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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

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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.”

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.

Photo Credit: Gerard Fritz via Compfight cc

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.

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.

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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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The Autism and Multisport Project (AMP)

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I recently published an essay about my son’s experiences with his first multisport race.  He is autistic and the experience, for him and my family, was transformative.  This essay has gotten a warm response.  Zachary’s experience with multisport is, of course, not unique.  In fact, I would argue that triathlon and related endurance sports, such as running, are uniquely well-suited to inclusion.

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Our own dignity and humanity are reflected in how we treat those who are disadvantaged.  I have personally witnessed beautiful acts of kindness and generosity at countless triathlons and marathons.  Sometimes, this brings me to weep even as I struggle with my own, rendered meaningless, discomfort, as I race.

I am interested in putting together a collection of essays about autism and triathlon and other endurance sports.  Perhaps this could be made into a book, with the proceeds going toward promoting inclusion.  For example, these proceeds could fund volunteers or adaptive bicycles.

Please share your thoughts and experiences.  If you can, please share in this blog, drbriansmart.com, so that it is easier to organize.  Also, if you have friends or family who may be interested in such a project, please spread the word.

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:

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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!]

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 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.

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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.

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 1, Mechanisms And Prevalence Of Use

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This article is the first part in a series about non-steroidal anti-inflammatory drugs (NSAIDs) and athletics.  I hope that this information is helpful to you.  As always, please consult with your physician before taking medications of any kind.

NSAIDs, such as ibuprofen and naproxen, are commonly used in athletics.  Many people take these medications while training and before, during, and after competitions. Unfortunately, many people believe that the over-the-counter status of many NSAIDs and their widespread use means that these medications are safe.  There is a growing body of evidence, however, that NSAIDs may not be appropriate or safe for many athletes in many situations. This article will review the mechanism of action of NSAIDs (how they work) and the prevalence of use of NSAIDs in amateur and elite athletes.  Subsequent articles will review such issues as the dangers of these medications to the health of athletes, effects on performance, effects on healing, effects on adaptation, and reasons why people may learn to depend on NSAIDs.

Ibuprofen and other NSAIDs have a number of important biological effects. The following is a very complex diagram showing the role of ibuprofen (and other NSAIDs) in several biochemical pathways. Copyright to PharmGKB, permission has been given by PharmGKB and Stanford University to use the Ibuprofen Pathway Pharmacodynamics. Click on the image to go to the most up-to-date interactive version of the pathway and a detailed legend.

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The upper right part of the diagram shows one of the mechanisms for relief of pain, by affecting the cannabinoid receptors.  The lower right part of the diagram shows how NSAIDs can affect the nitric oxide pathway.  The left part of the diagram, however, is the focus of our discussion. It shows how NSAIDs block the actions of cyclooxygenase (COX) enzymes (COX-1 and COX-2, which are called PTGS1 and PTGS2 in this diagram).  These COX enzymes mediate the conversion of arachidonic acid from cell membranes into biologically active substances called prostaglandins. These prostaglandins have a wide variety of effects, including the promotion of pain, fever, and inflammation (the effects that NSAIDs aim to prevent), and protection of the stomach lining, promotion of normal kidney function, and improved aggregation of platelets to form clots (the effects that are usually undesirable to block).  This is the main pathway by which NSAIDs cause beneficial and harmful effects.  These harmful effects and others, and their clinical relevance to athletes, will be discussed in depth in an upcoming article in this blog.

In spite of the risk of side effects, many NSAIDs are easily obtainable over-the-counter.  I reviewed published data from a range of sources and I was very surprised by the prevalence of use of these medications by athletes across sports, levels of ability, genders, and age groups.

For example, in the 2008 Ironman triathlon in Florianopolis, Brazil, approximately one quarter of athletes (n=327) participated in a survey about the use of NSAIDs.  59.9% reported using NSAIDs in the previous three months.  Of these athletes who had used NSAIDs, 25.5%, 17.9%, and 47.4% reported consuming NSAIDs the day before, immediately before, and during the race.  In other words, about a quarter of these Ironman participants used NSAIDS DURING THE RACE.  48.5% of NSAID users did so without a medical prescription.

In study of self-administered questionnaires given to 681 male high school football players, 75% had used NSAIDs in the past 3 months and 15% were daily users.

