run. Wilderness Environ Med. 2010 Dec;21(4):303-308.

Küster M, Renner B, Oppel P, et al. Consumption of analgesics before a marathon and the incidence of cardiovascular, gastrointestinal and renal problems: a cohort study. BMJ Open 2013;3:e002090.

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Page AJ, Reid SA, Speedy DB, et al. Exercise-associated hyponatremia, renal function, and nonsteroidal antiinflammatory drug use in an ultraendurance mountain run. Clin J Sport Med. 2007 Jan;17(1):43-48.

Smetanks RD, Lambert GP, Murray R. et al. Intestinal permeability in runners in the 1996 Chicago marathon. Int J Sport Nutr. 1999 Dec;9(4):426-433.

Van Wijck K, Lenaerts K, Van Bijnen AA, et al. Aggravation of exercise-induced intestinal injury by Ibuprofen in athletes. Med Sci Sports Exerc. 2012 Dec;44(12):2257-2262. Clin J Sport Med. 2007 Jan;17(1):43-8.

Wharam PC, Speedy DB, Noakes TD, et al. NSAID use increases the risk of developing hyponatremia during an Ironman triathlon. Med Sci Sports Exerc. 2006 Apr;38(4):618-622.

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NSAIDS And Athletes: Part 2, Harmful Effects

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This is part two of the series: NSAIDs And Athletes. The first part dealt with the biochemical mechanism of action of NSAIDs and the surprisingly high frequency of use of NSAIDs by athletes, even just before and during competitions. This part deals with the potential adverse effects of NSAIDs, with particular attention to athletes.

Most of the important effects of NSAIDs come from their ability to block the activity of the cyclooxygenase enzymes, called COX-1 and COX-2. These COX enzymes catalyze the rate-limiting step in the formation of prostaglandins. These prostaglandins, in turn, have undesirable effects, such as worsening of pain and inflammation. The goal, therefore, of NSAID use, is to reduce pain and inflammation. But prostaglandins also have desirable actions, such as protecting the lining of the stomach, protecting normal kidney function, and promoting normal aggregation of platelets to form clots.  So, NSAIDs, in blocking the production of prostaglandins, can have both beneficial and detrimental effects.

NSAIDs are not uniformly the same. Their differences lay in the relative degree of inhibition of the COX-1 vs COX-2 isoforms, which, in turn, determines the relative risk of side-effects. In this article, however, since all NSAIDs can have detrimental effects, NSAIDs will generally be grouped together as a whole. Your physician can help you make a more nuanced choice of a NSAID, if necessary for your care, with careful consideration of the balance between benefits and risks.

There are a number of side-effects of NSAIDs that are applicable to everyone regardless of level of athletic activity:

Gastrointestinal

All NSAIDs increase the risk of gastrointestinal injury, with up to 60% of users experiencing this effect. The level of severity can range from mild heartburn and an upset stomach to life-threatening events, such as bleeding in the upper-GI tract, perforation of the the upper-GI tract, and obstruction of the stomach. These side-effects are dose- and duration-related. In other words, higher doses (or the use of more than one NSAID) for longer durations increase the risk of GI side-effects.

Cardiovascular

NSAIDs increase the risk for cardiovascular side-effects, including myocardial infarction (heart attack) and cerebrovascular accident (stroke). While NSAIDs that selectively target COX-2, such as rofecoxib and celecoxib, have more often been associated with these risks, less-selective NSAIDs have also been shown to increase these risks, especially at higher doses and longer duration of use. In a recent nested case-control study of 8,852 nonfatal myocardial infarctions, patients taking NSAIDs had a 35% increased rate of myocardial infarctions. This finding was for all NSAIDs grouped together. When the individual NSAIDs were separated, naproxen was found to be the only NSAID that was not associated with increased risk of myocardial infarctions. Cardiovascular risk associated with NSAIDs has been shown to be higher in older individuals with preexisting cardiovascular disease. However, even in an apparently healthy population of people age 30-50, there has been shown to be an elevated (but still very small) risk of myocardial infarctions (63 deaths per million person-years) associated with taking NSAIDS. In another recent study, which involved the review of the records of more than 1 million healthy people, median age 39 years, there was a significant association between ischemic strokes and the use of diclofenac or high-dose ibuprofen. With regard to hemorrhagic strokes, this study showed that diclofenac or naproxen were associated with an increased rate of these events.

