Game 2 of the NBA finals is this weekend, and I’m sure the Miami Heat (despite their nickname) are hoping the air conditioning works. In truth, I think most of us are hoping that we witness a straight up basketball affair determined more by athletic skill and less by Exercise-Associated Muscle Cramping (EAMC).
If you need a primer to know what I’m talking about, here’s a brief rundown of Game 1 and LeBron’s EAMC.
‘Most of us’? I truly have no horse in this race (speaking of that….I most definitely am rooting for California Chrome to bring home the Triple Crown later today), but outside of Texas, it seems that most of the country may be leaning toward the Heat. At least that’s what ‘Big Data’ would suggest: check out this great, data-driven map from the New York Times showing the breakdown of team allegiances across the United States.
Truly though, aside perhaps from a pocket deep in the heart of Texas (who may want victory, no matter what!), I think most fans of the NBA would rather see the outcome of the games determined by the players and not by a lack of AC.
As a team physician, like many of you, I have had–along with my Athletic Trainers–to deal with plenty of muscle cramping in my career. Here in the States, I find it occurs most often in the very beginning of football season: during August pre-season, or the early September games that may be played in temperatures approaching 90 degrees. It seems the combination of relative deconditioning, environmental conditions, and plain foolishness (my adolescent athletes frequently forget to stay hydrated, despite constant reminders to do the same) gives rise to any number of trips on to the field to assist a player downed with quad or abdominal cramps. At some levels of the game, to circumvent that inability to maintain adequate oral hydration during a game, teams will turn to pre-game intravenous hydration, as has been discussed in literature published in this journal and blog.
Then again, perhaps there are other issues altogether different than these potential risk factors that give risk to EAMC. Despite the high incidence, the etiology of EAMC continues to be debated.
Yes, I am a believer in the powers of pickle juice, but EAMC remains a puzzle to me and others. And so I turned to the CJSM website this morning for guidance and found a great 2013 study: Collagen genes and exercise-associated muscle cramping, from a group of South African authors. I especially appreciated this article for its contribution to my basic science knowledge: I learned so much about the biology behind EAMC. I encourage you all, clinicians and non-clinicians, to check it out.
The authors begin the paper with an excellent overview of various hypotheses of EAMC, ranging from electrolyte depletion to altered neuromuscular control. They then explored the literature that points to the possibility that EAMC may be associated with a genetic predisposition to musculoskeletal soft tissue injury. Specifically, their research hypothesis was that “variants within collagen genes that code for components of the musculoskeletal system would increase susceptibility to EAMC.” To test this, the authors conducted a ‘retrospective case-control genetic association study’.
Subjects were recruited at a South African triathlon and ultra-marathon. The authors were able to recruit 116 individuals reporting a history of EAMC within the past 12 months and 150 controls with no history of ever having EAMC. Essentially, the authors looked at two phenotypes in these endurance athletes–those with and without a history of EAMC–and set out to determine if the phenotypes were an expression of an underlying genotype.
They performed venipuncture on the individuals, and with the blood samples they looked for the presence of various collagen gene polymorphisms. Specifically, the presence of polymorphisms in COL5A1, COL3A1, COL6A1, and COL12A1 were determined. They also looked at other purported risk factors including intensity of exercise (measured by finishing time); a history of tendon or ligament injury; weight and height.
Performing individual analyses of these risk factors on the cases and controls, as well a logistic regression analysis, the authors determined that indeed there was one genetic polymorphism associated with significantly increased risk of EAMC: the COL5A1 rs12722 genotype was found to contribute to a risk of developing EAMC in this model. The only other positive contributor the authors discovered was overall triathlon finishing time; this finding did not hold among the ultramarathoners.
The authors note the significant limitations of small sample size and self-reported history for EAMC (and history of tendon/ligament injury). Concerning the sample size, perhaps the study was underpowered to determine differences in expression of the other purported genotypic risk factors. One limitation the authors did not note was that all the study participants were white. I found this interesting for a variety of reasons. First, it does not appear that race was a specified inclusion criteria; I certainly did not note it to be so in the Methods section. Second, as an American, it leaves me wondering: were the South African Ironman triathlon and the Two Oceans ultra-marathon (the events included in the study) events with only white participants? I doubt that, given my knowledge of the Comrades Marathon, the legendary South African ultramarathon which was just run a couple of weeks ago. The authors state that “Two hundred sixty-eight white participants were recruited at….registration….” Were the only volunteers white racers? Come to think of it, after reading the article, I’m not sure about the gender breakdown of the participants. A table included in the article shows no statistically significant difference in age, BMI, country of origin of the cases and controls….but I’m not sure about gender.
I’ll have to write the authors and ask them these questions. After all, in Evidence-based medicine, we’re always looking for the generalizability of study findings. I began this post writing about Lebron James. If I were his personal physician, say, I’m not sure how applicable this study’s findings are to him. Then again, I am a decided novice when it comes to genetic polymorphisms. A clinician–yes! A basic scientist–most assuredly not!
I want to end with a few ‘editorial comments’ (see below), that I hope you find interesting. As ever, if you have comments in response by all means write them here on the blog, or tweet me @cjsmonline.
1) As I have indicated, I will be writing the authors. I encourage you all to do the same when you come across a study of interest. There is always a ‘corresponding author’ listed for CJSM published studies. Reach out to those authors: the medical literature is supposed to be interactive!
2) If you’re wondering about my use of a pic of LeBron in a Cleveland uniform……In this blog, I am committed as an Associated Editor for CJSM to use high quality media to which I/the journal has some ‘right.’ The images I mostly use will come from either media I have created or contacts/colleagues have freely given me. Not infrequently, when I am looking for a photo of a celebrity, like LeBron James, I will have none on hand. I often go to Wikimedia, where I find pictures in the public domain. The pic of LeBron I’m using in this post was uploaded to Wikimedia by Dave Hogg, who took this photo during a 2007 Cavaliers – Pistons basketball game. It is in the ‘public domain’ under a creative commons license. Thanks Wikiemedia, and thanks Dave! (p.s. I could find no pictures of LeBron wearing a Miami uniform in Wikimedia).
3) Finally, when you read the article on the CJSM website, you will notice that one Figure and one Table can be found only by clicking on hypertext. Such “Supplemental Digital Content (SDC)” allows both for greater flexibility for both authors and publishers (important content is accessible, but does not take up valuable print space) and demonstrates the increasing reliance we all place on staying ‘connected.’ If you have heretofore relied on the print version of CJSM only, here is a plug to get the iPad app and ensure easy access to such SDC and more!
I emailed the authors and got a prompt response. They did include only white males in their analyses. The authors explained that, regarding gender, they have found i) in previous work males are more prone to EAMC; ii) that the vast majority in the sample recruited at the two races were males. And so only males were included in the study.
Regarding race, the corresponding author wrote “Population group is an important factor in any genetic association study. The distribution of genetic variants can significantly differ between population groups. The variants tested in our article do. The inclusion of only white athletes was therefore by design.” He went on to tell me that whites, like males, were by far the largest group recruited, and that the ironman races specifically during the study years were notable for having predominantly white athletes. And so only whites, just as only males, were included in the study analyses.
The author noted that, as with most research, including other groups in future research will be important.
I certainly agree. It would be interesting to identify potential genetic polymorphisms that may contribute to EAMC seen in Africans, and African-Americans, such as LeBron.
As I think this through, obviously the pathology is quite different in ER, with SCT contributing to sickling of erythrocytes and vaso occlusion.
Anyone out in the blog universe with more knowledge about these issues, please comment! The Miami Heat certainly would want to figure out a way to keep LeBron on the court!