In FIFA international soccer, team physicians reported that 30.7% of female athletes were taking NSAIDs within 72 hours of matches.  In the male under-17 and under-20 groups, 17.3% and 21.4%, respectively, had taken NSAIDs within 72 hours of matches.

In another survey of the use of NSAIDs in international soccer, team physicians reported that more than half of adult male players used NSAIDs within 72 hours of matches.  Up to one third of the players  who took NSAIDs used them before every match, regardless of whether they took the field or not.

In a survey of data taken from doping control forms and drug exemption forms from the 2004 Athens Summer Olympic Games, 11.1% of athletes used NSAIDs.

With regard to elite track and field athletes, a review of doping control forms, which were submitted for 12 International Association of Athletics Federations World Championships and 1 out-of-competitions season, was performed.  The per-athlete use of NSAIDs was 0.27 (note that some athletes used more than one NSAID at a time, so the rate of use was not 27%). This use was higher in power and sprint disciplines than in middle- and long-distance runners.

In a study of amateur marathon runners, 3913 (of 7043 total) participants in the Bonn marathon in 2010 returned questionnaires about the use of analgesics immediately before the marathon.  49% of these participants reported using analgesics immediately before the race. The overwhelming majority of the analgesics used were NSAIDs.  Interestingly, 54% were taken without a prescription.  Also, significantly more women than men took analgesics (61% vs 42%). Of all respondents to the survey, 93% stated that they were not informed about the risks of using analgesics in connection with endurance sports.

The prevalence data between these studies is not easy to compare, since the studies drew data from different sources.  These sources, as described, above, included questionnaires of athletes, surveys of team physicians, and doping control submissions.  Furthermore, data was grouped in different ways.  For example, genders were not divided for the Ironman data and some other studies focused broadly on the 72 hours before competition. Nonetheless, it is clear that athletes, irrespective of sport, level of ability, gender, or age, use NSAIDs frequently. Furthermore, where data was available it appears that roughly half of athletes who use NSAIDs do so without the supervision of their physicians.

NSAIDs, as discussed, above, are potent medications with known beneficial and detrimental effects. These drugs are widely used by athletes.  The next article in this series will explore, in much more detail, the dangers of NSAIDs to athletes.

Stay tuned!  Be safe.

References:

Burian M and Geisslinger G. Cox-dependent mechanisms involved in the antinociceptive action of NSAIDs at central and peripheral sites. Pharmacol Ther. 2005 Aug;107(2):139-154.

Gorski T, Cadore EL, Pinto SS, et al. Use of NSAIDs in triathletes: prevalence, level of awareness and reasons for use. Br J Sports Med. 2011;45:85-90.

Kuster 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.

Mazaleuskaya LL, Theken KN, Gong L, et al. “PharmGKB summary: ibuprofen pathwaysPharmacogenetics and genomics (2014).

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Tscholl P, Alanso JM, Dolle G, et al. The use of drugs and nutritional supplements in top-level track and field athletes. Am J Sports Med. 2010 Jan;38(1):133-140.

Tscholl P, Feddermann N, Junge A, et al. The use and abuse of painkillers in international soccer: data from 6 FIFA tournaments for female and youth players. Am J Sports Med. 2009 Feb;37(2):260-265.

Tscholl PM, Vaso M, Weber A, et al. High prevalence of medication use in professional football tournaments including the World Cups between 2002 and 2014: a narrative review with a focus on NSAIDs. Br J Sports Med. 2015 May;49(9):580-582,

Tsitsimpikou C, Tsiokanos A, Tsarouhas K, et al. Medication use by athletes at the Athens 2004 Summer Olympic Games. Clin J Sport Med. 2009 Jan;19(1):33-38.

Warner DC, Schnepf G, Barrett MS, et al. Prevalence, attitudes, and behaviors related to the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in student athletes. J Adolesc Health. 2002 Mar;30(3):150-153.

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Sorry LeBron, Humans Are Born To Run Marathons.

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Watching a preternaturally talented athlete like LeBron James compete, it may be easy to think that human evolution was designed to create athletes with amazing skill, agility, and power.  But this is not so.  We humans exist today because our prehistoric ancestors evolved into creatures with unmatched ability to run great distances in hot weather.  That’s right.  We humans are supposed to be endurance athletes!