For athletes, there are additional specific dangers to using NSAIDs:

Renal (kidneys)

Prostaglandins are important to maintaining renal blood flow and glomerular filtration. While the effect of reducing the formation of prostaglandins on kidney function may not be very great in most non-exercise situations, this effect can become extremely important during strenuous exercise. This is because renal blood flow and glomerular filtration are reduced by 40-50% during strenuous exercise. This reduces the ability of the kidneys to remove free water. Taking NSAIDs, and, consequently, reducing the amount of prostaglandins, further reduces the ability of the kidneys to remove free water.  This leads to retention of water and dilution of the blood which, in turn, can lead to an elevated risk of developing potentially life-threatening hyponatremia (low blood sodium).

Hematologic (coagulation)

NSAIDs have variable effects on the function of platelets, which are essential to forming clots and controlling bleeding. Anti-platelet effects are especially potent for aspirin, which is similar to NSAIDs, but affects the COX enzymes in a different way. In athletes at risk for crashing, falling, and other other forceful impact, especially to the head, the use of aspirin and some other NSAIDs can lead to increased risk of dangerous bleeding.

Increased risk of injury

One of the intended effects of NSAIDs is to mask pain. But pain is an essential mechanism by which the body prevents injury. By reducing the ability of the body to signal, through pain, that an injury is imminent, the use of NSAIDs can lead an athlete to push too far and become injured.

Another effect of NSAIDs that can increase risk of injury has to do with musculoskeletal adaptation. As previously mentioned, NSAIDs, by blocking the COX enzymes, reduce the synthesis of prostaglandins. These prostaglandins are important in the synthesis of the extracellular matrix, containing collagen, which confers strength to musculoskeletal tissues. By reducing the formation of the extracellular matrix, there is increased risk for injury, such as stress fractures, and reduced tissue adaption to mechanical loading.

To elaborate, mechanical loading associated with exercise typically increases bone formation to increase skeletal strength. But a number of studies in animals and humans have shown that this load-induced formation of bone is reduced when NSAIDs are given before the challenge of a mechanical stimulus. Similarly, animal studies have shown that use of NSAIDs before exercise also reduces hypertrophy of muscle.

Reduced repair of musculoskeletal tissues after injury

Since prostaglandins are important in the formation of collagen, which is required in the repair of musculoskeletal injuries, NSAIDS, if taken before exercise or for extended durations of time, can lead to reduced repair of such injuries. Animal studies have shown that NSAID use delays healing after bone, ligament, tendon, and muscle injuries. Similar findings have been reported in human studies of the effect of NSAIDs on recovery from exercise-induced muscle damage. For example, NSAID use decreases the typical increase in prostaglandin formation after high-intensity eccentric exercise, which, in turn, decreases the exercise-induced increase in numbers of muscle satellite cells and increase in protein synthesis. These effects could potentially lead to reduced muscle hypertrophy after exercise and reduced muscle repair after injury.

Summary

By affecting the production of prostaglandins, NSAIDs have important beneficial and detrimental effects. The detrimental effects are not trivial and can undermine the intended effects of NSAIDs or even lead to death or permanent disability. As previously mentioned, NSAIDs are actually a spectrum of medications with variable effects on the COX-1 vs COX-2 isoforms and, therefore, different typical benefits and side-effects.  But all NSAIDs can cause harm.

This installment of this series has a largely theoretical tone. Stay tuned, because the next installment of this series will deal with the effects of NSAIDs as reported in real-life endurance race situations.

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References:

Brune K and Patrignani P. New insights into the use of currently available non-steroidal anti-inflammatory drugs. J Pain Res. 2015 Feb;8:105-118.

Fosbol EL, Olsen AM, Olesen JB, et al. Use of nonsteroidal anti-inflammatory drugs among healthy people and specific cerebrovascular safety. Int J Stroke. 2014 Oct;9(7):943-945.

Garcia Rodriguez LA, Tacconelli S, and Patrignani P. Role of dose potency in the prediction of risk of myocardial infarction associated with nonsteroidal anti-inflammatory drugs in the general population. J Am Coll Cardiol. 2008 Nov;52(20):1628-1636.

Lippi G, Franchini M, Guidi, GC, et al. Non-steroidal anti-inflammatory drugs in athletes. Br J Sports Med. 2006 Aug;40(8):661-662.

Warden SJ. Prophylactic use of NSAIDs by athletes: a risk/benefit assessment. Phys Sportsmed. 2010 Apr;38(1):132-138.

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Special Announcement: Article in May/June 2015 Issue of Endurance Racing Magazine

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I am delighted to announce that my article: “How Being Stubborn Nearly Cost Me My Life,” is in the current issue of Endurance Racing Magazine.  It also features a quote from my coach, Jennifer Harrison.

This is a nice magazine for the endurance racing community.  I hope you enjoy my contribution and the entire magazine.  Please consider subscribing and tell your friends!