Our prehistoric ancestors had to eat to survive.  But they were not remotely as strong and fast as predators of that time, like lions, leopards, and saber tooth tigers.  Our prehistoric ancestors also lacked the sorts of weapons that would even the playing field with other carnivores.  They had no bows and arrows, no atlatl, and their spears were only made of wood (no bone or stone points). The advantage they had, however, was endurance running.  We humans are unique among almost all other mammals in our ability to run great distances, even in very hot weather. Our prehistoric ancestors developed this ability and would track and chase prey to the point of exhaustion of the prey. The exhausted prey would then be vulnerable to attacks from the poor-quality weapons the hunters possessed.

How were our ancient ancestors able to do this?  Aren’t antelopes much faster than humans?

While much of the prey our ancestors hunted were much faster for short periods of time, pre-humans, in the end, had an advantage.  The most important advantage was their ability to resist overheating with extended exercise, even in very hot weather.

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This resistance to fatigue arises from a number of adaptations.  One of these adaptations is in muscle fibers.  Most mammals have more fast twitch than slow twitch muscles, whereas in humans the ratio is closer to 50:50.  With endurance training, however, humans can tip the balance to about 80% slow twitch.  This is one reason why most other mammals are so quick and explosively strong compared to humans (even LeBron James).

But strength comes with consequences.  Most mammals can only run at top speed (gallop) for 10-15 minutes before having to slow down or rest.  The most comfortable slower speed for most mammals is a trot and this speed is SLOWER than the speeds humans can maintain for extended periods of time.

Aside from having more slow-twitch musculature (and, therefore, better aerobic metabolism) there are a number of other adaptations that allow humans to be great endurance runners. One of the most important of these adaptations is the ability to sweat. Very few other animals can sweat (interestingly, kangaroos sweat).  Instead, they rely on panting to cool themselves. Panting occurs in the upper airway where gas exchange does not occur.  Panting also involves breathing approximately 10 times faster than normal.  Finally, in most animals the respiratory cycle is coupled 1:1 with movement of the limbs.  Therefore, when most mammals become overheated, they simply cannot gallop because they cannot both get the oxygen that they need (and remove carbon dioxide) and cool themselves at the same time.

Another interesting aspect of endurance that our ancient ancestors learned to exploit was the “sweet spot” of their prey’s gait.  For most mammals, there is a “U”- shaped curve of energy expenditure at both the gallop and trot speeds.  If these animals go much faster or slower than these two set speeds, they tire much faster.  In contrast, while walking, for humans, also has a “U”-shaped curve of energy expenditure, running does not. So, our ancient ancestors would chase their prey at speeds that would force them out of a comfortable trot.  This would create exhausted, vulnerable, prey much more efficiently.

This pattern of hunting went on for many thousands of years and it led to the evolution of pre-humans who were increasingly suited to endurance running.  As weapons, especially ranged weapons, became more effective and our ancient ancestors expanded out of regions that favored endurance hunting, this ability became less important.  Nonetheless, ability in endurance athletics is forever a part of all of our DNA.

We were born to run…marathons!

Reference:

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.

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Does Exercise Cause Allergy?

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Today’s article takes the concepts forward that were discussed in the first post on this blog (only 6 weeks ago: “Does Exercise Lead To Colds?”) with consideration of allergy as a cause of cold-like symptoms (upper respiratory tract symptoms, URS).  The idea for the previous article about exercise and colds (upper respiratory infections) had to do with the commonly-held impression, among athletes, coaches, and physicians, that athletes weaken their immune systems during peak training and races and, therefore, make themselves sick.  The evidence, however, does not support this idea.  Instead, it appears that URS may be a function of the release of inflammatory mediators and not, necessarily, infection.  Now, there is growing evidence that much of these URS associated with exercise may, actually, represent respiratory allergic disease.  Since respiratory allergic disease can be tested and treated, this concept has important implications for training and performance.

For researchers to begin to approach the question of the relationship between exercise and allergy, they first need a good tool to measure the incidence of allergy in athletes  Such a tool, the self-reported Allergy Questionnaire for Athletes (AQUA), was developed and validated, by Bonnini et al, in 2009.  The study group was professional soccer players (football for the rest of the world outside of the U.S.).  Skin testing for allergy (which is a gold standard) was positive for 46.8% of these athletes.  An AQUA score of 5 or higher gave a specificity for allergy of 97.1% (meaning that, for athletes with a score of 5 or higher, there is a 97.1% chance that they have allergy) and a sensitivity of 58.3% (meaning that this score only identifies 58.3% of athletes with allergy or, to put it another way, nearly 42% of athletes with allergy can be missed with a cutoff AQUA score of 5 or higher).  In other words, an AQUA score of 5 or higher almost always indicates allergy, but the rate of allergy can be under-reported.  The AQUA has been used for a number of studies since it was developed and validated.

Once such study was of 201 Brazilian elite marathon runners.  To be included in this study, athletes, between age 20 and 50, had to have completed, in the prior 18 months, a marathon in under 2:35 (men) or 3:00 (women) or a half-marathon in under 1:23 (men) or 1:35 (women). Since elite runners train outdoors for extended periods of time with a high ventilatory rate, this is an ideal group in which to consider the relationship between exercise and allergy.  This study found that 60% of these elite runners had allergy, as defined by an AQUA score of at least 5. There were no significant differences between the AQUA negative and the AQUA positive groups in gender, age, running experience, weekly training volume, and best performance time. This finding of 60% (which may be under-estimated, as explained, above) is higher than the estimated rate of allergy in the general population (which is roughly 10-30% of adults).

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In “average” marathoners, allergic respiratory disease is also important.  For example, 208 participants in the 2010 London Marathon were enrolled in a recently-published study.  The average age of participants was 40.3 years for males and 37.4 years for females.  On average, participants trained 7.6 hours per week for the race and the average finishing time was 5.1 hours.  It was found that 40% of runners in this study had allergy as defined by a positive AQUA questionnaire plus objective evidence of sensitization (allergy identified with a screen of blood samples for specific IgE, which is the “allergy antibody”).  This is higher than the rate of allergy for the general population.  The researchers also found that 47% of the runners experienced URS after the marathon, but only 19% of non-runners residing in the same households as study participants experienced URS.  Furthermore, a positive AQUA was a significant predictor of URS after the race.  Therefore, endurance running was associated with the development of URS and allergic respiratory disease was also associated with URS.

Aside from increased exposure to environmental allergens and increased rate of respiration with extended outdoor exercise, there is evidence that strenuous or excessive exercise can predispose individuals to a TH2 cytokine profile (this is found in people who have allergy).  In other words, strenuous or excessive exercise can “unbalance” athlete’s immune systems toward allergy.  Furthermore, one of the cytokines that has been shown to be increased after strenuous exercise (running, in fact) is IL-6.  Please recall the post “Does Exercise Lead To Colds,” in which it was discussed that IL-6 is elevated in athletes with URS.

Therefore, it appears that the rate of respiratory allergy is higher for both elite and non-elite runners.  Furthermore, there is a known mechanism that can explain this increased rate of allergy.  In the study of London Marathon participants, more than half of these athletes felt that they had allergic disease.  However, of this number, 77% were not using any form of medication, a quarter of whom did not do so for fear of affecting performance.  This fear is unfounded.  In fact, respiratory allergic disease can have negative effects upon exercise performance.   Therefore, for endurance athletes with upper respiratory symptoms associated with training and racing, it is worthwhile to be evaluated for allergy.  In the United States, Board-certified allergist/immunologists can be found at ACAAI and AAAAI.  But there are professional allergist’s societies around the world from whom an athlete can find help.

 Published February 17, 2015

 References:

Bonini M, Braido F, Baiardini I, et al. AQUA: Allergy Questionnaire for Athletes.  Development and validation. Med Sci Sports Exerc. 2009 May;41(5):1034-1041.

 Komarow HD and Postolache TT. Seasonal allergy and seasonal decrements in athletic performance. Clin Sports Med. 2005 Apr;24(2):e35-e50.

 Robson-Ansley P, Howatson G, Tallent J, et al. Prevalence of allergy and upper respiratory tract symptoms in runners of the London marathon. Med Sci Sports Exerc. 2012 Jun;44(6):999-1004.

 Smith LL. Overtraining, excessive exercise, and altered immunity: is this a T helper-1 versus T helper-2 lymphocyte response? Sports Med. 2003;33(5):347-364.

 Steensberg A, Toft AD, Bruunsgaard H, et al. Strenuous exercise decreases the percentage of type 1 T cells in the circulation. J Appl Physiol. 2001;91(4):1708-1712.

 Teixeira RN, Mendes FAR, Martins MA, et al. AQUA as predictor of allergy in elite marathon runners. World Allergy Organ J. 2014;7(1):7